Indian Journal Of Clinical Practice

IJCP

Medicolegal
1 Indian Journal of Clinical Practice, Vol. 35, No. 9, February 2025
Some Salient court obServationS
 Â The Counsel for Medical Council of India (MCI) 
stated that there is no prohibition in law to justify 
the attitude of doctors as complained. The affidavit 
filed on behalf of the MCI mentioned ‘Clause 10 – 
Obligations to the sick and Clause 13 – The patient 
must not be neglected’ of the Code of Medical Ethics 
Regulations and further stated: “… It should be the 
duty of a doctor in each and every casualty department 
of the hospital to attend such person first and thereafter 
take care of the formalities under the Criminal Procedure 
Code. The life of a person is far more important than the 
legal formalities.”
 Â The affidavit filed on behalf of the Union of 
India on 3rd August, 1989 also said: “There are no 
provisions in the Indian Penal Code, Criminal Procedure 
Code, Motor Vehicles Act, etc. which prevent Doctors 
from promptly attending seriously injured persons and 
accident case before the arrival of Police and their taking 
caSe Summary
Mr P, a human rights activist, filed a writ petition in 
the Supreme Court under Article 32 of the Constitution 
of India on the basis of a newspaper report titled ‘‘Law 
helps the injured to die”. According to the story, a 
bystander picked up an injured scooterist who had 
been hit by a speeding car. He took the injured to the 
hospital nearby, but the doctors refused to attend to 
the victim and instead asked him to take the injured 
person to another hospital located, 20 km away, that 
was authorised to handle medicolegal cases. 
The victim succumbed to his injuries before he 
could reach the hospital. Mr ‘P’ asked that every 
citizen brought to the hospital should be promptly 
administered treatment and the procedural criminal 
law should be allowed to operate after that. And, 
suitable compensation should be allowed in addition to 
any action taken for negligence in contravention of this 
directive.
Doctors are Required to Provide Emergency 
Medical Care without Waiting for the Police Report
Proceed
The Police  
have filed against this doctor  
who treated a patient of road  
traffic accident without waiting  
for the Police.
Lesson:  Doctors have the right to practice unencumbered in the best interest of patients even in medicolegal cases. In Pt. Parmanand Katara vs Union Of 
India & Ors on 28 August, 1989 AIR 2039, 1989 SCR (3) 997, the Supreme Court of India, in the context of medicolegal cases, has emphasised 
the need for rendering immediate medical aid to injured persons to preserve life and the obligations of the State as well as doctors in that 
regard. The Court observed: “Every doctor whether at a Government Hospital or otherwise has the professional obligation to extend his services 
with due expertise for protecting life. No law or State action can intervene to avoid/delay the discharge of the paramount obligation cast upon 
members of the medical profession.” Regulation 13 of the Code of Medical Ethics framed by the Medical Council of India also says that the 
patient must not be neglected. “A physician is free to choose whom he will serve. He should, however, respond to any request for his assistance 
in an emergency or whenever temperate public opinion expects the service…”
Yes,  
medical practitioners are  
required to provide  
emergency medical care  
without waiting for the  
Police report. 
I have  
the right to treat my  
patient without a police/ 
court order in any  
medicolegal case.
Medicolegal
2Indian Journal of Clinical Practice, Vol. 35, No. 9, February 2025
into cognisance of such cases, preparation of F.I.R. and 
other formalities by the Police.”
 Â “There can be no second opinion that preservation of 
human life is of paramount importance. This is so on 
account of the fact that once life is lost, the status quo 
ante cannot be restored, as resurrection is beyond the 
capacity of man.”
 Â “Every doctor whether at a Government hospital or 
otherwise has the professional obligation to extend his 
services with due expertise for protecting life. No law or 
State action can intervene to avoid/delay the discharge 
of the paramount obligation cast upon members of 
the medical profession. The obligation being total, 
absolute and paramount, laws of procedure whether in 
statutes or otherwise which would interfere with the 
discharge of this obligation cannot be sustained and 
must, therefore, give way.”
 Â “There is also no doubt that the effort to save the person 
should be the top priority not only of the medical 
professional but even of the Police or any other citizen 
who happens to be connected with the matter or who 
happens to notice such an incident or a situation.”
 Â The Court observed that there is an apprehension 
among doctors that they would be called as witness 
in medicolegal cases and also that they would be 
interrogated by the Police, which prevents them 
from helping such cases. It said, “…, the policy, the 
members of the legal profession, our law courts and 
everyone concerned will also keep in mind that a man 
in the medical profession should not be unnecessarily 
harassed for purposes of interrogation or for any 
other formality and should not be dragged during 
investigations at the Police station and it should be 
avoided as far as possible. We also hope and trust that 
our law courts will not summon a medical professional 
to give evidence unless the evidence is necessary and 
even if he is summoned, attempt should be made to see 
that the men in this profession are not made to wait and 
waste time unnecessarily…”
 Â “We have no hesitation in saying that it is expected of 
the members of the legal profession which is the other 
honourable profession to honour the persons in the medical 
profession and see that they are not called to give evidence 
so long as it is not necessary… where the facts are so clear 
it is expected that necessary harassment of the members 
of the medical profession either by way of requests for 
adjournments or by cross examination should be avoided 
so that the apprehension that the men in the medical 
profession have which prevents them from discharging 
their duty to a suffering person who needs their assistance 
utmost, is removed and a citizen needing the assistance of 
a man in the medical profession receives it.”
 Â “…if he finds that whatever assistance he could give 
is not sufficient really to save the life of the person but 
some better assistance is necessary-it is also the duty 
of the man in the medical profession so approached to 
render all the help which he could and also see that the 
person reaches the proper expert as early as possible.”
court order
The Court ordered that the guidelines indicated in the 
1985 decision of the Committee under the Chairmanship 
of the Director-General of Health Services should 
become operative.
1.  “Whenever any medicolegal case attends the hospital, 
the medical officer on duty should inform the Duty 
Constable, name, age, sex of the patient and place and 
time of occurrence of the incident, and should start 
the required treatment of the patient. It will be the 
duty of the Constable on duty to inform the concerned 
Police Station or higher police functionaries for 
further action. Full medical report should be prepared 
and given to the Police, as soon as examination and 
treatment of the patient is over. The treatment of the 
patient would not wait for the arrival of the Police or 
completing the legal formalities.
2.  Zonalisation as has been worked out for the hospitals 
to deal with medicolegal cases will only apply to those 
cases brought by the Police. The medicolegal cases 
coming to hospital of their own (even if the incident 
has occurred in the zone of other hospital) will not be 
denied the treatment by the hospital where the case 
reports, nor the case will be referred to other hospital 
because the incident has occurred in the area which 
belongs to the zone of any other hospital. The same 
police formalities as given in para 1 above will be 
followed in these cases.
All Government Hospitals, Medical Institutes should 
be asked to provide the immediate medical aid to all 
the cases irrespective of the fact whether they are 
medicolegal cases or otherwise. The practice of certain 
Government institutions to refuse even the primary 
medical aid to the patient and referring them to other 
hospitals simply because they are medicolegal cases is 
not desirable. However, after providing the primary 
medical aid to the patient, patient can be referred to 
the hospital if the expertise facilities required for the 
treatment are not available in that Institution.”
reference
1. Pt. Parmanand Katara vs Union of India & Ors on 28 
August, 1989; 1989 AIR 2039, 1989 SCR (3) 997.


English

Doctors are Required to Provide Emergency Medical Care without Waiting for the Police Report

Medication counseling is an integral part of clinical care. No prescription is complete unless accompanied by a comprehensiveexplanation of why, when, and how to take advised drugs. The 6E mnemonic provides a simple, yet sufficiency robustmethod of ensuring completeness of counseling. Expectations, effectiveness and efficiency, ease and endurance, economy,education, and engagement: these represent the six enduring pillars of medication counseling

Dr SANJAY KALRA

Dr SOURABH SHARMA

Dr NITIN KAPOOR

BRIEF COMMUNICATION
38 Indian Journal of Clinical Practice, Vol. 36, No. 4, September 2025
*Treasurer, International Society of Endocrinology (ISE); Vice President, South Asian 
Obesity Forum (SOF); Bharti Hospital, Karnal, Haryana, India
†Dept. of Nephrology, Vardhman Mahavir Medical College and Safdarjung Hospital, 
New Delhi, India
‡Dept. of Endocrinology, Diabetes and Metabolism, Christian Medical College, Vellore, 
Tamil Nadu, India; Noncommunicable Disease Unit, Baker Heart and Diabetes Institute, 
Melbourne, Victoria, Australia
Address for correspondence
Dr Sanjay Kalra
Treasurer, International Society of Endocrinology (ISE); Vice President, South Asian
Obesity Forum (SOF); Bharti Hospital, Karnal, Haryana, India
E-mail: brideknl@gmail.com
THE SOLUTION
We have previously suggested the BLACK mnemonic 
(Benefits, Limitations, Adverse effects, Cost, Knowledge) 
to create a clinical aid for counseling2. This can be used 
for all therapeutic interventions, irrespective of the 
clinical situation.
Here, we suggest a novel method, the 6E way, of 
systematic medication counseling. We have used it in 
our diabetes and obesity practice, with good results. 
The 6E way (Table 1) is a simple, step-wise method of 
guiding a clinical conversation regarding use of various 
drugs. It adds value, specifically in chronic diseases 
where patients need to practice active self-management.
THE UTILITY
The 6E checklist can be used by all health care professio-
nals, including physicians, pharmacist, nurse educators, 
and other paramedical staff. Though developed for use 
in diabetes and obesity, it is applicable to all other disease 
THE CHALLENGE
Medical prescription is incomplete unless accompanied 
by adequate medication counseling. Counseling serves 
as value-added therapy or VAT1, bringing strength and 
stability to management strategies.
Counseling is a Cinderella of sorts, being viewed as 
everyone’s responsibility. This leads to a paradoxical 
situation, where no health care professional views it 
as their sole obligation. Especially in situations where 
there are multiple health care providers, this may lead to 
inadequate education and explanation. 
In fact, conflicting advice may be received regarding 
importance, timing, or method of administration of 
various drugs. With the increasing exaptation of 
endocrine drugs, such as dapagliflozin, empagliflozin, 
semaglutide, and tirzepatide, for both glycemic and 
pan-metabolic effects, this scenario is becoming more 
and more common.
The 6E Way of Medication Counseling
SANJAY KALRA*, SOURABH SHARMA†, NITIN KAPOOR‡
ABSTRACT
Medication counseling is an integral part of clinical care. No prescription is complete unless accompanied by a comprehensive 
explanation of why, when, and how to take advised drugs. The 6E mnemonic provides a simple, yet sufficiency robust 
method of ensuring completeness of counseling. Expectations, effectiveness and efficiency, ease and endurance, economy, 
education, and engagement: these represent the six enduring pillars of medication counseling.
Keywords: Counseling, chronic disease, diabetes, motivational therapeutics, obesity, person-centered care
Table 1. The 6E Way of Medication Counseling
Expectation: outcomes expected by person living with disease, 
by health care team; level of concordance between them
Efficacy and Efficiency: anticipated efficacy and efficacy of 
proposed intervention
Ease and Endurance: possible side effects and adverse effects 
of proposed intervention; their mitigation
Economy: cost of therapy; cost containment 
Education: knowledge needed to administer therapy, mitigate 
side effects; sick day management
Engagement: continued engagement with health care team; 
mechanisms for trouble shooting, e.g., how to contact team in 
time of need 
BRIEF COMMUNICATION
39Indian Journal of Clinical Practice, Vol. 36, No. 4, September 2025
■ ■ ■ ■
states. Adding this as a checklist to printed prescriptions 
will help in ensuring adherence to counseling. This 
can also act as a foundation for good counseling 
practices (GCP), which must be made an integral part 
of good clinical practice3. GCP incorporates the ideas 
of “therapy by the ear”4, good clinical sense5, and 
motivational therapeutics6, in an easy-to-follow manner. 
The alliterative character of the list makes it easy to 
remember, and easy to practice as well. Counseling is 
not a one-off affair, and must be incorporated in every 
clinical encounter. Hence, this framework will have 
relevance for each and every prescription.
We take this opportunity to call for enhanced focus on 
medication counseling, especially in chronic disease 
management. The 6E rubric should help achieve this, 
and accomplish better health outcomes for all.
REFERENCES
1. Kalra S, Gupta Y, Baruah MP. Insulin and value-added 
therapy. J Soc Health Diabetes. 2014;2(02):059-61.
2. Kalra S, Aggarwal S, Kumar A. Counseling for growth 
hormone therapy. Turk Arch Pediatr. 2021;56(5):411-4.
3. Guerra-Farfan E, Garcia-Sanchez Y, Jornet-Gibert M, 
Nuñez JH, Balaguer-Castro M, Madden K. Clinical 
practice guidelines: The good, the bad, and the ugly. 
Injury. 2023;54 Suppl 3:S26-9.
4. Kalra S, Baruah MP, Das AK. Diabetes therapy by the 
ear: A bi-directional process. Indian J Endocrinol Metab. 
2015;19(Suppl 1):S4-5.
5. Kalra S, Gupta Y. Good clinical sense in diabetology. J Pak 
Med Assoc. 2015;65(8):904-6. 
6. Wu SS, Schoenfelder E, Hsiao RC. Cognitive behavioral 
therapy and motivational enhancement therapy. Child 
Adolesc Psychiatr Clin N Am. 2016;25(4):629-43.


The 6E Way of Medication Counseling

47Indian Journal of Clinical Practice, Vol. 36, No. 5, October 2025
MEDICAL VOICE FOR POLICY CHANGE
HCFI Dr KK Aggarwal Research Fund
≥100 mg/dL, glycated hemoglobin (HbA1c) ≥5.7%, 
blood pressure (BP) ≥130/85, plasma triglycerides 
≥150 mg/dL and plasma high-density lipoprotein 
(HDL) cholesterol ≤40 mg/dL.
 Â The MASLD continuum describes the progression 
of the disease, which begins from simple fatty liver 
with trivial or no inflammation and no hepato cyte 
ballooning (steatosis or “MAFL”), which progresses 
to significant inflammation and hepatocyte balloo-
ning (steatohepatitis or “MASH”) and finally, the 
increasing fibrosis leads to cirrhosis and HCC 
(cirrhosis).
 Â Physical inactivity and obesogenic diet increase 
adiposity and insulin resistance → increase in free 
fatty acids, glucose → type 2 diabetes → MASLD. 
Activation of Kupffer cells and stellate cells increases 
progression of fibrosis resulting in cirrhosis.
 Â The major risk factor for progression of fibrosis in 
MASLD is type 2 diabetes. Other factors include 
genetics, unhealthy diet and alcohol, gut dysbiosis 
and visceral obesity. 
 Â The major comorbidities are type 2 diabetes, dysli-
pidemia, obesity, and metabolic syndrome. Other 
associations include hypothyroidism, sleep apnea, 
hypopituitarism, hypogonadism, polycystic ovary 
syndrome (PCOS) and pancreatic resection.
 Â MASLD is a complex disease trait with genetic, 
environmental, and epigenetic modifiers. The 
environmental modifiers include sedentary lifestyle, 
snacking, fast food, saturated fats, trans fats, and 
processed red meat.
 Â Obesity and insulin resistance play a very impor-
tant part. An interplay of various factors such as 
hypertension, hyperuricemia, dyslipidemia, hyper-
glycemia, macrovascular disease, type 2 diabetes 
leads to MASLD.
 Â According to the multiple-hit hypothesis of MASLD, 
a single factor is not responsible; several interacting 
risk factors such as genetic predisposition, inflam-
matory cytokines, gut microbiota, dietary and 
environmental factors, oxidative stress, and insulin 
resistance are involved in the pathogenesis.
 Â Diagnostic evaluation includes assessment of fibro-
sis and hepatic inflammation, risk stratification, 
evaluation for comorbidities, screening for HCC 
and extrahepatic malignancies (thyroid, lung, colon, 
and pancreas).
Minutes of an International Weekly Meeting on 
“MASLD/MASH”
Speaker: Prof (Dr) Rajoo S Chhina, MBBS, MD, DM, 
MAMS, FAMS, Director & Head Gastroenterology, Fortis 
Hospital, Ludhiana
August 30, 2025 (Saturday, 9.30-10.30 AM)
 Â MASLD or metabolic dysfunction-associated steatotic 
liver disease is a new name for an old entity, but 
there are certain changes.
 Â It is defined as the presence of hepatic steatosis in 
conjunction with at least one cardiometabolic risk 
factor in the absence of harmful alcohol intake or 
other identifiable causes of steatotic liver disease.
 Â This definition marks a shift towards an inclusion-
based diagnosis, which focuses on metabolic 
dysfunction as the primary driver of the disease.
 Â The global prevalence is rising over the years. The 
prevalence in South East Asia is 33.07%. A very 
high prevalence is seen in Latin America (44%).
 Â MASLD is closely linked to diabetes. It is estimated 
that ~40% of individuals with diabetes have MASLD.
 Â It is the second leading cause of liver transplant in 
non-HCC (hepatocellular carcinoma) patients and 
most common in HCC patients.
 Â Individuals with obesity, diabetes, dyslipidemia, 
hyper tension, and of Hispanic heritage are at higher 
risk.
 Â Fatty liver was first described almost 200 years ago 
in 1836. In 2020, the name was changed to MAFLD 
(metabolic dysfunction-associated fatty liver disease). 
In 2023, the name MASLD was proposed. Non-
alcoholic steatohepatitis (NASH) was changed to 
MASH (metabolic dysfunction-associated steato-
hepatitis).
 Â Steatotic liver disease can be MASLD (which can 
progress to MASH), alcohol-associated liver disease, 
other causes such as drug-induced, celiac disease, 
and cryptogenic steatotic liver disease.
 Â If fatty liver is associated with low amount of alcohol 
intake (20 g/day for females and 30 g/day for males), 
it is metabolic and alcohol-associated liver disease 
(MetALD), but if high intake (50 g/day for females 
and 60 g/day for males) it is alcohol related MAFLD.
 Â The cardiometabolic criteria in adults, in addition 
to fatty liver, include fasting blood sugar (FBS) 
MEDICAL VOICE FOR POLICY CHANGE
48 Indian Journal of Clinical Practice, Vol. 36, No. 5, October 2025
 Â Assessment of fibrosis is important as it is the most 
accurate predictor of overall mortality, liver-related 
mortality and liver-related events in MASLD 
patients. Early diagnosis and management prevents 
progression to cirrhosis and its complications. 
 Â In an individual with suspected MASLD, the first 
step is risk identification (presence of metabolic 
syndrome or other high prevalence group such as 
type 2 diabetes, metabolic risk factors (body mass 
index [BMI] >25 or >23 in Asians, lipids, PCOS, 
obstructive sleep apnea) or first-degree relatives 
with MASLD, cirrhosis or HCC. 
 Â Ask about history of alcohol intake and any known 
pre-existing liver. 
 Â Investigations include liver biochemistry (alanine 
aminotransferase [ALT], aspartate aminotransferase 
[AST], etc.). Basing diagnosis only on abnormal 
liver enzymes is not enough.
 Â Tests to exclude other liver diseases – negative 
hepatitis B virus and hepatitis C virus serology, 
negative autoantibodies (ANA, AMA, SMA, ANCA), 
negative celiac serology, normal immunoglobulins, 
ferritin, copper, etc. 
 Â Liver ultrasound shows increased echogenicity 
(steatosis).
 Â Abnormal ALT may warrant workup for MASLD, 
but is not sensitive to confirm, rule out or characterize 
MASLD.
 Â Ultrasound can identify fatty liver (steatosis), but 
cannot distinguish between steatosis vs. MASH 
vs. fibrosis/early cirrhosis. The last stage, cirrhosis, 
can be picked up on USG, but not the intermediate 
stages of inflammation and fibrosis.
 Â Noninvasive blood-based scores include FIB-4 
index, aspartate transaminase-to-platelet ratio index 
(APRI), and NAFLD Fibrosis score (NFS).
 Â Commonest among these is the FIB-4 index; the 
cut-off is 1.30-2.67 with sensitivity ~84%. A score 
of <1.30 indicates low risk of fibrosis, while a score 
>2.67 indicates high risk of fibrosis. However, 
this may not be so clear in diabetes as in other 
individuals or in the elderly where a lower cut-off 
of 2.0 applies; its ability to detect fibrosis is limited 
in the intermediate range (1.30-2.67).
 Â NFS >0.676 indicates high risk of fibrosis. It 
incorporates age, BMI, impaired fasting glucose, 
AST/ALT ratio, platelet count, and albumin. 
 Â APRI calculated by the formula: AST/ULN AST) x 
(100/platelet count). Cut-off is 0.5-1.5 with sensitivity 
of 83%.
 Â Other noninvasive blood-based scores are Enhanced 
Liver Fibrosis (ELF) score and ADAPT score.
 Â Imaging techniques include elastography, vibration-
controlled transient elastography (VCTE) or Fibro-
Scan and two-dimensional shear wave elastography 
(2D-SWE) and point shear wave elastography 
(p-SWE). In FibroScan, if kPA is ≥8, it indicates 
advanced fibrosis risk.
 Â Magnetic resonance elastography (MRE) measures 
whole liver stiffness. It is more convenient and 
provides at least equal quality in fibrosis staging as 
USG-based elastography techniques. Cost, however, 
is a concern. Other magnetic resonance imaging 
(MRI)-based methods are MR-proton density fat 
fraction (PDFF) and corrected T1 (cT1).
 Â Combined scores using a combination of blood 
tests and imaging results can also be used for 
diagnosing fibrosis; these include MAST (MRE + 
MRI-PDFF + AST), FAST (VCTE + AST) and MEFIB 
(MRE + FIB-4).
 Â Liver biopsy is still the gold standard for definite 
diagnosis of steatohepatitis (MASH), but with 
limitations such as invasive, painful, expensive, 
associated morbidity/mortality, sampling variabi-
lity, observer variable, expertise to perform and 
impractical for population screening.
 Â In patients at risk or established fatty liver disease, 
do a primary risk assessment e.g., FIB-4. If score is 
<1.3, do not worry and re-assess the patient after 1 
to 2 years. If >1.3, then do a FibroScan; if >8, refer 
for gastrointestinal/hepatology care, if <8, then 
reassess periodically.
 Â Treatment of MASLD involves lifestyle interventions 
and pharmacotherapy. Lifestyle interventions are 
the cornerstone of treatment; the key components 
include weight loss, dietary changes, physical 
exercise, and quitting alcohol intake.
 Â In persons with MASLD and overweight/obesity, 
reduction of ≥5% of body weight reduces liver fat; 
reduction of 7%-10% improves liver inflammation 
and reduction of ≥10% improves fibrosis. In persons 
with MASLD and normal weight, reduction of 
3%-5% of body weight reduces liver fat.
 Â Sustained weight loss through lifestyle modification 
helps in NASH resolution, improvement of steatosis 
and inflammation, and fibrosis regression.
 Â Exercise has multisystemic effects on the muscles, 
adipose tissue, liver, and cardiovascular system. 
In the muscle, exercise increases muscle mass and 
glucose uptake; in the liver, it increases insulin 
sensitivity, glucose uptake and reduces oxidative 
MEDICAL VOICE FOR POLICY CHANGE
49Indian Journal of Clinical Practice, Vol. 36, No. 5, October 2025
stress; in the adipose tissue it increases insulin 
sensitivity, lipolysis and reduces visceral adiposity 
and in the cardiovascular system, it improves 
endothelial function, VO2 max and reduces heart 
rate.
 Â Ultra-processed foods are significantly associated 
with increased liver fat accumulation. The 
triglyceride glucose-waist to height ratio is a 
predictor of liver fibrosis.
 Â Pharmacotherapy in MASH targets steatosis, 
inflammation, insulin resistance, liver fibrosis.
 Â Drugs that reduce liver fat accumulation include 
glucagon-like peptide-1 receptor agonists (GLP-
1RAs) (semaglutide, tirzepatide), peroxisome 
proliferator-activated receptor (PPAR) agonists 
(pioglitazone, saroglitazar, lanifibranor), sodium-
glucose cotransporter-2 inhibitors (SGLT2i) (dapa-
gliflozin, empagliflozin), thyroid hormone receptor 
(THR)-β agonists (resmetirom), farnesoid X 
receptor (FXR) agonists (obeticholic acid, cilofexor) 
and omega-3 fatty acids.
 Â Drugs that improve insulin sensitivity include GLP-
1RAs (semaglutide, tirzepatide), PPAR agonists 
(pioglitazone, saroglitazar, lanifibranor), SGLT2i 
(dapagliflozin, empagliflozin), THR-β agonists 
(resmetirom), and fibroblast growth factor 21 
(FGF21) analogs (efruxifermin, pegozafermin).
 Â Drugs that reduce hepatic inflammation include 
vitamin E (antioxidant effect), GLP-1RAs (semaglu-
tide, tirzepatide), PPAR agonists (piogli tazone, 
saroglitazar, lanifibranor), FGF21 analogs (efruxi-
fermin, pegozafermin), and omega-3 fatty acids 
(anti-inflammatory properties).
 Â Drugs that have anti-fibrotic effects include PPAR 
agonists (pioglitazone, saroglitazar, lanifibranor), 
FGF21 analogs (efruxifermin, pegozafermin), THR-β 
agonists (resmetirom), FXR agonists (obeticholic 
acid), fatty acid synthase inhibitor (denifanstat) and 
GLP-1RAs (semaglutide).
 Â Resmetirom is a selective THR-β-agonist. It reduces 
fat in liver, fibrosis in the liver, intrahepatic 
inflammation and interferes with fibrogenesis in the 
liver. It was FDA approved for NASH treatment in 
March 2024.
 Â Resmetirom dose for patient <100 kg is 80 mg and 
in persons >100 kg, the dose is 100 mg. 
 Â PPAR agonists improve insulin sensitivity, glucose 
and lipid metabolism and reduces hepatic steatosis, 
inflammation, and fibrosis.
 Â Saroglitazar is a novel dual regulator of lipid and 
glucose homeostasis with >1,000-fold selectivity 
for PPAR-α over PPAR-γ. It significantly improved 
serum ALT, hepatic steatosis, insulin resistance and 
dyslipidemia in MASLD/MASH (EVIDENCE IV 
study).
 Â Saroglitazar treatment is effective and there is a 
significant difference in SGOT and SGPT, triglyce-
rides and liver stiffness measurement levels after 
treatment.
 Â Lanifibranor, a pan-PPAR agonist, which targets 
multiple pathways is undergoing phase III studies.
 Â GLP-1RAs (semaglutide, liraglutide, dulaglutide), 
dual (survodutide) and triple (retatrutide) agonists 
have mainly indirect benefit in MASLD (incretin 
effect). They lead to significant weight loss of 
5%-15%; ESSENCE phase 3 trial (semaglutide).
 Â SGLT-2i reduce hepatic steatosis and improve 
serum transaminases and noninvasive scores for 
fibrosis; dapagliflozin (DEAN trial).
 Â FGF21 analogs protect hepatocytes, reduce inflam-
mation and prevent progression of hepatic fibrosis; 
efruxifermin (HARMONY trial phase 2b) and 
pegozafermin (phase 2b). These are undergoing 
phase III trials.
 Â Fatty acid synthase inhibitors like denifanstat are 
currently in phase III trials.
 Â Some natural products like flavonoids, terpenoids, 
saponins, polyphenols, alkaloids, polysaccharides 
have also been used in MASLD because of their 
antioxidant, anti-inflammatory, and hepatoprotec-
tive properties.
 Â Applications of AI in MASLD: deep learning 
(EMRs, prediction models, NASHMap), digital 
pathology (WSI, SHG microscopy, qfibrosis, TPEF 
microscopy), ultrasound imaging (HRIA, TE, imple- 
 mented fat quantification), CT and MRI imaging 
(implement fat quantification), chatbots (patient 
education, histological diagnosis, clinician support), 
and drug development.
Participants – Member National Medical Associations: 
Dr Yeh Woei Chong, Singapore, Chair of Council 
CMAAO; Dr Akhtar Hussain, South Africa; Dr Prakash 
Budhathoki, Nepal
Invitees: Dr Monica Vasudev, USA; Dr Arpit Punetha; 
Dr Harbans Gulati; Dr Naorem Sharat Kumar; Dr Nishi 
Arora; Dr Poonam Chablani; Dr Ravindra Kuntal; Dr 
Shashi Khanna; Dr Ranjit Singh; Dr PC Pahwa; Dr Geeta 
Dutta; Dr Shagufta Yasmin; Dr Ashok Shukla; Dr S 
Sharma, Editor-IJCP Group
Moderator: Mr Saurabh Aggarwal


HCFI Dr KK Aggarwal Research Fund

Dr Veena Aggarwal

Indian Journal of Clinical Practice, Vol. 36, No. 6, November 2025 5
Medicine Update
FROM THE DESK OF GROUP EDITOR-IN-CHIEF
Dr Veena Aggarwal
Consultant, Womens’ Health
CMD and Group Editor-in-Chief, 
IJCP Group & Medtalks
Trustee, Dr KK’s Heart Care 
Foundation of India
POSTPARTUM BP: A PREDICTOR OF FUTURE 
HYPERTENSION AFTER HYPERTENSIVE DISORDER 
OF PREGNANCY
Women with a history of hypertensive disorder of 
pregnancy and raised systolic blood pressure (BP) 
15 to 90 days postpartum are at an 81% higher risk of 
incident hypertension in the first year after childbirth, 
according to a study published October 6, 2025 in the 
journal Hypertension1.
The retrospective cohort study examined the association 
between postpartum BP and new-onset hypertension 
in women after a hypertensive disorder of pregnancy. 
The study was conducted across two health systems in 
the southeastern United States from 2014 to 2017, and 
included women having a history of prior hypertensive 
disorder of pregnancy but no pre-existing hypertension. 
BP measurements were taken between 15 and 90 days 
postpartum.
Of the 5,657 women, only 2,520 (45%) underwent 
post partum BP measurement, while 39% of otherwise 
eligible participants did not have a BP check at 15 to 
90 days after childbirth. After a median follow-up 
of 9.9 months (median), the study found that higher 
post partum systolic BP was associated with a twofold 
increase in the risk of developing incident hypertension 
in the first year after childbirth with hazard ratio 
of 1.81. Women with BP of 140/90 mmHg had an 
estimated 12% cumulative incidence of hypertension at 
12 months, compared with 4.5% among those with BP 
of 110/65 mmHg.
The observations of this study emphasize the implication 
of early postpartum BP monitoring in women with 
hypertensive disorders of pregnancy, as nearly 40% of 
the at-risk participants did not have their BP measured 
within 15 to 90 days postpartum, according to the 
authors. Timely monitoring may prevent progression 
to chronic hypertension in this high-risk group.
Reference
1. Urrutia RP, Loop MS, Johnson JD, Wang TY, Price TM, 
Daubert MA. Blood pressure 15 to 90 days after a hyper-
tensive disorder of pregnancy and later hypertension. 
Hypertension. 2025 Oct 6.
MENTAL HEALTH OUTCOMES OF PRIMARY 
HEADACHES
Primary headaches are associated with at least a 50% 
increased risk for incident depression in both men and 
women, while tension-type headache was associated 
with a significantly higher risk of suicide, but only in 
men. These findings from a study were published in 
the Journal of Psychiatric Research1.
Data from the National Health Insurance Service-
National Health Screening Cohort database from 2002 to 
2019 in South Korea was utilized in this population-
based retrospective cohort study to determine the 
association of pre-existing primary headaches with 
higher risk of depression and suicide. Over 192,000 
individuals with primary headaches - tension-type 
headache or migraine - were followed from 2006 until 
the onset of depression, suicide, death, or the end of 
Indian Journal of Clinical Practice, Vol. 36, No. 6, November 20256
FROM THE DESK OF GROUP EDITOR-IN-CHIEF
the study period. The mean age was 52 years and 54% 
were men. They were age- and sex-matched to nearly 
460,000 individuals without primary headaches2.
A significant association was observed between primary 
headaches and greater risk of developing depression 
in both men and women with adjusted hazard ratios 
(aHR) of 1.55 for tension-type headache and 1.50 for 
migraine. The risk of suicide was significantly elevated 
in men (aHR 1.39) but not in women (aHR 1.11). 
Migraine was not significantly associated with the risk 
for suicide (aHR 1.16).
Headaches may occur secondary to various causes such 
as trauma, brain hemorrhage, or substance use; however, 
most headaches are primary headache disorders, 
mainly tension-type headache and migraine. This 
study highlights the adverse impact of pre-existing 
primary headaches on mental health, but it does not 
conclusively establish causality. It underscores the need 
for holistic management of headache that addresses not 
only the symptoms but also mental health in patients 
with headaches, both men and women.
References
1. Kim B, Park S, Lee SK, Shin HY, Kim KH, Park SJ, et al. 
Risk of depression and suicide in adults with pre-existing 
primary headaches. J Psychiatr Res. 2025;191:216-25. 
2. Chaphalkar A. Headache type tied to increased 
depression, suicide risk. Medscape. October 16, 2025.
■ ■ ■ ■


Medicine Update

Dr Surya Kant

Indian Journal of Clinical Practice, Vol. 36, No. 6, November 2025 7
Air Pollution: Leading Menace to Respiratory Health
EDITORIAL
Dr Surya Kant
Professor and Head 
Dept. of Respiratory Medicine,  
King George's Medical University, UP, 
Lucknow, India
President, Organization for Conservation 
of Environment and Nature (OCEAN) 
Member, National Core Committee, 
Doctors for Clean Air & Climate Action
Air pollution stands as one of the most pressing threats to human health today, particularly when it comes to our respiratory system. Every breath 
taken in cities like Delhi contains fine invisible particulate 
matter (PM2.5) that can damage our lungs over time1,2. 
According to the 2024 World Air Quality Report by 
IQAir (released March 2025), Delhi recorded the highest 
annual PM2.5 among capital cities at 91.6 µg/m³, far 
exceeding the World Health Organization’s (WHO) 
recommended safe limit of 5 µg/m³. This data is not 
just a statistic; it is a wake-up call for citizens as well 
as government. Globally, air pollution contributes to 
more than 8 million deaths annually, with respiratory 
diseases bearing much of the brunt. In India alone, 
it claims around 2 million death each year, fuelling a 
range of respiratory disorders, from everyday coughs 
to life-threatening conditions like chronic obstructive 
pulmonary disease (COPD)1,3-5. 
The roots of air pollution are all around us, stemming 
from both human activities and natural events ampli fied 
by our modern world. Fine particulate matter (PM2.5 and 
PM10) consists of particles small enough to penetrate 
deep into the lungs2,6. Then there are gases like nitrogen 
dioxide from traffic, sulfur dioxide from coal plants, 
ground-level ozone created by sunlight mixing with 
emissions, carbon monoxide from incomplete burning, 
and volatile organic compounds released during painting 
or cleaning2,3,7. Major outdoor sources include vehicular 
emissions, industrial processes, and crop-residue burning 
in northern India8. Indoor air pollution is also significant, 
particularly in rural households using biomass fuels 
(wood, dung, crop waste) for cooking8,9. The WHO has 
long warned that these everyday exposures add up, 
turning our shelters into unintended sources of harm. 
When these pollutants invade the lungs, the body 
mounts a defense, but it is often a losing battle. Inhaled 
particles trigger inflammation, much like a scrape on 
the skin swells to fight infection, except here it affects 
delicate airway linings8,9. This leads to oxidative stress, 
where free radicals overwhelm the natural antioxidants 
of the cells, causing widespread wear and tear. The 
immune system gets thrown off balance, producing 
too much mucus that clogs passages and impairs the 
tiny cilia, those hair-like sweepers in our airways, that 
normally clear out debris1,9. Over months or years, this 
cascade weakens lung defenses, making us prone to 
infections and chronic issues. Children breathe a higher 
volume of air per body weight and are therefore more 
vulnerable to long-term lung function. The elderly, 
whose repair mechanisms slow with age, and those 
already battling conditions like diabetes or heart disease 
find their risks compounded. Air pollution affects all 
parts of the body, and the effects even reach the fetus. 
Even short bursts of bad air, say during a smoggy winter 
day, can spike hospital visits for acute problems2,3,8.
Take allergies, for instance, a seemingly mild nuisance 
that pollution turns vicious. Pollen, dust mites or pet 
dander alone might cause a sniffle, but when coated in 
PM2.5 or nitrogen dioxide, they become supercharged 
allergens3,7. These altered particles burrow deeper, pro-
voking stronger immune overreactions that lead to hay 
fever symptoms: runny noses, itchy eyes, and relentless 
sneezing2,10. Air pollution in urban India, where traffic 
fumes mix with seasonal pollens, drives eczema flares and 
EDITORIAL
Indian Journal of Clinical Practice, Vol. 36, No. 6, November 20258
rhinitis cases to surge. Studies on allergy show how such 
exposures not only worsen symptoms, but also sensitize 
the body to new triggers, creating a vicious cycle for 
millions7,9,11,12.
Asthma offers another stark example. This chronic 
narrowing of the airways flares under the assault 
of pollution, with ozone and fine particles acting as 
direct irritants1,3,7. Wheezing, chest tightness, and 
breathlessness hit hard during attacks, often landing 
sufferers in emergency rooms. In Delhi, where nitrogen 
dioxide routinely surpasses WHO thresholds, winter 
smog correlates with a 20%-30% jump in asthma 
admissions. The indoor culprits compound this; second-
hand smoke or biomass cooking fumes in low-income 
homes provoke episodes that disrupt sleep and school8,13. 
Perhaps no condition illustrates the long-term toll of 
pollution like COPD14. Encompassing emphysema 
and chronic bronchitis, COPD scars the lungs with 
irreversible damage from repeated inflammation. PM2.5 
particles embed in alveoli, the tiny air sacs, fostering 
fibrosis that stiffens tissue and traps air. In India, 
where biomass burning is commonplace in villages and 
industrial haze blankets cities, COPD prevalence soars, 
often striking non-smokers in their prime working 
years. Symptoms creep in subtly; a nagging cough 
escalating to labored breathing on stairs, frequent 
infections, and exhaustion that side lines families7,14,15. 
The Global Burden of Disease Study, updated in 2024, 
links air pollution to a third of COPD cases in South 
Asia, with flare-ups driving up health care costs and 
mortality. A fresh analysis in Lung India from 2024 
ties higher COPD severity scores directly to years of 
biomass exposure, painting a grim picture for rural 
women who cook over open fires daily7,15,16. 
Lung cancer also emerges as a hidden threat in polluted 
air. The International Agency for Research on Cancer 
designates outdoor air pollution as a Group 1 carcinogen, 
equivalent to tobacco smoke. Polycyclic aromatic 
hydrocarbons, released from diesel engines and coal 
burning, damage DNA and trigger uncontrolled cell 
proliferation. Fine PM2.5 penetrates deep into the 
lungs, increasing adenocarcinoma incidence even in 
never-smokers. In India, air pollution contributes to 
roughly 10% of lung cancer cases, with the greatest 
impact on city residents and workers in high-exposure 
occupations such as driving1,3,7,17.
Beyond these, interstitial lung diseases scarring disor-
ders like idiopathic pulmonary fibrosis thrive in dusty, 
polluted environments. Coal miners or constru ction 
workers inhale silica-laden air, igniting fibrosis that 
thickens lung walls and starves the body of oxygen. 
Acute respiratory distress syndrome, a sudden lung 
failure, can erupt from toxic spikes, as seen in wildfire 
seasons or industrial accidents. These rarer but devasta-
ting outcomes remind us that the reach of pollution 
extends from bronchi to bloodstream3,7,9. 
The burden is not evenly spread; it carves deep lines 
of inequality. Poorer neighborhoods hug highways or 
factories, inhaling concentrated doses that wealthier 
suburbs escape3,7,12. Climate change pours fuel on the 
fire: warmer temperatures brew more ozone, droughts 
stir dust, and erratic monsoons trap pollutants low. 
Yet, glimmers of progress shine wealthier countries 
like those in Europe have slashed emissions through 
electric vehicles and scrubbers, dropping respiratory 
admissions by 20%-30% over decades1,3,4. 
India’s story is one of urgency laced with hope. Delhi’s 
perennial smog, born of parali burning in Punjab and 
Haryana plus vehicular sprawl, chokes visibility and 
spikes accidents18. The 2025 IQAir data shows not 
just Delhi, but Mumbai and Kolkata also in the global 
top 10, underscoring a national crisis. To tackle air 
pollution, governments must enforce tighter emission 
limits, shift to renewable energy sources, and expand 
urban tree planting, as trees naturally capture CO2 
and particulate matter18,19. Real-time air quality apps, 
like those used in Delhi, help people avoid outdoor 
activities during high-pollution periods. At home, 
simple measures include using kitchen exhaust fans, 
placing air purifiers in bedrooms, and selecting low-
emission paints. For vulnerable groups - children, the 
elderly, and those with asthma schools should seal 
windows on high-pollution days, and clinics must 
stock preventive medications3,8,10,19.
Additionally, initiatives like the National Clean Air 
Programme aim to cut PM levels by 40% by 2026, while 
the LiFE (Lifestyle for the Environment) movement 
launched by Prime Minister Narendra Modi in 2022 
nudges citizens toward eco-friendly habits: swapping 
bouquets for saplings at weddings, hopping buses 
over cars, and ditching smokes. Schemes such as the 
Ujjwala Yojana are helping families switch to cleaner 
cooking fuels, cutting down indoor smoke. Community 
drives, from NGO tree-planting to school anti-pollution 
pledges, build momentum1-4,19.
In the end, clean air is not a luxury; it is the very 
foundation of breath itself and a fundamental right of 
all human beings. Every child deserves skies free from 
poison, every elder the strength to walk without fear. 
By choosing renewal over ruin today, we gift tomorrow 
a world where lungs fill with hope, not harm.
EDITORIAL
Indian Journal of Clinical Practice, Vol. 36, No. 6, November 2025 9
■ ■ ■ ■
REFERENCES
1. Kant S. Air pollution: An invisible enemy of lung health. 
IP Indian J Immunol Respir Med. 2025;10(2):41-3.
2. India State-Level Disease Burden Initiative Air Pollution 
Collaborators: Pandey A, Brauer M, Cropper ML, 
Balakrishnan K, Mathur P, Dey S, et al. Health and 
economic impact of air pollution in the states of India: 
the Global Burden of Disease Study 2019. Lancet Planet 
Health. 2021;5(1):e25-38.
3. Kant S. Let us save our environment. IP Indian J Immunol 
Respir Med. 2022;7(2):47-9.
4. Kant S. Air pollution: An alarming threat to respiratory 
health. Indian J Allergy Asthma Immunol. 2025;39(1):1-3.
5. Lelieveld J, Haines A, Burnett R, Tonne C, Klingmüller K, 
Münzel T, et al. Air pollution deaths attributable to 
fossil fuels: observational and modelling study. BMJ. 
2023;383:e077784.
6. Di Bernardino A, Mevi G, Iannarelli AM, Falasca S, 
Cede A, Tiefengraber M, et al. Temporal variation of 
NO2 and O3 in Rome (Italy) from Pandora and in situ 
measurements. Atmosphere. 2023;14(3):594.
7. Qu S, Liang Y, Deng S, Li Y, Yang Y, Liu T, et al. Pharma-
cotherapeutic strategies for fine particulate matter-
induced lung and cardiovascular damage: marketed 
drugs, traditional Chinese medicine, and biological 
agents. Cardiovasc Toxicol. 2025;25(5);661-91.
8. India State-Level Disease Burden Initiative Air Pollution 
Collaborators: Balakrishnan K, Dey S, Gupta T, Dhaliwal 
RS, Brauer M, Cohen AJ, et al. The impact of air pollution 
on deaths, disease burden, and life expectancy across the 
states of India: the Global Burden of Disease Study 2017. 
Lancet Planet Health. 2019;3(1):e26-39.
9. Rajagopalan S, Vergara-Martel A, Zhong J, Khraishah H, 
Kosiborod M, Neeland IJ, et al. The urban environment 
and cardiometabolic health. Circulation. 2024;149(16): 
1298-314.
10. Solanki N. Air matters: the effect of ozone and traffic 
related air pollution on the airways. In: Lung Health and 
the Exposome: How Environmental Factors Influence 
Lung Health. Cham: Springer International Publishing; 
2022. pp. 1-21.
11. Herath Bandara SJ, Thilakarathne N. Economic and public 
health impacts of transportation-driven air pollution in 
South Asia. Sustainability. 2025;17(5):2306.
12. Rosario CS, Urrutia-Pereira M, Murrieta-Aguttes M, 
D’Amato G, Chong-Silva DC, Godoi RH, et al. Air pollution 
and rhinitis. Front Allergy. 2024 May 28; 5:1387525.
13. Bronte-Moreno O, González-Barcala FJ, Muñoz-Gall X, 
Pueyo-Bastida A, Ramos-González J, Urrutia-Landa I. 
Impact of air pollution on asthma: a scoping review. Open 
Respir Arch. 2023;5(2):100229.
14. Vu GV, Ha GH, Nguyen CT, Vu GT, Pham HQ, Latkin 
CA, et al. Interventions to improve the quality of life of 
patients with chronic obstructive pulmonary disease: 
a global mapping during 1990-2018. Int J Environ Res 
Public Health. 2020;17(9):3089.
15. Pandey AK, Verma AK, Singh A, Kant S, Chaudhary 
SC, Bajpai J, et al. The severity of non-smoking chronic 
obstructive pulmonary disease is correlated with biomass 
fuel exposure and COPD assessment test score. Lung 
India. 2024;41(4):251-8.
16. Wu Z, Zhang X, Zhang P, He Y, Ye Y, Pan Y, et al. The 
burden and risk factors of chronic obstructive pulmonary 
disease (COPD) in Asia and its countries from 1990 to 2021: 
a systematic analysis based on the 2021 Global Burden of 
Disease Study. Front Med (Lausanne). 2025;12:1641719. 
17. Sharma S, Kumar A, Gupta R. Air pollution and respira-
tory health: emerging evidence on bronchitis and 
pneumonia. J Environ Health Sci. 2023;15(4):112-20.
18. Kant S, Pandey AK, Singhal S, Tandon A. Air pollution: 
impact of sustained parali burning and myth of transient 
firecrackers. NMO J. 2024;18(2):65-6.
19. Squillacioti G, Bellisario V, Ghelli F, Marcon A, Marchetti P, 
Corsico AG, et al. Air pollution and oxidative stress in 
adults suffering from airway diseases. Insights from the 
Gene Environment Interactions in Respiratory Diseases 
(GEIRD) multi-case control study. Sci Total Environ. 
2024;909:168601.


Air Pollution: Leading Menace to Respiratory Health

54 Indian Journal of Clinical Practice, Vol. 36, No. 6, November 2025
Issu
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Sur
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Kan
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Issue Editors
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FounderDr KK Aggarwal
Group Editor-in-Chief
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October 2023, Pages 1–60
Volume 34, Number 5
Peer Reviewed Journal
Indexed with IndMED
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 Original Research 
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 Spiritual Update
 Inspirational Story
 Lighter Reading
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A Multispecialty Journal
Issue Editors
Dr Surya Kant & Dr Sanjay Kalra
Founder
Dr KK Aggarwal
Group Editor-in-Chief
Dr Veena Aggarwal
October 2023, Pages 1–60Volume 34, Number 5
Peer Reviewed Journal
Indexed with IndMED
Indexed with MedIND
Indian Citation Index (ICI)
ISSN 0971-0876
RNI 50798/1990
University Grants Commission 20737/15554
 Original Research 
 Retrospective Study
 Case Report
 Brief Communication
 Images in Clinical Practice 
 Medicolegal
 Medical Voice for Policy Change
 Conference Proceedings
 Around the Globe
 Spiritual Update
 Inspirational Story
 Lighter Reading
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Lighter Side of Medicine
HU
M
OR
A man goes to his doctor for a complete checkup. 
He hasn’t been feeling well and wants to find 
out if he is ill. 
After the checkup, the doctor comes out with the 
results of the examination and says, “I’m afraid 
I have some bad news. You’re dying and you 
don’t have much time.” 
The man says, “Oh no, that’s terrible. How long 
have I got?” 
The doctor looks down at the chart and says, 
“10…”
The man freaks out. “10? 10 what? Months? 
Weeks?” 
The doctor shakes his head and says, “10…9… 
8…7…”
One day, a woman walks into a doctor’s office. 
She has a cucumber in her nose, a carrot in her 
left ear, and a banana in her right ear. 
“Doctor, what’s wrong with me?” she says. 
He looks at her and says, “You’re not eating 
properly.”
One day, a man stumbled into his doctor’s office 
with a terrible cold. 
The doctor prescribed him some pills and sent 
him home. The man took the pills, but they 
didn’t help. When he went back, the doctor gave 
him a shot, but that didn’t help either. 
When the man returned the second time, the 
doctor told him, “Go home. Take a hot bath, and 
when you get out, open all the windows and 
stand in the draft.” 
The man frowned and said, “But if I do that, I’ll 
risk getting pneumonia!” 
The doctor nodded and said, “I know, but I can 
cure pneumonia.” 
The girl shrugged and said, “He made me wait 
45 minutes and then double-billed the insurance 
company.”
A woman calling Massachusetts General Hospital 
says, “Hello, I want to know if there’s any sign that a 
patient is improving at all.” 
The receptionist asks, “What is the patient’s name and 
room number?” 
The woman replied, “Sarah Finkel, Room 304.” 
The receptionist responds by saying, “Oh yes, Mrs. 
Finkel is doing very well. In fact, if her blood pressure 
continues to improve like it is, then Dr Cohen is 
looking to send her home on Tuesday!” 
The woman breathes a sigh of relief and says, “That’s 
fantastic!” 
The nurse says, “Are you a family member?” 
The woman replied, “No, I’m Sarah Finkel in 302. 
Dr Cohen doesn’t tell me anything.”
A man having trouble with his vision decides to visit 
his doctor. 
When he arrives at the office, the receptionist asks 
what’s wrong. “I keep seeing spots in front of my 
eyes,” 
The man complains. “Have you ever seen a doctor?” 
she asks. He frowns and says, “No, just spots.”
Dr. Good and Dr. Bad
©
 IJ
C
P 
G
R
O
U
P
LESSON: In patients with type 2 diabetes mellitus, 
progression of kidney disease as well as increased 
glycemic variability are known to contribute to the 
pathogenesis of coronary plaque formation via 
inflammatory pathways.
Cardiovasc Diabetol. 2017;16(1):131.
KIDNEY DISEASE IS COMMON
WITH ADVANCING AGE
SITUATION: A 70-year-old man with type 2 diabetes had 
increased glycemic variability. In addition, his kidney 
disease had worsened over a period of 2 years.
THESE FACTORS ARE LIKELY TO
INCREASE THE RISK FOR CORONARY
PLAQUE FORMATION


Lighter Side of Medicine

ConferenCe ProCeedings
1 Indian Journal of Clinical Practice, Vol. 35, No. 8, January 2025
Enhancing LongEvity in DiabEtEs – a 
thought from thE bEginning
Dr NK Singh, Dhanbad
Diabetes is a major cause of premature death and 
disability. One critical factor in the progression of 
type 2 diabetes complications is the interaction between 
oxidative stress and cellular dysfunction, particularly 
in the mitochondria. This leads to endothelial cell 
dysfunction. Additionally, chronic metabolic overload 
can damage the mitochondrial network, compromising 
mitochondrial DNA and function, which increases the 
risk of age-related diseases and premature functional 
decline. Fortunately, several strategies can help address 
and halt this progression:
 Â Lifestyle interventions: Lifestyle changes are among 
the most effective methods for managing diabetes. 
A balanced diet, regular exercise, and practices such 
as intermittent fasting can improve glucose control 
and reduce oxidative stress, thereby slowing the 
progression of diabetes and its complications.
 Â Respecting circadian rhythms: Following circadian 
rhythms, a principle rooted in ancient Indian 
wisdom, can significantly enhance metabolic 
health. Meal timing and dietary components 
(chrononutrition) play a crucial role in regulating 
circadian clocks, promoting longevity, and reducing 
the risk of type 2 diabetes.
 Â Pharmacological interventions: Certain medications 
can help maintain metabolic health and manage 
diabetes. Drugs like metformin, pioglitazone, 
glucagon-like peptide-1 receptor agonists, and 
sodium-glucose cotransporter 2 (SGLT2) inhibitors 
effectively control blood sugar, reduce oxidative 
stress, improve insulin sensitivity, and preserve 
endothelial function.
how to PrEvEnt Dfu with a rEguLar cLinicaL 
biochEmicaL Examination at aLL LEvELs of 
hEaLth carE
Dr Arun Bal, Mumbai
The mechanism behind diabetic foot ulcers (DFU) 
highlights that impulse loading, rather than just high 
DRS-WCPD: 11th World Congress on Prevention of 
Diabetes and Its Complications
pressure, plays a critical role. Impulse loading, defined 
as the product of pressure and ground contact time, is 
more relevant in causing injury. Patients with diabetes 
may need to adjust their exercise routines since pressure 
between 500 to 700 Kpa is the threshold for injury; 
faster gaits and longer strides increase pressure. Certain 
exercises are restricted for individuals with diabetic 
feet, including those with insensate or deformed feet, 
existing or previous ulcers, and activities like treadmill 
use, prolonged walking, jogging, and using stair 
masters. Unprotected walking can further damage 
the feet in diabetes, making it essential to go beyond 
wound healing and focus on biochemical correction to 
prevent a recurrence. To effectively reduce the risk of 
amputations, there is a need for comprehensive acute 
diabetic foot care units that address all aspects of foot 
care in diabetes.
rEvisiting gLobaL LanDmark triaLs for 
DiabEtEs PrEvEntion
Dr Amit Gupta, Noida
Global type 2 diabetes prevention trials have provided 
valuable insights into effective interventions. Dietary 
strategies across studies consistently aimed at energy 
restriction, fat reduction, and increased fiber intake, 
with significant weight loss observed in the Diabetes 
Prevention Program (DPP) and the Finnish Diabetes 
Prevention Study (DPS) studies. Physical activity 
was universally emphasized, with goals such as 
150 minutes per week in the DPP and daily walking 
in the Japanese impaired glucose tolerance (IGT) trial. 
Long-term follow-up was crucial for assessing the 
sustainability and impact of these interventions, which 
consistently showed that lifestyle changes outperformed 
other methods, including metformin alone, with the 
Japanese IGT trial achieving a 67% risk reduction. The 
reduction in diabetes incidence was independent of 
initial body weight, with those meeting multiple lifestyle 
targets benefiting the most, although weight reduction 
remained critical for overweight individuals. While 
lifestyle interventions delayed type 2 diabetes onset by 
at least 5 years, a residual risk persisted, particularly 
among those unable to fully adhere to lifestyle targets. 
Notably, individuals with a high genetic predisposition 
ConferenCe ProCeedings
2Indian Journal of Clinical Practice, Vol. 35, No. 8, January 2025
to diabetes have benefited significantly from these 
interventions. 
It can be concluded after revisiting the landmark 
trials; Pioneering studies like Da Qing, DPS, and DPP 
have demonstrated that lifestyle interventions can 
significantly reduce type 2 diabetes risk across diverse 
populations. These trials have a global impact, serving 
as the foundation for national and international type 2 
diabetes prevention programs. These studies have also 
shown the lasting impact of early lifestyle interventions 
in delaying or preventing type 2 diabetes onset. 
Real-world implementation continues to be an ongoing 
key challenge. Moving forward, building on the success 
of these trials, future efforts should focus on adapting 
proven strategies to diverse settings.
imPortancE of vitamin D in PrEDiabEtEs
Dr Anil Bhoraskar, Mumbai 
Vitamin D is vital in managing diabetes, prediabetes, 
and related health conditions. Its deficiency is linked 
to decreased insulin release and increased insulin 
resistance, key factors in developing type 2 diabetes. 
Studies have shown that maintaining sufficient 
vitamin D levels reduces the risk of progressing from 
prediabetes to diabetes, with supplementation showing 
a 10% to 13% reduction in this risk, regardless of initial 
levels. Moreover, vitamin D helps manage comorbidities 
like cardiovascular health, kidney function, obesity, and 
immune function.
Despite living in sun-rich areas, South Asians exhibit a 
high prevalence of vitamin D deficiency due to factors 
such as darker skin pigmentation, genetic variations 
affecting vitamin D metabolism, and limited sun 
exposure from indoor lifestyles and dietary choices. 
This deficiency often remains asymptomatic but 
increases the risk of type 2 diabetes, particularly in 
postmenopausal women, where it is associated with 
higher insulin resistance and poor glycemic control. 
Vitamin D supplementation can improve glycemic 
control, reduce HbA1c levels, and help manage FPG and 
PPG in diabetic patients. Long-term supplementation 
also enhances insulin sensitivity and lipid profiles, 
especially in those with deficiencies. Achieving adequate 
vitamin D levels is essential in preventing diabetes and 
improving overall metabolic health. However, excessive 
intake can cause hypervitaminosis D, which requires 
careful management, including halting vitamin D intake 
and adjusting calcium levels to prevent serious health 
consequences.
sitagLiPtin: thE LEgacy continuEs
Dr HN Chakravarti, Kolkata
It is well-established that a 1% reduction in glycated 
hemoglobin (HbA1c) can decrease the risk of diabetes-
related complications by 21%, lower the risk of 
myocardial infarction by 14%, and reduce diabetes-
related mortality by 21%. However, effective diabetes 
management extends beyond focusing on A1c levels 
or glucose control. It should encompass a broader 
approach, considering factors such as cardiovascular 
risk and mortality when choosing oral antidiabetic 
drugs. Current guidelines recommend metformin, either 
alone or in combination with SGLT2 inhibitors or DPP-
4 inhibitors, for treating diabetes. Notably, dipeptidyl 
peptidase-4 (DPP-4) inhibitors, such as gliptins, may 
be a better choice than SGLT2 inhibitors for several 
reasons, including:
 Â The use of SGLT2 inhibitors is associated with a 
higher risk of infections, osmotic diuresis, volume 
depletion, renal-related adverse effects, and 
increased blood ketone levels compared to placebo. 
 Â While SGLT2 inhibitors show consistent efficacy 
across different races, gliptins have demonstrated 
significant efficacy in Asian populations. 
 Â Additionally, some adverse effects of SGLT2 
inhibitors, like volume depletion and genital mycotic 
infections, are more common in warm and humid 
conditions.
Meanwhile, findings from landmark trials have shown 
that: Sitagliptin has well-established efficacy and safety 
through various landmark trials. Adding sitagliptin to 
treatment regimens is an effective and well-tolerated 
option for patients who cannot achieve glycemic 
control. Sitagliptin and its combinations are particularly 
valuable in the Indian setting for achieving glycemic 
control. Sitagliptin, in combination with dapagliflozin, 
has shown significant benefits in Indian patients with 
type 2 diabetes. It provides glycemic control along with 
pleiotropic benefits.
aPProach basED on “subtyPE of t2Dm”
Dr Piyush Desai, Surat
There is currently no international consensus on the 
subclassi fication of type 2 diabetes. As a result, clinical 
practice often distinguishes between obese and nonobese 
subtypes. However, the pathophysiological differences 
between these groups are still not fully understood.
ConferenCe ProCeedings
3 Indian Journal of Clinical Practice, Vol. 35, No. 8, January 2025
Cluster analysis offers an alternative approach, classifying 
adult-onset diabetes mellitus into five clusters: severe 
insulin-resistant diabetes (SIRD), mild obesity-related 
diabetes (MOD), mild age-related diabetes (MARD), 
severe insulin-deficient diabetes (SIDD), and severe 
autoimmune diabetes (SAID). 
In a study, 26.2% of Indians were diagnosed with SIDD, 
followed by 25.9% with MOD, 12.1% with SIRD, and 
35.8% with MARD. The phenotypic characteristics of 
these clusters varied significantly among the Indian 
population, though gender and diabetes duration did 
not affect the stability of the clusters.
key Points
 Â Compared to traditional classification, cluster-based 
subclassification better reflects the pathophysiology 
of type 2 diabetes and predicts future risk of 
complications and comorbidities.
 Â This approach may offer a more suitable tool for 
optimizing personalized therapeutic strategies.
 Â Over time, the leading causes of mortality in people 
with diabetes have shifted from vascular diseases 
to cancer and dementia, indicating the potential 
benefit of therapeutic strategies tailored to these 
emerging complications.
inDian DiabEtEs PrEvEntion Program
Dr Nanditha Arun, Chennai
Lifestyle modifications can often prevent type 2 diabetes, 
but such interventions are usually resource-intensive. In 
India, primary prevention trials have demonstrated that 
it is possible to prevent or delay the onset of diabetes. 
One promising approach to delivering educational 
and motivational support for lifestyle changes is 
mobile phone messaging, which offers a cost-effective 
alternative to traditional methods. 
Both lifestyle modification and metformin have been 
shown to be beneficial in diabetes prevention. A study 
in India that employed mobile technology for primary 
prevention produced significant results, highlighting 
the potential of this approach. The key takeaways 
from the Indian SMS prevention study include: (i) 
mobile technology’s capacity to influence behavior and 
reduce diabetes risk, (ii) the demonstration of a clinical 
outcome through information technology for the first 
time, and (iii) the observation that early improvements 
in a behavior predict better long-term outcomes.
Additionally, the study revealed ethnic differences in 
response to mobile technology between populations in 
India and the UK, emphasizing the need for tailored 
approaches in different cultural contexts. The findings 
confirm that mobile phone messaging is an effective and 
acceptable method for delivering advice and support to 
individuals at high risk of developing type 2 diabetes. 
This approach can successfully promote lifestyle modi-
fications necessary for diabetes prevention, especially in 
resource-limited settings where traditional interventions 
may not be feasible. 
In summary, using mobile technology in diabetes 
management offers a scalable and impactful strategy, 
particularly in regions like India, where it has shown 
promising results.
DiffErEnt tyPEs of miLks – unravELLing thE 
confusion
Dr Aditi Deshmane, Kolhapur
Milk has long been a dietary staple, but its various forms 
and impact on health, particularly for individuals with 
diabetes, have become confusing. Maintaining stable 
blood glucose levels is crucial for diabetes management, 
and milk’s carbohydrate content, primarily lactose, can 
complicate this effort. 
The rise in plant-based milk options, such as almond, 
soy, and oat, has added to the confusion. Each type 
varies in carbohydrates, fat, glycemic index, and overall 
effects on blood sugar levels. Cow’s milk, often high in 
lactose and fat, can raise concerns about blood sugar 
spikes, while alternatives like almond milk are low 
in calories and carbohydrates but may lack protein. 
Meanwhile, soy milk offers a good balance of protein 
and fat with fewer carbohydrates. Similarly, rice milk 
provides less protein but double the carbohydrate 
compared to cow’s milk. 
As a result, selecting the correct type of milk is a key 
dietary decision for managing blood glucose levels in 
diabetic patients. Some of the key considerations while 
choosing the milk are:
 Â Reduce saturated fat by selecting low-fat or skim 
milk, or try lactose-free and plant-based options.
 Â Keep milk intake moderate to manage calories and 
carbohydrates.
 Â Check blood sugar after drinking milk to gauge 
your tolerance.
 Â Consult a health care professional for personalized 
dietary advice.
 Â Always read labels to ensure milk alternatives fit 
your dietary preferences.
ConferenCe ProCeedings
4Indian Journal of Clinical Practice, Vol. 35, No. 8, January 2025
miLLEts – suPErfooD or hyPE
Dr Kavita Gupta, Nagpur
Millets, once considered “coarse grains”, have gained 
prominence as crucial parts of diabetes management due 
to their low glycemic index and high nutritional value. 
These ancient grains, such as finger millet (ragi), foxtail 
millet, and pearl millet (bajra), help control blood sugar 
levels and are a rich source of other micronutrients, 
such as iron, calcium, etc. Thus, they are a favorable 
food choice for those managing diabetes.
A meta-analysis of 99 studies has shown that long-term 
consumption of millets significantly reduces fasting 
blood glucose and postprandial blood glucose levels, 
contributing to better glycemic control. Additionally, 
millets have been found to lower HbA1c levels in 
prediabetic individuals, reducing the risk of developing 
type 2 diabetes.
The following study concluded that millet is beneficial in 
managing and reducing the risk of developing diabetes. 
Hence, the authors suggested that millet can be used to 
design appropriate meal plans for diabetic, prediabetic, 
and nondiabetic individuals as a preventive approach. 
Despite millet being a superfood, several points should 
be considered, such as:
 Â Moderation is the key to healthy eating.
 Â Millets do have an extraordinary nutritional value 
but try to include a variety of millets in the diet to 
ensure the adequacy of different nutrients.
 Â A balanced diet should provide not more than 45% 
calories from cereals and millet.
oiLs – which onE to choosE?
Dr Niti Desai, Mumbai
Diabetes is associated with a three- to fourfold increase 
in the risk of coronary heart disease. Additionally, 
nearly all individuals with diabetes exhibit one or 
more lipid abnormalities. Since fat intake provides the 
second-highest source of calories after carbohydrates, it 
is crucial to manage fat consumption in diabetes.
Some simple tips to help manage fat intake in diabetic 
patients:
 Â Limit visible fat (vegetable oil) to ½ kg per person 
per month.
 Â Consume 3-4 teaspoons of oil and 1-1½ teaspoons 
of ghee per day.
 Â Use two or more vegetable oils or blended oils.
 Â Nonvegetarians should consume oily fish (250 g/
week).
 Â Vegetarians should include algae oils, walnuts, 
flaxseed, or chia seeds in their diet.
 Â Avoid using vanaspati as a cooking medium and 
limit processed foods containing trans fats.
saLt anD sugar – gEtting thE facts right
Dr Naaznin Husein, Mumbai
Excessive sugar and salt consumption are key contri-
butors to global health challenges, including obesity, 
cardiovascular diseases, diabetes, and cognitive impair-
ments. Processed foods and sugary beverages have 
drastically increased dietary sugar intake since the mid-
20th century. 
However, the 21st Century witnessed a moderate 
decline in added sugar intake. These declines in sugar 
were accompanied by only a minimal 1% increase 
in dietary facts. Despite the decline in global sugar 
consumption, it is still high. Sugar-sweetened beverages 
(SSBs) are still the main source of daily added sugar in 
most Western countries. 
Studies have established a strong link between SSBs 
and adverse health outcomes, such as liver dysfunction, 
telomere shortening, and increased cardiometabolic 
risks. Reducing sugar intake, especially from SSBs, has 
been found to improve weight management and reduce 
the risk of metabolic disorders.
Similarly, excessive salt intake contributes to hyper-
tension, autoimmune disorders, and inflammatory 
diseases like rheumatoid arthritis and multiple sclerosis. 
Reducing salt intake to below 5 g/day, as recommended 
by the World Health Organization (WHO), could save 
millions of lives annually by mitigating the risks of 
cardiovascular diseases and cognitive decline. Always 
remember the SALT REBOOTING Mantra
 Â Control excess consumption
 Â Alter to healthy cooking methods
 Â Delete high-sodium foods.
■ ■ ■ ■


DRS-WCPD: 11th World Congress on Prevention of Diabetes and Its Complications

Vonoprazan helps in management and treatment of heartburn, peptic ulcers and gastroesophageal reflux disease. The structure,mechanism of action, and clinical applications have been discussed in this article. A brief review of literature is carried out

Dr Jyoti Yadav

Dr SHUBHRICA

1 Indian Journal of Clinical Practice, Vol. 35, No. 9, February 2025
NEW DRUG 
*Assistant Professor, Dept. of Ophthalmology, Maharaja Agrasen Medical College, 
Agroha, Haryana, India
†Senior Professor and Head, Dept. of Physiology, Pt BD Sharma PGIMS, Rohtak, 
Haryana, India
Address for correspondence
Dr Jyoti Yadav
Senior Professor and Head
Dept. of Physiology, Pt BD Sharma PGIMS, Rohtak, Haryana, India
E-mail: drjyotiyadav2008@yahoo.com
AbstrAct
Vonoprazan helps in management and treatment of heartburn, peptic ulcers and gastroesophageal reflux disease. The structure, 
mechanism of action, and clinical applications have been discussed in this article. A brief review of literature is carried out.
Keywords: Acid peptic disorders, gastroesophageal reflux disease, peptic ulcer
Vonoprazan – A Potassium-Competitive Acid 
Blocker: An Overview
SHUBHRICA*, JYOTI YADAV† 
esophagus, and esophageal adenocarcinoma. However, 
the frequency, severity, and complications of GERD 
depend on geographic and ethnic factors. Dietary factors 
are responsible to lower the frequency and severity of 
GERD and Barrett’s esophagus3.
POtAssIUM-cOMPEtItIVE AcID bLOcKErs
A novel treatment in acid-related diseases are potassium-
competitive acid blockers, which include fexuprazan, 
revaprazan, tegoprazan, and vonoprazan. Among these, 
vonoprazan has undergone extensive study and was 
initially approved in Japan in 2015 for various acid-
related diseases including gastric ulcer, duodenal ulcer, 
reflux esophagitis, and prevention of recurrence of 
ulcers as well as adjunct therapy for Helicobacter pylori 
eradication5. The US Food and Drug Administration 
(FDA) approved two vonoprazan-containing regimens 
for H. pylori treatment and also accepted a new drug 
application for vonoprazan for the treatment of erosive 
esophagitis5. Potassium-competitive acid blockers act at 
the final step in the acid secretory pathway by inhibiting 
the hydrogen potassium ATPase (H+/K+-ATPase) trans-
porter on the luminal membrane of gastric parietal 
cells, the same proton pump targeted by proton pump 
inhibitors (PPIs). After systemic absorption, potassium-
competitive acid blockers concentrate in parietal 
cell canaliculi and ionically bind to H+/K+-ATPase 
transporters to prevent acidifying proton secretion. 
Once bound, the potassium-competitive acid blockers 
block K+ ion access to the proton pump. Unlike PPIs, 
potassium-competitive acid blockers are acid stable and 
thus do not require enteric coating or optimal dosing 
administration 30 minutes prior to meals. Additionally, 
they are not prodrugs and act immediately at the 
Acid peptic disorders stem from unique yet inter-related pathogenic mechanisms, characterized by either heightened acid secretion or com-
promised mucosal defense. The diagnosis of gastro-
esophageal reflux disease (GERD), peptic ulcer disease 
and acid peptic disorders is further complicated by 
frequent overlap with conditions such as functional 
dyspepsia and irritable bowel syndrome posing 
challenges in clinical identification1. GERD is expected to 
remain a common cause for primary care consultations2.
The incidence of GERD is 15.6 (range 11.046-20.714). 
The risk factors are age, body mass index (BMI), 
nonvegetarian diet, tea and coffee, tobacco, and alcohol 
consumption3. Chavan and Bhaktavatsalam found the 
prevalence of acid peptic disease to be very high, i.e., 
38.1% in Indians4. Clinically, acid peptic disorders 
present as heartburn and regurgitation in GERD patients. 
They also experience extraesophageal symptoms with 
reflux cough syndrome, which is the most common 
symptom. Other symptoms include lower abdominal 
pain and constipation1.
The impact of acid peptic disorders affects quality of life 
and causes work absenteeism and if left untreated, it 
may lead to complications like peptic stricture, Barrett’s 
2Indian Journal of Clinical Practice, Vol. 35, No. 9, February 2025
NEW DRUG 
proton pump. These mechanistic differences facilitate 
more rapid attainment of peak plasma levels and onset 
of action5.
Patients in whom lifestyle modifications are ineffective in 
controlling GERD symptoms can benefit from pharma-
cologic therapy. Acid suppression forms the cornerstone 
of pharmacological management for GERD. Thera peutic 
agents include PPIs, histamine 2 receptor antagonists, 
and antacids. Additionally, medications affecting gastro-
intestinal motility such as prokinetics are also utilized in 
treatment of GERD6.
The alternative formulations of PPIs include immediate-
release omeprazole and modified-release dexlansoprazole 
in certain regions. Dexlansoprazole MR achieves a higher 
percentage of time with intragastric pH >4 compared to 
lansoprazole. However, these formulations offer only 
modest advantages in acid secretion control compared 
to conventional PPIs7.
There is growing interest in potassium-competitive acid 
blockers as promising alternatives, poised to overcome 
some limitations associated with PPIs5,7. When protons 
are transported by H+,K+-ATPase from cytoplasm to 
the canalicular space across the apical membrane of 
parietal cells, an equal amount of K+ ions are counter 
transported into cytoplasm of parietal cells, so that total 
process is electrically balanced. 
As a result, the activity of H+,K+-ATPase in the parietal 
cells is regulated by the availability of extracellular K+. 
Studies on molecular mechanisms of H+,K+-ATPase, 
therefore, led to discovery of potassium-competitive 
acid blockers, which is a new class of antisecretory 
agents and a novel treatment in acid-related diseases. 
This class of drugs exhibits their antisecretory effects 
by competitively blocking availability of K+ for H+,K+-
ATPase8.
VONOPrAZAN
Vonoprazan is a novel, orally active potassium-compe-
titive acid blocker that has demonstrated rapid, potent 
and long-lasting gastric acid suppression. It has been 
approved in Japan and 14 other countries in Asia and 
South America for a number of years for the treatment 
of a variety of acid-related diseases7.
Vonoprazan structure
Vonoprazan is a potassium-competitive acid blocker 
with the chemical structure C17H16FN3O2S. It is a pyrrole 
derivative that binds to the potassium ion binding site 
on the gastric proton pump, preventing the pump from 
activating and blocking gastric acid secretion.
Vonoprazan Uses
The principal use of vonoprazan is in management of 
GERD. It binds and inhibits H+,K+-ATPase at the final 
step in the acid secretory pathway in gastric parietal 
cells and it has different mechanisms of action than 
conventional PPIs. It can inhibit the proton pump even 
in neutral environments with an inhibitory constant (Ki) 
of 10 nM at pH 7 and 3 nM at pH 6.5. It has stronger 
potential to inhibit the gastric proton pump than other 
potassium-competitive acid blocker and lansoprazole7.
The treatment of acid peptic disease is based on 
providing symptomatic relief and enhancement of 
ulcer healing in affected area, i.e., esophagus, stomach 
and duodenum and to heal and maintain remission 
of erosive esophagitis. The aim of treatment is also to 
prevent complications and recurrence and to improve 
the quality of life6,9. The medical management of GERD 
comprises of lifestyle modifications and pharmacologic 
agents10. Lifestyle modifications to treat GERD should 
remain the first line of therapy and it includes weight 
loss, avoiding late night meals, elevating head of bed 
and steering clear of habits or foods that may worsen 
symptoms11.
PHArMAcODYNAMIcs AND PHArMAcOKINEtIc
The half-life of vonoprazan dissociation by potassium 
chloride is 12.5 hours in isolated proton pumps. 
Vonoprazan has high affinity and slow clearance from 
gastric parietal cells, accumulating in both resting and 
stimulated conditions. The acid dissociation constant 
of vonoprazan is 9.37, which is higher than that of 
conventional PPIs and other potassium-competitive 
acid blockers. When vonoprazan is exposed to acidic 
conditions, it is instantly protonated and remains stable. 
It can accumulate, function, and bind the proton pump 
N
N
N
S
H
O
O
F
Vonoprazan
3 Indian Journal of Clinical Practice, Vol. 35, No. 9, February 2025
NEW DRUG 
of gastric parietal cells in strongly acidic secretory 
canaliculi. The dissociation rate of vonoprazan from 
H+,K+-ATPase is slow and acid does not decompose it. 
Nonionic type of vonoprazan is decreased in a strong 
acidic secretory canaliculi and passive transport from 
the acidic secretory canaliculus to the cytoplasm is 
inhibited. It is therefore retained for a long time inside 
the parietal cells and can inhibit H+,K+-ATPase that is 
activated by further stimulation of acid secretion. The 
concentration of vonoprazan is up to 108-fold higher in 
secretory canaliculus of parietal cell than in plasma. It can 
stay in the protonated form and binds to H+,K+-ATPase 
subunit to compete with potassium binding and inhibits 
function of pump. The binding of vonoprazan to the 
proton pump is ionic, and its effects are reversible and 
dose-dependent. Vonoprazan can be taken regardless of 
meal ingestion and the rate of absorption is not affected 
by meals. It is rapidly absorbed and the time taken to 
reach maximum concentration in plasma is less than 
2 hours after oral administration. After absorption, 
the half-life in plasma is approximately 2 hours for 
conventional PPIs, but up to 9 hours for vonoprazan. 
Thus, vonoprazan stays in blood longer and can block 
acid secretion continuously7.
Vonoprazan demonstrated noninferiority and superio-
rity compared to PPI lansoprazole in both healing and 
maintenance of erosive esophagitis. This advantage 
was particularly notable in cases of more severe erosive 
esophagitis12. Vonoprazan has noninferior efficacy 
compared to lansoprazole in terms of erosive esophagitis 
healing rate13. Transitioning from a PPI to vonoprazan is 
significantly linked to symptom improvement in GERD 
patients resistant to PPI therapy. Hence, vonoprazan 
presents a promising treatment option for PPI-resistant 
GERD14. It significantly improved heartburn and 
patient satisfaction, among patients with PPI-resistant 
GERD15. Vonoprazan 20 mg shows a similar tolerability 
profile to lansoprazole 30 mg and is noninferior in 
terms of gastric ulcer healing. It also demonstrates 
similar efficacy for duodenal ulcer healing, despite 
not meeting the noninferiority criteria16. Vonoprazan 
10-20 mg demonstrated efficacy comparable to lanso-
prazole 15 mg in preventing peptic ulcer recurrence 
during low-dose aspirin therapy, exhibited a similar 
long-term safety profile and was well-tolerated17. 
A vonoprazan-based regimen is more effective than a 
PPI-based regimen as a first-line H. pylori eradication 
therapy18. Vonoprazan triple therapy and vonoprazan 
quadruple therapy regimens demonstrated increased 
H. pylori eradication rates compared to traditional 
quadruple therapy. Vonoprazan triple therapy exhibited 
fewer side effects, suggesting its potential applicability for 
H. pylori eradication in clinical practice19.
Vonoprazan Dosage and Administration
Vonoprazan film-coated tablets of 10 and 20 mg are 
available. They can be taken without regard to food or 
timing of food and should be swallowed and not chewed. 
The recommended dosage of vonoprazan is 20 mg once 
a day for 4 to 8 weeks in reflux esophagitis, 10 mg once a 
day for maintenance of healing esophagitis, 20 mg once 
a day for 8 weeks and 6 weeks for gastric and duodenal 
ulcers, respectively, 10 mg once a day for prevention of 
nonsteroidal anti-inflammatory drug (NSAID)-induced 
ulcer and 20 mg twice daily with triple drug regimen 
for 1 week for H. pylori eradication.
Vonoprazan contraindications
Vonoprazan is contraindicated in patients with known 
hypersensitivity to vonoprazan or any component 
of vonoprazan, rilpivirine containing products. As a 
precaution, vonoprazan should not be given during 
pregnancy and lactation. 
Vonoprazan side Effects
The side effects of vonoprazan include nausea, headache, 
dysgeusia, dyspepsia, gastritis, pain abdomen, abdominal 
distension, diarrhea, nasopharyngitis, vulvo vaginal 
candidiasis, urinary tract infection, and hypertension.
cONcLUsION
Vonoprazan plays a significant role in management 
of acid peptic diseases, especially in the treatment of 
GERD, peptic ulcer disease and H. pylori infection. It 
causes potent acid suppression, rapid symptom relief 
and has better outcome as compared to traditional PPI 
therapies. Further, it can be given empty stomach as 
well as after meals.
rEFErENcEs
1. Rai RR, Gangadhar A, Mayabhate MM. Clinical profiling of 
patients with acid peptic disorders (APD) in India: a cross 
sectional survey of clinicians. Int J Basic Clin Pharmacol. 
2017;6:194-202.
2. Zhang D, Liu S, Li Z Wang R. Global, regional and 
national burden of gastroesophageal reflux disease, 
1990-2019: update from the GBD 2019 study. Ann Med. 
2022;54(1):1372-84.
3. Rai S, Kulkarni A, Ghosal UC. Prevalence and risk 
factors for gastroesophageal reflux disease in the Indian 
population: a meta-analysis and meta-regression study. 
Indian J Gastroenterol. 2021;40(2):209-19.  
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4. Chavan MS, Bhaktavatsalam M. Prevalence and risk factors 
of acid peptic ulcer disease at a tertiary care hospital. Int J 
Adv Med. 2018;5(4):988-92.
5. Wong N, Reddy A, Patel A. Potassium-competitive 
acid blockers: present and potential utility in the 
armamentarium for acid peptic disorders. Gastroenterol 
Hepatol (N Y). 2022;18(12):693-700.
6. Rawla P, Sunkara T, Ofosu A, Gaduputi V. Potassium-
competitive acid blockers-are they the next generation of 
proton pump inhibitors? World J Gastrointest Pharmacol 
Ther. 2018;9(7):63-8.
7. Oshima T, Miwa H. Potent potassium-competitive acid 
blockers: a new era for the treatment of acid-related 
diseases. J Neurogastroenterol Motil. 2018;24(3):334-44.
8. Echizen H. The first-in-class potassium-competitive acid 
blocker, vonoprazan fumarate: pharmacokinetic and 
pharmacodynamic considerations. Clin Pharmacokinet. 
2016;55(4):409-18.
9. Mejia A, Kraft WK. Acid peptic diseases: pharmacological 
approach to treatment. Expert Rev Clin Pharmacol. 2009; 
2(3):295-314.
10. Kröner PT, Cortés P, Lukens FJ. The medical management 
of gastroesophageal reflux disease: a narrative review. J 
Prim Care Community Health. 2021;12:21501327211046736.
11. Katz PO, Dunbar KB, Schnoll-Sussman FH, Greer KB, 
Yadlapati R, Spechler SJ. ACG clinical guideline for the 
diagnosis and management of gastroesophageal reflux 
disease. Am J Gastroenterol. 2022;117(1):27-56.
12. Laine L, DeVault K, Katz P, Mitev S, Lowe J, Hunt B, et al. 
Vonoprazan versus lansoprazole for healing and main-
tenance of healing of erosive esophagitis: a randomized 
trial. Gastroenterology. 2023;164(1):61-71.
13. Xiao Y, Zhang S, Dai N, Fei G, Goh KL, Chun HJ, et al. 
Phase III, randomised, double-blind, multicentre study to 
evaluate the efficacy and safety of vonoprazan compared 
with lansoprazole in Asian patients with erosive 
oesophagitis. Gut. 2020;69(2):224-30.
14. Niikura R, Yamada A, Hirata Y, Hayakawa Y, Takahashi A, 
Shinozaki T, et al. Efficacy of vonoprazan for gastro-
esophageal reflux symptoms in patients with proton 
pump inhibitor-resistant non-erosive reflux disease. Intern 
Med. 2018;57(17):2443-50.
15. Gotoh Y, Ishibashi E, Honda S, Nakaya T, Noguchi C, 
Kagawa K, et al. Efficacy of vonoprazan for initial and 
maintenance therapy in reflux esophagitis, nonerosive 
esophagitis, and proton pump inhibitor-resistant gastro-
esophageal reflux disease. Medicine (Baltimore). 2020;99 
(11):e19520.
16. Miwa H, Uedo N, Watari J, Mori Y, Sakurai Y, Takanami Y, 
et al. Randomised clinical trial: efficacy and safety of 
vonoprazan vs. lansoprazole in patients with gastric or 
duodenal ulcers - results from two phase 3, non-inferiority 
randomised controlled trials. Aliment Pharmacol Ther. 
2017;45(2):240-52.
17. Kawai T, Oda K, Funao N, Nishimura A, Matsumoto Y, 
Mizokami Y, et al. Vonoprazan prevents low-dose aspirin-
associated ulcer recurrence: randomised phase 3 study. 
Gut. 2018;67(6):1033-41.
18. Maruyama M, Tanaka N, Kubota D, Miyajima M, 
Kimura T, Tokutake K, et al. Vonoprazan-based regimen is 
more useful than PPI-based one as a first-line Helicobacter 
pylori eradication: a randomized controlled trial. Can J 
Gastroenterol Hepatol. 2017;2017:4385161.
19. Huang J, Lin Y. Vonoprazan on the eradication of Helicobacter 
pylori infection. Turk J Gastroenterol. 2023;34(3):221-6.
■ ■ ■ ■


Vonoprazan – A Potassium-Competitive Acid Blocker: An Overview

20 Indian Journal of Clinical Practice, Vol. 35, No. 12, May 2025
NEW DRUG 
*Assistant Professor, Dept. of Ophthalmology, Maharaja Agrasen Medical College, 
Agroha, Haryana, India
†Senior Professor and Head, Dept. of Physiology, Pt BD Sharma PGIMS, Rohtak, 
Haryana, India
Address for correspondence
Dr Jyoti Yadav
Senior Professor and Head
Dept. of Physiology, Pt BD Sharma PGIMS, Rohtak, Haryana, India
E-mail: drjyotiyadav2008@yahoo.com
ABSTRACT
Vonoprazan helps in management and treatment of heartburn, peptic ulcers and gastroesophageal reflux disease. The structure, 
mechanism of action, and clinical applications have been discussed in this article. A brief review of literature is carried out.
Keywords: Acid peptic disorders, gastroesophageal reflux disease, peptic ulcer
Vonoprazan – A Potassium-Competitive Acid 
Blocker: An Overview
SHUBHRICA*, JYOTI YADAV† 
esophagus, and esophageal adenocarcinoma. However, 
the frequency, severity, and complications of GERD 
depend on geographic and ethnic factors. Dietary factors 
are responsible to lower the frequency and severity of 
GERD and Barrett’s esophagus3.
POTASSIUM-COMPETITIVE ACID BLOCKERS
A novel treatment in acid-related diseases are potassium-
competitive acid blockers, which include fexuprazan, 
revaprazan, tegoprazan, and vonoprazan. Among these, 
vonoprazan has undergone extensive study and was 
initially approved in Japan in 2015 for various acid-
related diseases including gastric ulcer, duodenal ulcer, 
reflux esophagitis, and prevention of recurrence of 
ulcers as well as adjunct therapy for Helicobacter pylori 
eradication5. The US Food and Drug Administration 
(FDA) approved two vonoprazan-containing regimens 
for H. pylori treatment and also accepted a new drug 
application for vonoprazan for the treatment of erosive 
esophagitis5. Potassium-competitive acid blockers act at 
the final step in the acid secretory pathway by inhibiting 
the hydrogen potassium ATPase (H+/K+-ATPase) trans-
porter on the luminal membrane of gastric parietal 
cells, the same proton pump targeted by proton pump 
inhibitors (PPIs). After systemic absorption, potassium-
competitive acid blockers concentrate in parietal 
cell canaliculi and ionically bind to H+/K+-ATPase 
transporters to prevent acidifying proton secretion. 
Once bound, the potassium-competitive acid blockers 
block K+ ion access to the proton pump. Unlike PPIs, 
potassium-competitive acid blockers are acid stable and 
thus do not require enteric coating or optimal dosing 
administration 30 minutes prior to meals. Additionally, 
they are not prodrugs and act immediately at the 
Acid peptic disorders stem from unique yet inter-related pathogenic mechanisms, characterized by either heightened acid secretion or com-
promised mucosal defense. The diagnosis of gastro-
esophageal reflux disease (GERD), peptic ulcer disease, 
and acid peptic disorders is further complicated by 
frequent overlap with conditions such as functional 
dyspepsia and irritable bowel syndrome posing 
challenges in clinical identification1. GERD is expected to 
remain a common cause for primary care consultations2.
The incidence of GERD is 15.6 (range 11.046-20.714). 
The risk factors are age, body mass index (BMI), 
nonvegetarian diet, tea and coffee, tobacco, and alcohol 
consumption3. Chavan and Bhaktavatsalam found the 
prevalence of acid peptic disease to be very high, i.e., 
38.1% in Indians4. Clinically, acid peptic disorders 
present as heartburn and regurgitation in GERD patients. 
They also experience extraesophageal symptoms with 
reflux cough syndrome, which is the most common 
symptom. Other symptoms include lower abdominal 
pain and constipation1.
The impact of acid peptic disorders affects quality of life 
and causes work absenteeism and if left untreated, it 
may lead to complications like peptic stricture, Barrett’s 
21Indian Journal of Clinical Practice, Vol. 35, No. 12, May 2025
NEW DRUG 
proton pump. These mechanistic differences facilitate 
more rapid attainment of peak plasma levels and onset 
of action5.
Patients in whom lifestyle modifications are ineffective in 
controlling GERD symptoms can benefit from pharma-
cologic therapy. Acid suppression forms the cornerstone 
of pharmacological management for GERD. Thera peutic 
agents include PPIs, histamine 2 receptor antagonists, 
and antacids. Additionally, medications affecting gastro-
intestinal motility such as prokinetics are also utilized in 
treatment of GERD6.
The alternative formulations of PPIs include immediate-
release omeprazole and modified-release dexlansoprazole 
in certain regions. Dexlansoprazole MR achieves a higher 
percentage of time with intragastric pH >4 compared to 
lansoprazole. However, these formulations offer only 
modest advantages in acid secretion control compared 
to conventional PPIs7.
There is growing interest in potassium-competitive acid 
blockers as promising alternatives, poised to overcome 
some limitations associated with PPIs5,7. When protons 
are transported by H+,K+-ATPase from cytoplasm to 
the canalicular space across the apical membrane of 
parietal cells, an equal amount of K+ ions are counter 
transported into cytoplasm of parietal cells, so that total 
process is electrically balanced. 
As a result, the activity of H+,K+-ATPase in the parietal 
cells is regulated by the availability of extracellular K+. 
Studies on molecular mechanisms of H+,K+-ATPase, 
therefore, led to discovery of potassium-competitive 
acid blockers, which is a new class of antisecretory 
agents and a novel treatment in acid-related diseases. 
This class of drugs exhibits their antisecretory effects 
by competitively blocking availability of K+ for H+,K+-
ATPase8.
VONOPRAZAN
Vonoprazan is a novel, orally active potassium-compe-
titive acid blocker that has demonstrated rapid, potent 
and long-lasting gastric acid suppression. It has been 
approved in Japan and 14 other countries in Asia and 
South America for a number of years for the treatment 
of a variety of acid-related diseases7.
Vonoprazan Structure
Vonoprazan is a potassium-competitive acid blocker 
with the chemical structure C17H16FN3O2S. It is a pyrrole 
derivative that binds to the potassium ion binding site 
on the gastric proton pump, preventing the pump from 
activating and blocking gastric acid secretion.
Vonoprazan Uses
The principal use of vonoprazan is in management of 
GERD. It binds and inhibits H+,K+-ATPase at the final 
step in the acid secretory pathway in gastric parietal 
cells and it has different mechanisms of action than 
conventional PPIs. It can inhibit the proton pump even 
in neutral environments with an inhibitory constant (Ki) 
of 10 nM at pH 7 and 3 nM at pH 6.5. It has stronger 
potential to inhibit the gastric proton pump than other 
potassium-competitive acid blocker and lansoprazole7.
The treatment of acid peptic disease is based on 
providing symptomatic relief and enhancement of 
ulcer healing in affected area, i.e., esophagus, stomach 
and duodenum and to heal and maintain remission 
of erosive esophagitis. The aim of treatment is also to 
prevent complications and recurrence and to improve 
the quality of life6,9. The medical management of GERD 
comprises of lifestyle modifications and pharmacologic 
agents10. Lifestyle modifications to treat GERD should 
remain the first line of therapy and it includes weight 
loss, avoiding late night meals, elevating head of bed 
and steering clear of habits or foods that may worsen 
symptoms11.
PHARMACODYNAMICS AND PHARMACOKINETIC
The half-life of vonoprazan dissociation by potassium 
chloride is 12.5 hours in isolated proton pumps. 
Vonoprazan has high affinity and slow clearance from 
gastric parietal cells, accumulating in both resting and 
stimulated conditions. The acid dissociation constant 
of vonoprazan is 9.37, which is higher than that of 
conventional PPIs and other potassium-competitive 
acid blockers. When vonoprazan is exposed to acidic 
conditions, it is instantly protonated and remains stable. 
It can accumulate, function, and bind the proton pump 
N
N
N
S
H
O
O
F
Vonoprazan
22 Indian Journal of Clinical Practice, Vol. 35, No. 12, May 2025
NEW DRUG 
of gastric parietal cells in strongly acidic secretory 
canaliculi. The dissociation rate of vonoprazan from 
H+,K+-ATPase is slow and acid does not decompose it. 
Nonionic type of vonoprazan is decreased in a strong 
acidic secretory canaliculi and passive transport from 
the acidic secretory canaliculus to the cytoplasm is 
inhibited. It is therefore retained for a long time inside 
the parietal cells and can inhibit H+,K+-ATPase that is 
activated by further stimulation of acid secretion. The 
concentration of vonoprazan is up to 108-fold higher in 
secretory canaliculus of parietal cell than in plasma. It can 
stay in the protonated form and binds to H+,K+-ATPase 
subunit to compete with potassium binding and inhibits 
function of pump. The binding of vonoprazan to the 
proton pump is ionic, and its effects are reversible and 
dose-dependent. Vonoprazan can be taken regardless of 
meal ingestion and the rate of absorption is not affected 
by meals. It is rapidly absorbed and the time taken to 
reach maximum concentration in plasma is less than 
2 hours after oral administration. After absorption, 
the half-life in plasma is approximately 2 hours for 
conventional PPIs, but up to 9 hours for vonoprazan. 
Thus, vonoprazan stays in blood longer and can block 
acid secretion continuously7.
Vonoprazan demonstrated noninferiority and superio-
rity compared to PPI lansoprazole in both healing and 
maintenance of erosive esophagitis. This advantage 
was particularly notable in cases of more severe erosive 
esophagitis12. Vonoprazan has noninferior efficacy 
compared to lansoprazole in terms of erosive esophagitis 
healing rate13. Transitioning from a PPI to vonoprazan is 
significantly linked to symptom improvement in GERD 
patients resistant to PPI therapy. Hence, vonoprazan 
presents a promising treatment option for PPI-resistant 
GERD14. It significantly improved heartburn and 
patient satisfaction, among patients with PPI-resistant 
GERD15. Vonoprazan 20 mg shows a similar tolerability 
profile to lansoprazole 30 mg and is noninferior in 
terms of gastric ulcer healing. It also demonstrates 
similar efficacy for duodenal ulcer healing, despite 
not meeting the noninferiority criteria16. Vonoprazan 
10-20 mg demonstrated efficacy comparable to lanso-
prazole 15 mg in preventing peptic ulcer recurrence 
during low-dose aspirin therapy, exhibited a similar 
long-term safety profile and was well-tolerated17. 
A vonoprazan-based regimen is more effective than a 
PPI-based regimen as a first-line H. pylori eradication 
therapy18. Vonoprazan triple therapy and vonoprazan 
quadruple therapy regimens demonstrated increased 
H. pylori eradication rates compared to traditional 
quadruple therapy. Vonoprazan triple therapy exhibited 
fewer side effects, suggesting its potential applicability for 
H. pylori eradication in clinical practice19.
Vonoprazan Dosage and Administration
Vonoprazan film-coated tablets of 10 and 20 mg are 
available. They can be taken without regard to food or 
timing of food and should be swallowed and not chewed. 
The recommended dosage of vonoprazan is 20 mg once 
a day for 4 to 8 weeks in reflux esophagitis, 10 mg once a 
day for maintenance of healing esophagitis, 20 mg once 
a day for 8 weeks and 6 weeks for gastric and duodenal 
ulcers, respectively, 10 mg once a day for prevention of 
nonsteroidal anti-inflammatory drug (NSAID)-induced 
ulcer and 20 mg twice daily with triple drug regimen 
for 1 week for H. pylori eradication.
Vonoprazan Contraindications
Vonoprazan is contraindicated in patients with known 
hypersensitivity to vonoprazan or any component 
of vonoprazan, rilpivirine containing products. As a 
precaution, vonoprazan should not be given during 
pregnancy and lactation. 
Vonoprazan Side Effects
The side effects of vonoprazan include nausea, headache, 
dysgeusia, dyspepsia, gastritis, pain abdomen, abdominal 
distension, diarrhea, nasopharyngitis, vulvo vaginal 
candidiasis, urinary tract infection, and hypertension.
CONCLUSION
Vonoprazan plays a significant role in management 
of acid peptic diseases, especially in the treatment of 
GERD, peptic ulcer disease, and H. pylori infection. It 
causes potent acid suppression, rapid symptom relief 
and has better outcome as compared to traditional PPI 
therapies. Further, it can be given empty stomach as 
well as after meals.
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patients with acid peptic disorders (APD) in India: a cross 
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2017;6:194-202.
2. Zhang D, Liu S, Li Z Wang R. Global, regional and 
national burden of gastroesophageal reflux disease, 
1990-2019: update from the GBD 2019 study. Ann Med. 
2022;54(1):1372-84.
3. Rai S, Kulkarni A, Ghosal UC. Prevalence and risk 
factors for gastroesophageal reflux disease in the Indian 
population: a meta-analysis and meta-regression study. 
Indian J Gastroenterol. 2021;40(2):209-19.  
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4. Chavan MS, Bhaktavatsalam M. Prevalence and risk factors 
of acid peptic ulcer disease at a tertiary care hospital. Int J 
Adv Med. 2018;5(4):988-92.
5. Wong N, Reddy A, Patel A. Potassium-competitive 
acid blockers: present and potential utility in the 
armamentarium for acid peptic disorders. Gastroenterol 
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6. Rawla P, Sunkara T, Ofosu A, Gaduputi V. Potassium-
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Ther. 2018;9(7):63-8.
7. Oshima T, Miwa H. Potent potassium-competitive acid 
blockers: a new era for the treatment of acid-related 
diseases. J Neurogastroenterol Motil. 2018;24(3):334-44.
8. Echizen H. The first-in-class potassium-competitive acid 
blocker, vonoprazan fumarate: pharmacokinetic and 
pharmacodynamic considerations. Clin Pharmacokinet. 
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9. Mejia A, Kraft WK. Acid peptic diseases: pharmacological 
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10. Kröner PT, Cortés P, Lukens FJ. The medical management 
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11. Katz PO, Dunbar KB, Schnoll-Sussman FH, Greer KB, 
Yadlapati R, Spechler SJ. ACG clinical guideline for the 
diagnosis and management of gastroesophageal reflux 
disease. Am J Gastroenterol. 2022;117(1):27-56.
12. Laine L, DeVault K, Katz P, Mitev S, Lowe J, Hunt B, et al. 
Vonoprazan versus lansoprazole for healing and main-
tenance of healing of erosive esophagitis: a randomized 
trial. Gastroenterology. 2023;164(1):61-71.
13. Xiao Y, Zhang S, Dai N, Fei G, Goh KL, Chun HJ, et al. 
Phase III, randomised, double-blind, multicentre study to 
evaluate the efficacy and safety of vonoprazan compared 
with lansoprazole in Asian patients with erosive 
oesophagitis. Gut. 2020;69(2):224-30.
14. Niikura R, Yamada A, Hirata Y, Hayakawa Y, Takahashi A, 
Shinozaki T, et al. Efficacy of vonoprazan for gastro-
esophageal reflux symptoms in patients with proton 
pump inhibitor-resistant non-erosive reflux disease. Intern 
Med. 2018;57(17):2443-50.
15. Gotoh Y, Ishibashi E, Honda S, Nakaya T, Noguchi C, 
Kagawa K, et al. Efficacy of vonoprazan for initial and 
maintenance therapy in reflux esophagitis, nonerosive 
esophagitis, and proton pump inhibitor-resistant gastro-
esophageal reflux disease. Medicine (Baltimore). 2020;99(11): 
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16. Miwa H, Uedo N, Watari J, Mori Y, Sakurai Y, Takanami Y, 
et al. Randomised clinical trial: efficacy and safety of 
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duodenal ulcers - results from two phase 3, non-inferiority 
randomised controlled trials. Aliment Pharmacol Ther. 
2017;45(2):240-52.
17. Kawai T, Oda K, Funao N, Nishimura A, Matsumoto Y, 
Mizokami Y, et al. Vonoprazan prevents low-dose aspirin-
associated ulcer recurrence: randomised phase 3 study. 
Gut. 2018;67(6):1033-41.
18. Maruyama M, Tanaka N, Kubota D, Miyajima M, 
Kimura T, Tokutake K, et al. Vonoprazan-based regimen is 
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Gastroenterol Hepatol. 2017;2017:4385161.
19. Huang J, Lin Y. Vonoprazan on the eradication of Helicobacter 
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42 Indian Journal of Clinical Practice, Vol. 35, No. 12, May 2025
MEDICOLEGAL 
The fact that the doctor found it convenient to perform 
the sterilization operation without consent as the patient 
was already under general anesthetic, was held to be not 
a valid defense. A somewhat similar view was expressed 
by Courts of Appeal in England in Re: F. (supra). It 
was held that the additional or further treatment which 
can be given (outside the consented procedure) should be 
confined to only such treatment as is necessary to meet 
the emergency, and as such needs to be carried out at 
once and before the patient is likely to be in a position to 
make a decision for himself. Lord Goff observed:
   ‘Where, for example, a surgeon performs an opera­
tion without his consent on a patient temporarily 
rendered unconscious in an accident, he should 
do no more than is reasonably required, in the 
best interests of the patient, before he recovers 
consciousness. I can see no practical difficulty 
arising from this requirement, which derives from 
the fact that the patient is expected before long to 
regain consciousness and can then be consulted 
about longer term measures.’
   The decision in Marshell vs. Curry ­ 1933 (3) 
DLR 260 decided by the Supreme Court of NS, 
Canada, illustrates the exception to the rule, that 
an unauthorized procedure may be justified if the 
patient’s medical condition brooks no delay and 
warrants immediate action without waiting for the 
patient to regain consciousness and take a decision 
for himself. In that case the doctor discovered 
a grossly diseased testicle while performing a 
hernia operation. As the doctor considered it to be 
gangrenous, posing a threat to patient’s life and 
health, the doctor removed it without consent, as a 
part of the hernia operation. An action for battery 
was brought on the ground that the consent was for 
a hernia operation and removal of testicle was not 
consent. The claim was dismissed. The court was 
of the view that the doctor can act without the 
consent of the patient where it is necessary to save 
the life or preserve the health of the patient. Thus, 
the principle of necessity by which the doctor is 
permitted to perform further or additional procedure 
(unauthorized) is restricted to cases where the patient 
is temporarily incompetent (being unconscious), to 
permit the procedure delaying of which would be 
unreasonable because of the imminent danger to the 
life or health of the patient.”
Question: Whether consent given for diagnostic surgery, 
can be construed as consent for performing additional 
or further surgical procedure?
Answer: If in the course of one operation, there is a 
medical emergency requiring a medical procedure, 
the doctor can operate on the patient without his or 
her consent and is protected by the defense of medical 
necessity. 
The 3 Judges Constitution Bench of Hon’ble Supreme 
Court of India in the landmark judgment titled as 
“Samira Kohli versus Prabha Manchanda, AIR 2008 
SC 1385” has held that the doctor can act without the 
consent of the patient where it is necessary to save 
the life or preserve the health of the patient. However, 
the principle of necessity by which the doctor is 
permitted to perform further or additional procedure 
(unauthorized) is restricted to cases where the patient is 
temporarily incompetent (being unconscious), to permit 
the procedure delaying of which would be unreasonable 
because of the imminent danger to the life or health of 
the patient. Thus, unless the unauthorized additional 
or further procedure is necessary in order to save the 
life or preserve the health of the patient and it would 
be unreasonable (as contrasted from being merely 
inconvenient) to delay the further procedure until the 
patient regains consciousness and takes a decision, a 
doctor cannot perform such procedure without the 
consent of the patient. The relevant paragraphs of the 
judgment are reproduced hereunder:
  “16. The next question is whether in an action for 
negligence/battery for performance of an unauthorized 
surgical procedure, the Doctor can put forth as defense 
the consent given for a particular operative procedure, as 
consent for any additional or further operative procedures 
performed in the interests of the patient. In Murray vs. 
McMurchy ­ 1949 (2) DLR 442, the Supreme Court 
of BC, Canada, was considering a claim for battery by 
a patient who underwent a cesarean section. During 
the course of cesarean section, the doctor found fibroid 
tumors in the patient’s uterus. Being of the view that such 
tumors would be a danger in case of future pregnancy, he 
performed a sterilization operation. The court upheld the 
claim for damages for battery. It held that sterilization 
could not be justified under the principle of necessity, as 
there was no immediate threat or danger to the patient’s 
health or life and it would not have been unreasonable to 
postpone the operation to secure the patient’s consent. 
Insights on Medicolegal Issues
MEDICOLEGAL 
43Indian Journal of Clinical Practice, Vol. 35, No. 12, May 2025
  “17. It is quite possible that if the patient been conscious, 
and informed about the need for the additional procedure, 
the patient might have agreed to it. It may be that the 
additional procedure is beneficial and in the interests of 
the patient. It may be that postponement of the additional 
procedure (say removal of an organ) may require another 
surgery, whereas removal of the affected organ during 
the initial diagnostic or exploratory surgery, would save 
the patient from the pain and cost of a second operation. 
Howsoever, practical or convenient the reasons may be, 
they are not relevant. What is relevant and of importance 
is the inviolable nature of the patient’s right in regard 
to his body and his right to decide whether he should 
undergo the particular treatment or surgery or not. 
Therefore at the risk of repetition, we may add that 
unless the unauthorized additional or further procedure 
is necessary in order to save the life or preserve the 
health of the patient and it would be unreasonable (as 
contrasted from being merely inconvenient) to delay the 
further procedure until the patient regains consciousness 
and takes a decision, a doctor cannot perform such 
procedure without the consent of the patient.”
The Hon’ble National Consumer Disputes Redressal 
Commission in the matter titled as “Saroj Chandhoke 
versus Ganag Ram Hospital, 2007 (3) CPJ 189 (NCDRC)” 
has held that:
 “VI. Conclusion:
 In conclusion it is held that:
 (i)  In a simple Hysterectomy operation, the Complainant 
lost her ovaries and left kidney. She was required to 
undergo other operations for control of fecal discharge 
from vagina. She was required to stay in the hospital 
for complete cure for months.
 (ii)  Informed consent was obtained only for total abdo­
minal hysterectomy (TAH). There was no necessity 
of trying to operate via vaginal route.
 (iii)  No consent was obtained for removal of ovaries in 
advance planned surgery.
 (iv)  In the present case, the question is not whether 
TAH is preferable to vaginal hysterectomy (VH). 
The patient was prepared for TAH and had given 
written consent for TAH and no consent was 
obtained or no information was given to the patient 
that her ovaries would be removed. In such set of 
circumstances, it cannot be said that because a 
surgeon is expert in the field he/she can carry out 
the surgery of his choice. If he/she does so, he/she 
does it at his/her risk in case of mishap.
   No doubt, in case of emergency there can be deviation 
in mode of surgery, but not in a planned surgery 
where express consent for a particular mode is taken 
from the patient, particularly, when there is no 
emergency.
 (v)  Before performing surgery, properly informed 
written consent is must. No doubt, while operating, 
to control adverse situation or to save the life of the 
patient or for benefit of the patient, other procedure 
could be followed or other part of the body could be 
operated.
 (vi)  As held in Spring Meadows Hospital (supra) it is to 
be seen that superiority of the Doctor is not abused 
in any manner. Further, if during the operation any 
mishap occurs because of error of judgment, it would 
be deficiency in service or negligence, if that would 
not have been committed by a reasonably competent 
professional man professing the standard and type 
of skill that a surgeon held out as having. The 
Opposite Party No. 2 is an expert Gynecologist who 
has performed many such operations as contended 
by her and Opposite Party No. 1 is a known big 
Hospital. In such a case, it is difficult to accept that 
for no fault there was avulsion of vein to such an 
extent that left kidney was required to be removed. 
Inference could be that there was some error which 
resulted in cut of a vein.”
Question: Whether the doctor is required to obtain 
consent of the patient in case of accident?
Answer: In Re F (Mental Patient: Sterilization), 1990 
(2) AC 1, Lord Bridge has observed that doctors and 
other health care professionals would otherwise face on 
intolerable dilemma, if they administer the treatment 
which they believe to be in the interest of the patient, 
they might face an action for trespass to the person, but 
if they withhold that treatment they could be in breach 
of duty of care in negligence. 
The Indian Medical Council (Professional Conduct, 
Etiquette & Ethics) Regulations, 2002 casts a duty on all 
medical practitioners, i.e., all medical practitioners must 
attend to sick and injured immediately and it is the 
duty of the medical practitioners to make immediate 
and timely medical care available to every injured 
person whether he is injured in accident or otherwise. 
The relevant provisions of Indian Medical Council 
(Professional Conduct, Etiquette & Ethics) Regulations, 
2002 is reproduced hereunder:
 “2. Duties of physicians to their patients
 2.1 Obligations to the sick
  2.1.1 Though a physician is not bound to treat each and 
every person asking his services, he should not only be 
MEDICOLEGAL 
44 Indian Journal of Clinical Practice, Vol. 35, No. 12, May 2025
ever ready to respond to the calls of the sick and the 
injured, but should be mindful of the high character 
of his mission and the responsibility he discharges in 
the course of his professional duties. In his treatment, he 
should never forget that the health and the lives of those 
entrusted to his care depend on his skill and attention. 
A physician should endeavor to add to the comfort of 
the sick by making his visits at the hour indicated to 
the patients. A physician advising a patient to seek 
service of another physician is acceptable, however, in 
case of emergency a physician must treat the patient. 
No physician shall arbitrarily refuse treatment to a 
patient. However for good reason, when a patient is 
suffering from an ailment which is not within the range 
of experience of the treating physician, the physician 
may refuse treatment and refer the patient to another 
physician.
  2.1.2 Medical practitioner having any incapacity 
detrimental to the patient or which can affect his 
performance vis-à-vis the patient is not permitted to 
practice his profession.
 2.4 The Patient must not be neglected
  A physician is free to choose whom he will serve. He 
should, however, respond to any request for his assistance 
in an emergency. Once having undertaken a case, the 
physician should not neglect the patient, nor should 
he withdraw from the case without giving adequate 
notice to the patient and his family. Provisionally or 
fully registered medical practitioner shall not willfully 
commit an act of negligence that may deprive his patient 
or patients from necessary medical care.
 3.5 Treatment after Consultation
  No decision should restrain the attending physician from 
making such subsequent variations in the treatment if any 
unexpected change occurs, but at the next consultation, 
reasons for the variations should be discussed/explained. 
The same privilege, with its obligations, belongs to the 
consultant when sent for in an emergency during the 
absence of attending physician. The attending physician 
may prescribe medicine at any time for the patient, 
whereas the consultant may prescribe only in case of 
emergency or as an expert when called for.”
The Hon’ble Supreme Court of India in the matter titled 
as “Parmanand Katara versus Union of India, AIR 1989 
SC 2039” has held that:
  “There can be no second opinion that preservation of 
human life is of paramount importance. That is so on 
account of the fact that once life is lost, the status quo 
ante cannot be restored as resurrection is beyond the 
capacity of man. The patient whether he be an innocent 
person or be a criminal liable to punishment under the 
laws of the society, it is the obligation of those who are 
in­charge of the health of the community to preserve life 
so that the innocent may be protected and the guilty may 
be punished. Social laws do not contemplate death by 
negligence to tantamount to legal punishment.”
  “Article 21 of the Constitution casts the obligation on the 
State to preserve life. The provision as explained by this 
Court in scores of decisions has emphasized and reiterated 
with gradually increasing emphasis that position. A doctor 
at the Government hospital positioned to meet this State 
obligation is, therefore, duty­bound to extend medical 
assistance for preserving life. Every doctor whether at 
a Government hospital or otherwise has the professional 
obligation to extend his services with due expertise for 
protecting life. No law or State action can intervene to 
avoid/delay the discharge of the paramount obligation cast 
upon members of the medical profession. The obligation 
being total, absolute and paramount, laws of procedure 
whether in statutes or otherwise which would interfere 
with the discharge of this obligation cannot be sustained 
and must, therefore, give way. On this basis, we have 
not issued notices to the States and Union Territories 
for affording them an opportunity of being heard before 
we accepted the statement made in the affidavit of the 
Union of India that there is no impediment in the law. 
The matter is extremely urgent and in our view, brooks 
no delay to remind every doctor of his total obligation and 
assure him of the position that he does not contravene 
the law of the land by proceeding to treat the injured 
victim on his appearance before him either by himself 
or being carried by others. We must make it clear that 
zonal regulations and classifications cannot also operate 
as fetters in the process of discharge of the obligation 
and irrespective of the fact whether under instructions 
or rules, the victim has to be sent elsewhere or how the 
police shall be contacted, the guideline indicated in the 
1985 decision of the Committee, as extracted above, is to 
become operative. We order accordingly.”
The Hon’ble National Consumer Dispute Redressal 
Commission in the matter titled as “Pravat Kumar 
Mukherjee versus Ruby General Hospital & Ors., 
2005 (2) CPJ 35” has held that:
 “ Considering the aforesaid law, it is apparent that: 
emergency treatment was required to be given to 
the deceased who was brought in a seriously injured 
condition; there was no question of waiting for the 
consent of the patient or a passer by who brought the 
patient to the hospital, and was not necessary to wait 
for consent to be given for treatment;
MEDICOLEGAL 
45Indian Journal of Clinical Practice, Vol. 35, No. 12, May 2025
  There is nothing on record to suggest that the Doctor 
has informed the patient or the relatives or the person 
who has brought him to the hospital with regard to 
dangers ahead or the risk involved by going without the 
operation/treatment at the earliest. 
  Consent is implicit in such cases when patient is brought 
to the hospital for treatment, and a surgeon who fails to 
perform an emergency operation must prove that the patient 
refused to undergo the operation not only at the initial stage 
but even after the patient was informed about the dangerous 
consequences of not undergoing the operation.”
Thus, the patient’s consent is not necessary in case of 
accident/emergency as in such cases, the consent is 
implied when the patient is brought to the hospital. 
Further, it is an obligation on the doctor to treat his 
patient without any delay. 
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