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Melanie Rodacki

Dytz et al. Diabetol Metab Syndr  (2017) 9:4 
DOI 10.1186/s13098-017-0203-7
SHORT REPORT
Clinical aspects of pancreatogenic 
diabetes secondary to hereditary pancreatitis
Marcio Garrison Dytz1,2,3,4*, Pedro Arthur Hamamoto Marcelino3, Olga de Castro Santos1, Lenita Zajdenverg3, 
Flavia Lucia Conceição1, Tânia Maria Ortiga‑Carvalho2 and Melanie Rodacki3
Abstract 
Background: Hereditary pancreatitis is a rare inherited form of pancreatitis, characterized by recurrent episodes of 
acute pancreatitis with early onset and/or chronic pancreatitis, and presenting brittle diabetes, composed of epi‑
sodes of nonketotic hyperglycemia and severe hypoglycemia. The existing literature regarding this form of diabetes is 
scarce. In this report, clinical features of pancreatogenic diabetes secondary to hereditary pancreatitis are presented 
along with recommendations for appropriate medical treatment.
Results: Clinical data from five patients of a family with pancreatogenic diabetes secondary to hereditary pancreatitis 
were analyzed. The average time between hereditary pancreatitis and diabetes diagnosis was 80 ± 24 months (range: 
60–180 months) with a mean age of 25.6 ± 14.7 years (range: 8–42 years), four patients used antidiabetic agents 
for 46 ± 45 months and all progressed to insulin therapy with a mean dose of 0.71 ± 0.63 IU/kg (range: 0.3–1.76 IU/
kg). The glycemic control had a high variability with average capillary blood glucose of 217.00 ± 69.44 mg/dl (range: 
145–306 mg/dl) and the average HbA1c was 9.9 ± 1.9% (range: 7.6–11.6%). No ketoacidosis episodes occurred and 
there were several episodes of hospitalization for severe hypoglycemia.
Conclusions: Diabetes mellitus secondary to hereditary pancreatitis presents with early onset, diverse clinical pres‑
entation and with extremely labile glycemic control. Diabetes treatment varies according to the presentation and 
insulin is frequently necessary for glycemic control.
Keywords: Hereditary pancreatitis, Cationic trypsinogen, Pancreatogenic diabetes, Beta‑cell
© The Author(s) 2017. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License 
(http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, 
provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, 
and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/
publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Background
Hereditary pancreatitis (HP) is a rare autosomal domi-
nant disease characterized by recurrent episodes of acute 
pancreatitis that leads to permanent chronic pancreatitis. 
Common clinical manifestations are: abdominal pain, 
disabsorptive syndrome, diabetes mellitus (DM) and pan-
creatic cancer [1].
Pancreatic inflammation results in destruction of 
pancreatic islet with loss of β-cells (insulin), α-cells 
(glucagon), δ-cells (somatostatin) and PP-cells (pancre-
atic-polypeptide) [2] that can lead to the development of 
brittle diabetes, which is characterized by extreme blood 
glucose levels fluctuations, causing hyperglycemia or 
hypoglycemia [3]. This article focuses on clinical features 
and treatment of pancreatogenic diabetes secondary to 
HP.
Methods
Clinical data from a family with confirmed molecular 
diagnosis of HP was evaluated. A retrospective analysis 
of their medical records assessed weight, age, DM dura-
tion, interval between the diagnosis of HP and DM, use 
and dose of insulin, use of oral antidiabetic medications, 
HbA1c values, episodes of severe hypoglycemia, hospi-
talization for ketoacidosis and presence of chronic com-
plications of DM. Download of data obtained through 
thirty days of self-monitoring of blood glucose using 
the Accu-Check Smart Pix Software®, was performed 
in order to measure and calculate average and standard 
Open Access
Diabetology &
Metabolic Syndrome
*Correspondence:  marcio@ideb.med.br 
4 Endocrinology Section, Hospital Universitário Clementino Fraga Filho, 
Rua Rodolpho Paulo Rocco 255, Ilha do Fundão, Rio de Janeiro, RJ 
21941‑913, Brazil
Full list of author information is available at the end of the article
Page 2 of 6Dytz et al. Diabetol Metab Syndr  (2017) 9:4 
deviation (SD) of capillary blood glucose (CBG). The 
mutation screening has been previously described [4].
The local ethics committee approved the study proto-
col (169 11-CEP), in accordance with institutional ethi-
cal standards and national research committee. Patient 
informed consent form was obtained before initiating the 
study.
Results
The study evaluated five patients from a family with HP 
secondary to N29T mutation in exon 2 of the PRSS1 
gene (Fig. 1) [4]. In 3 patients, the HP diagnosis preceded 
DM, while in 2 the opposite occurred. The average time 
between HP and DM diagnosis was 80  ±  24  months 
(range: 60–180 months) (Table 1).
All patients used insulin. The mean dose was 
0.71 ± 0.63 IU/kg (range: 0.27–1.76 IU/kg). In 4 patients, 
other drugs (Metformin and Glyburide) were used before 
insulin therapy was started, mean time of 46 ± 45 months 
(range: 4–96 months).
The average CBG was 217.00  ±  69.44  mg/dl (range: 
145–306 mg/dl) with SD of 104.75 ± 15.56 mg/dl (range: 
94–127 mg/dl). There was a high variability of CBG in all 
cases, with frequent hypoglycemic events and hypergly-
cemic excursions. HbA1c levels demonstrated the het-
erogeneity between patients, but most patients showed 
elevated levels (Fig. 2).
The average diabetes duration was 
120.80  ±  80.32  months (range: 24–228  months). No 
ketoacidosis episodes occurred, although there were 
Table 1 Clinical features of pancreatogenic diabetes in affected patients
BMI body mass index, CBG capillary blood glucose, SD standard deviation
a Mean of 5 years, method high-performance liquid chromatography (HPLC)
Patient Age of onset 
(years)
Duration 
of pancreatitis 
(years)
Duration 
of diabetes 
(years)
BMI (kg/m2) Mean CBG/SD Insulin dose 
(IU/kg)
HbA1ca (mean) 
(%)
Chronic 
diabetes com-
plications
1 8 53 19 25.4 184/94 0.3 7.6 No
2 5 36 13 21.7 233/104.4 0.83 11.6 Retinopathy
3 14 25 2 29.7 – 0.27 8.2 No
4 2 16 10 22.6 145/94.8 0.41 11.5 No
5 4 12 5 22.7 306/127.5 1.76 10.9 Neuropathy
1
3
4 5
2
NM
NMNMNMNM
NM
NM
NMNM
NM NNNNNN
NN
NNNN
Fig. 1 Pedigree of the reported family demonstrating 5 members with diabetes (blue) and exocrine pancreatic dysfunction (red), 1 member with 
only exocrine pancreatic dysfunction, 2 members with acute pancreatitis (yellow) and 2 clinically unaffected mutation carrier. NN no mutation, NM 
heterozygous mutation
Page 3 of 6Dytz et al. Diabetol Metab Syndr  (2017) 9:4 
episodes of hospitalization because of severe hypogly-
cemia. Surgical procedures were performed on patients 
4 and 5, respectively, for refractory pain and abdominal 
complication. Patients 2 and 5 presented microvascular 
lesions secondary to diabetes with nonproliferative dia-
betic retinopathy with macular edema and distal sym-
metrical sensorimotor polyneuropathy accompanied by 
autonomic neuropathy, respectively.
Discussion
In this study, we describe the glycemic pattern of five 
patients with diabetes secondary to a mutation in the 
PRSS1 gene, which leads to an increased autocatalytic 
conversion of trypsinogen to active trypsin, that results 
in autodigestion and damage to the acinar cells [5, 6].
Mutations in the PRSS1 gene (R122H, N29I, A16V, and 
other less prevalent) are responsible for greater than 70% 
0
100
200
300
400
500
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
G
lu
co
se
(m
g/
dl
)
Days
a
Jan 10 Jan 11 Jan 12 Jan 13 Jan 14 Jan 15
6
7
10
8
9
16
15
18
17
12
11
14
13
Pt 3
Pt 1
Pt 2
Pt 4
Pt 5
b
H
bA
1c
 (%
)
Fig. 2 a Capillary blood glucose (CBG) of the patient 4 in 2 weeks with high glycemic variability. b HbA1c measurements of patients with Heredi‑
tary Pancreatitis over 5 years
Page 4 of 6Dytz et al. Diabetol Metab Syndr  (2017) 9:4 
of mutations in HP kindreds [7, 8], but other mutations 
have also been described (Fig. 3) [9–11].
A high rate of hypoglycemia and CBG variability was 
observed in these patients with diabetes secondary to HP. 
The marked glycemic lability is probably due not only to 
a continued loss of insulin secreting β-cells but also from 
counter regulatory glucagon secreting α-cells. Addition-
ally, nutrients malabsorption resulted in impaired incre-
tin secretion and thereby diminished insulin release. 
Moreover, the lack of other paracrine or endocrine fac-
tors secreted by the pancreatic cells may also contribute 
to this glycemic pattern [12].
Unlike type 1 DM, even with high glucose levels no 
patient developed ketoacidosis. The reasons that may 
warrant this is that the β-cell deficit is seldom absolute 
and it occurs concomitantly with the loss of α-cells [13].
All patients required insulin therapy, but the progres-
sion of the pancreatic endocrine failure was extremely 
variable. In some of the cases, insulin was necessary 
shortly after the diabetes diagnosis, while in others, oral 
drug therapy without insulin was possible for years.
Oral antidiabetic agents may be appropriate in early 
pancreatogenic diabetes (HbA1c  <  8.0%). Metformin 
should be the drug of first choice, in the absence of con-
traindications, especially if concomitant insulin resistance 
is evidenced, and if it is tolerated due to common gas-
trointestinal adverse effects and weight loss [14]. Besides 
that, it is possible that Metformin might reduce the risk of 
pancreatic cancer, and therefore would have a theoretical 
rationale in chronic pancreatitis [15]. Oral therapy with 
insulin secretagogues (sulfonylurea and glinides) may 
also be considered as second-line therapy, but should be 
Fig. 3 Schematic mechanism underling mutations‑associated pancreatitis. The PRSS1 (Cationic Trypsinogen) mutation leads to a gain‑of‑function 
with an increased conversion of intrapancreatic trypsinogen to trypsin. The SPINK1 (Serine Protease Inhibitor Kazal type 1) and CTRC (Chymotrypsin 
C) mutations lead to loss of defenses against the activation of trypsinogen. Mutations in CPA1 (carboxypeptidase A1) generate misfolded proteins 
leading to endoplasmic reticulum stress
Page 5 of 6Dytz et al. Diabetol Metab Syndr  (2017) 9:4 
aware of hypoglycemia in patients with inconsistent meal 
ingestion [3]. Thiazolidinediones, incretin based therapies 
and SGLT2 inhibitors should be avoided because of side 
effects and lack of data in this context [3, 16].
In advanced pancreatogenic diabetes, insulin therapy is 
the preferred treatment, and especially during acute epi-
sodes of pancreatitis or hospitalized patients, and severe 
malnutrition patients in which the anabolic effects of 
insulin are desired. Patients should be treated using gen-
eral insulin dosing and regimen guidelines for type 1 dia-
betes [3, 16]. The patients studied used NPH and regular 
insulin because it is the first choice in the local healthcare 
public system. Despite the use of human insulin, glyce-
mic control was more unpredictable than expected with 
high glycemic variability. The insulin analogues or insu-
lin pump therapy are treatment options that may allow a 
more stable glycemic control.
Moreover, the islet autotransplant might be an option 
for patients with severe chronic pancreatitis, who have 
debilitating abdominal pain refractory to medical or 
endoscopic interventions and for which total pancreatec-
tomy is indicated [17, 18]. Patient 4 underwent pancrea-
tectomy and could have benefited from this therapy to 
preserve the function of the remaining β-cells.
In summary, these data indicate that DM second-
ary to HP presents clinical heterogeneity among 
patients, but with high glycemic variability and diffi-
cult management. Hence, molecular diagnosis should 
be performed in suspicious patients of HP because it 
allows the proper approach. Strategies to improve the 
glycemic control in affected patients should also be 
pursued.
Abbreviations
HP: hereditary pancreatitis; DM: diabetes mellitus; SD: standard deviation; CBG: 
capillary blood glucose; NN: no mutation; NM: heterozygous mutation; BMI: 
body mass index; HPLC: high‑performance liquid chromatography; PRSS1: 
cationic trypsinogen; SPINK1: Serine Protease Inhibitor Kazal type 1; CTRC: 
Chymotrypsin C; CPA1: carboxypeptidase A1.
Authors’ contributions
MGD, FLC, TMOC and MR participated in the design of the study; MGD, PAHM 
and OCS collected patient data; MGD, LZ, TMOC and MR analyzed data; and 
MGD, TMOC and MR wrote the paper. All authors read and approved the final 
manuscript.
Author details
1 Endocrinology Section, Department of Internal Medicine, Medical School, 
Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil. 2 Labora‑
tory of Translational Endocrinology, Instituto de Biofísica Carlos Chagas Filho, 
Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil. 3 Diabetes 
and Nutrology Section, Department of Internal Medicine, Medical School, 
Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil. 4 Endocri‑
nology Section, Hospital Universitário Clementino Fraga Filho, Rua Rodolpho 
Paulo Rocco 255, Ilha do Fundão, Rio de Janeiro, RJ 21941‑913, Brazil. 
Acknowledgements
Not applicable.
Competing interests
The authors declare that they have no competing interests.
Availability of data and materials
All data generated or analysed during this study are included in this published 
article and in the article [4].
Consent for publication
All patients signed a consent form, in which they agree with the publication of 
the results of the study.
Ethics approval and consent to participate
The ethics committee of Federal University of Rio de Janeiro approved 
the study protocol (169 11‑CEP) on April 24th, 2012, in accordance with 
institutional ethical standards (Declaration of Helsinki) and national research 
committee. Patient informed consent form was obtained before initiating the 
study.
Funding
This work was supported by the FAPERJ (Foundation for Research Support of 
the State of Rio de Janeiro) and the CNPq (National Council for Scientific and 
Technological Development).
Received: 23 April 2016   Accepted: 7 January 2017
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Clinical aspects of pancreatogenic diabetes secondary to hereditary pancreatitis

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LETTER TO EDITOR/LED REPLY
Quality of Life and Weight Loss in Bariatric Patients
Michał Robert Janik1
Published online: 18 February 2017
# The Author(s) 2017. This article is published with open access at Springerlink.com
Dr. Scott Shikora
Editor in Chief
Obesity Surgery
Dear Dr. Scott Shikora
We are glad that our article has attracted the interest of readers
and opened an important discussion about quality of life in
bariatric patients. Moreover, we are honoured that our study
has raised the interest of Álvares, R. S. R et al. who present
their results on the relationship between weight loss and quality
of life in group of patients after Roux-en Y Gastric Bypass
(RYGB) in long-term follow-up [1]. This cross-sectional study
investigated 101 patients who had undergone RYGB from
1998 to 2011 in Brazilian bariatric center. Quality of life
(QoL) was assessed by the Moorehead-Ardelt (MA) quality
of life questionnaire. In order to investigate the determinants
of long-term QoL after BS, they performed a binary logistic
regression model with QoL (improved or not improved) as
the outcome variable adjusted for age, gender, partnered status
%EBMIL, hypertension, diabetes, history of gastroesophageal
reflux, smoking status, and physical activity. The results
showed that %EBMIL was the only significant quality of life
determinant. This observation was discussed with the results
presented in our paper titled: BQuality of Life and Bariatric
Surgery: Cross Sectional Study and Analysis of Factors
Influencing Outcome^. In our study, we performed correlation
analysis between total score in MA and the following psycho-
metric variables: %TWL (r = −0.122, p = 0.36), ΔBMI
(r = −0.107, p = 0.42), and %EWL (r = −0.064, p = 0.63)
[2]. Álvares, R. S. R et al. pointed out that differences regarding
the postoperative times of QoL assessment, comorbidities prev-
alence, and cultural differences explain these different findings.
Clearly, those two studies are not comparable.We agree on that.
However, few more issues should be discussed.
First, we used correlation analysis. The aim of this statisti-
cal method is to quantify the association between two contin-
uous variables. It is not the same method as binary logistic
regression which is used to assess the association between
dependent categorical variable with one or more predictor
(or independent) variables. Please mind that in Álvares, R.
S. R et al. study, the dependent categorical variable was de-
fined by authors (improved/non-improved). Different type of
statistical method used in the studies can affect the results.
Second, both analyses did not include the information re-
garding body contouring after bariatric surgery. Many patients
after massive weight loss are disappointed due to an excess
skin folds. This might have an impact on QoL [3]. It is more
likely that patients who are more than 5 years after bariatric
procedure underwent also abdominoplasty, especially in coun-
try where plastic surgery is very popular [4]. In our opinion,
future studies on QoL in bariatric patients should also include
information about body contouring after massive weight loss.
Third, both studies were cross-sectional design. This type of
study is not intended to assess the impact of weight loss onQoL.
The aims in our study were to compare QOL in obese patients
12–18 months after bariatric surgery to control seeking surgery
and to investigate which factors influence QOL outcomes in the
MA II in obese patients. We found that QoL is significantly
better in patients after bariatric surgery (1.70 ± 0.76 in the oper-
ated group versus 0.59 ± 1.17 in the control group; p < 0.01).We
also stated that the fact of underwent bariatric surgery is only
significant factor affecting QoL scoring in obese patients (OR
0.113; 95% CI 0.044–0.290). The analysis of correlation be-
tween %EWL and QoL scoring was performed in addition.
* Michał Robert Janik
janiken@gmail.com; mjanik@wim.mil.pl
1 Department of General, Oncologic, Metabolic and Thoracic Surgery,
Military Institute of Medicine, Szaserów 128 Street,
04-141 Warsaw, Poland
OBES SURG (2017) 27:1074–1075
DOI 10.1007/s11695-017-2587-8
The lack of correlation was consistent with other studies [5, 6].
We decided to present it in the manuscript because wewanted to
show that surgeons should not be only a BBMI-hunter .^ Yet,
there is a need for longitudinal study to obtain a reliable answer
on a question about the relationship between weight loss and
QoL in bariatric patients.
To sum it up, there is agreement that weight loss leads to
better quality of life. Yet, it is not clear what exactly contribute
to this improvement. It seems reasonable that the amount of
weight loss does not play a significant role after crossing cer-
tain threshold. This threshold can be specific for each patient.
In our opinion, other factors should be taken into the account
like improvement of comorbidities or changes in body image.
Compliance with Ethical Standards
Conflict of Interest The author declares that he has no conflict of
interest.
Open Access This article is distributed under the terms of the Creative
Commons At t r ibut ion 4 .0 In te rna t ional License (h t tp : / /
creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
distribution, and reproduction in any medium, provided you give appro-
priate credit to the original author(s) and the source, provide a link to the
Creative Commons license, and indicate if changes were made.
References
1. Álvares RSR, Beleigoli AMR, Cançado AGM, et al. Quality of life
and weight loss in the long-term after gastric. Obes Surg 2017.
2. Janik MR, Rogula T, Bielecka I, et al. Quality of life and bar-
iatric surgery: cross-sectional study and analysis of factors
influencing outcome. Obes Surg. 2016; doi:10.1007/s11695-
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3. Cintra W, Modolin MLA, Gemperli R, et al. Quality of life after
abdominoplasty in women after bariatric surgery. Obes Surg.
2008;18:728–32. doi:10.1007/s11695-007-9280-2.
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Surg. 2012;130:967–8. doi:10.1097/PRS.0b013e31826703b1.
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and body image after gastric bypass surgery. Surg Obes Relat Dis.
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OBES SURG (2017) 27:1074–1075 1075


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