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Lipoprotein(a), apolipoprotein(a) polymorphism and coronary atherosclerosis severity in type 2 diabetic patients.
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Lipoprotein(a), apolipoprotein(a) polymorphism and coronary atherosclerosis severity in type 2 diabetic patients
Author(s): Gazzaruso, C (Gazzaruso, C); Bruno, R (Bruno, R); Pujia, A (Pujia, A); De Amici, E (De Amici, E); Fratino, P (Fratino, P); Solerte, SB (Solerte, SB); Garzaniti, A (Garzaniti, A)
Source: INTERNATIONAL JOURNAL OF CARDIOLOGY Volume: 108 Issue: 3 Pages: 354-358 DOI: 10.1016/j.ijcard.2005.05.022 Published: APR 14 2006
Times Cited: 8 (from Web of Science)
Cited References: 27 [ view related records ] Citation Map
Abstract: Background: Few and conflicting data are available in the literature on the association between Lp(a) levels and the severity of coronary artery disease (CAD) in diabetic patients. In addition, no studies took into account the role of apo(a) polymorphism. The purpose of the present study was to analyse the association of the degree of coronary atherosclerosis with Lp(a) levels and apo(a) polymorphism in a large group of type 2 diabetic patients.
Methods: The study population consisted of 227 consecutive type 2 diabetic patients undergoing a routine coronary angiography to evaluate chest pain or suspected CAD. The patients were subdivided into four subgroups according to the number of coronary arteries diseased: normal arteries (n = 26), mono-vessel disease (n = 67), bi-vessel disease (n = 54) and multi-vessel disease (n = 80).
Results: Lp(a) levels (normal arteries: 14.6 +/- 19.6 mg/dl; mono-vessel disease: 19.0 +/- 16.4 mg/dl; bi-vessel disease: 19.3 +/- 15.1 mg/dl; multi-vessel disease: 26.5 +/- 16.8 mg/dl; p < 0.001) and the percentages of patients with at least one isoform of low molecular weight (normal arteries: 23.1%; mono-vessel disease: 38.8%; bi-vessel disease: 75.9%; multi-vessel disease: 81.2%; p < 0.001) were significantly correlated with increasing number of coronary vessels diseased. Multiple logistic regression analysis showed that both Lp(a) levels (OR: 1.31; 95% CI: 1.02-4.11) and apo(a) polymorphism (OR: 3.43; 95% CI: 1.67-7.05) were independent predictors of CAD severity.
Conclusions: Our data suggest that Lp(a) levels and apo(a) polymorphism may be reliable predictors of CAD severity in type 2 diabetic patients
LIFE EXPECTANCY IN ALZHEIMER'S DISEASE (AD)
No full textSurvival following a diagnosis of AD is important information for health planners, caregivers, patients, and their families. AD is associated with variable, but shortened life expectancy. Knowing the expected survival time may empower people with AD and their families, but clinicians currently have limited predictive information. A better knowledge about prognosis in patients affected by AD and related disorders should be of paramount importance in order to improve care plans and assist in medical decisions, above all for patients in the moderate-severe stages of the disease. Life expectancy for patients with AD can vary between 3 to 10 years. Many studies have tried to identify predictive factors that can be of help for clinicians. The main predictor of life expectancy is the age. Therefore caregivers, patients, and their families could plan on a median life span as long as 7 to 10 years for patients whose conditions are diagnosed when they are in their 60s and early 70s, to only about 3 years or less for patients whose conditions are diagnosed when they are in their 90s. Dementias with prominent psychiatric-behavioral manifestations and gait impairment have a faster progression compared to AD. However the many variables that influence life expectancy make difficult to define prognosis at the bedside and more studies are needed to assist clinicians in they daily routine with patients and caregivers
Reply to letter to the editor regarding “Use of DPP-4 inhibitors in patients with COVID-19”
No full textVariability of Interactions Between Neuroendocrine and Immunological Functions in Physiological Aging and Dementia of the Alzheimer's Type
No full text: A link between neuroendocrine and immunological changes has been suggested in the pathophysiology of dementia of the Alzheimer's type (DAT). Healthy young and old subjects and patients with DAT were recruited to evaluate the chrononeuroendocrine organization of cortisol, GH, and melatonin (MLT) secretions. The study was carried out together with the evaluation of natural killer (NK) cell function: cytotoxic activity (NKCC) and TNF-alpha and IFN-gamma release after exposure to IL-2 (100 U/mL). Moreover, a cerebral morphometric analysis of hippocampus and temporal lobe (MRI) was performed. The activation of hypothalamo-pituitary-adrenal (HPA) axis and the decrease of GH, and MLT nocturnal peaks were associated with normal NKCC and TNF-alpha/IFN-gamma in healthy elderly subjects, whereas in DAT patients the same neuroendocrine changes occurred together with abnormal NKCC (spontaneous and IL-2/IFN-beta-modulated) and with alterations of TNF-alpha/INF-gamma generation from NK. Moreover significant correlations among the increase of NKCC and TNF-alpha and the decrease of cognitive function were found in the DAT group. These correlations were associated with the impairment of nocturnal GH and MLT levels and with the relatively higher serum cortisol concentrations. Moreover, the impairment of cortisol suppression after dexamethasone (1 mg orally at 23:00) was significantly correlated with the increase of spontaneous release of TNF-alpha and with IL-2-modulated NKCC. Finally the imunoneuroendocrine alterations found in DAT were associated with the reduction of cerebral volume in hippocampus and temporal lobes. Taken together these data indicate that the immunoneuroendocrine balance is maintained in physiological aging, whereas NK immune dysregulation in DAT could contribute to altering the neuroendocrine functions and to extend the progression of neurodegeneration and dementia
The relevance of biochemical index of nutritional status in elderly obese subjects
No full text“IFCC-WORLDLAB XVII International Congress of Clinical Chemistry and Laboratory Medicine”, Firenze 6-11 Giugno 199
Dipeptidyl peptidase-4 (DPP4) inhibition in COVID-19
No full textAims: SARS–CoV-2 causes severe respiratory syndrome (COVID-19) with high mortality due to a direct cytotoxic viral effect and a severe systemic inflammation. We are herein discussing a possible novel therapeutic tool for COVID-19. Methods: Virus binds to the cell surface receptor ACE2; indeed, recent evidences suggested that SARS–CoV-2 may be using as co-receptor, when entering the cells, the same one used by MERS–Co-V, namely the DPP4/CD26 receptor. The aforementioned observation underlined that mechanism of cell entry is supposedly similar among different coronavirus, that the co-expression of ACE2 and DPP4/CD26 could identify those cells targeted by different human coronaviruses and that clinical complications may be similar. Results: The DPP4 family/system was implicated in various physiological processes and diseases of the immune system, and DPP4/CD26 is variously expressed on epithelia and endothelia of the systemic vasculature, lung, kidney, small intestine and heart. In particular, DPP4 distribution in the human respiratory tract may facilitate the entrance of the virus into the airway tract itself and could contribute to the development of cytokine storm and immunopathology in causing fatal COVID-19 pneumonia. Conclusions: The use of DPP4 inhibitors, such as gliptins, in patients with COVID-19 with, or even without, type 2 diabetes, may offer a simple way to reduce the virus entry and replication into the airways and to hamper the sustained cytokine storm and inflammation within the lung in patients diagnosed with COVID-19 infection
Branching fraction and CP asymmetry of the decays B+→K0Sπ+ and B+→K0SK+
No full textAn analysis of B+ → K0
Sπ+ and B+ → K0
S K+ decays is performed with the LHCb experiment. The pp
collision data used correspond to integrated luminosities of 1 fb−1 and 2 fb−1 collected at centre-ofmass
energies of
√
s = 7 TeV and
√
s = 8 TeV, respectively. The ratio of branching fractions and the
direct CP asymmetries are measured to be B(B+ → K0
S K+
)/B(B+ → K0
Sπ+
) = 0.064 ± 0.009 (stat.) ±
0.004 (syst.), ACP(B+ → K0
Sπ+
) = −0.022 ± 0.025 (stat.) ± 0.010 (syst.) and ACP(B+ → K0
S K+
) =
−0.21 ± 0.14 (stat.) ± 0.01 (syst.). The data sample taken at
√
s = 7 TeV is used to search for
B+
c
→ K0
S K+ decays and results in the upper limit ( fc · B(B+
c
→ K0
S K+
))/( fu · B(B+ → K0
Sπ+
)) <
5.8 × 10−2 at 90% confidence level, where fc and fu denote the hadronisation fractions of a ¯b
quark
into a B+
c or a B+ meson, respectively
Influence of Triphasic Oral-contraceptives On Blood Rheology and Hemostatic and Metabolic Patterns In Young-women - Results of A 3-year Study
No full textLong-term (three-ear) variations in clinical, hemorheologic, hemostatic and blood lipid parameters were evaluated in 20 young healthy women taking a triphasic oral contraceptive. Body weight, arterial blood pressure, whole blood, plasma and serum viscosity, erythrocyte deformability, fibrinogen, fibronectin, alpha-2 macroglobulin Von Willebrand factor antigen, triglycerides, nonesterified fatty acids, total and low density lipoprotein cholesterol, very low density lipoprotein, low density and apolipoprotein B levels remained unchanged throughout the study. However, high density lipoprotein cholesterol, high density lipoprotein and apolipoprotein Al serum concentrations increased significantly during treatment. Long-term use of the triphasic oral contraceptive does not seem to adversely affect the blood rheology pattern or vascular endothelium function, which are the main factors responsible for the development of thromboembolic complications
Observations of Bºs→ψ(2S)η and Bº(s)→ψ(2S)π+π- decays
No full textFirst observations of the B0s
→ψ(2S)η, B0 →ψ(2S)π
+
π
− and B0s
→ψ(2S)π
+
π
− decays are made
using a dataset corresponding to an integrated luminosity of 1.0 fb−1 collected by the LHCb experiment in
proton–proton collisions at a centre-of-mass energy of
√
s = 7 TeV. The ratios of the branching fractions
of each of the ψ(2S) modes with respect to the corresponding J/ψ decays are
B(B0s
→ψ(2S)η)
÷
B(B0s
→J/ψη)
= 0.83± 0.14 (stat)±0.12 (syst) ±0.02 (B),
;
B(B0→ψ(2S)π
+
π
−
)
÷
B(B0→J/ψπ
+
π
−
)
= 0.56± 0.07 (stat)±0.05 (syst)± 0.01 (B),
;
B(B0s
→ψ(2S)π
+
π
−
)
÷
B(B0s
→J/ψπ
+
π
−
)
= 0.34± 0.04 (stat)±0.03 (syst)± 0.01 (B),
where the third uncertainty corresponds to the uncertainties of the dilepton branching fractions of the J/ψ
and ψ(2S) meson decays
Twenty-four-week effects of liraglutide on body composition, adherence to appetite, and lipid profile in overweight and obese patients with type 2 diabetes mellitus
No full textMariangela Rondanelli,1 Simone Perna,1 Paolo Astrone,2 Annalisa Grugnetti,2 Sebastiano Bruno Solerte,2 Davide Guido3,4 1Endocrinology and Nutrition Unit, Section of Human Nutrition, Department of Public Health, Experimental and Forensic Medicine, Agency for Elderly People Services, Santa Margherita Hospital, University of Pavia, Pavia, Italy; 2Section of Geriatrics and Gerontology, Department of Internal Medicine, Agency for Elderly People Services, Santa Margherita Hospital, University of Pavia, Pavia, Italy; 3Medical and Genomics Statistics Unit, Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy; 4Biostatistics and Clinical Epidemiology Unit, Department of Public Health, Experimental and Forensic Medicine, University of Pavia, Pavia, Italy Background: Liraglutide has well-known effects on glucose patterns. However, its several other metabolic properties are still controversial. Given this background, the aims of the present study are to evaluate the effects of 24-week liraglutide treatment on body composition, appetite, and lipid profile in overweight and obese type 2 diabetes mellitus (T2DM) patients. Methods: A cohort study was carried out on overweight and obese T2DM patients with glycosylated hemoglobin A1c equal to 6% (42 mmol/mol)-10% (86 mmol/mol), under a 3-month treatment (at least) with maximal dose of metformin as stable regime, by adding liraglutide at doses up to 3 mg/d. Body composition markers were measured by dual-energy X-ray densitometry at baseline and after 24 weeks of liraglutide treatment. Glucose control was monitored by glucose, glycosylated hemoglobin A1c, insulin, and homeostasis model assessment. Finally, the appetite sensation and plasma lipids were also evaluated. Results: Twenty-eight subjects (male/female: 16/12, mean age: 58.75±9.33 years, body mass index: 34.13±5.46 kg/m2) were evaluated. Accounting for the adjustment for age, sex, and duration of diabetes, we noted significant decreases in body mass index (-0.86 kg/m2, P=0.024), fat mass (-2.01 kg, P=0.015), fat mass index (-0.71 kg/m2, P=0.014), android fat (-1.72%, P=0.022), trunk fat (-1.52%, P=0.016), and waist circumference (-6.86 cm, P<0.001) from the baseline values. Haber score was increased by 3.82 units (P=0.009), and the number of metabolic syndrome risk factors was decreased (-0.69 units, P=0.012). The glucose control variables and total cholesterol/high-density lipoprotein cholesterol ratio also showed significant decreases from baseline values. Conclusion: The 24-week liraglutide treatment leads to the reduction of fat mass, android fat, trunk fat, and appetite by improving the lipid profile, glucose control, and insulin sensitivity. Keywords: liraglutide, weight loss, body composition, fat mass, type 2 diabetes mellitus, appetit
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