Early Alterations in Glycemic Control and Pancreatic Endocrine Function in Nondiabetic Patients With Chronic Pancreatitis

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Abstract

<div class="section"> <a class="named-anchor" id="S1">  </a> <h5 class="section-title" id="d5181895e178">Objectives</h5> <p id="P1">Diabetes mellitus (DM) is a frequent consequence of chronic pancreatitis (CP). Little is known about pancreatic endocrine function before the development of DM in CP, particularly in females, or those without calcific and/or alcoholic pancreatitis. </p> </div><div class="section"> <a class="named-anchor" id="S2">  </a> <h5 class="section-title" id="d5181895e183">Methods</h5> <p id="P2">Twenty-five non-diabetic adult CP patients (19 female, age 34.2 ± 2.4 yrs) were compared to 25 healthy controls matched for age, gender, and BMI. Subjects underwent frequent sample intravenous glucose tolerance testing (FSIVGTT) and mixed meal tolerance testing (MMTT). </p> </div><div class="section"> <a class="named-anchor" id="S3">  </a> <h5 class="section-title" id="d5181895e188">Results</h5> <p id="P3">Mean fasting glucose was higher in CP patients (89.5 ±2.3 mg/dL) than in controls (84.4 ±1.2 mg/dL, p=0.04). On MMTT, CP patients had a higher area under the curve (AUC) glucose and AUC glucagon compared to controls (p≤0.01). AUC C-peptide was equivalent (p=0.6) but stimulated C-peptide at 30 minutes was lower in CP patients (p=0.04). Mean insulin sensitivity index calculated from the FSIVGTT was lower in CP group, indicating reduced insulin sensitivity (p≤0.01). Disposition index (insulin secretion adjusted for insulin sensitivity on FSIVGTT) was lower in CP patients (p=0.01). </p> </div><div class="section"> <a class="named-anchor" id="S4">  </a> <h5 class="section-title" id="d5181895e193">Conclusions</h5> <p id="P4">CP patients had higher fasting and MMTT glucose levels, without a compensatory increase in insulin secretion suggesting subtle early islet dysfunction. Our cohort had relative hyperglucagonemia and were less insulin sensitive than controls. </p> </div>

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Clinical and genetic characteristics of hereditary pancreatitis in Europe.

Richard M. Charnley, Jan O Jansen, Giorgio Cavallini … (2004)

Hereditary pancreatitis is an autosomal dominant disease that is mostly caused by cationic trypsinogen (PRSS1) gene mutations. The aim was to determine phenotype-genotype correlations of families in Europe. Analysis of data obtained by the European Registry of Hereditary Pancreatitis and Pancreatic Cancer was undertaken using multilevel proportional hazards modelling. There were 112 families in 14 countries (418 affected individuals): 58 (52%) families carried the R122H, 24 (21%) the N29I, and 5 (4%) the A16V mutation, 2 had rare mutations, and 21 (19%) had no PRSS1 mutation. The median (95% confidence interval [CI]) time to first symptoms for R122H was 10 (8, 12) years of age, 14 (11, 18) years for N29I, and 14.5 (10, 21) years for mutation negative patients (P = 0.032). The cumulative risk (95% CI) at 50 years of age for exocrine failure was 37.2% (28.5%, 45.8%), 47.6% (37.1%, 58.1%) for endocrine failure, and 17.5% (12.2%, 22.7%) for pancreatic resection for pain. Time to resection was significantly reduced for females (P < 0.001) and those with the N29I mutation (P = 0.014). The cumulative risk (95% CI) of pancreatic cancer was 44.0% (8.0%, 80.0%) at 70 years from symptom onset with a standardized incidence ratio of 67% (50%, 82%). Symptoms in hereditary pancreatitis start in younger patients and endpoints take longer to be reached compared with other forms of chronic pancreatitis but the cumulative levels of exocrine and endocrine failure are much higher. There is an increasingly high risk of pancreatic cancer after the age of 50 years unrelated to the genotype.

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MINMOD Millennium: a computer program to calculate glucose effectiveness and insulin sensitivity from the frequently sampled intravenous glucose tolerance test.

Darko Stefanovski, Raymond C. Boston, Peter J Moate … (2002)

The Bergman Minimal Model enables estimation of two key indices of glucose/insulin dynamics: glucose effectiveness and insulin sensitivity. In this paper we describe MINMOD Millennium, the latest Windows-based version of minimal model software. Extensive beta testing of MINMOD Millennium has shown that it is user-friendly, fully automatic, fast, accurate, reproducible, repeatable, and highly concordant with past versions of MINMOD. It has a simple interface, a comprehensive help system, an input file editor, a file converter, an intelligent processing kernel, and a file exporter. It provides publication-quality charts of glucose and insulin and a table of all minimal model parameters and their error estimates. In contrast to earlier versions of MINMOD and some other minimal model programs, Millennium provides identified estimates of insulin sensitivity and glucose effectiveness for almost every subject.

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MINMOD: a computer program to calculate insulin sensitivity and pancreatic responsivity from the frequently sampled intravenous glucose tolerance test.

G. Pacini, R N Bergman (1986)

Insulin sensitivity and pancreatic responsivity are the two main factors controlling glucose tolerance. We have proposed a method for measuring these two factors, using computer analysis of a frequently-sampled intravenous glucose tolerance test (FSIGT). This 'minimal modelling approach' fits two mathematical models with FSIGT glucose and insulin data: one of glucose disappearance and one of insulin kinetics. MINMOD is the computer program which identifies the model parameters for each individual. A nonlinear least squares estimation technique is used, employing a gradient-type of estimation algorithm, and the first derivatives (not known analytically) are computed according to the 'sensitivity approach'. The program yields the parameter estimates and the precision of their estimation. From the model parameters, it is possible to extract four indices: SG, the ability of glucose per se to enhance its own disappearance at basal insulin, SI, the tissue insulin sensitivity index, phi 1, first phase pancreatic responsivity, and phi 2, second phase pancreatic responsivity. These four characteristic parameters have been shown to represent an integrated metabolic portrait of a single individual.