Quantitative determination of pancreas size using anatomical landmarks and its clinical relevance: A systematic literature review.

There have been many reports of altered pancreas size in diseases of the endocrine and exocrine pancreas, but few attempts to quantify such changes. The aim of this study was to conduct a systematic literature review, documenting the methodology, and quantitative data in studies reporting on pancreas size. Three electronic databases (Embase, Scopus, and MEDLINE) were searched by two reviewers independently. Studies of humans were included if they compared pancreas size (reported as pancreas diameters, areas, and/or lengths) between diseased populations and controls. A total of 28 studies with 3,810 individuals were included. Among these, 22 measured pancreas diameters, seven measured pancreas areas, and one measured pancreas lengths. The most common landmark for the head of the pancreas was the confluence of the superior mesenteric and splenic veins (three out of nine studies, 33.3%); for the body it was the superior mesenteric artery (seven out of nine, 77.8%); for the tail it was the internal border of the left kidney (two out of six, 33.3%). Pancreas diameters and areas tended to be smaller in diabetes mellitus, the extent of reduction being greater in individuals with type 1 than type 2 diabetes. Pancreas diameters tended to be greater in acute pancreatitis and pancreatic cancer but not in chronic pancreatitis. Pancreas diameters are a clinically relevant measure for diseases of the endocrine and exocrine pancreas. Consensus guidelines need to be developed to standardize their measurements. Clin. Anat. 31:913-926, 2018. © 2018 Wiley Periodicals, Inc.

The effect of parental imprinting on the INS-IGF2 locus of Korean type I diabetic patients.

BACKGROUND: Insulin-dependent diabetes mellitus (IDDM) is caused by the autoimmune destruction of pancreatic beta-cells. Susceptibility to IDDM appears to depend on more than one genetic locus. Evidence of a genetic linkage for IDDM2 was found in male meioses from French and North American populations. It is linked to maternal imprinting (i.e. monoalleleic expression of the insulin gene) that is considered the most likely cause of these gender-related differences. IGF2 is expressed only in the paternal allele and, therefore, is considered a candidate gene for IDDM2 transmission because of its important autocrine/paracrine effects on the thymus, lymphocytes and pancreas. Nevertheless, it remains controversial whether the parental origin of IDDM2 influences IDDM susceptibility. METHODS: Using PCR and semi-quantitative RT-PCR, we analyzed the INS/Pstl + 1127 and IGF2/Apal polymorphisms and RNA expression level between Pstl (+/-) and Pstl (+/+) to determine genotype and allele-specific expression of the INS and IGF2 genes. RESULTS: INS/Pstl (+/+) and IGF2/Apal (+/-) were observed in 36 (97.3%) of 37 IDDM patients and in 29 (72.5%) of 40 IDDM patients, respectively. The presence of both IGF2 alleles in RNA was observed in 21 (91.6%) of 24 IDDM patients. Our results show a 3-fold increase in RNA expression from Pstl (+/-) allele over Pstl (+/+) allele. CONCLUSION: Our conclusion does not entirely exclude IGF2 as the gene involved in IDDM2, even though the parental effect of IDDM2 transmission is not related to IGF2 maternal imprinting. The INS genotype appeared mostly in the Pstl (+/+) homozygote and, therefore, we could not explain the INS imprinting pattern in Korean type 1 diabetic patients. Genetic differences between populations may account for the discrepancy between Korean type I diabetic patients and American or French type I diabetic patients.