A study of pancreatic function among subjects over ninety years of age.

BACKGROUND: Among the various studies of pancreatic function in the elderly published so far, none have dealt with subjects over 90 years of age. The aim of this study was to examine pancreatic function in healthy individuals over 90 years old. METHODS: Sixty-eight healthy noninstitutionalized elderly persons, aged 91-104 years, with a mean age of 95 years, and 63 younger controls were studied. Pancreatic function was studied by determining fecal elastase 1 concentration. In addition to this test, we also measured serum amylase, pancreatic isoamylase and lipase in 53 of the 68 elderly subjects. RESULTS: All but 1 of the 68 elderly subjects had normal elastase 1 values; the one who did not had a value slightly below normal. No significant difference with controls was found. Serum pancreatic enzymes were normal in almost all of the 53 elderly studied; 3 had a mild elevation only of amylase and 1 had a persistent elevation of amylase, pancreatic isoamylase and lipase. CONCLUSIONS: In subjects over 90 years of age, exocrine pancreatic function continues to be normal; if an impairment occurs, it is mild and not significant for digestion of food. In addition, serum pancreatic enzymes remain within normal limits in the vast majority of cases.

Magnetic resonance cholangiopancreatography in asymptomatic pancreatic hyperenzymemia.

OBJECTIVES: To determine the type and frequency of pancreatic lesions detected by magnetic resonance cholangiopancreatography (MRCP) in subjects with asymptomatic pancreatic hyperenzymemia and to assess for a possible relationship between these lesions and the hyperenzymemia. METHODS: From January 2005 to May 2008, 63 subjects with asymptomatic pancreatic hyperenzymemia were studied by MRCP. In addition, amylase, pancreatic isoamylase, and lipase were determined for 5 consecutive days. RESULTS: In most subjects (n = 57, 90.5%), MRCP showed a normal pancreas. In the remaining 6 subjects (9.5%), the following alterations were found: pancreas divisum in 2, small intrapancreatic cyst in 2, anatomic variant of the Wirsung in 1, and mild dilatation of 3 secondary ducts in 1. In these 6 subjects, hyperenzymemia was highly variable from day to day, with frequent normalizations, as was also true for the 30 subjects with no MRCP alterations in whom diurnal enzyme determinations were made. CONCLUSIONS: Most of the subjects with asymptomatic pancreatic hyperenzymemia did not have pancreatic lesions detectable by MRCP. In the few subjects in whom a lesion was found, the great variability and the frequent transient normalization of serum enzyme levels tend to exclude a relation between the lesion and the hyperenzymemia.

[Benign pancreatic hyperenzynemia or Gullo's syndrome]. / Iperenzimemia pancreatica benigna o sindrome di Gullo.

Benign pancreatic hyperenzymemia is a newly identified syndrome characterized by abnormal increase in serum pancreatic enzymes in absence of pancreatic disease. The hyperenzymemia can occur sporadically or in a familial form, and all of the pancreatic enzymes show elevations. Although the condition is persistent, the enzyme elevations fluctuate considerably, even temporarily returning to normal levels at times. In this paper the main characteristics of this syndrome are described.

SPINK1 and PRSS1 mutations in benign pancreatic hyperenzymemia.

UNLABELLED: The aim of this study was to determine whether mutations in SPINK1/PRSS1 genes are associated with benign pancreatic hyperenzymemia (BPH). METHODS: Sixty-eight subjects with BPH (including 13 familial cases) were studied. In all, we sequenced germline DNA for all the exons and intro-exon boundaries of PRSS1 and SPINK1. RESULTS: Nine (13.2%) of the 68 subjects harbored PRSS1 or SPINK1 mutations. As to PRSS1, no hereditary pancreatitis-associated variant was detected, whereas previously undescribed mutations (p.Ala148Val and c.40+1G>A) were respectively found in 2 subjects (2.9%). SPINK1 mutations were detected in 7 subjects (10.3%). Five of them exhibited known mutations (3 p.Asn34Ser, 1 p.Pro55Ser, and 1 c.88-23A>T), whereas 2 had a newly found variant (p.Arg67Gly and c.*32C>T, respectively). Only 2 familial BPH, belonging to 2 different families, were found to carry a mutation (1 with p.Ala148Val for PRSS1 and 1 with p.Asn34Ser for SPINK1). CONCLUSIONS: No known mutations of PRSS1 have been found in BPH, whereas the frequency of known SPINK1 variants is similar to that reported in the general population. No segregation of PRSS1/SPINK1 variants occurs in BPH families. Benign pancreatic hyperenzymemia cannot be explained by mutations in genes whose variants are known to be associated with pancreatitis or by mutations in other PRSS1/SPINK1 genes.