Histopathology and immunohistochemistry of pancreatic islets in fibrocalculous pancreatic diabetes

• Published in: Diabetes research and clinical practice 2001, Vol.51 (1), p.29-38
• Main Authors: Govindarajan, Meera, Mohan, Viswanathan, Deepa, Raj, Ashok, Sundararaman, Pitchumoni, Capecomarin S.
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Atrophy; Biological and medical sciences; Biopsy; Blood Glucose - analysis; Chronic Disease; Diabetes Mellitus - blood; Diabetes Mellitus - pathology; Diabetes. Impaired glucose tolerance; Endocrine pancreas; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Exocrine; Female; Fibrocalculous pancreatic diabetes; Gastrins - analysis; Glucagon - analysis; Humans; Hyperplasia; Immunohistochemistry; Insulin - analysis; Islets of Langerhans - pathology; Ketosis resistance; Male; Medical sciences; Middle Aged; Pancreas - pathology; Pancreatic Ducts - pathology; Pancreatic Polypeptide - analysis; Pancreatitis - blood; Pancreatitis - pathology; Pathology; Tropical chronic pancreatitis; Vasoactive Intestinal Peptide - analysis
• ISSN: 0168-8227; 1872-8227
• DOI: 10.1016/S0168-8227(00)00204-7

The histopathology of Fibrocalculous Pancreatic Diabetes (FCPD) has been extensively studied, but there are no reports on alteration in patterns of hormone secreting cells using immunohistochemistry in islets of FCPD patients. In this study, we report on the histopathology and immunohistochemistry of islets of FCPD patients and its possible correlation with the clinical picture. Pancreatic biopsies were carried out in six patients with FCPD at the time of surgery for abdominal pain. Routine histopathology and immunohistochemistry studies were carried out with six primary antibodies namely insulin, glucagon, pancreatic polypeptide (PP), somatostatin, vasoactive intestinal peptide and gastrin. Histopathology of the pancreas showed a spectrum of changes ranging from moderate to severe atrophy, fibrosis of the parenchyma and degeneration of the ducts. Nesidioblastosis was present in three patients. Immunohistochemical studies showed a decrease in the number of islets but some patients showed evidence of hyperplasia. There was an overall decrease in the percent of insulin cells and the positivity in the islets correlated with plasma C-peptide levels and the duration of diabetes. There was no consistent relationship with glucagon with some patients showing increased and other decreased positivity. There was a marked decrease in PP and somatostatin positivity, the significance of which is not clear. The reduction, but partial preservation of insulin positivity is consistent with the ketosis resistance shown by patients with Fibrocalculous Pancreatic Diabetes.