To date, only few studies characterized histopathological features of feline diabetic pancreas. The aim was the assessment of pancreatic lesions in diabetic cats, in comparison to a well-matched control population. Formalin-fixed, paraffin-embedded pancreatic samples were collected from post-mortem examination of 37 diabetic and 20 control cats, selected to be matched for age, sex, breed and body weight. Sections were stained with HE and Congo Red. Double-labeled immunohistochemistry was performed for: insulin/myeloperoxidase, insulin/CD3, insulin/CD20, insulin/PCNA, glucagon/Ki-67. Cell counting and morphometric analysis were performed manually and with software, respectively. Data were analyzed with contingency tables and t-tests. The mean insulin-positive cross sectional area was 40% lower in diabetic than control cats (P<0.01), that of glucagon was similar. Compared to control, the amount of islet amyloid in diabetic cats, based on cross-sectional analysis of the islets, was similar. Proliferation of insulin and glucagon positive cells and the average counts of inflammatory cells in the islets did not differ between groups. The presence of (T and B) lymphocytes, in general, tended to be more frequent in diabetic (21.6%) than control cats (5%), as well as an increased presence of necrosis and fibrosis (P=0.07) Proliferation of acinar cells was 3-fold higher in diabetic cats (P<0.01), notably nearby islets (6-fold, P<0.001). The results confirm previous observations that loss of β-cells occurs in diabetic cats. In addition, a subset of diabetic cats shows islets lymphocytic infiltration that might have contributed to β-cell loss. Necrosis and fibrosis of the exocrine tissue may suggest a concurrent pancreatitis. Finally, evidence of an increased proliferation rate of acinar cells, as reported in humans, could be associated with chronic pancreatitis as well as with transdifferentiation into islet cells.
Detection of Cytomegalovirus-related gastrointestinal tract lesions in a series of 45 xenotransplanted primates
CAVICCHIOLI, LAURA;ZANETTI, ROSSELLA;FERRARESSO, SERENA;DE BENEDICTIS, GIULIA MARIA;Emanuele Cozzi
2013
Abstract
To date, only few studies characterized histopathological features of feline diabetic pancreas. The aim was the assessment of pancreatic lesions in diabetic cats, in comparison to a well-matched control population. Formalin-fixed, paraffin-embedded pancreatic samples were collected from post-mortem examination of 37 diabetic and 20 control cats, selected to be matched for age, sex, breed and body weight. Sections were stained with HE and Congo Red. Double-labeled immunohistochemistry was performed for: insulin/myeloperoxidase, insulin/CD3, insulin/CD20, insulin/PCNA, glucagon/Ki-67. Cell counting and morphometric analysis were performed manually and with software, respectively. Data were analyzed with contingency tables and t-tests. The mean insulin-positive cross sectional area was 40% lower in diabetic than control cats (P<0.01), that of glucagon was similar. Compared to control, the amount of islet amyloid in diabetic cats, based on cross-sectional analysis of the islets, was similar. Proliferation of insulin and glucagon positive cells and the average counts of inflammatory cells in the islets did not differ between groups. The presence of (T and B) lymphocytes, in general, tended to be more frequent in diabetic (21.6%) than control cats (5%), as well as an increased presence of necrosis and fibrosis (P=0.07) Proliferation of acinar cells was 3-fold higher in diabetic cats (P<0.01), notably nearby islets (6-fold, P<0.001). The results confirm previous observations that loss of β-cells occurs in diabetic cats. In addition, a subset of diabetic cats shows islets lymphocytic infiltration that might have contributed to β-cell loss. Necrosis and fibrosis of the exocrine tissue may suggest a concurrent pancreatitis. Finally, evidence of an increased proliferation rate of acinar cells, as reported in humans, could be associated with chronic pancreatitis as well as with transdifferentiation into islet cells.
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