Zini E, Ferro S, Lunardi F, Zanetti R, Heller R S, Coppola L M, Guscetti F, Osto M, Lutz T A, Cavicchioli L, Reusch C E
Clinic for Small Animal Internal Medicine, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland Department of Animal Medicine, Production, and Health, University of Padova, Legnaro, Italy Istituto Veterinario di Novara, Granozzo con Monticello, Italy
Department of Comparative Biomedicine and Food Sciences, University of Padova, Legnaro, Italy.
Vet Pathol. 2016 Jan;53(1):145-52. doi: 10.1177/0300985815603434. Epub 2015 Aug 28.
Pancreatitis has been described in cats with diabetes mellitus, although the number of studies currently available is very limited. In addition, ketoacidosis has been hypothesized to be associated with pancreatitis in diabetic cats. The aims of the present study were to investigate whether diabetic cats have pancreatitis and to determine if pancreatitis is more frequent with ketoacidosis. Samples of pancreas were collected postmortem from 37 diabetic cats, including 15 with ketoacidosis, and 20 control cats matched for age, sex, breed, and body weight. Sections were stained with hematoxylin and eosin, double-labeled for insulin/CD3, insulin/CD20, insulin/myeloperoxidase, insulin/PCNA, and glucagon/Ki67, and single-labeled for Iba1. A previously proposed semiquantitative score was used to characterize pancreatitis, along with counts of inflammatory cells. Scores of pancreatitis and the number of neutrophils, macrophages, and lymphocytes in the exocrine pancreas did not differ between diabetic and control cats or between diabetic cats with and without ketoacidosis. Of note, PCNA-positive acinar cells were increased (P = .002) in diabetic cats, particularly near islets (P < .001). Ki67-positive acinar cells were increased only near islets (P = .038). Ketoacidosis was not linked to proliferation. The results suggest that histopathologic evidence of pancreatitis may not be more frequent in diabetic cats and that ketoacidosis may not be associated with it at the time of death. Augmented PCNA-positive acinar cells might indicate increased proliferation due to chronic pancreatitis. The reason behind the prevalent proliferation of acinar cells surrounding pancreatic islets deserves further investigation.
胰腺炎在患有糖尿病的猫中已有描述，尽管目前可用的研究数量非常有限。此外，有人推测酮症酸中毒与糖尿病猫的胰腺炎有关。本研究的目的是调查糖尿病猫是否患有胰腺炎，并确定胰腺炎在酮症酸中毒时是否更常见。从37只糖尿病猫（包括15只患有酮症酸中毒的猫）以及20只年龄、性别、品种和体重匹配的对照猫身上在死后采集胰腺样本。切片用苏木精和伊红染色，进行胰岛素/CD3、胰岛素/CD20、胰岛素/髓过氧化物酶、胰岛素/增殖细胞核抗原（PCNA）和胰高血糖素/Ki67的双标记，以及离子钙结合衔接分子1（Iba1）的单标记。使用先前提出的半定量评分来表征胰腺炎，并对炎症细胞进行计数。糖尿病猫和对照猫之间，以及有和没有酮症酸中毒的糖尿病猫之间，胰腺炎评分以及外分泌胰腺中中性粒细胞、巨噬细胞和淋巴细胞的数量没有差异。值得注意的是，糖尿病猫中PCNA阳性腺泡细胞增加（P = .002），特别是在胰岛附近（P < .001）。Ki67阳性腺泡细胞仅在胰岛附近增加（P = .038）。酮症酸中毒与增殖无关。结果表明，糖尿病猫中胰腺炎的组织病理学证据可能并不更常见，并且酮症酸中毒在死亡时可能与之无关。PCNA阳性腺泡细胞增多可能表明由于慢性胰腺炎导致增殖增加。胰岛周围腺泡细胞普遍增殖的背后原因值得进一步研究。
