Diabetes mellitus bei der Katze: Ein Überblick

Reusch, Claudia E; Tschuor, F; Kley, Saskia; Boretti, Felicitas S; Sieber-Ruckstuhl, N.

doi:10.1024/0036-7281.148.3.130

Cited by 5 publications

(1 citation statement)

References 15 publications

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“…There are less commonly reported cases of primary hypoadrenocorticism in cats caused by trauma15 or primary adrenal lymphoma 11 12. Secondary hypoadrenocorticism is due to a pituitary insufficiency with decreased ACTH secretion resulting in insufficient glucocorticoid production, while mineralocorticoid secretion is not affected.…”

Section: Discussionmentioning

confidence: 99%

Hypoadrenocorticism in two cats successfully treated with desoxycorticosterone pivalate

Reimann¹,

Siol²,

Schlüter³

et al. 2018

Vet Rec Case Rep

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Two cats were presented with lethargy and anorexia. Clinically, the cats showed hypothermia and dehydration. Blood examination in both cats showed hyponatraemia, hyperkalaemia and additionally azotaemia in case 1 and hypercalcaemia in case 2. In both cats, an adrenocorticotropic hormone (ACTH) stimulation test showed an insufficient stimulation of the adrenal glands. In case 1, markedly elevated endogenous ACTH was additionally measured. Both cats were successfully treated with a combination of desoxycorticosterone pivalate (DOCP) and prednisolone (0.15 mg/kg daily). Case 1 received a final concentration of 2.6 mg/kg DOCP every 30 days, while case 2 was successfully managed with 2.2 mg/kg every 28 days. These rare cases of feline hypoadrenocorticism demonstrate that DOCP can be used similarly as in dogs.

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Section: Discussionmentioning

confidence: 99%

Hypoadrenocorticism in two cats successfully treated with desoxycorticosterone pivalate

Reimann¹,

Siol²,

Schlüter³

et al. 2018

Vet Rec Case Rep

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Endocrine Pancreas in Cats With Diabetes Mellitus

et al. 2015

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Pancreatic amyloidosis and loss of α and β cells have been shown to occur in cats with diabetes mellitus, although the number of studies currently available is very limited. Furthermore, it is not known whether pancreatic islet inflammation is a common feature. The aims of the present study were to characterize islet lesions and to investigate whether diabetic cats have inflammation of the pancreatic islets. Samples of pancreas were collected postmortem from 37 diabetic and 20 control cats matched for age, sex, breed, and body weight. Histologic sections were stained with hematoxylin and eosin and Congo red; double labeled for insulin/CD3, insulin/CD20, insulin/myeloperoxidase, insulin/proliferating cell nuclear antigen, and glucagon/Ki67; and single labeled for amylin and Iba1. Mean insulin-positive cross-sectional area was approximately 65% lower in diabetic than control cats (P = .009), while that of amylin and glucagon was similar. Surprisingly, amyloid deposition was similar between groups (P = .408). Proliferation of insulin- and glucagon-positive cells and the number of neutrophils, macrophages, and T (CD3) and B (CD20) lymphocytes in the islets did not differ. The presence of T and B lymphocytes combined tended to be more frequent in diabetic cats (n = 8 of 37; 21.6%) than control cats (n = 1 of 20; 5.0%). The results confirm previous observations that loss of β cells but not α cells occurs in diabetic cats. Islet amyloidosis was present in diabetic cats but was not greater than in controls. A subset of diabetic cats had lymphocytic infiltration of the islets, which might be associated with β-cell loss.

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Exocrine Pancreas in Cats With Diabetes Mellitus

et al. 2015

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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 ¼ .002) in diabetic cats, particularly near islets (P < .001). Ki67-positive acinar cells were increased only near islets (P ¼ .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.

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Diabetes mellitus bei der Katze: Ein Überblick

Cited by 5 publications

References 15 publications

Hypoadrenocorticism in two cats successfully treated with desoxycorticosterone pivalate

Hypoadrenocorticism in two cats successfully treated with desoxycorticosterone pivalate

Endocrine Pancreas in Cats With Diabetes Mellitus

Exocrine Pancreas in Cats With Diabetes Mellitus

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