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E C Feldman

Publications and source records attributed to E C Feldman.

129 records · Page 8Linked to original sources
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Frequency and risk factors for urinary tract infection in cats with diabetes mellitus.

BACKGROUND: Identification and control of infections are important in the management of diabetic cats. Urinary tract infections have not been well characterized in diabetic cats. This retrospective study was performed to review and characterize urinary tract infections in diabetic cats. HYPOTHESIS: Urinary tract infections are common in diabetic cats. ANIMALS: A review was made of the medical records of 141 diabetic cats that had had urine obtained for culture by antepubic cystocentesis and that had not been treated with antibiotics, undergone urinary tract catheterization or urinary tract surgery within 2 weeks of urine collection or had urethral obstruction at the time of urine collection. METHODS: A review of medical records. RESULTS: Urinary tract infection was identified in 18 of 141 diabetic cats. Escherichia coli was the most common isolate (67%). Female cats were at increased risk (prevalence odds ratios [POR], 3.7; 95% confidence interval [CI], 1.3 to 10.2; P = .013). Clinical signs of lower urinary tract disease and findings on urine sediment examination were good predictors of positive urine cultures. CONCLUSIONS AND CLINICAL IMPORTANCE: Urinary tract infections are common in diabetic cats regardless of status of diabetic control, suggesting routine monitoring with urine sediment exams or urine culture is warranted.

Animals↗
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Subcutaneous administration of desoxycorticosterone pivalate for the treatment of canine hypoadrenocorticism.

Twelve dogs with hypoadrenocorticism were treated with subcutaneous desoxycorticosterone pivalate (DOCP). Eight of these dogs were recently diagnosed and had not yet been treated. Four dogs previously had been diagnosed and treated (three with intramuscular DOCP, one with oral fludrocortisone acetate). History, physical examination, serum electrolytes, and blood urea nitrogen (BUN) were evaluated. Desoxycorticosterone pivalate (2.2 mg/kg body weight) was administered every 25 days. On day 0, recently diagnosed dogs had a median serum sodium concentration of 131.5 mEq/L, median serum potassium concentration of 6.6 mEq/L, and median BUN of 41.5 mg/dl. All subsequent median serum electrolyte and BUN concentrations were normal. All previously treated dogs had normal blood values which were maintained throughout the study.

Adrenal Insufficiency↗
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Transient clinical diabetes mellitus in cats: 10 cases (1989-1991).

Medical records of 10 cats with transient clinical diabetes mellitus were reviewed. At the time diabetes was diagnosed, clinical signs included polyuria and polydipsia (10 cats), weight loss (8 cats), polyphagia (3 cats), lethargy (2 cats), and inappetence (1 cat). Mean (+/- SD) fasting blood glucose concentration was 454 +/- 121 mg/dL, mean blood glucose concentration during an 8-hour period (MBG/8 hours) was 378 +/- 72 mg/dL, and glycosuria and trace ketonuria were identified in 10 and 5 cats, respectively. Baseline serum insulin concentration was undetectable (6 cats) or within the reference range (4 cats) and serum insulin concentration did not increase after i.v. glucagon administration in any cat. Insulin-antagonistic drugs were being administered to 5 cats and concurrent disorders were identified in all cats. Management of diabetes included administration of glipizide (6 cats), insulin (3 cats), or both (1 cat), discontinuation of insulin-antagonistic drugs, and treatment of concurrent disorders. Insulin and glipizide treatment was discontinued 4-16 weeks (mean, 7 weeks) after the initial diagnosis of diabetes was confirmed. At the time treatment for diabetes was discontinued, clinical signs had resolved, mean fasting blood glucose concentration was 102 +/- 48 mg/dL, MBG/ 8 hours was 96 +/- 32 mg/dL, glycosuria and ketonuria were not identified in any cat, and concurrent disorders (except mild renal insufficiency in 1 cat) had resolved. Significant (P < .05) increases occurred in postglucagon serum insulin concentrations, insulin peak response, and total insulin secretion, compared with values obtained when clinical diabetes was diagnosed. Histologic abnormalities were identified in pancreatic islets of 5 cats in which pancreatic biopsies were obtained and included decreased number of islets (4 cats), islet amyloidosis (3 cats), and vacuolar degeneration of islet cells (3 cats). Mean beta cell density was significantly (P < .001) decreased in diabetic cats compared with control cats (1.4 +/- 0.7 versus 2.6 +/- 0.5%, respectively). Cells within islets stained positive for insulin, however, the number of insulin-staining cells per islet and the intensity of insulin staining were decreased in 5 and 2 cats, respectively. Clinical diabetes had not recurred in 1 cat after 6 years, in 4 cats lost to follow-up after 1.5, 1.5, 2.0, and 2.5 years, and in 2 cats that died 6 months and 5.5 years after clinical diabetes resolved. Clinical diabetes recurred in 3 cats after 6 months, 14 months, and 3.4 years, respectively. These findings suggest that cats with transient clinical diabetes have pancreatic islet pathology, including decreased beta cell density, and that treatment of diabetes and concurrent disorders results in improved beta cell function, reestablishment of euglycemia, and a transition from a clinical to subclinical diabetic state.

Animals↗