The use of portable blood glucose meters (PBGM) has become common in veterinary medicine as a rapid means of monitoring animals' blood glucose in a variety of medical conditions. These hand-held monitors allow for diagnostic and therapeutic decisions to be made quickly and relatively inexpensively using only a small amount of blood. Both in conditions resulting in hyperglycemia, such as diabetes mellitus, and in those resulting in hypoglycemia, such as sepsis or the presence of an insulinoma, veterinarians have come to rely on PBGM to provide critical information on the status of their animal patients. In particular, PBGM are frequently used to measure individual blood glucose values in an animal over a period to create a blood glucose curve when evaluating the effectiveness of insulin therapy in diabetic dogs and cats.

Accurate assessment of diabetic patients requires cooperation between owners and veterinarians as well as evaluation of all data, including resolution of clinical signs, serial blood glucose levels, and possibly serum glycosylated protein concentrations. in evaluating serial blood glucose curves, both the duration of action and nadir of glucose concentration must be assessed and changes in insulin dose or frequency made accordingly. Glycosylated protein concentrations may help determine the adequacy of ongoing control. Development of hypoglycemia or hyperglycemia in a previously well-controlled patient suggests a change in either endogenous or exogenous factors, and a cause should be determined. Hypoglycemia should he avoided and treated aggressively if it does occur. If insulin resistance is present, the cause should be delineated and removed if possible.

Diabetes mellitus can be particularly frustrating for veterinarians and clients. Weight management plays a large role in diabetes control, but the recommended high-fiber foods can be unpalatable and are associated with other adverse effects. Rotation of diets and other solutions may help to avoid these problems. Deciding whether to use insulin or hypoglycemic agents can be difficult. Glipizide, vanadium, chromium, and acarbose are oral hypoglycemic agents that may be tried as therapy.

A blinded, multicenter, prospective clinical trial assessed the effects of enalapril (EN) versus standard care in dogs with naturally occurring, idiopathic glomerulonephritis (GN). Twenty-nine adult dogs with membranous (n = 16) and membranoproliferative (n = 13) GN were studied. Dogs were randomly assigned to receive either EN (0.5 mg/kg PO q12-24h; n = 16) or placebo (n = 14) for 6 months (1 dog was treated first with the placebo and then with EN). All dogs were treated with low-dose aspirin (0.5-5 mg/kg PO q12-24h) and fed a commercial diet. At baseline, serum creatinine (SrCr), systolic blood pressure (SBP), and glomerular histologic grade were not different between groups, but the urine protein/creatinine ratio (UP/C) was greater in the EN group compared with the placebo group (8.7 +/- 4.4 versus 4.7 +/- 2.3). After 6 months of treatment, the change in UP/C from baseline was significantly different between groups (EN = -4.2 +/- 1.4 versus 1.9 +/- 0.9 in the placebo group). When data were adjusted for changes in SrCr (SrCr X UP/C) a similar significant reduction was noted ( 2.2 +/- 15.2 versus 8.4 +/- 10.1). The change in SBP after 6 months of treatment also was significantly different between groups (EN = -12.8 +/- 27.3 versus 5.9 +/- 21.5 mm Hg in the placebo group). Response to treatment was categorized as improvement (assigned a value of 2), no progression (assigned a value of 1), and progression (assigned a value of 0). Response was significantly better in the EN group (1.4 +/- 0.8) compared with the placebo group (0.3 +/- 0.5). These results suggest that EN treatment is beneficial in dogs with naturally occurring idiopathic GN.

Objective-To describe the clinicopathologic characteristics of dogs with hyperadrenocorticism and concurrent pituitary and adrenal tumors.Design-Retrospective study.Animals-17 client-owned dogs.Procedure-Signalment, response to treatment, and results of CBC, serum biochemical analysis, urinalysis, endocrine testing, and histologic examinations were obtained from medical records of dogs with hyperadrenocorticism and concurrent adrenal and chromophobe pituitary tumors.Results-On the basis of results of adrenal function tests and histologic examination of tissue specimens collected during surgery and necropsy, concurrent pituitary and adrenal tumors were identified in 17 of approximately 1,500 dogs with hyperadrenocorticism. Twelve were neutered females, 5 were males (3 sexually intact, 2 neutered); and median age was 12 years (range, 7 to 16 years). Hyperadrenocorticism had been diagnosed by use of low-dose dexamethasone suppression tests and ACTH stimulation tests. During high-dose dexamethasone suppression testing of 16 dogs, serum cortisol concentrations remained high in 11 dogs but decreased in 5 dogs. Plasma concentrations of endogenous ACTH were either high or within the higher limits of the reference range (12/16 dogs), within the lower limits of the reference range (2/16), or low (2/16). Adrenal lesions identified by histologic examination included unilateral cortical adenoma with contralateral hyperplasia (10/17), bilateral cortical adenomas (4/17), and unilateral carcinoma with contralateral hyperplasia (3/17). Pituitary lesions included a chromophobe microadenoma (12/17), macroadenoma (4/17), and carcinoma (1/17).Clinical Implications-Pituitary and adrenal tumors can coexist in dogs with hyperadrenocorticism. resulting in a confusing mixture of test results that may complicate diagnosis and treatment of hyperadrenocorticism.

Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation DS Greco; Insulin therapy in cats. J Am Anim Hosp Assoc 1 July 1999; 35 (4): 269–270. doi: https://doi.org/10.5326/15473317-35-4-269 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search

The use of oral hypoglycemic agents for the treatment of noninsulin-dependent diabetes mellitus (NIDDM) is still in its infancy. The purpose of this article is to summarize the current knowledge regarding the use of oral hypoglycemic agents in cats. Oral hypoglycemic therapy is more successful when the veterinarian is aware of the mechanism of action of the drug, as well as its dosage, side effects, and drug interactions. A short section on combining insulin with oral hypoglycemics and monitoring therapy with oral hypoglycemic agents is also included.

Addisonian crisis is well-recognized endocrine emergency in small animals. Electrolyte abnormalities consisting of severe hyponatremia and hypochloremia associated with hyperkalemia are the hallmarks of hypoadrenocorticism. This article describes the corticotropin stimulation lest used to confirm hypoadrenocorticism and the management of addisonian crisis. Pulmonary thromboembolism can occur secondary to hyperadrenocorticism and is often fatal. Treatment consists of oxygen therapy and medical management to prevent the formation of more blood clots. Thyrotoxic crisis might occur in cats with thyrotoxicosis. Therapy for the crisis consists of efforts to inhibit hormone synthesis and release and to antagonize adrenergically mediated aspects of peripheral thyroid hormone action. Myxedema coma can be a complication of hypothyroidism in dogs. Therapy should be initiated immediately (before the diagnosis is confirmed) and should consist of intravenous administration of levothyroxine. Supportive care may be indicated. Slow, passive rewarming should be considered only after thyroid hormone supplementation. Hypocalcemia requires prompt treatment, which rapidly resolves clinical signs. Calcitriol can be given to prevent hypocalcemia in patients undergoing thyroidectomy. Initial treatment of hypercalcemia includes fluid diuresis. Management depends on the cause.

Objective-Comparison of diagnostic accuracy of results of low-dose dexamethasone suppression (LDDS) and ACTH stimulation tests with necropsy findings in 81 dogs.Design-Retrospective study.Animals-81 dogs that had undergone screening tests for hyperadrenocorticism and that had a complete necropsy report.Procedure-Medical records were evaluated for results of CBC, serum biochemical analysis, urinalysis, endocrine testing, signalment, treatment, and necropsy findings. Each dog was definitively classified as having true-positive, true-negative, false-positive, or false-negative results. Statistical analyses included determination of prevalence, apparent prevalence, accuracy, number of dogs misclassified, sensitivity, specificity, and positive- and negative-predictive values.Results-Of the 81 dogs that fit the criteria for selection, 40 (49%) were confirmed as having hyperadrenocorticism (30 had pituitary-dependent disease and 10 had adrenal gland tumors). Forty-one dogs had illnesses attributable to a cause other than disease of the adrenal glands. Sensitivity of ACTH stimulation and LDDS tests were 95 and 96%, respectively. Specificity for the ACTH stimulation test was higher (91%) than that of the LDDS test (70%). When prevalence of the disease in the study population was taken into consideration, the positive-predictive value for the ACTH stimulation test was 91%, compared with 76% for the LDDS test.Clinical Implications-The ACTH stimulation test was more specific than the LDDS test, although sensitivity was similar for both tests. The ACTH stimulation test also had a significantly higher positive-predictive value than the LDDS test when a prevalence of 25% was taken into consideration.

Pancreatic disorders often cause emergencies in small animal practice. The most common of these emergencies is diabetic ketoacidosis. As insulin deficiency culminates in diabetic ketoacidosis, ketones and lactic acid accumulate in the blood, and electrolytes and water are lost via urine. The result is profound dehydration, hypovolemia, metabolic acidosis, and shock. This article presents a four-step protocol for the management of diabetic ketoacidosis: fluid therapy with 0.9% saline, insulin therapy (low-dose intramuscular or intravenous), electrolyte supplementation (potassium and magnesium), and reversal of metabolic acidosis. Hyperosmolar nonketotic syndrome may also occur in diabetic cats or dogs. Treatment of this condition is difficult. Fluid therapy should be approached cautiously, and low doses of insulin should be used. Hypoglycemic seizures can result from various causes. Treatment consists at a slow intravenous bolus of 50% dextrose. If no vein is readily available, corn syrup or pancake syrup can be applied to the oral mucous membranes. Long-term management of hypoglycemia depends on the cause.

Platelet aggregation in response to collagen (1 or 3 micrograms/ml), arachidonic acid (10(-2) M), and adenosine diphosphate (ADP, 2 microM) was compared in healthy cats treated with diltiazem (approximately 2 mg/kg body weight, q 8 hrs for 10 doses), aspirin (approximately 21 mg/kg body weight [1 baby aspirin], q 72 hrs for three doses), or a combination of diltiazem and aspirin. Baseline values obtained prior to treatment served as controls. Addition of arachidonic acid to blood resulted in an impedance change (i.e., aggregation) with time in samples from the nontreated cats and the cats treated with diltiazem, but the addition had no effect in blood from cats treated with aspirin alone or with a combination of diltiazem and aspirin. Platelet aggregation in response to either concentration of collagen or to ADP was not altered by any treatment. Secretion of adenosine triphosphate (ATP) from the platelets was measured when the aggregating agent was 3 micrograms/ml collagen; secretion was not affected by any treatment.

OBJECTIVE:To evaluate the protective effects of dietary n-3 fatty acid supplementation versus treatment with a thromboxane synthetase inhibitor (TXSI) in dogs given high-dose gentamicin.DESIGN:Clinicopathologic and renal histopathologic changes induced by gentamicin (10 mg/kg of body weight, IM, q 8 h, for 8 days) were compared in dogs fed an n-3 fatty acid-supplemented diet containing a fatty acid ratio of 5.7:1 (n-6:n-3), dogs treated with CGS 12970 (a specific TXSI given at 30 mg/kg, PO, q 8 h, beginning 2 days prior to gentamicin administration), and control dogs. The TXSI-treated and control dogs were fed a diet with a fatty acid ratio of 51.5:1 (n-6:n-3). Both diets were fed beginning 42 days prior to and during the 8-day course of gentamicin administration.ANIMALS:Eighteen 6-month-old male Beagles, 6 in each group.RESULTS:After 8 days of gentamicin administration, differences existed among groups. Compared with n-3-supplemented and control dogs. TXSI-treated dogs had higher creatinine clearance. Both TXSI-treated and n-3-supplemented dogs had higher urinary prostaglandin E2 and E3 (PGE2/3) and 6-keto prostaglandin F1a (PGF1a) excretion, compared with control dogs. Urinary thromboxane B2 (TXB2) excretion was higher in n-3-supplemented and control dogs, compared with TXSI-treated dogs. Urine PGE2/3-to-TXB2 and PGF(in)-to-TXB2, ratios were increased in TXSI-treated dogs, compared with n-3-supplemented and control dogs, and these ratios were increased in n-3-supplemented dogs, compared with control dogs. In addition, TXSI-treated and n-3-supplemented dogs had lower urinary protein excretion, compared with control dogs. Proximal tubular necrosis was less severe in TXSI-treated dogs, compared with control dogs.CONCLUSION:Treatment with CGS 12970 prior to and during gentamicin administration prevented increases in urinary TXB2 excretion and reduced nephrotoxicosis.CLINICAL RELEVANCE:Increased renal production/excretion of thromboxane is important in the pathogenesis of gentamicin-induced nephrotoxicosis.

OBJECTIVE:To determine the pharmacokinetics of gentamicin sulfate in healthy llamas after i.v. administration of a single bolus and after repeated parenteral administration.DESIGN:Prospective clinical trial.ANIMALS:19 clinically normal, adult male llamas for the single-dose trial and 10 of the 19 llamas for the multiple-dose trial.PROCEDURE:In the first trial, llamas were given gentamicin (5 mg/kg of body weight, i.v.) as a single bolus, and serum gentamicin concentration was monitored over the next 48 hours. 2 months later, llamas were given gentamicin (2.5 mg/kg) i.v. for the first day, then IM every 8 hours for 7 days. Serum gentamicin concentration and indices of renal function and damage were monitored during the 7 days.RESULTS:There were no significant dose- or time-related differences in clearance of the drug; volume of distribution; apparent coefficients of the distribution and elimination phases, alpha and beta, respectively; mean residence time; or distribution (t1/2 alpha) and elimination phase (t1/2 beta) half-lives. The 5 mg/kg i.v. kinetic study revealed t1/2 alpha of 14.5 +/- 5.06 minutes and t1/2 beta of 166 +/- 20.5 minutes. The 2.5 mg/kg i.v. kinetic study revealed t1/2 alpha of 17.7 +/- 6.59 minutes and t1/2 beta of 165 +/- 40.3 minutes. Peak serum gentamicin concentration averaged 10.10 micrograms/ml in the multiple-dose trial, and trough concentration averaged 1.50 micrograms/ml.CONCLUSIONS:Dose effects were not observed for gentamicin clearance, volume of distribution, or half-lives. Multiple dosing at 2.5 mg/kg every 8 hours does not appear to cause renal impairment in healthy llamas.CLINICAL RELEVANCE:Gentamicin pharmacokinetic variables in llamas appear to resemble those in other ruminant species.

Hypertrophic cardiomyopathy is the most common acquired heart disease in the cat. Middle-aged to older male castrated cats are most commonly affected. Clinical signs associated with hypertrophic cardiomyopathy are usually attributable to decreased left ventricular diastolic filling and myocardial ischemia with resultant heart failure. Radiography, echocardiography, and electrocardiography are important tools used for the diagnosis of hypertrophic cardiomyopathy. Calcium channel blockers represent a new mode of treatment that may reverse the pathogenesis of hypertrophic cardiomyopathy in addition to improving clinical signs. Arterial thromboembolism is a complication occurring in up to 50% of cats with hypertrophic cardiomyopathy and remains extremely difficult to treat.

Objective-To assess factors associated with development of hospital-acquired acute renal failure (HARF) and to determine outcome of and prognostic indicators for dogs with HARF.Design-Retrospective case series.Animals-29 dogs.Results-The most common inciting causes for development of HARF were exposure to a nephrotoxicant and advanced age. Mortality was 62%, and factors that contributed to mortality were age and initial urine output. Dogs greater than or equal to 7 years old and dogs that were initially oliguric had an odds ratio of mortality of 8.8 and 20, respectively. The effect of preexisting heart disease on mortality approached significance (P = 0.053). The magnitude of azotemia at the time of diagnosis was not related to the chance for survival. Dogs that died had a significantly higher initial anion gap and serum phosphorus concentration than did dogs that survived. We did not detect a relationship between cause of HARF and outcome (survived vs died or euthanatized).Clinical Implications-In most cases, HARF is associated with a poor outcome. Older dogs may be at increased risk for development of HARF, and once HARF has developed, have a greater chance of dying. Prognosis can not be determined on the magnitude of azotemia al the time of diagnosis or on the inciting cause of HARF.

Insulin therapy is the most important treatment aspect of diabetes mellitus. Since the discovery of insulin in 1921, a variety of insulin formulations have been developed. The purpose of this article is to describe the current sources, formulations, and types of insulins available for therapy of diabetes mellitus in small animals and to provide the veterinarian with guidelines for insulin therapy in dogs and cats.

The correlation between 24-hour urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) and gamma-glutamyl transferase (GGT) with urine NAG and GGT/creatinine ratios was assessed in dogs with gentamicin-induced nephrotoxicosis. Eighteen 6-month-old male Beagles with normal renal function were randomly divided into 3 groups of 6. Each group was fed a different concentration of protein (high protein, 27.3%; medium protein, 13.7%; and low protein, 9.4%) for 21 days. After dietary conditioning, gentamicin was administered at a dose of 10 mg/kg IM tid for 8 days and each group was continued on its respective diet. Endogenous creatinine clearance and 24-hour urinary excretion of NAG and GGT were determined after dietary conditioning (day 0) and on days 2, 4, 6, and 8 of gentamicin administration. In addition, urine NAG and GGT/creatinine ratios (IU/L divided by mg/dL) were determined from catheterized spot urine samples obtained between 7 and 10 AM on the same days. The correlation between 24-hour urinary enzyme excretion and urine enzyme/creatinine ratio in the spot urine samples was evaluated by simple linear regression analysis. Spot sample urine enzyme/creatinine ratios were significantly correlated with 24-hour urinary enzyme excretion through day 4 for dogs on low dietary protein, through day 6 for those on medium protein, and through day 8 for those on high dietary protein. Mean +/- SD baseline values for urine NAG/creatinine ratio and 24-hour urinary NAG excretion were 0.06 +/- 0.04 and 0.19 +/- 0.14 IU/kg/24 hr, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Eighteen, six-month-old male Beagles with normal renal function were randomly divided into three groups of 6. Each group was fed a diet that was similar except for protein content (high = 26%, medium = 13% and low = 9%, all on an as fed basis) throughout the experimental period. After a 21 day dietary protein conditioning period (including a terminal 2 day testing period), gentamicin was administered at a dosage of 10 mg/kg q. 8 h for 8 days. The first dose on days 1 and 7 was administered i.v. and all others were given i.m. Pharmacokinetic parameters were determined using blood samples collected over an 8 h period following the i.v. dose on day 1. The elimination rate constant was calculated on days 1 and 7. The data best fit a two-compartment open model for all dogs on day 1. The volume of distribution was higher and the clearance greater in the high protein group compared to the other two groups. No difference was found in the rate of elimination between days 1 and 7 for the high protein group; however, in the medium and low protein groups the rate of elimination decreased over the 7 days of treatment. Therefore, high dietary protein prior to and during gent-amicin administration induced faster gentamicin clearance and a larger volume of distribution and preserved the ability to eliminate gentamicin in dogs with normal renal function.

Exogenous creatinine clearance rate was determined in 8 partially (approx 75%) nephrectomized dogs fed 2 concentrations of dietary sodium, beginning 9 weeks after partial nephrectomy was performed. In a double crossover design, dogs were then fed low-sodium diet (0.18% sodium on a dry-weight basis) or high-sodium diet (1.3% sodium on a dry-weight basis) in 2 sequences (L/H/L or H/L/H) for 3 consecutive 4-week observation periods. Glomerular filtration rate (GFR) was measured by exogenous creatinine clearance before and after partial nephrectomy, and every 2 weeks during the experimental diet periods. Initial mean +/- SD GFR (3.76 +/- 0.78 ml/min/kg of body weight) decreased precipitously after nephrectomy (1.25 +/- 0.45 ml/min/kg); however, during the postnephrectomy and experimental diet periods, GFR gradually increased in all dogs to nearly half the prenephrectomy values (1.87 +/- 0.22 ml/min/kg). Significant differences in GFR were not observed when dogs were fed the L/H/L or the H/L/H sequence. Therefore, it was concluded that abrupt changes from high dietary sodium (1.3%) to restricted dietary sodium (0.18%), or vice versa, does not cause deterioration of renal function in dogs with moderate renal impairment. However, caution should be used in extrapolating these findings to dogs with clinically evident (azotemia, isosthenuria) renal failure.