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- Author or Editor: Richard W. Nelson x
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Abstract
Objective—To evaluate the clinical features and heritability of naturally occurring hypoadrenocorticism in Nova Scotia Duck Tolling Retrievers (NSDTRs).
Design—Retrospective case series.
Animals—25 NSDTRs with hypoadrenocorticism.
Procedures—Questionnaires completed by owners of NSDTRs with hypoadrenocorticism and medical records from veterinarians were reviewed for information regarding diagnosis, age at diagnosis, concurrent diseases, age at death, and cause of death. Pedigrees were analyzed for heritability and mode of inheritance of hypoadrenocorticism (including complex segregation analysis of pedigrees of 1,515 dogs).
Results—On the basis of results of ACTH stimulation testing, hypoadrenocorticism was diagnosed in 16 female and 9 male NSDTRs (including 6 full siblings). Median age at diagnosis was 2.6 years; the diagnosis was made prior to 2 years of age in 11 dogs. Seventeen dogs had hyponatremia, hyperkalemia, or both, and serum electrolyte concentrations were within reference ranges for 8 dogs at the time of diagnosis. Median survival time after diagnosis for 4 dogs that died or were euthanized as a result of medical causes was 1.6 years. Heritability was calculated at 0.98 with no sex effect, and complex segregation analysis fit a major gene model with an autosomal recessive mode of inheritance.
Conclusions and Clinical Relevance—In NSDTRs, hypoadrenocorticism was diagnosed at an earlier age, compared with published reports of age at diagnosis among the general dog population. Among the study dogs, 32% had no serum electrolyte abnormalities at the time of diagnosis, and the disease appeared to have an autosomal recessive mode of inheritance in the breed.
Abstract
Objective—To evaluate effect of acarbose on control of glycemia in dogs with diabetes mellitus.
Design—Prospective randomized crossover controlled trial.
Animals—5 dogs with naturally acquired diabetes mellitus.
Procedure—Dogs were treated with acarbose and placebo for 2 months each: in 1 of 2 randomly assigned treatment sequences. Dogs that weighed ≤ 10 kg (22 lb; n = 3) or > 10 kg (2) were given 25 or 50 mg of acarbose, respectively, at each meal for 2 weeks, then 50 or 100 mg of acarbose, respectively, at each meal for 6 weeks, with a 1-month interval between treatments. Caloric intake, type of insulin, and frequency of insulin administration were kept constant, and insulin dosage was adjusted as needed to maintain control of glycemia. Serum glucose concentrations, blood glycosylated hemoglobin concentration, and serum fructosamine concentration were determined.
Results—Significant differences in mean body weight and daily insulin dosage among dogs treated with acarbose and placebo were not found. Mean preprandial serum glucose concentration, 8-hour mean serum glucose concentration, and blood glycosylated hemoglobin concentration were significantly lower in dogs treated with insulin and acarbose, compared with insulin and placebo. Semisoft to watery feces developed in 3 dogs treated with acarbose.
Conclusions and Clinical Relevance—Acarbose may be useful as an adjunctive treatment in diabetic dogs in which cause for poor glycemic control cannot be identified, and insulin treatment alone is ineffective. (J Am Vet Med Assoc 2000;216:1265–1269)
Objective
To determine magnesium (Mg) status in cats with naturally acquired diabetes mellitus (DM) and diabetic ketoacidosis (DKA), evaluate changes in Mg status after treatment for DKA, and correlate Mg status with systemic blood pressure and degree of glycemic control.
Design
Case series and cohort study.
Animals
12 healthy cats (controls), 21 cats with DM, and 7 cats with DKA.
Procedure
Serum total magnesium (tMg) and ionized magnesium (iMg) concentrations and spot urinary fractional excretion of magnesium (FEmg) were determined, using serum and urine samples obtained from all cats when they were entered in the study and from cats with DKA 12, 24, and 48 hours after initiating treatment. Indirect blood pressure and degree of glycemic control were determined in 10 and 21 cats with DM, respectively.
Results
Initially, 2 and 13 cats with DM and 1 and 4 cats with DKA had serum tMg and iMg concentrations, respectively, less than the low reference limit (mean — 2 SD) determined for controls. In cats with DKA, serum tMg concentration decreased significantly over time after initiating treatment. Urinary FEmg was significantly higher in cats with DM or DKA, compared with controls. Systemic hypertension was not detected nor was there a correlation between Mg status and degree of glycemic control in cats with DM.
Conclusions and Clinical Relevance
Hypomagnesemia was a common finding in cats with DM and DKA and was more readily identified by measuring serum iMg concentration than tMg concentration. The clinical ramifications of hypomagnesemia in such cats remain to be determined. (J Am Vet Med Assoc 1999;215:1455–1459)
Abstract
Objective
To evaluate the efficacy of using serum total and ionized magnesium (Mg) concentrations and urine Mg concentrations to identify Mg deficiency in cats.
Animals
6 healthy castrated male cats.
Procedure
A Mg-replete diet was fed for 37 days, followed by a Mg-deficient diet for 37 days. On days 1, 3, and 7 of the last week of each diet, serum ionized and total Mg concentrations were determined; in addition, urine Mg concentration was determined each day of the last week. Serum total and ionized Mg concentrations were compared with urine Mg concentration, amount of Mg excreted during 24 hours (24-hour urine Mg excretion), ratio of urine Mg concentration to urine creatinine concentration (Umg:Ucr), and urinary fractional excretion of Mg (FEmg) to determine which variable best predicted Mg status.
Results
Cats fed Mg-deficient diets had significantly lower serum total and ionized Mg concentrations and 24-hour urine Mg excretion values, compared with cats fed Mg-replete diets. Serum total Mg concentration was the best predictor of Mg status. Twenty-four-hour urine Mg excretion was a repeatable, reliable measurement and had the best correlation with serum total Mg concentration. Serum total Mg concentration also correlated with urine Mg concentration, Umg:Ucr, and FEmg.
Conclusions and Clinical Relevance
Serum total and ionized Mg concentrations can be used to identify cats with dietary-induced Mg deficiencies. Twenty-four-hour urine Mg excretion and urine Mg concentration correlated best with serum total Mg concentration and, therefore, may be the most useful urine variables for identifying Mg deficiency. (Am J Vet Res 1999;60:1159–1163)
Summary
Pituitary neoplasm was identified in 43 dogs with pituitary-dependent hyperadrenocorticism via necropsy (n = 33), diagnostic imaging with computerized tomography or magnetic resonance imaging (n = 5), or diagnostic imaging and necropsy (n = 5). All dogs had clinical signs and clinicopathologic test results typical of hyperadrenocorticism. Thirty-seven dogs had grossly visible pituitary tumors, and 6 dogs had microscopic pituitary tumors. Fifteen dogs had developed neurologic signs typical of those resulting from an enlarging pituitary mass. Twenty-three dogs had pituitary tumors ≥ 1 cm in diameter. Provocative testing of the pituitary-adrenocortical axis was performed on all dogs.
Dogs with grossly visible pituitary tumors and dogs with neurologic signs had Significantly (P < 0.05) higher mean plasma endogenous acth concentrations, compared with values from dogs with microscopic tumors and dogs without neurologic signs, respectively. Dogs with grossly visible pituitary tumors and dogs with tumors ≥ 1 cm in diameter had Significantly (P < 0.05) lower adrenocortical responsiveness to exogenous acth, compared with dogs with microscopic pituitary tumors and dogs with tumors < 1 cm in diameter, respectively. Despite these differences, there was overlap between test results among dogs. On the basis of endocrine test results, it would appear difficult to distinguish dogs with pituitary-dependent hyperadrenocorticism and large pituitary tumors from those with pituitary-dependent hyperadrenocorticism and microscopic pituitary tumors prior to onset of neurologic signs.
Summary:
The efficacy of microcrystalline desoxycorticosterone pivalate (docp) therapy was evaluated in 60 dogs with hypoadrenocorticism. Fifty-one of the dogs were being treated with either docp or fludrocortisone acetate prior to entering the study. The disease had been recently diagnosed in 9 dogs that were not under maintenance treatment prior to entering the study. Desoxycorticosterone pivalate (2.2 mg/kg of body weight, im) was administered on days 0, 25, and 50. Physical examination was performed, and blood samples were obtained for serum biochemical analysis (Na+, K+, and bun concentrations) on days 0, 14, 25, 39, 50, 64, and 75. On day 75 of the study, a final physical examination was performed and the course of treatment was evaluated.
Sixty-eight percent (41/60) of the dogs had normal physical findings on day 0 vs 87% (52/60) on day 75. Mean (±sd) body weight increased from 24.8 ± 12.7 kg on day 0 to 26.2 ± 13.7 kg on day 75. Mean serum Na+ (137.7 ± 8.5 mEq/L) and K+ (5.6 1.0 mEq/L) concentrations and Na+-to-K+ ratio (25.4 ± 5.0:1) were outside normal reference limits on day 0. By day 75, serum Na+ (144.3 ± 4.8 mEq/L) and K+ (4.9 ± 0.8 mEq/L) concentrations and Na+-to-K+ ratio (30.4 ± 5.1:1) were normal and were significantly (P < 0.01) improved, compared with the corresponding values on day 0.
Of the 60 dogs, 58 (97%) regained the loss in body weight, appetite, and muscular strength while given docp; once achieved, these improvements were maintained. These 58 dogs did not vomit or have diarrhea, common problems in dogs with hypoadrenocorticism. The mineralocorticoid (docp) alone was not adequate to correct all clinical signs associated with endogenous mineralocorticoid and glucocorticoid deficiencies, which are typical of hypoadrenocorticism in dogs. Thus, 22 of the 58 dogs had glucocorticoid-responsive clinical signs of disease (lethargy, n = 10; anorexia, n = 8; weakness and hypoadrenal crisis, n = 2 each). These signs resolved in response to initiation of glucocorticoid therapy (prednisolone, 2.5 mg/d, po) and/or adjustments in docp dose or dosing interval. Ten dogs developed polyuria, polydipsia, or both during the study; these signs improved when the dose of prednisolone (n = 9) or docp (n = 1) was reduced. All owners but 1 chose to continue docp therapy after the trial ended, and all dogs remained free of clinical signs associated with hypoadrenocorticism for at least 1 year after the study ended.
Objective
To evaluate use of urine cortisol-to-creatinine ratio (UC:C) as a means of monitoring response to long-term mitotane treatment in dogs with pituitary-dependent hyperadrenocorticism.
Design
Prospective uncontrolled study.
Animals
101 dogs with pituitary-dependent hyperadrenocorticism.
Procedure
Urine samples were obtained from dogs on the morning an ACTH stimulation test was performed, and owners were asked their opinion on the health of their dog to monitor response to mitotane treatment. Urine was assayed for cortisol and creatinine concentrations, and UC:C was calculated. The UC:C was compared with post-ACTH plasma cortisol concentration.
Results
Post-ACTH plasma cortisol concentration was used to categorize each dog's response to mitotane treatment. The UC:C did not correlate satisfactorily with results of ACTH stimulation testing. Twenty-seven of 85 (32%) dogs would have been incorrectly considered as having received appropriate doses using UC:C. In addition, 16 dogs that received overdoses could not be distinguished from 29 dogs that received appropriate doses.
Clinical Implications
UC:C does not provide a consistent, correct assessment of mitotane-induced adrenocortical destruction. The ACTH stimulation test, although more time-consuming and expensive, is recommended for monitoring response to mitotane treatment. (J Am Vet Med Assoc 1997;211:1002–1004)
Objective
To characterize glycosylated hemoglobin (GHb) concentrations in the blood of dogs with disorders that may affect serum glucose or blood GHb concentrations, and to determine whether changes in GHb concentration correlate with changes in control of diabetes in dogs.
Design
Prospective study.
Animals
63 healthy dogs, 9 dogs with anemia, 24 dogs with untreated hyperadrenocorticism, 12 dogs with pancreatic β-cell neoplasia, 23 dogs with newly diagnosed diabetes mellitus, and 77 diabetic dogs treated with insulin.
Procedure
Control of diabetes in dogs treated with insulin was classified as good or poor on the basis of history, physical examination findings, changes in body weight, and measurement of serum glucose concentrations. Sequential evaluations of control were performed and GHb concentration in blood was measured, by means of affinity chromatography, for 5 untreated diabetic dogs before and after initiating insulin treatment, for 10 poorly controlled diabetic dogs before and after increasing insulin dosage, and for 5 diabetic dogs before and after pancreatic islet cell transplantation.
Results
Mean (± SD) GHb concentration was 3.3 ± 0.8% in the blood of healthy dogs. Compared with results from healthy dogs, mean GHb concentration was significantly lower in the blood of dogs with anemia and pancreatic β-cell neoplasia and significantly higher in the blood of untreated diabetic dogs. Mean GHb concentration was significantly higher in the blood of 46 poorly controlled diabetic dogs, compared with 31 well-controlled diabetic dogs (7.3 ± 1.8 vs 5.7 ± 1.7%, respectively). Mean GHb concentration in blood decreased significantly in 5 untreated diabetic dogs after treatment (8.7 ± 1.9 vs 5.3 ± 1.9%). Mean GHb concentration in blood also decreased significantly in 10 poorly controlled diabetic dogs after control was improved and in 5 diabetic dogs after they had received a pancreatic islet cell transplant.
Clinical Implications
Measurement of GHb concentration in blood may assist in monitoring control of diabetes in dogs. (J Am Vet Med Assoc 1997; 211:723–727)
Objective—
To determine prevalence and severity of systemic arterial hypertension and proteinuria in dogs with naturally developing diabetes mellitus (DM) and to determine whether these abnormalities were related to age, sex, duration of DM, or degree of control of glycemia.
Design—
Case series and cohort study.
Animals—
Fifty dogs with naturally developing DM.
Procedures—
Blood pressure was measured in all 50 dogs. Thirty-eight dogs were evaluated once, and 12 were evaluated sequentially. Thirty-five were evaluated for proteinuria by determining protein-to-creatinine ratio in urine (n = 35) or by electrophoresis of urine (33).
Results—
Hypertension was detected in 23 on the basis of a systolic pressure > 160 mm HG (12 dogs), a diastolic pressure > 100 mm HG (21), or a mean pressure > 120 mm HG (23). All dogs with systolic hypertension had concurrent diastolic and mean hypertension, and 19 of 21 dogs with diastolic hypertension had concurrent high mean pressure. Ten of 12 dogs reevaluated at subsequent visits had no change in blood pressure. Blood pressure remained consistent in 3 dogs tested at different times during the day on a single visit. Duration of DM and presence of proteinuria were significant predictors of hypertension. Seven of 35 (20%) dogs had an increased protein-to-creatinine ratio in their urine. Albumin concentration and albumin-to-creatinine ratio were significantly higher in urine from diabetic dogs, compared with healthy, nondiabetic dogs. Hypertension was associated with an increased albumin-to-creatinine ratio.
Clinical Implications—
Systemic hypertension and proteinuria may be common in diabetic dogs, but the clinical importance of these findings are, as yet, unknown. (J Am Vet Med Assoc 1998;213:822-825)
Objective—
To determine clinical signs, clinicopathologic abnormalities, prevalence of concurrent disease, treatment, complications of treatment, and outcome in cats with diabetic ketosis (DK) or diabetic ketoacidosis (DKA).
Design—
Retrospective study.
Animals—
42 cats with DK or DKA.
Procedure—
Medical records of diabetic cats with ketonuria were reviewed.
Results—
In 26 cats, diabetes was newly diagnosed; in 16, diabetes had been diagnosed previously and cats had been treated with insulin (n = 14) or sulfonylurea drugs (2). Common clinical findings were lethargy, anorexia, polyuria, polydipsia, and weight loss. Common laboratory findings were hyperglycemia, hyponatremia, hypochloremia, hypokalemia, hypocalcemia, hypophosphatemia, low total CO2 content, hyperosmolality, high serum alanine transaminase activity, azotemia, glycosuria, and ketonuria. Concurrent disorders were identified in 39 cats and included hepatic lipidosis, cholangiohepatitis, pancreatitis, chronic renal failure, urinary tract infection, and neoplasia. Treatment of DK and DKA included administration of regular crystalline (34 cats), NPH (6), or ultralente (2) insulin, intravenous (38) or subcutaneous (4) administration of fluids, and enterall parenteral or administration of antibiotics (42). Complications during treatment included abnormalities in serum electrolyte concentrations (27 cats), hemolytic anemia (4), hypoglycemia (3), and neurologic abnormalities unrelated to hypoglycemia (2). Eleven cats died or were euthanatized during the initial hospitalization period for treatment of DK or DKA. Azotemia, metabolic acidosis, and hyperosmolality were more severe in cats that died than in cats that survived. Differences in regard to treatment or complications were not apparent between cats that died and cats that survived. The 31 cats that survived were discharged 1 to 16 days (median, 5 days) after initiation of insulin treatment. Diabetic ketosis or ketoacidosis recurred in 13 (42%) of these cats.
Clinical Implications—
A thorough diagnostic evaluation should be performed on cats with DK or DKA to identify concurrent disorders, formulate an appropriate treatment plan, and provide prognostic information to the owner. (J Am Vet Med Assoc 1997;211: 188–192)
