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- Author or Editor: Richard W. Nelson x
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Abstract
Objective—To determine ultrasonographic characteristics of the thyroid gland in healthy small-, medium-, and large-breed dogs and evaluate the relationships of thyroid gland size and volume with body weight and body surface area (BSA).
Animals—72 dogs of small (6 Toy and 6 Miniature Poodles), medium (12 Beagles), and large breeds (12 Akitas and 36 Golden Retrievers).
Procedure—Each dog's thyroid gland was examined ultrasonographically with a 10- to 5-MHz multifrequency linear-array transducer. Size, shape, echogenicity, and homogeneity of thyroid lobes were evaluated on longitudinal and transverse images. Thyroid lobe volume was estimated by use of the equation for an ellipsoid (π/6 [length × height × width]).
Results—Thyroid lobes appeared fusiform or elliptical on longitudinal images and triangular or round to oval on transverse images. In most dogs, thyroid lobes were hyperechoic or isoechoic, compared with surrounding musculature, and had a homogeneous echogenic pattern. Mean length, width, height, and volume of thyroid lobes were significantly greater in Akitas and Golden Retrievers, compared with findings in Beagles or Poodles; mean length, width, and height were significantly greater in Beagles, compared with findings in Poodles. Total thyroid gland volume correlated with body weight (r = 0.73) and BSA (r = 0.74).
Conclusions and Clinical Relevance—Among the dog breeds examined ultrasonographically, thyroid lobe size and volume were more variable than shape, echogenicity, and homogeneity. The correlation of thyroid gland volume with BSA suggests that size of the dog, rather than breed, should be considered when assessing thyroid glands ultrasonographically.
Abstract
Objective—To compare aesthesiometer-determined corneal sensitivity between diabetic and nondiabetic dogs and to investigate the correlation between corneal sensitivity and duration of diabetes or status of glycemic control, as estimated by use of glycated blood protein concentrations.
Animals—23 diabetic and 29 nondiabetic normoglycemic dogs.
Procedure—A Cochet-Bonnet aesthesiometer was used to measure corneal touch threshold (CTT) in 5 corneal regions of each dog. At the time of ocular examination, duration of diabetes mellitus was estimated from the history, and blood was drawn for assessment of blood glycosylated hemoglobin and serum fructosamine concentrations.
Results—Median CTT for central, nasal, dorsal, temporal, and ventral corneal regions in nondiabetic dogs (1.6, 2.3, 2.8, 2.8, and 5.1 g/mm2, respectively) was significantly lower than in diabetic dogs (2.8, 4.0, 5.1, 5.1, and 6.6 g/mm2, respectively). Median regional CTT in diabetic dogs was not significantly correlated with estimated duration of diabetes mellitus or blood glycated protein concentrations. No significant difference was found in regional CTT between eyes of normoglycemic dogs with unilateral cataracts.
Conclusion and Clinical Relevance—Diabetic dogs have significantly reduced corneal sensitivity in all regions, compared with nondiabetic normoglycemic dogs. Regional variation in corneal sensitivity is similar in diabetic and normoglycemic dogs. Neither glycemic control nor duration of diabetes, as estimated, is significantly correlated with corneal hyposensitivity. Corneal nerve dysfunction may be associated with recurrent or nonhealing ulcers in diabetic dogs for which no other underlying cause can be found. (Am J Vet Res 2003;64:7–11)
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
Serum glucose and immunoreactive insulin concentrations were monitored after topical administration of an insulin-containing ophthalmic solution in 20 clinically normal cats. Three ophthalmic surface-acting agents, benzalkonium chloride, dimethyl sulfoxide, and proparacaine hydrochloride, were evaluated individually for their effectiveness in enhancing absorption of topically applied insulin. The ophthalmic effects of insulin-containing ophthalmic preparations were assessed by complete ophthalmic examination before and at the conclusion of each test period. Withholding of food overnight (12 hours) preceded each topical application of insulin-containing ophthalmic solution (12.25 to 26.4 U/cat), either alone or in combination with surface-acting agents, after which blood samples were drawn serially from an indwelling iv catheter over a period of 8 hours. Baseline serum insulin concentration, after food was withheld for 12 hours, in nonstressed cats was 6.0 μU/ml (geometric mean), and an exponentiation of the logarithmic quantity (mean ± sd) yielded values of 1.5 to 23.0 μU/ml. All ophthalmic solutions tested failed to significantly lower serum glucose concentration or increase serum insulin concentration. Solutions used did not induce deleterious effect on ocular structures. Results indicate that topical administration of insulin-containing ophthalmic solution, either alone at the concentrations used or in combination with surfaceacting agents, did not result in effective absorption of insulin across the conjunctival and lacrimal nasal mucosa in biologically relevent quantities. Thus, this route of insulin administration, under these specific conditions, is not an effective alternative or adjunct to SC administration of insulin for treatment of cats with insulin-dependent diabetes mellitus or severe noninsulin-dependent diabetes mellitus.
Summary
Outcome of and complications associated with bilateral adrenalectomy in 8 cats with pituitary-dependent hyperadrenocorticism and bilateral adrenocortical hyperplasia and outcome of and complications associated with unilateral adrenalectomy in 2 cats with adrenocortical tumor (adrenocortical adenoma, 1 cat; adrenocortical carcinoma, 1 cat) and unilateral adrenomegaly were determined. Glucocorticoids were administered to all cats at the time of surgery, and mineralocorticoids were administered to the 8 cats that underwent bilateral adrenalectomy. A ventral midline celiotomy was performed in all cats.
Intraoperative complications did not develop in any cat. Postoperative complications developed in all cats and included abnormal serum electrolyte concentrations (n = 8), skin lacerations (n = 5), pancreatitis (n = 3), hypoglycemia (n = 2), pneumonia (n = 1), and venous thrombosis (n = 1). Three cats died within 5 weeks after surgery of complications associated with sepsis (n = 2) or thromboembolism (n = 1). Clinical signs and physical abnormalities caused by hyperadrenocorticism resolved in the remaining 7 cats 2 to 4 months after adrenalectomy. Insulin treatment was discontinued in 4 of 6 cats with diabetes mellitus. Median survival time for these 7 cats was 12 months (range, 3 to > 30 months). Two cats died of acute adrenocortical insufficiency 3 and 6 months after bilateral adrenalectomy, 2 cats were euthanatized because of chronic renal failure 3 and 12 months after bilateral (n = 1) or unilateral (n = 1) adrenalectomy, and 2 cats were alive 9 and 14 months after bilateral adrenalectomy. In the remaining cat, clinical signs recurred 10 months after the cat had undergone unilateral adrenalectomy. The remaining adrenal gland was found to contain an adrenocortical adenoma and was removed. The cat was doing well when it was lost to follow-up 15 months after the second surgery.
Objective—
To assess clinical signs, biochemical findings, results of modified water deprivation and other diagnostic tests, response to treatment, and survival time in dogs with central diabetes insipidus (CDI).
Design—
Retrospective study.
Animals—
20 dogs with CDI.
Procedure—
Signalment, history, physical examination, results of diagnostic tests, response to treatment, and survival time were extracted from the medical record of each dog and supplemented with information obtained from owners via telephone.
Results—
Isosthenuria or hyposthenuria was a consistent finding. Seven dogs with complete CDI and 13 dogs with partial CDI were identified on the basis of results of a modified water deprivation test. Dogs treated with desmopressin acetate responded well to treatment. Seven dogs were alive 18 to 72 months (median, 36 months) after diagnosis, and 10 dogs died or were euthanatized 1 week to 2 years (median, 2 months) after diagnosis. Seven of 10 dogs that died developed neurologic signs after diagnosis of CDI. Computed tomography revealed a mass in the region of the pituitary gland in 5 of 7 dogs. Necropsy of 6 dogs, including 2 dogs on which computed tomography had been performed, revealed neoplasia in the pituitary gland.
Clinical Implications—
Onset of neurologic signs after diagnosis of CDI in middle- to old-aged dogs indicates that CDI may not be a benign disease that is treated easily. Brain imaging is recommended after diagnosis of CDI in middle- to old-aged dogs. Also, because many dogs are isosthenuric on initial examination, CDI cannot be ruled out as a cause of polyuria and polydipsia on the basis of lack of hyposthenuria. (J Am Vet Med Assoc 1996;209:1884–1888)
Objective
To determine whether measuring change in serum thyroid-stimulating hormone (TSH) concentration in response to thyrotropin-releasing hormone (TRH) administration can be used as a test of thyroid function in dogs suspected of having hypothyroidism.
Design
Case-cohort study.
Animals
13 healthy dogs, 20 hypothyroid dogs, and 18 euthyroid dogs with concurrent diseases.
Procedure
Blood samples were collected before and 30 minutes after TRH administration, and serum TSH concentration was measured. The 13 healthy dogs were used to establish a reference range for change in TSH concentration after TRH administration. The remaining 38 dogs were categorized as hypothyroid or euthyroid on the basis of baseline total thyroxine (T4) and TSH concentrations, T4 concentration 4 hours after TRH administration, and clinical response to administration of sodium levothyroxine.
Results
Median baseline TSH concentration was 0.25 ng/ml (range, 0.03 to 0.44 ng/ml) in healthy dogs, 0.93 ng/ml (0.21 to 3.5 ng/ml) in hypothyroid dogs, and 0.21 ng/ml (0.03 to 0.63 ng/ml) in euthyroid dogs with concurrent diseases. Median percentage change in TSH concentration after TRH administration was 207% (range, 25 to 2,200%) in healthy dogs, 24% (-21 to 134%) in hypothyroid dogs, and 167% (69 to 1,800%) in euthyroid dogs with concurrent diseases. Overall accuracy of using the TRH-induced change in TSH concentration to identify hypothyroid dogs was 90%.
Clinical Implications
Although percentage change in TSH concentration in response to TRH administration can be used to differentiate euthyroid from hypothyroid dogs, the test has little advantage over measurement of baseline TSH and total or free T4concentration. (J Am Vet Med Assoc 1998;213:1435-1438)
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.
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The most common cause of naturally developing acromegaly in cats is a growth hormone-secreting adenoma of the pituitary pars distalis somatotropic cells.
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Irradiation of pituitary gland tumors in cats with acromegaly may result in transient or long-term resolution of acromegaly and diabetes mellitus.
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Diabetic cats with acromegaly may have a history of weight loss instead of weight gain.
Summary
The purpose of this study was to determine the sensitivity of dogs with hyperadrenocorticism to treatment with the adrenocorticolytic agent mitotane. Specifically, we looked for differences in response to treatment using this drug in dogs with adrenocortical tumors (adrenal tumor hyperadrenocorticism, ath) vs those with pituitary-dependent hyperadrenocorticism (pdh). For inclusion in this study, each dog must have had clinical signs, data base laboratory abnormalities, and endocrine screening test results consistent with the diagnosis of hyperadrenocorticism. Further, each dog had to have been treated for at least 6 months with mitotane and have histologic evidence for adrenocortical or pituitary neoplasia (all dogs were necropsied). Thirteen dogs with ath (8 carcinomas, 5 adenomas) were identified. The ages and body weights of these 13 dogs were computer-matched to 13 dogs with pdh. All dogs were initially treated with approximately 50 mg of mitotane/kg/d of body weight. Reexaminations were performed after 7, 30, 90, and 180 days of treatment.
Individual dosages varied widely after the initial 5 to 12 days of treatment. The mean (± sd) dose of mitotane (mg/kg/d) for the first 7 days of treatment was 47.5 ± 9.4 for dogs with ath vs 45.7 ± 11.9 for dogs with pdh. The mean plasma cortisol concentrations 1 hour after acth administration at the 7-day recheck were significantly higher in dogs with ath (502 ± 386 nmol/L) than in dogs with pdh (88 ± 94 nmol/L). At 30 days, the mean daily dose of mitotane and post-acth cortisol concentration were significantly greater in dogs with ath (28.8 ± 15.4 mg/kg/d; 392 ± 356 nmol/L, respectively) than in dogs with pdh (10.5 ± 7.5 mg/kg/d; 99 ± 72 nmol/L, respectively). After 90 days of treatment, these values were larger (25.3 ± 16.8 mg/kg/d; 340 ±193 nmol/L in dogs with ath vs those in dogs with pdh (5.4 ± 2.5 mg/kg/d, 110 ± 94 nmol/L) and again after 180 days (26.0 ± 22.1 mg/kg/d, 268 ± 152 nmol/L in dogs with ath vs 6.3 ± 3.4 mg/kg/d, 80 ± 116 nmol/L in dogs with pdh). Clinical signs were consistent with laboratory values, that is, cortisol control was not as good in dogs with ath as in the dogs with pdh. On the basis of these findings, we suggest that dogs with hyperadrenocorticism caused by ath are more resistant to mitotane than are dogs with pdh.