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Objective
To evaluate use of an assay for measuring serum concentration of canine thyroid-stimulating hormone (cTSH) as an aid for diagnosing thyroid disease in a population of dogs suspected of having hypothyroidism.
Design
Case-cohort study.
Animals
62 healthy dogs and 49 dogs with clinical signs consistent with hypothyroidism (16 were hypothyroid and 33 were euthyroid with concurrent disease).
Procedure
Samples from healthy dogs were used to establish a reference range for serum cTSH concentration. The 49 dogs were categorized as hypothyroid or euthyroid with concurrent disease on the basis of clinical signs, results of additional diagnostic and thyroid-stimulating hormone (TSH) response tests, and response to administration of levothyroxine sodium. Function of the thyroid gland was considered normal when serum total thyroxine (T4) concentration 6 hours after TSH administration was > 2.5 µg/dl. Hypothyroidism was diagnosed when serum T4 concentration after TSH administration was ≤ 1.5 µg/dl.
Results
Serum cTSH concentration differed significantly among all 3 groups. Four of 33 (12%) euthyroid dogs had cTSH concentrations that were greater than the reference range, whereas 6 of 16 (38%) hypothyroid dogs had cTSH concentrations within the reference range. Specificity for serum cTSH concentration was 0.88 and sensitivity was 0.63. When interpreted in combination with serum T4 concentration, specificity increased to 1.0.
Clinical Implications
cTSH assay had good specificity for use in the diagnosis of hypothyroidism in dogs. Because this assay had low sensitivity, a diagnosis of hypothyroidism could not be excluded on the basis of a serum cTSH concentration that was within the reference range. (J Am Vet Med Assoc 1998; 212:387-391)
Objective
To compare outcome of surgical versus medical treatment of dogs with beta cell neoplasia.
Design
Retrospective study.
Animals
39 dogs with clinical signs of hypoglycemia and serum glucose and insulin concentrations consistent with a diagnosis of beta cell neoplasia.
Procedure
Information on signalment; clinical history; physical examination findings; results of CBC, serum biochemical analyses, and urinalysis; serum glucose and insulin concentrations; results of thoracic radiography and abdominal ultrasonography; treatment and treatment complications; survival time; and cause of death were obtained from medical records.
Results
26 dogs underwent exploratory celiotomy and partial pancreatectomy; 13 dogs were treated medically (ie, dietary change and prednisone). Median survival time was significantly longer for dogs treated surgically than for dogs treated medically. Significant differences were not found in mean age, body weight, duration of clinical signs prior to diagnosis, serum glucose and insulin concentration, or results of other serum biochemical tests between dogs treated surgically and dogs treated medically; also, there was no significant correlation between any of these parameters and survival time for either group of dogs.
Conclusions and Clinical Relevance
Results suggest that exploratory celiotomy and partial pancreatectomy are indicated once a tentative diagnosis of beta cell neoplasia is established in dogs. (J Am Vet Med Assoc 1999;215:226–230)
Objective
To correlate serum fructosamine concentrations with established measures of glycemic control and to compare serum fructosamine and blood glycosylated hemoglobin (GHb) concentrations as a means for assessing glycemic control in diabetic cats.
Design
Longitudinal cohort study.
Animals
26 healthy cats, 5 cats with stress-induced hyperglycemia, 15 untreated diabetic cats, and 36 treated diabetic cats.
Procedure
Control of glycemia was classified and monitored and serum fructosamine and blood GHb concentrations were measured for 12 poorly controlled diabetic cats before and after improving glycemic control, 8 well-controlled treated diabetic cats before and after glycemic control deteriorated, and 5 cats with diabetes mellitus before and after onset of stress-induced hyperglycemia.
Results
Mean serum fructosamine and blood GHb concentrations were significantly higher in untreated diabetic cats, compared with healthy cats, and in 24 poorly controlled diabetic cats, compared with 12 well-controlled diabetic cats. Mean serum fructosamine and blood GHb concentrations decreased significantly in 12 poorly controlled diabetic cats after improving glycemic control and increased significantly in 8 well-controlled diabetic cats after glycemic control deteriorated. A significant stress-induced increase in mean blood glucose concentration was evident 12 hours after insulin administration, but not in 5 docile diabetic cats that became fractious.
Clinical Implications
Serum fructosamine and blood GHb concentrations are clinically useful tools for monitoring control of glycemia in cats with diabetes mellitus. (J Am Vet Med Assoc 1999;214:1794-1798)
Objective
To evaluate the effect of a high insolublefiber (HF) diet containing 12% cellulose in dry matter and a low insoluble-fiber (LF) diet on control of glycemia in dogs with naturally acquired insulin-dependent diabetes mellitus.
Design
Prospective randomized crossover controlled trial.
Animals
11 dogs with naturally acquired diabetes mellitus.
Procedure
Dogs were fed HF and LF diets for 8 months each in 1 of 2 randomly assigned diet sequences. Caloric intake and insulin treatment were adjusted as needed to maintain stable body weight and control of glycemia, respectively. After a 2-month adaptation period, control of glycemia was evaluated every 6 weeks for 6 months. Variables assessed included serum glucose concentration measured during the preprandial state, blood glycosylated hemoglobin concentration, serum glucose concentration measured every 2 hours for 24 hours beginning at the time of the morning insulin injection, 24-hour mean serum glucose concentration, mean serum glucose concentration fluctuation from the 24-hour mean serum glucose concentration, and 24-hour urinary excretion of glucose.
Results
Significant differences in mean daily caloric intake, body weight, or daily insulin dosage among dogs fed HF and LF diets were not found. Mean preprandial serum glucose concentration, most postprandial serum glucose concentrations, 24-hour mean serum glucose concentration, and 24-hour urinary excretion of glucose were significantly lower in dogs fed the HF diet, compared with the LF diet.
Clinical Implications
Results of this study support feeding of commercially available insoluble fiber diets to dogs with naturally acquired diabetes mellitus. (J Am Vet Med Assoc 1998; 212:380-386)
Objective—
To determine prevalence and severity of systemic arterial hypertension and proteinuria in dogs with naturally developing hyperadrenocorticism and to determine whether these abnormalities resolve with adequate management of the disease.
Design—
Case series and cohort study.
Animals—
77 dogs with naturally developing hyperadrenocorticism examined once; 15 dogs examined before and after treatment.
Results—
Among dogs examined only once, hypertension was diagnosed in 21 of 26 dogs with untreated pituitary-dependent hyperadrenocorticism (PDH), 17 of 21 with inadequately controlled PDH, 8 of 16 with well-controlled PDH, 10 of 10 with an untreated adrenocortical tumor, and 0 of 4 that had undergone adrenalectomy because of an adrenocortical tumor. Untreated dogs and dogs with inadequately controlled PDH had significantly higher blood pressures than did other dogs. Proteinuria was documented in 12 of 26 dogs with untreated PDH, 5 of 16 with inadequately controlled PDH, 3 of 14 with well-controlled PDH, 5 of 8 with an untreated adrenocortical tumor, and 1 of 3 that had undergone adrenalectomy. Dogs with untreated PDH and dogs with an untreated adrenocortical tumor had higher urine protein/creatinine ratios than did dogs with well-controlled PDH. Among dogs evaluated before and after treatment, blood pressure and urine protein/creatinine ratio did not change in 8 dogs with inadequately controlled hyperadrenocorticism, but decreased in 7 dogs with well-controlled disease.
Clinical Implications—
Results suggest that systemic hypertension and proteinuria are common in dogs with untreated hyperadrenocorticism and that successful treatment of hyperadrenocorticism will result in resolution of these abnormalities in many, but not all, dogs. (J Am Vet Med Assoc 1996;209:1724–1729)
Objective—
To compare a technique in which samples obtained from selected venous sites are analyzed for parathyroid hormone (PTH) concentration versus usefulness of cervical ultrasonography for localizing primary hyperparathyroidism (PHP) in dogs.
Design—
Prospective study.
Animals—
12 dogs with PHP.
Procedure—
For each dog, blood samples were collected from the left and right jugular veins and 1 cephalic vein for determination of serum PTH concentration. Ultrasonography of the neck was performed in each dog. Each dog underwent exploratory surgery of the neck. Abnormal appearing parathyroid tissue was removed. Dogs were included in the study if serum calcium concentration decreased within 12 hours after surgery, hypercalcemia completely resolved within 96 hours after surgery, and serum calcium concentration was maintained within the reference range for at least 6 months after surgery.
Results—
Serum PTH concentrations from the 3 veins were similar in 11 of 12 dogs with PHP. In 1 dog, the serum PTH concentration from the jugular vein ipsilateral to a parathyroid adenoma was greater than that from the contralateral jugular or cephalic vein. Ultrasonography correctly identified a parathyroid mass and its location in 10 of 11 dogs with a solitary abnormal parathyroid gland and in 1 dog in which both parathyroid glands were enlarged.
Clinical Implications—
Surgeons may benefit from knowing the location of abnormal parathyroid tissue in dogs with PHP before surgical exploration. Ultrasonography has potential value for identifying and localizing abnormal parathyroid tissue, whereas sample collection from selected sites for PTH analysis is not likely to be helpful. (J Am Vet Med Assoc 1997;211:54–56)
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)
Summary
The value of magnetic resonance imaging (MRI) for the evaluation of dogs with pituitary-dependent hyperadrenocorticism (pdh) and cns signs was assessed. Magnetic resonance imaging of the brain was performed in 13 dogs with pdh and neurologic signs. The diagnosis of pdh was made on the basis of results of adrenocortical function tests and abdominal ultrasonography, in conjunction with appropriate history, clinical signs, and clinicopathologic alterations. Eight dogs had been treated with the adrenocorticolytic agent, mitotane, for 1 to 30 months before the development of neurologic signs.
Prior to mri, each dog had progressive neurologic signs that could not be attributed to hypocortisolism or mitotane toxicosis. The neurologic signs most frequently detected were disorientation and ataxia. Mean age of dogs at the time neurologic signs developed was 9.5 years. Sex predilection was not detected; however, most were large-breed dogs, with 11 of the 13 dogs weighing more than 20 kg.
A large mass in the pituitary gland, suprasellar region, or both was easily identified on the magnetic resonance images of each dog. The masses ranged from 8 to 24 mm in size. Expansion of tumors into the suprasellar region and compression of structures adjacent to the pituitary gland were readily detected by MRI. Contrast enhancement did not improve tumor identification, but did enable better delineation between tumor and surrounding structures.
After the diagnosis of a macrotumor was made by MRI, radiotherapy was initiated in 9 dogs and was successfully completed in 6. Three dogs had a relapse of neurologic signs 8, 11, and 26 months after radiotherapy was completed. Three dogs are alive 8, 15, and 32 months after radiotherapy. Postmortem examinations performed on 7 dogs confirmed the diagnosis of pituitary macroadenomas. In 4 dogs, postmortem examination was performed within 1 month of MRI, providing a means to substantiate results. Magnetic resonance imaging provided accurate information on tumor size and the extent of tumor expansion into the surrounding structures.
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 evaluate magnetic resonance imaging (MRI) brain scans of dogs with pituitary-dependent hyperadrenocorticism (PDH) and no signs of CNS dysfunction 1 year after diagnosis and initial MRI.
Design
Prospective study of surviving dogs from a previous study.
Animals
13 dogs underwent MRI of the brain at the time that PDH was diagnosed and prior to treatment. At that time, none of the dogs had clinical signs suggestive of an intracranial mass. Approximately 1 year after diagnosis and MRI, the brain was again evaluated by MRI.
Results
On the initial MRI scan, 5 of the 13 dogs had normal findings, and 8 had evidence of a mass (tumor) in the area of the pituitary gland. Of the 5 dogs that had no visible pituitary mass on the initial MRI scan, 3 had a normal MRI brain scan 1 year later. Of the 5 dogs that had no visible pituitary mass on initial MRI scan, 2 had a visible pituitary mass at 1 year. The 8 dogs that had a visible mass on the initial MRI brain scan had easily identified pituitary masses on the second MRI scan. Of these 8 dogs, 4 had no apparent change in pituitary mass size, and 4 had obvious increase in vertical height of the pituitary mass. Of the 4 dogs, 2 developed signs of neurologic dysfunction within 1 year after diagnosis of PDH, presumably attributable to that mass. Of the 13 dogs, 12 were treated with mitotane soon after completion of the initial MRI scan. Sensitivity to mitotane and initial pituitary mass size or growth were not correlated. Of the 13 dogs evaluated initially and 1 year after diagnosis, 10 had pituitary masses identified on MRI brain scans.
Clinical Implications
The incidence of visible pituitary masses among dogs with PDH at the time of or within a year of diagnosis was > 75%. In 2 dogs, signs of CNS dysfunction developed within 1 year of PDH diagnosis when pituitary masses were ≥ 10 mm. (J Am Vet Med Assoc 1996;208: 1268–1273)
