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The objectives of this study were to determine which serum thyroid hormone test best identifies iatrogenic hypothyroidism in cats that develop azotaemia after radioiodine treatment and to determine which thyroid test best differentiates these azotaemic, hypothyroid cats from azotaemic, radioiodine-treated euthyroid cats, as well as from azotaemic cats with chronic kidney disease and no history of thyroid disease.A total of 42 hyperthyroid cats that developed azotaemia (serum creatinine ê220 µmol/L) after radioiodine treatment had serum concentrations of thyroxine and free thyroxine by dialysis and thyroid--stimulating hormone measured at 3, 6 and 12 months. Iatrogenic hypothyroidism was confirmed (n=28) or excluded (n=14) on the basis of thyroid scintigraphy. A total of 14 cats with chronic kidney disease and 166 clinically normal cats underwent similar serum thyroid testing and scintigraphy.Concentrations of thyroxine and free thyroxine were lower and thyroid-stimulating hormone higher in hypothyroid cats than in all three groups of euthyroid cats (P0·0001). Of the hypothyroid cats, thyroxine and free thyroxine concentrations were low in 15 (53·6%) and seven (25%), respectively. Low serum thyroxine and free thyroxine concentrations were also detected in seven (50%) and two (14·3%) of the cats with chronic kidney disease. Thyroid-stimulating hormone concentrations were elevated in all hypothyroid cats but remained within the reference interval in all three groups of euthyroid cats. Serum thyroid--stimulating hormone had a higher test sensitivity and specificity than either thyroxine or free thyroxine concentration.The finding of high serum thyroid-stimulating hormone concentrations best identifies feline iatrogenic hypothyroidism and differentiates it from non-thyroidal illness syndrome in cats that develop azotaemia after treatment.

Microbiological and chemical changes were determined during the smoking and drying of salmon strips processed at 29 to 318C for 4 days at a facility in Alaska in 1993. During the process, Staphylococcus aureus populations increased to more than 10 5 CFU/g after 2 to 3 days of processing. Subsequent laboratory studies showed that a pellicle (dried skinlike surface) formed rapidly on the strips when there was rapid air circulation in the smokehouse and that bacteria embedded in or under the pellicle were able to grow even when heavy smoke deposition occurred. Under these conditions, an inoculum of 26 CFU/ g of S. aureus increased to 10 5 CFU/g after 3 days of processing. Elimination of preprocess drying and reduction in air e ow during smoking resulted in smoke deposition before pellicle formation and enabled the product to reach levels of water-phase salt and water activity that inhibit the growth of S. aureus and Listeria monocytogenes. In 1994, these modie cations were then applied during processing at an Alaskan facility, and S. aureus could not be detected in the e nished product. L. monocytogenes was detected in the raw product area, on the processing tables, and on the raw salmon strips, but it was not detected in the e nished product when the smoke was applied before pellicle formation. Smoking and drying are among the oldest methods of food preservation. Even though we have had considerable experience with these processes, food poisoning outbreaks occasionally occur. Improperly processed products and the lack of understanding that some products may become hazardous if they are stored at temperatures that permit the growth of microbial pathogens have caused these food poisoning outbreaks. In Alaska, native smoked and dried salmon products are processed during the summer months when the e sh are returning to the rivers during the spawning season. Since processing is done under ambient temperature and humidity, the processing time can vary from 4 days to 1 or 2 weeks, depending on weather conditions. This long drying time raises concern, because the drying temperatures are ideal for the growth of bacterial pathogens. During processing, there is a race between the product reaching inhibitory levels of water-phase salt (WPS), moisture, and water activity (aw) and the growth of pathogenic and spoilagetype bacteria. If the product is processed at temperatures of 608C or higher, the nonspore-forming bacteria are usually inactivated. In 1993, we worked with an Alaskan native processor along the Yukon River to learn more about the processes used and the microbiological and chemical composition of smoked and dried salmon. The processor had developed a fairly modern processing facility with stainless steel tabletops, a chlorinated water supply, a refrigeration room, and walls and e oors that could be cleaned and sanitized.

The potential to use adult Artemia to deliver erythromycin to first-feeding sockeye salmon, Oncorhynchus nerka (Walbaum), was investigated in three trials. In the first trial, first-feeding sockeye were fed live erythromycin enriched adult Artemia or pellets containing equal amounts of erythromycin for 35 days. At the end of the trial, tissue erythromycin concentration of the fish fed the live Artemia was significantly greater (P < 0.05, 25.52 +/- 1.29 microg mL(-1); mean +/- SEM), than the tissue concentration of the fish fed the pellets (0.72 +/- 0.01 microg mL(-1)). In the second trial, first-feeding sockeye were fed either live or freeze-dried bioencapsulated erythromycin (adult Artemia) or pellets containing erythromycin daily for 21 days. Mean daily erythromycin concentration in fish fed the freeze-dried Artemia, live Artemia, or pellets did not differ significantly. In the third trial, apparent erythromycin digestibility was determined. Significantly more (P < 0.05) erythromycin was retained by juvenile sockeye fed freeze-dried bioencapsulated erythromycin (98.3 +/- 1.0%) compared with medicated pellets (89.2 +/- 1.7%). Uptake of bioencapsulated erythromycin from adult Artemia (live or freeze-dried) appears to be greater than uptake from pellets. Freeze-dried and live Artemia were equally effective at delivery suggesting enriched freeze-dried adult Artemia could be produced into a highly palatable, consistent, off-the-shelf product.

Water phase sodium chloride (WPS) levels of 1.8 to 3.0% in combination with heat pasteurization for 15 min at temperatures of 75, 80, 85, and 90 degrees C were evaluated as methods for the inactivation or inhibition of nonproteolytic, psychrotrophic Clostridium botulinum types B and E in crab analogs (imitation crab legs) subsequently stored at 10 and 25 degrees C. Samples inoculated with 10(2) type B or E spores per g prior to pasteurization remained nontoxic for 120 days at 10 degrees C and for 15 days at 25 degrees C. With 10(4) type E spores per g and 80 degrees C pasteurization, > or = 2.4 and 2.7% WPS was required for inhibition at 10 and 25 degrees C storage, respectively. Pasteurization at 85 degrees C decreased the inhibitory level of WPS to 2.1% at 10 degrees C and to 2.4% at 25 degrees C. When the inoculum was 10(4) type B spores per g, samples with 2.7% WPS were toxic after 80 days of storage at 10 degrees C. Samples inoculated with 10(3) type B spores per g and processed at 85 degrees C remained nontoxic for 15 days at 25 degrees C with a WPS of > or = 2.4%. When pasteurization was carried out before inoculation and packaging, 1.8% WPS prevented toxin production by 10(2) and 10(4) type E spores per g for 30 days at 10 degrees C, and this time period increased as the WPS concentrations increased. Three percent WPS prevented toxin production by 10(4) type E spores per g in vacuum-packaged analogs stored 110 days at 10 degrees C. Pasteurization processes used in these experiments, however, do not inactivate the heat-resistant proteolytic types of Clostridium botulinum. Therefore, the most important factor controlling the growth of this bacterium is continuous refrigeration below 3.0 degrees C or frozen storage of the finished product.

The purpose of this study was to investigate the occurrence of ocular abnormalities in hyperthyroid cats. One hundred hyperthyroid cats and 30 clinically normal, geriatric cats were studied. In both groups, ophthalmic examination was performed by use of slit-lamp biomicroscopy and indirect ophthalmoscopy after application of 1% tropicamide to dilate the pupil. Ocular abnormalities were common in both the hyperthyroid and euthyroid cats. Approximately 75% of all eyes were affected with 1 or more abnormalities, and the range of abnormalities involved all structures of the eye. Significant differences between the euthyroid and hyperthyroid cats were found in the prevalence of prominent suture lines, nonpigmented deposits on the posterior lens capsule, hyperreflective ring around the optic nerve, and hyperpigmentation of the area centralis, but all of these abnormalities were more common in the euthyroid cats than in the cats with hyperthyroidism. Active retinal lesions were only observed in 3 hyperthyroid cats (3%). The results of this study indicate that hyperthyroidism does not seem to be a frequent cause of abnormalities in the eyes of cats.

The pathologic changes associated with hyperthyroidism (adenomatous hyperplasia, adenoma of the thyroid gland) have been well characterized in cats, but the pathogenesis of these changes remains unclear. In this research, we undertook a case-control study to search for potential risk factors for this disease. Owners of 379 hyperthyroid and 351 control cats were questioned about their cats' exposure to potential risk factors including breed, demographic factors, medical history, indoor environment, chemicals applied to the cat and environment, and diet. The association between these hypothesized risk factors and outcome of disease was evaluated by conditional logistic regression. Two genetically related cat breeds (ie, Siamese and Himalayan) were found to have diminished risk of developing hyperthyroidism. Cats that used litter had higher risk of developing hyperthyroidism than those that did not. Use of topical ectoparasite preparations was associated with increased risk of developing hyperthyroidism. Compared with cats that did not eat canned food, those that ate commercially prepared canned food had an approximate 2-fold increase in risk of disease. When these 4 variables (breed, use of cat litter, consumption of canned cat food, and use of topical ectoparasite preparations) from the univariate analysis were selected for further study as candidate risk factors and analyzed by multivariate conditional logistic regression, a persistent protective effect of breed (ie, Siamese or Himalayan) was found. In addition, results suggested a 2- to 3-fold increase in risk of developing hyperthyroidism among cats eating a diet composed mostly of canned cat food and a 3-fold increase in risk among those using cat litter. In contrast, the use of commercial flea products did not retain a strong association. The results of this study indicate that further research into dietary and other potentially important environmental factors (eg, cat litter) is warranted.

To determine whether administration of phenobarbital, potassium bromide, or both drugs concurrently was associated with abnormalities in baseline serum total thyroxine (T4), triiodothyronine (T3), free T4, or thyrotropin (thyroid-stimulating hormone; TSH) concentrations in epileptic dogs.Prospective case series.78 dogs with seizure disorders that did not have any evidence of a thyroid disorder (55 treated with phenobarbital alone, 15 treated with phenobarbital and bromide, and 8 treated with bromide alone) and 150 clinically normal dogs that were not receiving any medication.Serum total T4, total T3, free T4, and TSH concentrations, as well as serum concentrations of anticonvulsant drugs, were measured in the 78 dogs with seizure disorders. Reference ranges for hormone concentrations were established on the basis of results from the 150 clinically normal dogs.Total and free T4 concentrations were significantly lower in dogs receiving phenobarbital (alone or with bromide), compared with concentrations in clinically normal dogs. Administration of bromide alone was not associated with low total or free T4 concentration. Total T3 and TSH concentrations did not differ among groups of dogs.Results indicate that serum total and free T4 concentrations may be low (i.e., in the range typical for dogs with hypothyroidism) in dogs treated with phenobarbital. Serum total T3 and TSH concentrations were not changed significantly in association with phenobarbital administration. Bromide treatment was not associated with any significant change in these serum thyroid hormone concentrations.

To determine whether low doses of synthetic ACTH could induce a maximal cortisol response in clinically normal dogs and to compare a low-dose ACTH stimulation protocol to a standard high-dose ACTH stimulation protocol in dogs with hyperadrenocorticism.Cohort study.6 clinically normal dogs and 7 dogs with hyperadrenocorticism.Each clinically normal dog was given 1 of 3 doses of cosyntropin (1, 5, or 10 micrograms/kg [0.45, 2.3, or 4.5 micrograms/lb] of body weight, i.v.) in random order at 2-week intervals. Samples for determination of plasma cortisol and ACTH concentrations were obtained before and 30, 60, 90, and 120 minutes after ACTH administration. Each dog with hyperadrenocorticism was given 2 doses of cosyntropin (5 micrograms/kg or 250 micrograms/dog) in random order at 2-week intervals. In these dogs, samples for determination of plasma cortisol concentrations were obtained before and 60 minutes after ACTH administration.In the clinically normal dogs, peak cortisol concentration and area under the plasma cortisol response curve did not differ significantly among the 3 doses. However, mean plasma cortisol concentration in dogs given 1 microgram/kg peaked at 60 minutes, whereas dogs given doses of 5 or 10 micrograms/kg had peak cortisol values at 90 minutes. In dogs with hyperadrenocorticism, significant differences were not detected between cortisol concentrations after administration of the low or high dose of cosyntropin.Administration of cosyntropin at a rate of 5 micrograms/kg resulted in maximal stimulation of the adrenal cortex in clinically normal dogs and dogs with hyperadrenocorticism.

Hypoadrenocorticism secondary to bilateral lymphomatous invasion of adrenocortical tissue was diagnosed in 2 adult castrated domestic shorthair cats. In both cats, findings during initial physical examination (ie, lethargy, anorexia, weight loss, and severe weakness) were consistent with severe hypoadrenocorticism. Hyperkalemia, hyponatremia, and azotemia were also detected, which were consistent with hypoadrenocorticism. Hypoadrenocorticism was documented on the basis of finding low baseline and ACTH-stimulated serum cortisol concentrations. The cats initially responded well to treatment, but both owners chose to have the cat euthanatized. Multicentric lymphoma with infiltration and destruction of the adrenal glands was confirmed during necropsy.

To identify factors regulating secretion of alpha-melanocyte-stimulating hormone (alpha-MSH) from the pars intermedia (PI) of the pituitary gland of cats.28 healthy adult cats.Indwelling catheters were placed in 1 jugular vein of each of 7 to 10 cats, depending on treatment group. Sixteen hours later, 3 blood samples were collected for determination of baseline plasma hormone concentrations, and saline solution or a test substance (haloperidol, corticotropin-releasing hormone, bromocriptine, isoproterenol, insulin, or dexamethasone) was administered via the catheter. Subsequent blood samples were collected at regular intervals for up to 240 minutes after injection. Concentrations of ACTH, cortisol, and alpha-MSH were measured in plasma by use of specific radioimmunoassays. Cats were rested for at least 3 weeks between experiments.Administration of haloperidol and isoproterenol resulted in increased, and bromocriptine and insulin in decreased, circulating concentrations of alpha-MSH from baseline. ACTH and plasma cortisol concentrations increased after administration of all test substances except dexamethasone. Dexamethasone injection resulted in decreased plasma concentrations of ACTH and cortisol.Secretion of alpha-MSH from the PI of cats appears to be inhibited by dopaminergic activity and stimulated by beta-adrenergic influences. Activation of secretion of alpha-MSH from the PI can be dissociated from activation of secretion of other pro-opiomelanocortin-derived peptides, such as ACTH, arising from the pars distalis. Regulation of secretory activity of the PI of cats resembles that of rats.

To determine whether measurement of baseline serum concentrations of total thyroxine (T4), and triiodothyronine (T3), free T4, and thyrotropin (thyroid-stimulating hormone; TSH) would aid in the diagnosis of hypothyroidism in dogs.Prospective case series.54 dogs with hypothyroidism, 54 euthyroid dogs with nonthyroidal disease initially suspected to have hypothyroidism, and 150 clinically normal dogs.In the 54 dogs with hypothyroidism, diagnosis was established on the basis of clinical signs, results of routine laboratory and TSH stimulation tests, exclusion of concurrent nonthyroidal disease, and a good clinical response to treatment with L-thyroxine. Blood samples were collected from all dogs and were tested for thyroid hormone and TSH concentrations. Reference ranges for hormone concentrations were established on the basis of results for the 150 clinically normal dogs.Of the 54 hypothyroid dogs, 48 (89%) had low total T4 concentrations, 3 had low-normal concentrations, and 3 had high concentrations because of T4 autoantibodies. In contrast, only 10 (18%) euthyroid dogs had low total T4 concentrations. Only 3 of 31 (10%) hypothyroid dogs had low T3 concentrations; 23 had concentrations within the reference range, and 5 had high concentrations because of T3 autoantibodies. Only 3 of 38 euthyroid dogs had low T3 concentrations. Of the hypothyroid dogs, 53 (98%) had low free T4 concentrations and 1 had a low-normal concentration. Only 4 (7%) euthyroid dogs had low free T4 concentrations. Of the hypothyroid dogs, 41 (76%) had high TSH concentrations, and 13 had TSH concentrations within the reference range. Of the euthyroid dogs, only 4 (8%) had high TSH concentrations. Of all single hormone measurements evaluated, measurement of free T4 concentration had the highest sensitivity (0.98), specificity (0.93), and accuracy (0.95) as a test for hypothyroidism; measurement of total T4 concentration had a lower sensitivity (0.89), specificity (0.82), and accuracy (0.85). Compared with measurement of total or free T4 concentration, measurement of TSH concentration had a lower sensitivity (0.76) and accuracy (0.84) but specificity (0.93) equal to that for measurement of free T4 concentration. When T4 (total or free) and TSH concentrations were evaluated together, specificity was higher than when T4 or TSH concentration was evaluated alone. Only 1 euthyroid dog had low T4 (total and free) and high TSH concentrations.Results indicate that measurement of serum free T4 and TSH concentrations is useful for diagnosis of hypothyroidism in dogs. About a quarter of the dogs with confirmed hypothyroidism, however, will have serum TSH concentrations within reference limits.

To evaluate the efficacy and safety of ipodate in the treatment of hyperthyroidism in cats.Prospective case series.12 cats with hyperthyroidism treated at The Animal Medical Center between November 1994 and March 1996.Each cat initially received 100 mg of ipodate/d, PO. The drug's effects on clinical signs, body weight, heart rate, and serum triiodothyronine (T3) and thyroxine concentrations were evaluated 2, 4, 6, 10, and 14 weeks after initiation of treatment. A CBC and serum biochemical analyses were performed at each evaluation to monitor potential adverse effects of the drug. Dosage of ipodate was increased to 150 mg/d and then to 200 mg/d at 2-week intervals if a good clinical response was not observed.8 cats responded to treatment and 4 did not. Among cats that responded, mean body weight increased and mean heart rate and serum T3 concentration decreased during the study period. Among cats that did not respond, mean body weight decreased and mean heart rate and serum T3 concentration were not significantly changed. Serum thyroxine concentration remained high in all cats. Adverse clinical signs or hematologic abnormalities attributable to ipodate treatment were not reported in any of the cats.Ipodate may be a feasible alternative to methimazole for medical treatment of hyperthyroidism in cats, particularly those that cannot tolerate methimazole and are not candidates for surgery or radiotherapy. Cats with severe hyperthyroidism are less likely to respond to ipodate than are cats with mild or moderate disease, and cats in which serum T3 concentration does not return to the reference range are unlikely to have an adequate improvement in clinical signs.

The nonpolymorphic, nonclassical class II molecule DM has been shown to be important in the processing and presentation of antigenic epitopes by MHC class II molecules. The dependence of class II molecules on the coexpression of DM varies with the particular allele or epitope studied. In an effort to resolve disparities that exist for some alleles of class II in their requirements for DM, we have constructed a species-matched murine transfection model with which we can test both the functional and biochemical consequences of DM expression for different alleles of murine class II. When we evaluated the ability of class II molecules to form SDS-stable dimer and release CLIP, we find that while I-A(d) requires DM for the formation of SDS-stable dimers and the release of CLIP, I-A(k) is capable of both SDS-stable dimer formation and CLIP release in the absence of DM. Despite the apparent differences in the biochemical consequences of DM expression for I-A(d) and I-A(k), we find that Ag presentation by both alleles can be enhanced by the expression of DM. Interestingly, we find that DM can facilitate the removal of a natural intermediate in Ii processing (p12). The ability of DM to catalyze the dissociation of p12 and possibly larger Ii fragments from class II in vivo offers a possible mechanism to account for the observed DM enhancement of Ag presentation for alleles that have a low affinity for CLIP. Our findings indicate that DM may function in multiple compartments and on multiple class II/Ii substrates.

To evaluate clinical, laboratory, radiographic, ultrasonographic, surgical, and histologic findings in ferrets with insulinoma and to determine their long-term outcome.Retrospective study.57 ferrets with a histopathologic diagnosis of pancreatic islet cell tumor.Medical records of ferrets with pancreatic islet cell tumors were reviewed.Lethargy, weakness, and collapse were the most common clinical signs. All ferrets had hypoglycemia, and hyperinsulinemia was documented in 39 of 47 (83%) ferrets. Ultrasonographic examination of the abdomen revealed pancreatic nodules in 5 of 23 ferrets. Surgical treatment was performed in 50 ferrets, 3 were treated by medical management alone, and 4 did not have treatment. At the time of surgery, 1 pancreatic nodule was found in 13 (26%) ferrets and multiple nodules were found in 37 (74%) ferrets. Pancreatic carcinoma alone was found in 34 ferrets. Whereas a combination of carcinoma and either hyperplasia or adenoma was found in 23 ferrets; 4 ferrets had metastasis to regional lymph nodes or liver. In 26 (53%) ferrets, hypoglycemia persisted after surgery, necessitating medical treatment with prednisone, diazoxide, or both. Sixteen (33%) ferrets had redevelopment of hypoglycemia at 1 to 23.5 months (median, 10.6 months) after surgery. Only 7 of the 50 (14%) ferrets remained euglycemic after surgery.In ferrets, surgical removal of insulin-secreting pancreatic islet cell tumors is recommended as definitive treatment; however, multiple pancreatic nodules are common, making complete excision of all tumor tissue difficult. Persistent hypoglycemia after surgical treatment indicates that lifelong medical management with prednisone or diazoxide or both may be necessary in many ferrets. Finally, because the insulin-secreting tumors are malignant, long-term cure and survival are not likely.

To determine plasma concentrations of steroid hormones in ferrets with hyperadrenocorticism associated with adrenocortical neoplasia or nodular hyperplasia of the adrenal gland, the effect of surgical removal of the affected adrenal gland on concentrations of these hormones, and whether any hormone concentrations could be used as a marker for the disease.Prospective case series.32 ferrets with hyperadrenocorticism associated with adrenocortical neoplasia or nodular hyperplasia of the adrenal gland.A blood sample was obtained from each ferret before adrenalectomy. In 26 of the 32 ferrets, a second blood sample was collected 24 to 48 hours after adrenalectomy. Plasma concentrations of 7 hormones were measured (cortisol, estradiol, testosterone, progesterone, 17-hydroxyprogesterone, androstenedione, and dehydroepiandrosterone sulfate).Median plasma concentrations of 17-hydroxyprogesterone, androstenedione, and dehydroepiandrosterone sulfate were significantly higher in ferrets with adrenal gland disease, compared with concentrations in clinically normal ferrets. After adrenalectomy, median concentrations of estradiol, 17-hydroxyprogesterone, and androstenedione decreased significantly. Of 23 ferrets in which concentrations of estradiol, 17-hydroxyprogesterone, and androstenedione all were measured, 22 (96%) had high concentrations of at least 1 of these 3 hormones, but only 5 (22%) ferrets had high concentrations of all 3 hormones.The condition that develops in ferrets with adrenal gland disease apparently is caused by excessive secretion of 1 or more steroids other than cortisol. Because concentration of a particular hormone was not high in all ferrets, we recommend determining plasma concentrations of several sex steroids, including androstenedione, 17-hydroxyprogesterone, and estradiol.

To assess pretreatment clinical and laboratory findings in cats with diabetes mellitus and to determine the influence of ketoacidosis on pretreatment findings.Retrospective case series.104 cats with diabetes mellitus, 38 of which had ketoacidosis.Medical records of cats with diabetes mellitus examined over a 20-month period were reviewed. Cats that had received previous treatment for diabetes mellitus, or for which medical records were incomplete, were excluded from this study.Cats ranged in age from 1 to 19 years (median, 11 years). Male cats were twice as likely to develop diabetes as females. The most common historical signs were polyuria, polydipsia, weight loss, and diminished activity. Anorexia or poor appetite was reported more commonly than polyphagia, especially in cats with ketoacidosis. Diminished activity, anorexia, weakness, and vomiting were all significantly more common in ketoacidotic cats than in nonketoacidotic cats. Forty-four cats were considered thin, and 34 were considered obese. All cats had hyperglycemia and most had hypercholesterolemia and high activities of 1 or more hepatic enzymes. Compared with nonketoacidotic cats, ketoacidotic cats were more likely to have had low serum electrolyte values. All cats had glucosuria and 42 (40.4%) had ketonuria. Baseline serum insulin concentrations were measured in 18 cats and were low or at the low end of the reference range in 14 (77.8%) cats. Serum fructosamine concentration, determined in 22 cats, was high in 20 (90.9%) cats. Twenty-three of the 104 (22.1%) cats had concurrent disease, the most common of which were hyperthyroidism, inflammatory bowel disease, and eosinophilic granuloma complex.In more than a third of cats, diabetes mellitus is complicated by development of ketoacidosis, which increases the severity of clinical and laboratory abnormalities. Diagnosis of diabetes mellitus is made on the basis of signalment (e.g., middle-aged to old male cats), owner complaints (e.g., polyuria, polydipsia, and weight loss), physical examination findings (e.g., lethargy or muscle wasting), and laboratory findings (e.g., hyperglycemia and glucosuria).

To evaluate clinical and laboratory findings in 225 dogs with naturally occurring hypoadrenocorticism diagnosed over a 14-year period.Retrospective case series.220 dogs with primary hypoadrenocorticism and 5 dogs with secondary hypoadrenocorticism (primary ACTH deficiency).We reviewed medical records of all dogs with naturally occurring hypoadrenocorticism examined at The Animal Medical Center between 1979 and 1993 or at Tufts University, Foster Hospital for Small Animals, between 1987 and 1993.Dogs ranged from 4 months to 14 years old. Most (71%) were female, and female dogs had a significantly higher relative risk of developing hypoadrenocorticism than did males. Great Danes, Portuguese Water Dogs, Rottweilers, Standard Poodles, West Highland White Terriers, and Wheaton Terriers had a significantly higher relative risk of developing hypoadrenocorticism than did dogs of other breeds. Common owner complaints included lethargy, poor appetite, and vomiting, whereas lethargy, weakness, and dehydration were common abnormalities detected on physical examination. Serum biochemical testing at the time of diagnosis revealed moderate-to-severe azotemia and hyperphosphatemia in most dogs. In 99 of 172 (57.6%) dogs that had a pretreatment urinalysis performed, urine specific gravity was1.030 even though dogs were azotemic. Serum electrolyte changes included hyperkalemia (n = 215), hyponatremia (183), hypochloremia (94), and hypercalcemia (69). Five of the 220 dogs with primary hypoadrenocorticism and the 5 dogs with secondary hypoadrenocorticism did not have hyperkalemia at time of diagnosis. In all dogs, ACTH stimulation testing revealed a low to low-normal baseline serum cortisol concentration with little to no rise after ACTH administration. Endogenous plasma ACTH concentration measured in 35 dogs with primary hypoadrenocorticism was markedly high; whereas ACTH concentration was undetectable to low in the 5 dogs with secondary hypoadrenocorticism.hypoadrenocorticism is a rare disease in dogs, most commonly affecting young to middle-aged females; some breeds are at greater risk of developing the disease than others. In general, clinical signs are nonspecific and similar to manifestations of more common diseases. Serum electrolyte disturbances of hyperkalemia and hypernatremia are characteristic in dogs with primary hypoadrenocorticism, but concentrations may be normal in dogs with early or mild primary or secondary hypoadrenocorticism. Diagnosis of hypoadrenocorticism is best confirmed by demonstration of a low baseline serum cortisol concentration with a subnormal or negligible response to ACTH administration. Determination of endogenous plasma ACTH concentrations is valuable in differentiating primary from secondary hypoadrenocorticism, particularly in dogs with normal serum electrolyte concentrations.

To evaluate a protocol for subcutaneous radioiodine treatment of cats with hyperthyroidism in which the dose was determined on the basis of severity of the cat's clinical signs, thyroid tumor size, and magnitude of the serum thyroxine (T4) concentration.Prospective case series.524 cats with hyperthyroidism.A scoring system based on 3 factors (severity of clinical signs, size of the thyroid gland, and magnitude of the serum T4 concentration) was used to select the dose of radioiodine to be administered subcutaneously.On the basis of the scoring system, 310 (59%) cats were treated with a low dose of radioiodine (3.5 mCi; median, 3.0 mCi), 158 (30%) were treated with a moderate dose (3.5 to 4.4 mCi; median, 4.0 mCi), and 56 (11%) were treated with a high dose (or = 4.5 mCi; median, 5.0 mCi). At time of discharge from the hospital, serum T4 concentration was still high in 80 (15.3%) cats, but by 6 months after administration of radioiodine, the serum T4 concentration had decreased to within or below reference range in all but 8 (1.5%) cats with persistent hyperthyroidism. Many cats had low serum T4 concentrations at some time after radioiodine treatment, but only 11 (2.1%) cats developed clinical and clinicopathologic features of hypothyroidism and required supplementation with L-thyroxine. Thirteen (2.5%) cats had a relapse of hyperthyroidism 1.1 to 6.5 years after initial radioiodine treatment. Overall, the response to treatment was considered good in 94.2% of the cats. Median survival time in the cats was 2.0 years; the percentage of cats alive after 1, 2, and 3 years of treatment was 89, 72, and 52%, respectively.Results of the study suggest that this method of dose estimation works well and that subcutaneous administration of radioiodine provides a safe and effective means of treating hyperthyroidism in cats.

The purpose of the study reported here was to assess 3 commonly used screening tests for hyperadrenocorticism (low-dose dexamethasone suppression test, ACTH stimulation test, and urinary cortisol:creatinine ratio) in dogs with various diseases other than those of the adrenal glands (nonadrenal diseases). A group of 100 dogs was studied: 59 dogs with nonadrenal disease, 21 clinically normal dogs, and 20 dogs with pituitary-dependent hyperadrenocorticism. Of 59 dogs with nonadrenal disease, 20 (34%) had high baseline cortisol concentration (greater than reference range limits), and 22 (38%) and 33 (56%) had inadequate serum cortisol suppression at 4 and 8 hours, respectively, after administration of a low dose of dexamethasone. Compared with clinically normal dogs, dogs with nonadrenal disease had significantly (P0.05) higher mean serum cortisol concentration at 4 and 8 hours after administration of a low dose of dexamethasone; however, significant differences were not detected between the mean cortisol concentration at 8 hours after administration for dogs with nonadrenal disease and for dogs with hyperadrenocorticism. After ACTH stimulation, only 8 of 59 (14%) dogs with nonadrenal disease had high serum cortisol concentrations. Significant differences did not exist after ACTH stimulation between mean cortisol concentration of clinically normal dogs and that of dogs with nonadrenal disease. Of 59 dogs with nonadrenal disease, 45 (76%) had a high urinary cortisol:creatinine ratio. When compared with clinically normal dogs, dogs with nonadrenal disease had a significantly higher mean urinary cortisol:creatinine ratio, but significant differences did not exist between the mean urinary cortisol:creatinine ratio of dogs with nonadrenal disease and that of dogs with hyperadrenocorticism.(ABSTRACT TRUNCATED AT 250 WORDS)

A study was designed to evaluate the effects of desoxycorticosterone pivalate (DOCP) on blood pressure in 8 dogs with primary hypoadrenocorticism, and to attempt to identify other factors that might suggest overdosage of the drug. In 4 dogs, primary hypoadrenocorticism had been diagnosed immediately before entry of the dog into the study, and the dogs had not received any mineralocorticoid supplementation. In the other 4 dogs, primary hypoadrenocorticism had been diagnosed 1 to 6 years previously, and dogs were being treated with DOCP at the time of entry into the study. In all 8 dogs, DOCP (2.2 mg/kg of body weight, IM) was administered on days 0, 30, 60, and 90 of the study; each dog was examined on days 0, 30, 60, 75, 90, and 105. At the time of each visit, a medical history was obtained, a complete physical examination and serum biochemical analyses were performed, and body weight and blood pressure were measured. Doppler-shift ultrasonic sphygmomanometry was used to indirectly record systemic systolic and diastolic pressures. None of the dogs developed hypernatremia or hypokalemia or any clinical signs suggestive of hypoadrenocorticism during the study. However, in 6 dogs (3 that had not been previously treated with mineralocorticoids and 3 that had been), there was a significant increase in body weight over the course of the study. Compared with baseline (day 0) arterial blood pressure, neither systolic nor diastolic blood pressure was significantly increased during the study, and all systolic and diastolic blood pressure measurements were within reference ranges at all evaluation times.(ABSTRACT TRUNCATED AT 250 WORDS)

Thirty-two dogs with hyperadrenocorticism caused by cortisol-secreting adrenocortical neoplasia were treated with mitotane at an initial daily induction dosage of 27.5 to 75.0 mg/kg of body weight (mean, 46.3 mg/kg) for 10 to 14 days. All dogs received daily maintenance glucocorticoid supplementation during the induction period. After 2 weeks, the ACTH-stimulated serum cortisol concentration had decreased to within or below the reference range for baseline cortisol concentration in 18 (56.3%) of the 32 dogs; the remaining 14 (43.7%) still responded to ACTH administration with serum cortisol concentrations above the reference range. In these 14 dogs, mitotane was continued at a higher daily dosage (mean, 60.7 mg/kg) for an additional 1 to 9 weeks. Serum cortisol concentration subsequently fell within or below the reference range for baseline cortisol concentration in all but 1 dog. In 30 of the 32 dogs, mitotane was continued at an initial mean maintenance dosage of 101.6 mg/kg/wk, divided into 2 to 5 doses. Twenty-two dogs received prednisone daily (0.2 mg/kg) throughout the maintenance period. One or more relapses occurred in 19 (63%) of the 30 dogs. In dogs with relapse, the mean maintenance mitotane dosage was increased from 98.1 mg/kg/wk to a high of 212.4 mg/kg/wk. After a mean maintenance treatment time of 13.2 months, final mean maintenance dosage required in the 30 dogs ranged from 35.3 to 1,273 mg/kg/wk. Adverse effects were seen in 19 (59.4%) of the 32 dogs as a result of a drug toxicosis associated with high-dosage administration of mitotane, low serum cortisol concentration, or both.(ABSTRACT TRUNCATED AT 250 WORDS)

Nuclear medicine may have both diagnostic and therapeutic utility during the evaluation and management of thyroid disease. This article will focus on the use of radionuclide scintigraphy and radioactive iodine therapy in the diagnosis and treatment of thyroid disease in the dog and cat.

We measured immunoreactive (IR) plasma concentrations of the proopiomelanocortin (POMC)-derived peptides (adrenocorticotropic hormone [ACTH]; beta-endorphin/beta-lipotropin [beta END/beta LPH]; and alpha-melanocyte stimulating hormone [alpha MSH]) and of cortisol in 100 clinically normal cats. Median plasma concentration of IR-ACTH was 2.7 pmol/L (range,or = 1.1 to 22 pmol/L), of beta END/beta LPH was 28 pmol/L (range, 3.8 to 130 pmol/L), of alpha MSH was 36 pmol/L (range,or = 3.6 to 200 pmol/L), and of cortisol was 35 nmol/L (range, 5 to 140 nmol/L). Plasma concentrations of IR-ACTH, alpha MSH, and beta END/beta LPH were at or below the assay sensitivity in 34, 3, and 0% of the cats, respectively. We did not detect a correlation between plasma concentrations of IR-ACTH and beta END/beta LPH (r = 0.23) or between plasma concentrations of IR-ACTH and alpha MSH (r = 0.19). However, there was a significant (P0.001) correlation between plasma concentrations of IR-beta END/beta LPH and alpha MSH (r = 0.81). There was not a significant correlation between plasma concentration of cortisol and plasma concentration of any of the IR-POMC peptides. High plasma concentrations of IR-alpha MSH and beta END, POMC peptides secreted predominantly by melanotrophs in other species, indicate that clinically normal cats have an actively secreting pars intermedia.(ABSTRACT TRUNCATED AT 250 WORDS)

The absorption kinetics and glycemic effects of 3 long-acting insulin preparations (protamine zinc beef-pork insulin, ultralente beef-pork insulin, and ultralente human insulin) were evaluated in 9 healthy, adult, domestic shorthair cats (6 males, 3 females). A triple crossover study was performed, in which the serial serum concentrations of insulin and glucose were determined over a 24-hour period after SC administration of the 3 insulin preparations (dosage, 1.0 U/kg of body weight) at 3-week intervals. A control study was also performed in 4 of the cats by serially collecting samples for insulin and glucose determinations after administration of insulin diluent. After administration of protamine zinc insulin (PZI), mean (+/- SEM) serum insulin concentration increased significantly (P0.05) above baseline, reached a peak value (484 +/- 287 pmol/L) at 1 hour, and remained significantly (P0.05) higher than baseline at 24 hours. After administration of ultralente human insulin, the serum insulin curve was similar to that obtained after PZI administration, but mean serum insulin concentration took longer to peak (538 +/- 177 pmol/L at 4 hours). After administration of ultralente beef-pork insulin, mean peak serum insulin concentration was lower (220 +/- 54 pmol/L, not statistically significant) than that obtained after administration of PZI and ultralente human insulins; it then decreased to values statistically indistinguishable from baseline by 16 hours. The area under the serum insulin concentration curve for PZI (5,063 +/- 681 pmol x h/L) and ultralente human insulin (4,138 +/- 439 pmol x h/L) was significantly (P0.05) larger than that for ultralente beef-pork insulin (2,378 +/- 561 pmol x h/L).(ABSTRACT TRUNCATED AT 250 WORDS)

Concentration of dexamethasone was determined in plasma or serum samples from dogs after i.v. administration of a low dose (0.01 mg/kg of body weight) or high dose (0.1 mg/kg) of dexamethasone. On the basis of history, clinical signs of disease, and degree of cortisol suppression in response to dexamethasone, dogs were assigned to these groups: healthy dogs, dogs with nonadrenal illness, and dogs with hyperadrenocorticism. Four hours after administration of the low dose of dexamethasone, concentration of the steroid was reduced (P0.05) in dogs with hyperadrenocorticism, compared with healthy dogs, but not compared with values from dogs with nonadrenal illness. By 8 hours after dexamethasone administration, values were similar across groups. Dexamethasone concentration 4 and 8 hours after high-dose administration was similar between healthy dogs and dogs with hyperadrenocorticism. Concentration of dexamethasone 4 and 8 hours after its administration overlapped after the 2 doses. For example, in 11 of 66 dogs from all groups, concentration measured 4 hours after the low dose was greater than the minimal concentration determined in the 18 dogs given the high dose. These data indicate that dexamethasone metabolism may be altered in dogs with hyperadrenocorticism, and that individuals may have appreciable variability in dexamethasone clearance. Such variability provides a possible explanation for false-positive and false-negative results associated with dexamethasone suppression testing in dogs.

We compared the plasma cortisol and immunoreactive corticotropin (IR-ACTH) responses to incremental doses (1.25, 12.5 and 125 micrograms) of synthetic ACTH (cosyntropin) administered IV to 6 clinically normal cats. Mean plasma cortisol concentration increased significantly (P0.0001) after administration of all 3 doses of cosyntropin. After administration of the 1.25- and 12.5-microgram doses, plasma cortisol concentration peaked at 30 minutes, then decreased to values not significantly different from baseline concentration by 90 and 120 minutes, respectively. In contrast, after administration of the 125-micrograms dose, mean cortisol concentration peaked at 60 minutes and remained significantly (P0.05) higher than baseline values at 120 minutes. Compared with the 1.25- and 12.5-micrograms doses, administration of the 125-micrograms dose of cosyntropin induced significantly (P0.05) higher cortisol responses at 60, 90, and 120 minutes. Although individual cat's peak plasma cortisol concentration after administration of the 125-micrograms dose was higher than the peak value determined after administration of the 2 lower doses of cosyntropin, these differences were not statistically significant. Mean plasma IR-ACTH concentration increased significantly (P0.0001) and reached a maximal value at 30 minutes after administration of all 3 doses of cosyntropin. After administration of the 1.25- and 12.5-micrograms doses, plasma IR-ACTH concentration decreased to values not significantly different from baseline concentration by 60 and 120 minutes, respectively, whereas mean IR-ACTH concentration remained significantly (P0.05) higher than baseline values 120 minutes after administration of the 125-micrograms dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma cortisol and immunoreactive (IR)-ACTH responses to 125 micrograms of tetracosactrin and cosyntropin--the formulation of synthetic ACTH available in Europe and the United States, respectively--were compared in 10 clinically normal cats. After administration of tetracosactrin or cosyntropin, mean plasma cortisol concentration reached a peak and plateaued between 60 and 120 minutes, then gradually decreased to values not significantly different from baseline concentration by 5 hours. Mean plasma IR-ACTH concentration reached a maximal value at 15 minutes after administration of tetracosactrin or cosyntropin and was still higher than baseline concentration at 6 hours. Difference between mean plasma cortisol and IR-ACTH concentrations for the tetracosactrin or cosyntropin trials was not significant at any of the sample collection times. Individual cats had some variation in the time of peak cortisol response after administration of either ACTH preparation. About half the cats had peak cortisol concentration at 60 to 90 minutes, whereas the remainder had the peak response at 2 to 4 hours. In general, however, peak cortisol concentration in the cats with delayed response was not much higher than the cortisol concentration at 60 to 90 minutes. Overall, these results indicate that tetracosactrin or cosyntropin induce a comparable, if not identical, pattern of adrenocortical responses when administered to healthy cats.

Serum concentrations of total and free thyroxine (T4 and FT4, respectively), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3) were measured in 42 dogs with hyperadrenocorticism, and were compared with values determined in clinically normal dogs. Mean total T4 concentration in dogs with hyperadrenocorticism (14.3 nmol/L) was significantly (P less than 0.001) lower than the normal value (25.7 nmol/L), with 38% of the dogs having low serum T4 concentration. Although 16 (38%) of the 42 dogs with hyperadrenocorticism had a high FT4 fraction, indicative of diminished serum T4 binding, normal FT4 concentration was found in only 6 of the 16 dogs (38%) with low total T4 values. Mean serum T3 concentration in dogs with hyperadrenocorticism (0.79 nmol/L) was also significantly (P less than 0.001) lower than the normal value (1.16 nmol/L), with 39% of the dogs having T3 values below the normal range. Individual T3-to-T4 and T3-to-FT4 ratios, indices of T3 production and/or clearance, were above the normal range in 29 and 24% of dogs with hyperadrenocorticism, respectively. Mean reverse T3 concentration in dogs with hyperadrenocorticism (0.17 nmol/L) was also significantly (P less than 0.001) lower than the normal mean value (0.39 nmol/L), with 48% of the dogs having reverse T3 values below the normal range. Of the 21 dogs in which all iodothyronines were measured, 6 (29%) had undetectable values for all hormones.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma cortisol and immunoreactive (IR)-ACTH responses to 125 micrograms of synthetic ACTH (cosyntropin) administered IV or IM were compared in 10 clinically normal cats. After IM administration of cosyntropin, mean plasma cortisol concentration increased significantly (P less than 0.05) within 15 minutes, reached maximal concentration at 45 minutes, and decreased to values not significantly different from baseline concentration by 2 hours. After IV administration of cosyntropin, mean plasma cortisol concentration also increased significantly (P less than 0.05) at 15 minutes, but in contrast to IM administration, the maximal cortisol response took longer (75 minutes) and cortisol concentration remained significantly (P less than 0.05) higher than baseline cortisol concentration for 4 hours. Mean peak cortisol concentration (298 nmol/L) after IV administration of cosyntropin was significantly (P less than 0.05) higher than the peak value (248 nmol/L) after IM administration. All individual peak plasma cortisol concentrations and areas under the plasma cortisol response curve were significantly (P less than 0.05) higher after IV administration of cosyntropin than after IM administration. Mean plasma IR-ACTH concentration returned to values not statistically different from baseline by 60 minutes after IM administration of cosyntropin, whereas IR-ACTH concentration still was higher than baseline concentration 6 hours after IV administration. Peak plasma IR-ACTH concentration and area under the plasma IR-ACTH response curve also were significantly (P less than 0.05) higher after IV administration of cosyntropin. Results of the study confirmed that IV administration of cosyntropin induces significantly (P less than 0.05) greater and more prolonged adrenocortical stimulation than does IM administration.(ABSTRACT TRUNCATED AT 250 WORDS)

We evaluated the effect of ovine corticotropin-releasing hormone (CRH) on plasma immunoreactive (IR) concentrations of ACTH, alpha-melanocyte-stimulating hormone, and cortisol in 8 dogs with naturally acquired adrenocortical insufficiency. Of the 7 dogs with primary adrenal insufficiency, 6 had markedly high basal plasma IR-ACTH concentrations and exaggerated ACTH responses to CRH administration, whereas 1 dog that was receiving replacement doses of prednisone at the time of testing had normal basal IR-ACTH concentrations and a nearly normal response to CRH. In contrast, the 1 dog with secondary adrenocortical insufficiency had undetectable basal plasma IR-ACTH concentrations, which failed to increase after administration of CRH. Basal plasma alpha-melanocyte-stimulating hormone concentrations in the dogs with adrenal insufficiency were within normal range and were unaffected by CRH administration. In all 8 dogs with adrenal insufficiency, plasma cortisol concentrations were low and did not increase after administration of CRH. Therefore, stimulation with CRH produced 2 patterns of plasma IR-ACTH response when administered to dogs with naturally acquired adrenal insufficiency. Dogs with primary adrenal insufficiency had high basal plasma IR-ACTH concentrations and exaggerated responses to CRH, whereas the dog with secondary adrenal insufficiency had undetectable basal plasma concentrations of IR-ACTH that did not increase after stimulation with CRH.

Erythrocyte insulin receptor binding measurements were evaluated in 8 dogs with spontaneous hyperadrenocorticism. These dogs had normal serum glucose concentration, with normal to high serum insulin concentration (range, 45 to 1,400 pmol/L; normal, 40 to 170 pmol/L). Dogs with hyperadrenocorticism had significant (P less than 0.01) decrease in mean +/- SEM percentage of maximal binding for erythrocyte insulin receptors (2.25 +/- 0.21%), compared with results in 11 clinically normal pet dogs (4.29 +/- 0.42%). The decrease in erythrocyte receptor binding was attributed to significant (P less than 0.01) decrease in high-affinity receptor sites in dogs with hyperadrenocorticism (14.5 +/- 2.8), compared with clinically normal dogs (31.2 +/- 4.3). Significant differences in receptor affinity were not apparent between the 2 groups. Percentage of maximal binding for erythrocyte insulin receptors for dogs with hyperadrenocorticism was inversely correlated with serum insulin concentration (r = -0.85, P less than 0.01). Results indicate that the observed decrease in erythrocyte insulin receptor binding could contribute to insulin resistance and hyperinsulinemia associated with hyperadrenocorticism. Alternatively, decreased binding of insulin receptors in animals with hyperadrenocorticism may result from down-regulation secondary to hyperinsulinemia itself caused by insulin resistance at a postreceptor site (decreased responsiveness).

Unbound or free cortisol constitutes a small fraction of total plasma cortisol, but is believed to represent the biologically active portion of this circulating glucocorticoid. We tested the hypothesis that the percentage free cortisol was altered in plasma from dogs with hyperadrenocorticism, which could account for a greater target tissue response to this circulating hormone. The percentage free cortisol in plasma samples from human beings, healthy dogs, and dogs with hyperadrenocorticism was estimated, using centrifugal ultrafiltration-dialysis. Total cortisol concentrations were determined by use of radioimmunoassay. Total cortisol concentrations appeared greater in plasma from human beings than in plasma from either group of dogs. However, the percentage free cortisol was lower in plasma from human beings, resulting in a calculated concentration of free cortisol that was quite similar between plasma from human beings and healthy dogs. Total plasma cortisol concentrations were greater (P less than 0.01) in samples from dogs with hyperadrenocorticism (190 +/- 113 nmol/L; mean +/- SD) than in healthy dogs (102 +/- 85 nmol/L), but the percentage free cortisol was not different between these 2 groups (dogs with hyperadrenocorticism, 16 +/- 9%; healthy dogs, 13 +/- 6%). However, plasma free cortisol concentrations (product of total and the percentage of free cortisol) were greater (P less than 0.01) in samples from dogs with hyperadrenocorticism (36 +/- 41 nmol/L) than in those from healthy dogs (16 +/- 9 nmol/L). Significant (P less than 0.001) positive linear relationships were found between total cortisol concentrations and percentage free cortisol in plasma samples from healthy dogs and dogs with hyperadrenocorticism.(ABSTRACT TRUNCATED AT 250 WORDS)

As expertise among small animal practitioners grows, feline hyperthyroidism is being diagnosed earlier in the course of the disease. There are, in fact, a growing number of cats with clinical signs of hyperthyroidism and palpably large thyroid glands whose serum total thyroxine (T4) and triiodothyronine (T3) concentrations are within the normal or borderline range. This condition can be referred to as "occult" hyperthyroidism. Early detection and treatment of feline hyperthyroidism presents an obvious advantage in avoiding some of the deleterious effects of chronic thyroid hormone excess (eg, cardiomyopathy). Recent advances have been made in the diagnosis of occult hyperthyroidism in cats. It has been found, for instance, that serum thyroid hormone concentrations can fluctuate in and out of the normal range in some cats with hyperthyroidism. Recent work also has laid the groundwork for use of a T3 suppression test as an aid in the diagnosis of early, mild, or occult hyperthyroidism in cats. The purpose of this chapter is to discuss these and other developments, as well as to discuss some of the problems confronted in diagnosing occult hyperthyroidism in cats.

We reviewed the medical records of 494 cats with a variety of nonthyroidal diseases in which serum thyroxine (T4) concentration was determined as part of diagnostic evaluation. The cats were grouped by category of disease (ie, renal disease, congestive heart failure, diabetes mellitus, focal neoplasia, systemic neoplasia, hepatopathy, inflammatory bowel disease, inflammatory pulmonary disease, miscellaneous diseases, or undiagnosed disease), degree of illness (ie, mild, moderate, or severe), survival (ie, lived, died, or euthanatized), and presence or absence of a palpable thyroid gland. The mean (+/- SD) serum T4 concentrations in all 10 groups of cats, which ranged from 10.5 +/- 11.1 nmol/L in cats with diabetes mellitus to 18.7 +/- 7.8 nmol/L in cats with focal neoplasia, were significantly (P less than 0.001) lower than those of normal cats (27.0 +/- 10.4 nmol/L). The number of ill cats with low serum T4 concentrations (less than 10 nmol/L) was highest in the cats with diabetes mellitus (59%), hepatopathy (54%), renal failure (48%), and systemic neoplasia (41%). When the serum T4 concentrations in cats with mild, moderate, and severe illness were compared, mean concentrations were progressively lower (21.3 +/- 6.8, 14.8 +/- 8.1, and 6.5 +/- 5.8 nmol/L, respectively) as degree of illness increased. Severity of illness had a more significant (P less than 0.001) effect in lowering serum T4 concentrations than did disease category. Mean serum T4 concentrations in the cats that died (7.8 +/- 9.8 nmol/L) or were euthanatized (10.0 +/- 7.0 nmol/L) were also significantly (P less than 0.001) lower than those of cats that survived (15.2 +/- 8.8 nmol/L).(ABSTRACT TRUNCATED AT 250 WORDS)

Concentrations of serum thyroxine (T4) and 3,3',5-triiodothyronine (T3) were determined in 7 clinically healthy adult dogs before and after administration of freshly reconstituted thyrotropin (TSH) and TSH that had been previously reconstituted and frozen for 1, 2, and 3 months. The 4 TSH response tests were performed at 30-day intervals by collecting blood samples for serum T4 and T3 determinations before and 4 and 6 hours after IV administration of TSH (0.1 U/kg of body weight). Baseline serum concentrations of T4 and T3 were similar at each of the 4 sample collection times over the 3-month period of the study. Mean serum concentrations of T4 and T3 increased significantly (P less than 0.01) over baseline values after administration of freshly reconstituted TSH or TSH that had been previously frozen for 1, 2, or 3 months. Significant difference was not found in the mean post-TSH serum T4 or T3 concentration after injection of freshly reconstituted TSH or TSH that had been previously frozen for 1, 2, or 3 months. In 2 of the 7 dogs, mild reactions--mild ataxia and weakness--were observed during the last of the series of TSH response tests (ie, after IV administration of TSH that had been previously frozen for 3 months). Results of this study suggest that for use in dogs, reconstituted TSH stored at -20 C maintains adequate biological activity for at least 3 months. The ability to store reconstituted TSH for a longer period than the recommended 48 hours represents an economic advantage, because it allows clinicians to perform more TSH response tests per vial of TSH.

The purpose of this study was to develop a T3 suppression test to help in the diagnosis of mild hyperthyroidism in cats. We evaluated the response in circulating T4 concentrations to exogenous T3 (liothyronine) administration in 44 clinically normal cats, 77 cats with hyperthyroidism, and 22 cats with nonthyroidal disease. The test was performed by first collecting blood samples for basal serum T4 and T3 determinations, administering liothyronine at an oral dosage of 25 micrograms three times daily for seven doses, and, on the morning of the third day, again collecting serum samples for T4 and T3 determinations 2 to 4 hours after the seventh dose of liothyronine. The mean basal serum concentrations of T4 (53.1 nmol/L) and T3 (1.8 nmol/L) were significantly higher in the cats with hyperthyroidism than in the normal cats (T4 = 25.3 nmol/L, T3 = 1.3 nmol/L) and the cats with nonthyroidal disease (T4 = 29.5 nmol/L, T3 = 1.4 nmol/L); however, there was a great deal of overlap of basal values between the three groups of cats. Of the 77 cats with mild hyperthyroidism, 41 (53%) had serum T4 values and 55 (71%) had T3 values that were within the established normal ranges. After administration of liothyronine, mean serum T4 concentrations fell much more markedly in the normal cats and the cats with nonthyroidal disease than in the hyperthyroid cats.(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin-secreting tumor of the pancreas was diagnosed in 55 dogs. Diagnosis was based mainly on the increase of serum insulin concentrations in the presence of hypoglycemia. The use of the amended insulin/glucose ratio to diagnose the tumor, although providing less false-negative results than did increased serum insulin concentrations alone, appeared less specific and gave false-positive results in dogs without insulin-secreting tumors. Management of the disease included surgical intervention alone (26 dogs), surgery plus medical management with diazoxide (14 dogs), and medical management with diazoxide alone (4 dogs). Eleven dogs were euthanatized at the time of diagnosis. Diazoxide therapy controlled hypoglycemia in about 70% of the dogs.

An M-mode echocardiographic examination was performed in a consistent manner in 30 clinically healthy cats under light ketamine hydrochloride sedation. There was a significant linear relationship between increasing body size and increasing cardiac dimensions for several echocardiographic values. Positive correlation existed between body weight and body surface area with aortic root, left ventricular caudal wall thickness (LVCW), interventricular septal thickness (IVS), IVS/LVCW, and mean velocity of circumferential fiber shortening (Vcf); there was a negative correlation between body weight and body surface area with left ventricular ejection time (LVET). Body surface area also correlated positively with percentage of ventricular minor axis dimensional change (% delta D). Positive correlations were recorded between left ventricular end-diastolic dimension (LVEDD) and left ventricular endsystolic dimension (LVESD), LVESD and LVET, LVCW and IVS, LVET (calculated by LVCW motion) and LVET (calculated by aortic valve motion), % delta D and Vcf, heart rate and Vcf, and Vcf (calculated using aortic valve motion to compute LVET) and Vcf (using LVCW motion to compute LVET). There were negative correlations between LVEDD and % delta D, LVEDD and Vcf, LVESD and Vcf, LVET and Vcf, LVET and heart rate, LVET and % delta D. Significant differences were recorded between means of echocardiographic reference values generated in this and other studies, except for LVESD.

Severe polycythemia was found in 3 dogs with PCV 68% to 70%. Direct RBC mass determinations were increased in all dogs, confirming absolute polycythemia. Cause for secondary polycythemia was not found in any of the dogs; serum erythropoietin concentrations were undetectable, consistent with primary polycythemia. The polycythemia and associated clinical signs were controlled successfully for extended periods (mean, 16.6 months), using phlebotomy followed by oral administration of hydroxyurea in loading and in daily maintenance dosages.

Invasive tumors of the pituitary gland were diagnosed in 8 dogs. Seven of the dogs had been treated for pituitary-dependent hyperadrenocorticism before the onset of neurologic signs. All 8 dogs had behavior abnormalities and similar neurologic signs: 6 dogs had rotary nystagmus and 7 dogs had symmetric tetraparesis. Once neurologic signs developed, the clinical course in all 8 dogs had a mean duration of 4.7 +/- 2.0 months before death or euthanasia; 5 dogs had a clinical course of less than or equal to 2 months. Necropsy was performed in 7 dogs. The histologic diagnosis was malignant pituitary adenocarcinoma in 2 dogs and pituitary adenoma in 5 dogs.