Adrenal corticotropin hormone and nestling bald eagle corticosterone levels.
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Adrenocorticotropic Hormone↗
Biomedical subjects
K R Refsal
Publications and source records attributed to K R Refsal.
Lymphocytic thyroiditis.
Lymphocytic thyroiditis is a common canine condition that can lead to functional hypothyroidism. It is associated with more than 50% of cases of canine hypothyroidism. Evidence in human beings and experimental situations suggests that it is a disease of defective immunoregulation, but specific investigation of the molecular pathogenesis of the naturally occurring disease in dogs has not yet been carried out. The condition is heritable in those breeds that have been studied, and progression to hypothyroidism, if it occurs, can be slow. Factors that influence the progression from subclinical thyroiditis to hypothyroidism in dogs are still to be identified, but excessive iodine intake is an important factor in other species.
Animals↗
Update on the diagnosis and treatment of disorders of calcium regulation.
The availability of PTH, iCa, PTHrP, and 25OHD assays for evaluation of calcium abnormalities in companion animals has been well received [table: see text] by clinicians and diagnosticians. Use of these assays has heightened awareness that some of these disorders are more common than originally thought. Also, there is added insight of alterations of calcium homeostasis as a consequence of other illness or environmental factors such as diet. Animal counterparts of other disorders of calcium metabolism in people are likely to be identified, and use of these assays should play a significant role. As already emphasized, the foundation of using [table: see text] these assays is first assessing whether the calcium abnormality is of a parathyroid-dependent or parathyroid-independent classification.
Animals↗
Salivary and plasma concentration of cortisol in normal horses and horses with Cushing's disease.
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Adrenal Cortex Function Tests↗
The postmortem diagnosis of cholecalciferol toxicosis: a novel approach and differentiation from ethylene glycol toxicosis.
The objectives of this study were to develop a novel approach to postmortem diagnosis of cholecalciferol (CCF) toxicosis in dogs using kidney, bile, and urine samples, and to differentiate CCF from ethylene glycol (EG) toxicosis. To achieve these objectives, specimens collected from 2 previous laboratory studies in which dogs were given a single oral toxic dose of CCF (8.0 mg/kg) were used. For EG toxicosis, historical data from the previous 13 years (1985-1998) were reviewed and confirmed cases of EG toxicosis were selected. The historical data were used to compare trace mineral concentrations, specifically of calcium and phosphorus to differentiate between intoxications caused by CCF from that caused by EG in dogs. Kidneys, bile, and urine from dogs that died of CCF toxicosis were analyzed for 25 monohydroxy vitamin D3 (25(OH)D3) and 1,25 dihydroxy vitamin D3 (1,25(OH)2D3) and compared to known control unexposed dogs. Results of this study show that biliary and renal 25(OH)D3 concentrations and renal calcium to phosphorus ratio are of diagnostic value in dogs exposed to toxic concentrations of CCF. The renal calcium to phosphorus ratio was <0.1 in normal dogs, 0.4-0.9 in dogs that died of CCF toxicosis, and >2.5 in dogs that died of EG toxicosis.
Animals↗
Effects of electrolyte and glycerol supplementation on recovery from endurance exercise.
Incomplete recovery from endurance exercise after an overnight rest period is reflected by persisting weight loss and an elevated plasma aldosterone concentration, even in successful competitors. To determine whether supplementation with high doses of electrolytes, with or without glycerol, enhances recovery, the following were measured in 6 Arabian horses before and after completion of a 60 km treadmill exercise test simulating an endurance ride and after 12, 24, 48, and 72 h of recovery: bodyweight; plasma osmolality; plasma concentrations of protein, electrolytes, aldosterone and cortisol; and urine and faecal electrolyte concentrations. Before and during the exercise test, horses were supplemented with a total of 2.4 ml/kg bwt of water (W); 0.2 g/kg bwt KCl and 0.4 g/kg bwt NaCl in 2.4 ml/kg bwt of water (E); or 0.2 g/kg bwt KCl and 0.4 g/kg bwt NaCl in 2.4 ml/kg bwt (3 g/kg bwt) of glycerol (GE). Although weight loss after completion of the simulated ride was greater (P < 0.01) for W (3.2%) than for E and GE (1.0 and 0.9%, respectively), horses supplemented with E or GE experienced further weight loss by 24 h after the simulated ride (2.2 and 2.1% for E and GE, respectively) while bodyweight with W remained unchanged (3.0%) from the finish value. After 48 h of recovery, bodyweight was not different from the starting values with E and GE but remained decreased (P < 0.01) with W throughout the recovery period (2.2% persisting weight loss after 72 h of recovery). Plasma osmolality and plasma Na+ and Cl- concentrations increased (P < 0.01) and plasma protein concentration decreased (P < 0.01) after the exercise test with E and GE but were unchanged with W. Plasma osmolality and protein and electrolyte concentrations returned to pre-exercise values within 12 h of recovery with the exception of a persistent increase in plasma Na+ concentration with GE. The greatest plasma aldosterone concentration was measured after 12 h of recovery with W (1357 pmol/l) and was greater (P < 0.02) than that with E and GE (24 and 304 pmol/l, respectively). Urine production during the simulated ride increased (P < 0.01) with GE and resulted in loss of approximately 20% and essentially 100% of supplemented Na+ and K+, respectively. In contrast, electrolyte losses in faeces were unaffected by electrolyte or glycerol supplementation. In conclusion, supplementation with high doses of electrolytes as hypertonic oral pastes attenuated weight loss during a simulated endurance ride (by enhancing voluntary water intake); however, it did not prevent development of significant weight loss during the initial 24 h of recovery. Glycerol administration resulted in no benefits, and actually increased urine electrolyte losses, in comparison to supplementation with electrolytes alone.
Animal Feed↗
Short-term influence of prednisone and phenobarbital on thyroid function in euthyroid dogs.
The short-term effects of prednisone and phenobarbital on serum total thyroxine (tT4), free thyroxine (fT4), and thyroid stimulating hormone (TSH) were evaluated in euthyroid dogs. Twenty-six beagles were randomly divided into 3 groups receiving, respectively, a placebo, prednisone (1.2 to 2 mg/kg body weight, per os, every 12 hours for 3 weeks), or phenobarbital (1.8 to 3 mg/kg body weight for 1 week, then 2.7 to 4.5 mg/kg body weight, per os, every 12 hours for 2 weeks). Blood samples taken over a 6-week period were assayed for serum tT4, fT4, and TSH. Phenobarbital therapy in our study did not affect serum tT4, fT4, or TSH concentrations. Prednisone therapy, however, significantly decreased serum tT4 and fT4, but did not affect serum TSH concentrations.
Animals↗
Prevalence of autoantibodies to thyroglobulin in dogs with nonthyroidal illness.
OBJECTIVE: To evaluate a thyroglobulin autoantibody (TgAA) assay and determine a diagnostic threshold. SAMPLE POPULATION: Serum samples from dogs with various endocrine abnormalities and from 30 obese adult female Beagles. PROCEDURE: TgAA were determined by use of the ELISA. Six experiments were done: 1, definition of positive results for TgAA using samples from normal and T3 autoantibody (T3AA) positive dogs; 2, establishment of prevalence of positive results in 91 clinically normal dogs; 3, evaluation of positive results for sera from dogs with nonthyroidal illnesses; 4, testing of samples from dogs with primary hypothyroidism but absence of T4AA or T3AA, or both; 5, determination of prevalence of false-negative results in dogs that are T4AA and/or T3AA positive, which were (18 dogs) or were not (22 dogs) receiving L-thyroxine replacement therapy; and 6, examination of thyroid biopsy specimens from 18 dogs (8 TgAA positive and 10 TgAA negative). RESULTS: Positive results were defined as at least twice (200%) the optical density of the negative-control sample. False-positive results were obtained for only 3.4% of 146 dogs with nonthyroidal illness. Thirty-seven percent of dogs with primary hypothyroidism, but no evidence of T4AA or T3AA, or both, were TgAA positive. False-negative results were found in 1 of 22 and 2 of 18 T3AA-positive dogs with and without thyroid replacement therapy, respectively. Thyroid biopsy specimens from 8 TgAA-positive dogs had evidence of lymphocytic thyroiditis, whereas those from 10 TgAA-negative dogs did not. CONCLUSION AND CLINICAL RELEVANCE: The assay is sensitive and specific for identification of lymphocytic autoimmune thyroiditis in dogs, and has potential for aiding early diagnosis of thyroiditis in dogs and identifying dogs likely to perpetuate hypothyroidism in breeding programs.
Animals↗
Ovarian steroid cell tumor resembling luteoma associated with hyperadrenocorticism (Cushing's disease) in a dog.
An ovarian steroid cell tumor was diagnosed in a 6.5-year-old female Rottweiler. The animal was polydipsic and polyuric, with an enlarged, pot-bellied abdomen. Radiographs and ultrasound examinations revealed an approximately 13-cm-diameter cystic mass below the right kidney. A low-dose dexamethasone suppression test was consistent with hyperadrenocorticism. Surgical exploration revealed an enlarged, lobulated left ovary approximately 10 cm in diameter, weighing 550 gs. Histologically, the ovarian tumor consisted of dense sheets and nests of round to polyhedral cells with abundant, finely vesiculated cytoplasm. The overall features were most consistent with ovarian steroid cells tumor resembling luteoma and associated with hyperadrenocorticism.
Animals↗
Hypercalcemia and renal failure. Etiology, pathophysiology, diagnosis, and treatment.
Hypercalcemia is a frequent disorder of calcium metabolism in dogs and cats. Hypercalcemia-induced alterations in renal function and morphology are linked to many of the clinical manifestations observed in hypercalcemic patients. Since many renal effects induced by hypercalcemia are potentially reversible, early recognition and characterization of the problem facilitates rapid therapeutic intervention.
Animals↗
Effects of sample handling temperatures on bovine skim milk progesterone concentrations.
The effect of incubation of whole milk at various temperatures and times on the amount of progesterone (nmol/l) in the skim milk fraction was determined. For this study, milk samples were obtained from 10 pregnant Holstein cows. The whole milk samples were incubated at 37 degrees C (near normal body temperature of the cow) for 4 h and the initial skim milk progesterone concentration was determined. After that, the experiment was carried out in two main steps: (I) The test tubes containing the whole milk were divided into 4 groups and incubated at different temperatures (0, 4, 20 and 37 degrees C). Samples were removed at 30, 60, 90 and 120 min. (II) After 120 min of incubation at different temperatures, the remaining test tubes were returned to the water bath at 37 degrees C for another 30, 60 and 90 min. The initial average of skim milk progesterone concentrations after incubating the whole milk at 37 degrees C for 4 h was 11.0 +/- 4.4 nmol/l. When the whole milk was incubated at 0 degrees C, the skim milk progesterone concentration increased (P < 0.05) to 14.6 nmol/l at 30 min and reached 16.2 nmol/l at 60 min of incubation. At 4 degrees C incubation temperature, skim milk progesterone increased significantly (P < 0.05) to 15.3 nmol/l and reached 16.9 nmol/l after 90 min. When the whole milk was left at 20 degrees C, the initial skim milk progesterone values decreased to 9.5 nmol/l after 30 min incubation and no further decreases were found even if the whole milk was returned to 37 degrees C for 90 min.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effect of food deprivation on baseline iodothyronine and cortisol concentrations in healthy, adult horses.
Six healthy, adult horses, with normal (mean +/- SEM) baseline serum concentrations of total triiodothyronine (T3, 1.02 +/- 0.16 nmol/L), free T3 (FT3, 2.05 +/- 0.33 pmol/L), total thyroxine (T4, 19.87 +/- 1.74 nmol/L), free T4 (FT4, 11.55 +/- 0.70 pmol/L), total reverse T3 (rT3, 0.68 +/- 0.06 nmol/L), and cortisol (152.75 +/- 17.50 nmol/L), were judged to be euthyroid on the basis of response to a standardized thyroid-stimulating hormone response test. Serum concentrations of T3, FT3, T4, FT4, rT3, and cortisol were determined immediately before and every 24 hours during a 4-day period of food deprivation, when water was available ad libitum. Similar variables were measured 72 hours after refeeding. Decreases (to percentage of baseline, prefood deprivation value) in circulating T3 (42%), T4 (38%), FT3 (30%), and FT4 (24%) concentrations were maximal after 2, 4, 2, and 4 days of food deprivation, respectively (P < 0.05). Increases (compared with baseline, prefood deprivation value) in rT3 (31%) and cortisol (41%) concentrations were maximal after 1 and 2 days of food deprivation, respectively (P < 0.05). Refeeding resulted in increase in serum T4 and FT4, and decrease in rT3 and cortisol concentrations toward baseline values, after 72 hours (P < 0.05). Refeeding did not effect a return of T3 or FT3 concentration to baseline values after 72 hours (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Analysis of Variance↗
Isolation of thyroid peroxidase and lack of autoantibodies to the enzyme in dogs with autoimmune thyroid disease.
Fifty serum samples from dogs with clinical signs of hypothyroidism and autoantibodies (AA) to thyroglobulin (Tg), thyroxine, or triiodothyronine were screened for AA to thyroid peroxidase (TPO). Thyroid peroxidase is the antigen against which microsomal AA are formed in human beings with lymphocytic thyroiditis. The TPO was isolated from canine thyroid tissue, using a modification of the procedure for purifying porcine TPO. The enzyme was solubilized from the membrane, using a deoxycholate-trypsin solution, followed by ammonium sulfate precipitation and diethylaminoethyl Sephadex chromatography. Activity of TPO was determined, using an iodide oxidation assay and a guaiacol assay. A monoclonal antibody to canine Tg, coupled to an immunoaffinity column, was used to eliminate the contaminating Tg from the TPO preparation. Using the TPO preparation as an antigen, an ELISA was performed on 10 serum samples and immunoblot assays were performed on 50 canine sera. Autoantibodies to TPO were not found in any of the sera. Assays also were performed, using purified porcine and human TPO and evidence of cross-reactivity with canine TPO was not identified. The absence of AA to TPO in dogs suggests a different pathogenesis for autoimmune thyroid disease in dogs than that hypothesized for lymphocytic thyroiditis in human beings.
Animals↗
Skim milk progesterone in pregnant cows from insemination throughout lactation.
The skim milk progesterone profile was assessed by radioimmunoassay, without extraction, from the day of insemination (day 0) until the cows were dried off on day 225 of gestation. A total of 418 samples were collected from 154 pregnant Holstein cows. The daily variation in skim milk progesterone was recorded from day 1 until day 45 of pregnancy to detect the commencement of progesterone secretion from the corpus luteum after insemination. Subsequent determinations were made every 2 weeks from day 46 until lactation ceased. On the day of artificial insemination and for the first 2 days after insemination, all the cows had a basal progesterone concentration < 0.1 ng/ml. A rise in progesterone (0.2 +/- 0.1 ng/ml) was first detected on the third day after insemination. The progesterone values then increased significantly (p < 0.001) until day 15. The values then remained nearly constant (2.5-3.5 ng/ml) until day 106 of pregnancy, when they began to decline. Between days 120 and 180 of gestation, progesterone was significantly decreased (2.2-2.9 ng/ml) before it rose again to the previous plateau (3.5-3.9 ng/ml) around day 180. The progesterone concentration then remained at the higher level until the animals were dried off.
Animals↗
Thyroid function in dogs with spontaneous and induced congestive heart failure.
The effects of spontaneous and experimentally induced congestive heart failure on serum thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3'5'-triiodothyronine (reverse T3), free T4, free T3 concentrations, and the serum T4 and T3 concentrations in response to administration of thyrotropin were studied. Serum thyroid hormone concentrations were not different between eight dogs with spontaneous congestive heart failure and normal age matched control dogs. Seven dogs with experimental heart failure were tested before and after induction of congestive heart failure by rapid ventricular pacing. Mean serum T4 and free T3 concentrations were decreased and mean serum reverse T3 concentration was increased following induction of heart failure. The serum T4 and T3 responses to thyrotropin were not altered. Thyroid gland morphology appeared normal in dogs with experimental heart failure. Experimental congestive heart failure, similar to some other nonthyroidal illnesses, alters thyroid hormone secretion and metabolism in dogs.
Animals↗
Pharmacokinetics of L-thyroxine after its oral administration in dogs.
Twelve mature (5 sexually intact males, 4 castrated males, and 3 females) mixed-breed dogs were surgically thyroidectomized and used in a Latin-square design pharmacokinetic study of orally administered L-thyroxine. The dogs were treated with 44, 22, and 11 micrograms of L-thyroxine/kg as a single morning dose or in divided doses, morning and evening. Serum concentration of thyroxine (T4) was evaluated to determine a number of pharmacokinetic variables for comparison. Mean steady-state concentrations (Css) were determined from the area under the curve. Variables were analyzed for comparisons between dosages by use of ANOVA. Concentration at steady state was highest for dogs of the 44-micrograms/kg of body weight once-daily group and was lowest for dogs of the group given 11 micrograms/kg in 2 daily doses. Single daily administration resulted in higher Css, except at the 22-micrograms/kg/d dosage. Clearance was faster for the 22- and 44-micrograms/kg/d dosages than for the 11-micrograms/kg/d dosage. The half-life (t1/2) and mean residence time (MRT) also were shorter for the 44-micrograms/kg/d dosage, possibly indicating more rapid elimination of the drug at higher doses and dose-dependent kinetics. Perhaps, as the dogs' metabolism increased with higher iodothyronine concentrations, hormone degradation was accelerated. Interval (divided vs single dose) caused some expected changes: maximal concentration was higher and minimal concentration was lower when single administration was used. These undulations resulted in iodothyronine concentrations above the physiologic range for a number of hours, whereas concentration closer to physiologic ranges was achieved by use of divided doses.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Oral↗
Radioimmunoassay monitoring of thyroid hormone concentrations in dogs on thyroid replacement therapy: 2,674 cases (1985-1987).
Serum iodothyronine concentrations from 4,064 samples submitted for monitoring of thyroid replacement therapy were evaluated in a retrospective study. After exclusion of samples because of the presence of 3,5,3' triiodothyronine (T3) autoantibodies, insufficient numbers of dogs on some commercial preparations or medication with corticosteroids or synthetic T3 preparations, data from 2,674 dogs remained. Data were analyzed by using information on dose, time after dosing, commercial product, and once-a-day or twice-a-day dosing regimens. Serum total thyroxine (T4) and total T3 and estimates of free T4 and free T3 were significantly high in serum from dogs given higher doses of synthetic L-thyroxine orally. Doubling the oral dosage did not double the serum iodothyronine concentrations, perhaps because of poor absorption or more rapid catabolism of the hormones at higher L-thyroxine doses. Wide variation in the therapeutic hormone concentrations was found. Some dogs given low dosages of L-thyroxine had normal iodothyronine concentrations whereas some others given higher dosages had low normal to low concentrations. Monitoring the serum concentrations is an objective way to ensure adequate concentrations for successful therapy. When a therapeutic trial is used as a diagnostic procedure, one should not rule out hypothyroidism unless a therapeutic monitoring sample has indicated that replacement dose and absorption of the exogenous iodothyronine has been adequate. Thyroid hormone concentrations peaked at 4 to 6 hours after oral administration of L-thyroxine for once-a-day and twice-a-day dosage regimens. Higher concentrations were achieved with once-a-day than with twice-a-day regimens at the same total daily dose.(ABSTRACT TRUNCATED AT 250 WORDS)
Analysis of Variance↗
Prevalence of autoantibodies to thyroglobulin, thyroxine, or triiodothyronine and relationship of autoantibodies and serum concentrations of iodothyronines in dogs.
Assays were developed to detect and measure autoantibodies (AA) to thyroglobulin (Tg) and to the thyroid hormones, thyroxine (T4) and triiodothyronine (T3). An ELISA to detect AA to Tg was developed, using purified canine Tg as the antigen and goat anti-canine IgG conjugated with alkaline phosphatase as the second antibody. A highly charged agarose electrophoresis assay was used for determination of AA to T4 and T3. Sera from dogs (n = 119) with clinical signs consistent with hypothyroidism were tested for AA to Tg, T4, and T3. Autoantibodies to at least 1 of the 3 thyroid antigens were detected in 58 of the 119 (48.7%) sera tested. Autoantibodies to Tg were detected more frequently in samples with low serum concentrations of thyroid hormones than in samples with normal concentrations. The presence of AA to T4, T3, or both was not significantly associated with low thyroid hormone concentrations, but this lack of association may have been attributable to binding of AA in the measurement of thyroid hormones by radioimmunoassay.
Animals↗