Thyroid-stimulating hormone and total thyroxine concentrations in euthyroid, sick euthyroid and hypothyroid dogs

Canine thyroid-stimulating hormone (cTSH) was measured in a variety of clinical cases (n= 72). The cases were classified as euthyroid, sick euthyroid, hypothyroid or hypothyroid on non-thyroidal therapy on the basis of their history, clinical signs, laboratory results (including total thyroxine concentrations and, where indicated, thyroid-releasing hormone [TRH] stimulation tests) and response to appropriate therapy. Additional samples were taken during some of the TRH stimulation tests to measure the response of cTSH concentrations following TRH administration. A reference range (0 to 0–41 ng/ml) was calculated from the basal concentrations of cTSH in a group of 41 euthyroid dogs. Six of nine cases of confirmed hypothyroidism had basal cTSH concentrations above the reference range, whereas the remainder were within the normal range. One of these three remaining cases was a pituitary dwarf and did not show a rise in cTSH concentration following TRH stimulation. In contrast, only one of a group of six hypothyroid dogs that had been on non-thyroidal treatment within the previous four weeks had increased concentrations of basal cTSH. This study also found that five of a group of 16 dogs with sick euthyroid syndrome had increased cTSH concentrations. It was concluded that cTSH measurements are a useful additional diagnostic test in cases of suspected hypothyroidism in dogs but that dynamic testing is still required to confirm the diagnosis of hypothyroidism.     

Evaluation of serum free thyroxine and thyrotropin concentrations in the diagnosis of canine hypothyroidism

Canine thyroid-stimulating hormone (cTSH), total thyroxine (T4) and free T4 by equilibrium dialysis (fT4d) were measured in serum samples from 107 dogs with clinical signs suggestive of hypothyroidism in which the diagnosis was either confirmed (n = 30) or excluded (n = 77) by exogenous TSH response testing. Median serum total T4 and fT4d concentrations were significantly lower and cTSH significantly higher (P < 0.001) in hypothyroid compared with euthyroid dogs. Differential positive rate analysis determined optimal cut-off values of less than 14.9 nmol/litre (total T4), less than 5.42 pmol/litre (fT4d), greater than 0.68 ng/ml (cTSH), less than 17.3 (T4 to cTSH ratio), and less than 7.5 (fT4d to cTSH ratio) for hypothyroidism. These had a sensitivity and specificity of 100 and 75.3 per cent, 80 and 93.5 per cent, 86.7 and 81.8 per cent, 86.7 and 92.2 per cent, and 80 and 97.4 per cent, respectively, for diagnosing hypothyroidism. Corresponding areas under the receiver operating characteristic curves were 0.92, 0.93, 0.87, 0.93 and 0.93. Unexpectedly low cTSH values in hypothyroid dogs may have resulted from concurrent non-thyroidal illness. Unexpectedly high serum cTSH values in the euthyroid dogs might have resulted from recovery from illness or concurrent potentiated sulphonamide therapy. Measurement of endogenous cTSH concentration is a valuable diagnostic tool for canine hypothyroidism if used in association with assessment of T4. Estimation of fT4d added only limited additional information over total T4 measurement.     

Evaluation of recombinant human thyroid-stimulating hormone to test thyroid function in dogs suspected of having hypothyroidism

OBJECTIVE: To evaluate the use of recombinant human (rh) thyroid-stimulating hormone (TSH) in dogs with suspected hypothyroidism. ANIMALS: 64 dogs with clinical signs of hypothyroidism. PROCEDURES: Dogs received rhTSH (75 microg/dog, IV) at a dose independent of their body weight. Blood samples were taken before and 6 hours after rhTSH administration for determination of total serum thyroxine (T(4)) concentration. Dogs were placed into 1 of 3 groups as follows: those with normal (ie, poststimulation values indicative of euthyroidism), unchanged (ie, poststimulation values indicative of hypothyroidism; no thyroid gland stimulation), or intermediate (ie, poststimulation values between unchanged and normal values) post-TSH T(4) concentrations. Serum canine TSH (cTSH) concentration was determined in prestimulation serum (ie, before TSH administration). RESULTS: 14, 35, and 15 dogs had unchanged, normal, and intermediate post-TSH T(4) concentrations, respectively. Basal T(4) and post-TSH T(4) concentrations were significantly different among groups. On the basis of basal serum T(4) and cTSH concentrations alone, 1 euthyroid (normal post-TSH T(4), low basal T(4), and high cTSH concentrations) and 1 hypothyroid dog (unchanged post-TSH T(4) concentration and low to with-in reference range T(4) and cTSH concentrations) would have been misinterpreted as hypothyroid and euthyroid, respectively. Nine of the 15 dogs with intermediate post-TSHT(4) concentrations had received medication known to affect thyroid function prior to the test, and 2 of them had severe nonthyroidal disease. CONCLUSIONS AND CLINICAL RELEVANCE: The TSH-stimulation test with rhTSH is a valuable diagnostic tool to assess thyroid function in selected dogs in which a diagnosis of hypothyroidism cannot be based on basal T(4) and cTSH concentrations alone.     

Effects of sulfamethoxazole-trimethoprim on thyroid function in dogs

OBJECTIVE: To evaluate effects of trimethoprim-sulfamethoxazole (T/SMX) on thyroid function in dogs. ANIMALS: 6 healthy euthyroid dogs. PROCEDURE: Dogs were administered T/SMX (14.1 to 16 mg/kg, PO, q 12 h) for 3 weeks. Blood was collected weekly for 6 weeks for determination of total thyroxine (TT4), free thyroxine (fT4), and canine thyroid-stimulating hormone (cTSH) concentrations. Schirmer tear tests were performed weekly. Blood was collected for CBC prior to antimicrobial treatment and at 3 and 6 weeks. RESULTS: 5 dogs had serum TT4 concentrations equal to or less than the lower reference limit, and 4 dogs had serum fT4 less than the lower reference limit after 3 weeks of T/SMX administration; cTSH concentrations were greater than the upper reference limit in 4 dogs. All dogs had TT4 and fT4 concentrations greater than the lower reference limit after T/SMX administration was discontinued for 1 week, and cTSH concentrations were less than reference range after T/SMX administration was discontinued for 2 weeks. Two dogs developed decreased tear production, which returned to normal after discontinuing administration. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that administration of T/SMX at a dosage of 14.1 to 16 mg/kg, PO, every 12 hours for 3 weeks caused decreased TT4 and fT4 concentrations and increased cTSH concentration, conditions that would be compatible with a diagnosis of hypothyroidism. Therefore, dogs should not have thyroid function evaluated while receiving this dosage of T/SMX for >2 weeks. These results are in contrast to those of a previous study of trimethoprim-sulfadiazine.     

Clinical,hematological, biochemical and endocrinological aspects of 32 dogs with hypothyroidism

During the years of 1996-2001, hypothyroidism was diagnosed at the clinic for small animal internal medicine, University of Zurich, in 32 dogs. Most of the dogs were large breeds. The most frequent clinical characteristics observed were exercise intolerance, obesity, dermatological, neurological and gastrointestinal signs. Predominant laboratory abnormalities were a low red blood cell count, increased concentration of cholesterol, triglycerides and fructosamin. 29 dogs had a T4 below the reference range (< 1.5 micrograms/dl), one dog had a T4 at the lower limit thereof (1.6 micrograms/dl). One dog had a T4 within the reference range (3.4 micrograms/dl), another had a very high T4 of 206.8 micrograms/dl; the results of the latter 2 dogs were interpreted as incorrectly increased T4 values due to in vitro interference with T4-autoantibodies. Diagnosis was confirmed in all of the dogs based on TSH-stimulation testing. Endogenous TSH (cTSH) measured parallelly, was elevated in only 60% of the dogs. In about 67% of the dogs, hypothyroidism was associated with thyroglobulin-autoantibodies. Canine hypothyroidism is a rather rare endocrine disorder in Switzerland. The TSH-stimulation test remains the gold standard in confirming the disease; a definitive diagnosis can be challenging for practitioners because bovine TSH, used for the TSH-stimulation test is not licensed for use in dogs. Since assessment of cTSH using current assays shows normal values in a high percentage of hypothyroid dogs, the diagnostic value is only limited. In most of the hypothyroid dogs T4 is decreased, with the presence of autoantibodies to T4, it can be normal or increased.     

Thyroid sonography as an effective tool to discriminate between euthyroid sick and hypothyroid dogs

The diagnosis of canine hypothyroidism and its differentiation from euthyroid sick syndrome still is a major diagnostic challenge. In this study, ultrasonography was shown to be an effective tool for the investigation of thyroid gland diseases. Healthy control dogs (n = 87), dogs with euthyroid sick syndrome (n = 26), thyroglobulin autoantibody-positive (TgAA-positive, n = 30) hypothyroid dogs, and TgAA-negative (n = 23) hypothyroid dogs were examined by thyroid ultrasonography. Maximal cross sectional area (MCSA), thyroid volume, and echogenicity were measured. Statistical analysis identified highly significant (P < .001) differences between euthyroid and hypothyroid dogs both in thyroid volume and in MCSA, whereas no significant differences in thyroid size were detected between healthy euthyroid dogs and dogs with euthyroid sick syndrome. In euthyroid and euthyroid sick dogs, parenchymal echotexture was homogeneous and hyperechoic, whereas relative thyroid echogenicity of both TgAA-positive and TgAA-negative hypothyroid dogs was significantly lower (P < .001). When using arbitrarily chosen cutoff values for relative thyroid volume, MCSA, and echogenicity, thyroid volume especially was found to have highly specific predictive value for canine hypothyroidism. In summary, the data reveal that thyroid sonography is an effective ancillary diagnostic tool to differentiate between canine hypothyroidism and euthyroid sick syndrome.     

The Effect of Levothyroxine Treatment on Resting Energy Expenditure of Hypothyroid Dogs

Thirty adult, client-owned dogs were diagnosed with hypothyroidism based on history, physical examination findings, hematologic and biochemical abnormalities, thyrotropin (TSH) response testing, endogenous canine thyrotropin (cTSH) concentration, or both, and total serum thryoxine concentration. All dogs received levothyroxine (L-thyroxine) at an initial dose of 22 μg/kg PO sid in either a tablet (13 dogs) or chewable form (17 dogs). Energy expenditure of each dog during apparent rest was estimated with an open-flow indirect calorimetry system by determining the rates of carbon dioxide production and oxygen consumption. Energy expenditure of apparent rest (EE) was lower in untreated hypothyroid dogs compared with reference values for EE. After treatment with L-thyroxine, EE of the hypothyroid dogs was significantly ( P < .05) higher than pretreatment values.     

Exercise-induced hyperkalemia in hypothyroid dogs

We investigated the effect of hypothyroidism in dogs on (1) the Na+-, K+ -ATPase concentration in skeletal muscle, and (2) potassium (K+) homeostasis at rest and during exercise. Prior to and 1 year after induction of hypothyroidism by surgery and subsequent radiothyroidectomy, the Na+-, K+ -ATPase concentrations were quantified in biopsies of sternothyroid muscles of seven Beagle dogs by measuring [3H]ouabain binding capacity. In addition, plasma K+ concentrations were measured at rest and after treadmill exercise in six hypothyroid and seven euthyroid Beagle dogs. During hypothyroidism, the mean Na+ -, K+ -ATPase concentration in muscle biopsies was 41% lower than during euthyroidism. The mean resting plasma K+ value of the hypothyroid dogs was significantly (14%) higher than that of the euthyroid dogs. In the hypothyroid dogs, plasma K+ concentration increased significantly during exercise, whereas there was no rise in the euthyroid dogs. The rise in plasma K+ concentration could not be ascribed to muscle damage, as plasma creatine kinase concentrations remained within reference range. Also renal K+ retention was an unlikely explanation, as plasma aldosterone concentration and plasma renin activity rather increased than decreased during exercise. In conclusion, hypothyroid dogs tend to develop hyperkalemia during exercise, which for a large part can be explained by the severe reduction of the Na+ -, K+ -ATPase capacity in the skeletal muscle pool.     

Evaluation of thyroid function in dogs suffering from recurrent flank alopecia

Thyroid function was assessed in euthyroid dogs (n = 20), dogs suffering from canine recurrent flank alopecia (CRFA, n = 18), and hypothyroid dogs (n = 21). Blood samples obtained from all dogs in each group were assayed for total thyroxine (TT4), thyrotropin (TSH), and thyroglobulin autoantibody (TgAA) serum concentrations. Total T4 and TSH serum concentrations were significantly decreased and increased, respectively, in the hypothyroid group compared with the other 2 groups. No significant differences in TT4 and TSH serum values were found between the euthyroid and CRFA groups. Thyroglobulin autoantibodies were detected in 10, 11.1, and 61.9% of euthyroid dogs, dogs with CRFA, and hypothyroid dogs, respectively. In conclusion, dogs suffering from CRFA have a normal thyroid function, and the determination of TT4 and TSH serum concentrations allows differentiation of these dogs from dogs with hypothyroidism, in most cases. Occasionally, the 2 diseases can be concomitant.     

Altered Serum Thyrotropin Concentrations in Dogs with Primary Hypoadrenocorticism before and during Treatment

Background

Thyrotropin (TSH) can be increased in humans with primary hypoadrenocorticism (HA) before glucocorticoid treatment. Increase in TSH is a typical finding of primary hypothyroidism and both diseases can occur concurrently (Schmidt's syndrome); therefore, care must be taken in assessing thyroid function in untreated human patients with HA.

Objective

Evaluate whether alterations in cTSH can be observed in dogs with HA in absence of primary hypothyroidism.

Animals

Thirty dogs with newly diagnosed HA, and 30 dogs in which HA was suspected but excluded based on a normal ACTH stimulation test (controls) were prospectively enrolled.

Methods

cTSH and T4 concentrations were determined in all dogs and at selected time points during treatment (prednisolone, fludrocortisone, or DOCP) in dogs with HA.

Results

cTSH concentrations ranged from 0.01 to 2.6 ng/mL (median 0.29) and were increased in 11/30 dogs with HA; values in controls were all within the reference interval (range: 0.01–0.2 ng/dL; median 0.06). There was no difference in T4 between dogs with increased cTSH (T4 range 1.0‐2.1; median 1.3 μg/dL) compared to those with normal cTSH (T4 range 0.5‐3.4, median 1.4 μg/dL; P=0.69) and controls (T4 range 0.3‐3.8, median 1.8 μg/dL; P=0.35). After starting treatment, cTSH normalized after 2–4 weeks in 9 dogs and after 3 and 4 months in 2 without thyroxine supplementation.

Conclusions and Clinical Relevance

Evaluation of thyroid function in untreated dogs with HA can lead to misdiagnosis of hypothyroidism; treatment with glucocorticoids for up to 4 months can be necessary to normalize cTSH.     

Treatment and therapeutic monitoring of canine hypothyroidism

Thirty-one dogs with spontaneous hypothyroidism were treated with thyroid hormone replacement therapy (THRT) and monitored for approximately three months. Good clinical and laboratory control was ultimately achieved in all cases with a mean L-thyroxine (T4) dose of 0.026 mg/kg administered once daily. There was a significant increase and decrease in circulating total T4 and canine thyroid stimulating hormone (cTSH) concentrations, respectively, after starting THRT. After commencing treatment, 11 cases subsequently required an increase and three cases required a decrease in dose to achieve optimal clinical control. Median (semi interquartile range [SIR]) circulating six-hour post-pill total T4 (53.6 [27.91 nmol/litre) and cTSH (0.03 [0] microg/litre) concentrations were significantly increased and decreased, respectively, in treated dogs that did not require a dose change; corresponding values in treated dogs in which an increase in dose was required were 29.3 (12.7) nmol/litre and 0.15 (0.62) microg/litre, respectively. However, circulating cTSH measurement was of limited value in assessing therapeutic control because, although increased values were associated with inadequate therapy, reference range cTSH values were common in inadequately treated dogs. Lethargy and mental demeanour were typically the first clinical signs to improve, with significant bodyweight reduction occurring within two weeks of commencing THRT. Routine clinicopathological monitoring was of value in confirming a general metabolic response to THRT, but was of limited value in accurately monitoring cases or tailoring therapy in individual cases.     

Plasma von Willebrand factor concentration and thyroid function in dogs

Plasma von Willebrand factor antigen concentration was determined in 15 dogs with suspected hypothyroidism, in 1 dog with hyperthyroidism, and in 14 euthyroid dogs. The mean +/- SEM von Willebrand factor:antigen concentration in hypothyroid dogs (47.1% +/- 12.6%) was significantly decreased (P less than 0.0005), compared with that in euthyroid dogs (94.7 +/- 5.6%). Four hypothyroid dogs were given thyroxine for 1 month and all 4 had an increase in von Willebrand factor:antigen concentration. The plasma von Willebrand factor:antigen concentration was 200% in the hyperthyroid dog. Seemingly, reduced concentrations of plasma von Willebrand factor:antigen can be found in dogs in association with congenital von Willebrand disease or with von Willebrand disease acquired through hypothyroidism.     

Effect of dosing and sampling time on serum thyroxine, free thyroxine, and thyrotropin concentrations in dogs following multidose etodolac administration

Thirty-eight dogs with orthopedic disorders received etodolac, an NSAID, at 10.0 to 13.3 mg/kg PO once daily for 14 to 19 days. Mean total thyroxine (T4), free thyroxine (fT4), and canine thyrotropin (cTSH) values before and after etodolac administration were compared using paired t-tests. A significant (P <.05) decrease in T4 values occurred after etodolac administration with 21% of these values falling below the reference range. A significant (P <.05) increase in cTSH following etodolac administration, but none of the values was above the reference range. No significant changes occurred in mean fT4 values; however, 10% of the values fell below the reference range. In conclusion, T4 and fT4 test results should be interpreted with caution in dogs receiving etodolac.     

The effects of thyroid hormones on the skin of beagle dogs

The effects of hypothyroidism on canine skin were determined by comparing morphologic, morphometric, and hair cycle differences in skin biopsy samples from 3 groups of age- and gender-matched Beagle dogs: (1) euthyroid dogs; (2) dogs made hypothyroid by administration of 131I; and (3) dogs made hypothyroid and maintained in a euthyroid state by treatment with synthetic thyroxine. After 10 months of observation, there was slower regrowth of hair 2 months after clipping in the untreated-hypothyroid dogs. Untreated-hypothyroid dogs had a greater number of follicles in telogen and fewer hair shafts (ie, a greater number of hairless telogen follicles) than did the control group. The control dogs had a greater number of telogen follicles but the same number of hair shafts as the treated-hypothyroid group. Treated-hypothyroid dogs had the greatest number of follicles in the growing stage of the hair cycle (anagen). This study suggests that, at least in Beagles, induced hypothyroidism does not affect the pelage as dramatically as has been described in naturally occurring disease. This is because normal Beagles retain hair shafts in follicles for long periods, and the alopecia of hypothyroidism appears to evolve slowly because of the prolongation of this haired telogen stage. The evaluation of thyroxine-treated hypothyroid dogs demonstrates that thyroid hormone supplementation of Beagle dogs with induced hypothyroidism stimulates hair growth.     

Effect of 131I-induced hypothyroidism on indices of reproductive function in adult male dogs

Hypothyroidism has been cited as a cause of infertility, abnormal semen quality, and poor libido in people and animals. The purpose of this study was to evaluate the effect of hypothyroidism on variables indicative of reproductive function in adult male dogs. Nine normal dogs were randomly assigned to 2 groups. Hypothyroidism was induced with 131I in 6 dogs. Three dogs remained untreated, normal, and euthyroid. Thyroid hormone concentrations, body weight, clinical signs, and reproductive function were determined for each dog every 3 months for 2 years. Reproductive function was assessed by determining daily sperm output, total scrotal width, spermatozoal motility and morphology, libido, and serum testosterone and luteinizing hormone concentration responses to exogenous gonadotropin-releasing hormone. The 131I-treated dogs developed clinical and laboratory signs of hypothyroidism. In the hypothyroid dogs, serum concentrations of thyroid hormones were consistently below the reference range and were significantly lower than that in the euthyroid dogs. There was no difference in reproductive function between the hypothyroid and euthyroid dogs. The results of this study show that 131I-induced hypothyroidism does not affect indices of reproductive function in adult male dogs.     

Thyroid function testing in Greyhounds.

OBJECTIVE: To evaluate thyroid function in healthy Greyhounds, compared with healthy non-Greyhound pet dogs, and to establish appropriate reference range values for Greyhounds. ANIMALS: 98 clinically normal Greyhounds and 19 clinically normal non-Greyhounds. PROCEDURES: Greyhounds were in 2 groups as follows: those receiving testosterone for estrus suppression (T-group Greyhounds) and those not receiving estrus suppressive medication (NT-group Greyhounds). Serum thyroxine (T4) and free thyroxine (fT4) concentrations were determined before and after administration of thyroid-stimulating hormone (TSH) and thyroid-releasing hormone (TRH). Basal serum canine thyroid stimulating hormone (cTSH) concentrations were determined on available stored sera. RESULTS: Basal serum T4 and fT4 concentrations were significantly lower in Greyhounds than in non-Greyhounds. Serum T4 concentrations after TSH and TRH administration were significantly lower in Greyhounds than in non-Greyhounds. Serum fT4 concentrations after TSH and TRH administration were significantly lower in NT-group than T-group Greyhounds and non-Greyhounds. Mean cTSH concentrations were not different between Greyhounds and non-Greyhounds. CONCLUSIONS AND CLINICAL RELEVANCE: Previously established canine reference range values for basal serum T4 and fT4 may not be appropriate for use in Greyhounds. Greyhound-specific reference range values for basal serum T4 and fT4 concentrations should be applied when evaluating thyroid function in Greyhounds. Basal cTSH concentrations in Greyhounds are similar to non-Greyhound pet dogs.     

Blood–brain‐barrier disruption in chronic canine hypothyroidism

Background: Central nervous system (CNS) manifestations of hypothyroidism have been associated with cerebrovascular complications. Reports of cerebrospinal fluid (CSF) abnormalities are rare in hypothyroid dogs. Objective: The aim of this study was to determine if chronic hypothyroidism causes blood–brain‐barrier (BBB) abnormalities that are detectable using indirect CSF biomarkers. Methods: The study included 18 normal, euthyroid, female mixed‐breed dogs. Hypothyroidism was induced by ¹³¹iodine administration in 9 dogs; 9 served as untreated controls. Evaluations included physical and neurologic examination, complete CSF analysis, serum and CSF protein electrophoresis, measurement of plasma vascular endothelial growth factor (VEGF) and serum S‐100B concentrations, and calculation of CSF albumin quota (AQ) and were conducted at baseline and 6, 12, and 18 months after induction of hypothyroidism. Data were analyzed using repeated measures ANOVA. Results: At baseline, differences between groups were not detected for any variable. Throughout the study, controls dogs remained free of neurologic disease and had test variables that remained within reference intervals. Two hypothyroid dogs developed CNS signs during the study, and evidence of cerebrovascular disease was found at necropsy. At 12 and 18 months, the CSF total protein, VEGF, S‐100B, and fractional albumin concentrations, and AQ were significantly higher (P<.04) in hypothyroid dogs than controls. Among test variables assayed in serum or plasma, the only significant difference was a higher S‐100B concentration in hypothyroid dogs (P=.003) at 18 months. Conclusions: BBB integrity is disrupted in chronic hypothyroidism. Significant increases in CSF concentrations of VEGF and S100‐B in hypothyroid dogs indicate dysfunction in both endothelial and glial elements of the BBB.     

Proliferative responses to canine thyroglobulin of peripheral blood mononuclear cells from hypothyroid dogs

The immune responses of hypothyroid dogs to canine thyroglobulin (cTg) were evaluated for the proliferative ability of peripheral blood mononuclear cells (PBMC). PBMC from three hypothyroid dogs with high titers of thyroglobulin autoantibody (TgAA) and 3 clinically normal dogs were cultured with 5, 10, or 20 microg/ml of cTg for 72 hr. The proliferative responses of the cells were determined by the level of incorporated BrdU. The numbers of cells expressing Thy-1, CD4, CD8 and IgG in the PBMC were counted by the immunofluorescence method. Proliferative responses to cTg were observed in the cells from hypothyroid dogs. The number of cells expressing IgG and CD8 in the hypothyroid dogs tended to be high compared with the clinically normal dogs. The CD4+ cells in cultures from hypothyroid dogs increased depending upon the amount of cTg. There was a significant (P<0.05) positive correlation between the number of CD4+ cells and the concentration of cTg in the cultures from hypothyroid dogs. These findings suggest a possible relationship between canine hypothyroidism and cellular immunity. Loss of self tolerance to thyroid antigens in CD4+ T cells may play an important role in the development of canine hypothyroidism.     

Serum thyroid hormone concentrations and thyrotropin responsiveness in dogs with generalized dermatologic disease.

Fifty-eight dogs with generalized dermatologic disease that had not been given glucocorticoids systemically or topically within 6 weeks of entering the study were evaluated for thyroid function by use of the thyrotropin-response test. Dogs were classified as euthyroid or hypothyroid on the basis of test results and response to thyroid hormone replacement therapy. Baseline serum thyroxine (T4), free T4 (fT4), and triiodothyronine (T3) concentrations were evaluated in the 58 dogs. Serum T4, fT4, and T3 concentrations were evaluated in 200 healthy dogs to establish normal values. Hormone concentrations were considered low if they were less than the mean -2 SD of the values for control dogs. Specificity of T4 and fT4 concentrations was 100% in predicting hypothyroidism; none of the euthyroid dogs with generalized skin disease had baseline serum T4 or fT4 concentration in the low range. Sensitivity was better for fT4 (89%) than for T4 (44%) concentration. Significant difference was not observed in serum T4 and fT4 concentrations between euthyroid dogs with generalized skin disease and healthy control dogs without skin disease. Serum T3 concentration was not accurate in predicting thyroid function; most of the euthyroid and hypothyroid dogs with skin disease had serum T3 concentration within the normal range.     

Use of recombinant human thyroid-stimulating hormone for thyrotropin stimulation test in healthy, hypothyroid and euthyroid sick dogs

Recombinant human thyroid-stimulating hormone (rhTSH) was evaluated for the diagnosis of canine hypothyroidism, using TSH response tests. Phase I stimulation tests were performed in 6 healthy dogs weighing over 20 kg, using 50 and then 100 microg of freshly reconstituted rhTSH administered intravenously. In phase II, the same dogs were stimulated by using 100 microg of rhTSH frozen for 3 months at -20 degrees C. Phase III stimulation tests were performed by using 50 or 100 microg of freshly reconstituted or frozen rhTSH in healthy (n = 14), euthyroid sick (n = 11) and hypothyroid dogs (n = 9). A dose of 100 microg of rhTSH was judged more appropriate for dogs weighing more than 20 kg. Biological activity of rhTSH after freezing at -20 degrees C for up to 12 weeks was maintained. When stimulated, significant (P < 0.05) increases in total thyroxine concentration were observed only in healthy and euthyroid sick dogs. Results of this study show that the rhTSH stimulation test is able to differentiate euthyroidism from hypothyroidism in dogs.