Methimazole-induced hypothyroidism is a clinical problem in the treatment of hyperthyroidism in people and animals and is an example of metabolic disease that can lead to fertility disorders and can give elastographic testicular changes. Ultrasound elastography using the Esaote MyLab Twice ultrasound system and a morphological examination of testes were performed in seven methimazole-administered (group E) and seven healthy rats (group C). The elasticity ratio of strains in the scrotal wall of the near-field test area to testicular tissue (ELX-T-RAT) and hardness percentage of strained tissues in the defined area of a testicle (ELX-T%HRD) in group E were statistically significantly lower than in group C. The degree of spermatogenesis was statistically significantly higher in group E than in group C and similarly seminiferous tubule diameters in group E were statistically significantly higher than in group C. Body weight and testicular weight in group E were statistically significantly lower than in group C. Changes in the elastographical parameters of testes may result from disorders secondary to hypothyroidism. The usefulness of elastography is noteworthy in the case of evaluation of testis function in patients with some metabolic disorders.

Introduction: Thyroid hormones affect protein turnover, and in the case of hypothyroidism a decrease in protein synthesis and reduced release of certain amino acids from skeletal muscles are observed. Changes in the amino acid system of skeletal muscles may be responsible for the occurrence of muscle disorders. Material and Methods: The study measured the content of selected amino acids in the gastrocnemius muscle of Wistar rats during experimental hypothyroidism induced by oral administration of methimazole at a concentration of 0.05% in drinking water for 90 d. The rats were divided into four groups: E1 (n = 6) - experimental males, E2 (n = 6) - experimental females, C1 (n = 6) - control males, and C2 (n = 6) control females. Results: A statistically significant reduction occurred in leucine, isoleucine, and 1-methylhistidine levels in males, and 1-methylhistidine in females, in comparison to the control groups. Conclusion: The hypothyroidism-induced changes in amino acid content may be responsible for the occurrence of skeletal muscle function disorders.

Introduction: Thyroid hormones play a major role in the regulation of testicular maturation and growth and in the control of Sertoli and Leydig cell functions in adulthood. When naturally occurring, hypothyroidism causes male hypogonadotropic hypogonadism and Sertoli cell function disorders, but when iatrogenic and methimazole-induced its influence on the pituitary-testicular axis function with respect to Sertoli cells is poorly known. Material and Methods: Male adult Wistar rats (n = 14) were divided into two groups: E – taking methimazole orally for 60 days, and C – control animals. After 60 d, the concentrations in serum of testosterone, follicle-stimulating and luteinising hormones, and inhibins A and B were measured. Testicles were examined morphologically: the apoptotic Sertoli cell percentage (ASC%) and number of these cells functional per tubular mm² (FSCN/Tmm²) were calculated. Results: In group E, inhibin A was higher while inhibin B was lower than in group C. ASC% was higher and FSCN/Tmm² lower in group E than in group C. Conclusion: A specific modulation of Sertoli cell function in the course of methimazole-induced hypothyroidism leads to a simultaneous concentration increase in inhibin A and decrease in B. Inhibin A might share responsibility for pituitary-testicular axis dysfunction and hypogonadotropic hypogonadism in this model of hypothyroidism.

Methimazole-induced hypothyroidism is a clinical problem in the treatment of hyperthyroidism in people and animals and is an example of metabolic disease that can lead to fertility disorders and can give elastographic testicular changes.

Introduction: Thyroid hormones affect protein turnover, and in the case of hypothyroidism a decrease in protein synthesis and reduced release of certain amino acids from skeletal muscles are observed. Changes in the amino acid system of skeletal muscles may be responsible for the occurrence of muscle disorders. Material and Methods: The study measured the content of selected amino acids in the gastrocnemius muscle of Wistar rats during experimental hypothyroidism induced by oral administration of methimazole at a concentration of 0.05% in drinking water for 90 d. The rats were divided into four groups: E1 (n = 6) - experimental males, E2 (n = 6) - experimental females, C1 (n = 6) - control males, and C2 (n = 6) control females. Results: A statistically significant reduction occurred in leucine, isoleucine, and 1-methylhistidine levels in males, and 1-methylhistidine in females, in comparison to the control groups. Conclusion: The hypothyroidism-induced changes in amino acid content may be responsible for the occurrence of skeletal muscle function disorders.

Hypothyroidism is a possible predisposing factor in a number of disorders of companion psittacine birds. We developed and validated a thyroid-stimulating hormone (TSH) response testing protocol for cockatiels (Nymphicus hollandicus), using 0.1 IU of TSH/bird given IM, with blood sample collection at 0 and 6 hours after TSH, and a commercial radioimmunoassay for thyroxine T4). This protocol was used to document a seasonal sex difference in stimulated T4 values-females responded with higher T4 values than those in males in summer- and a stress-induced depression of baseline T4 values was detected in a group of cockatiels with normal TSH response. An experimental model for mature-onset hypothyroidism in cockatiels was created by radiothyroidectomizing cockatiels with 3.7 MBq (100 microCi) of 131I/bird given IV. Induction of the hypothyroid state was confirmed by baseline T4 concentration, TSH response test results, thyroid pertechnetate scintigraphy, and gross and microscopic examinations. Classical signs of hypothyroidism (eg, hypercholesterolemia, obesity, poor feathering) were lacking or mild at 48 days after thyroid ablation.

The objectives of this experiment were to determine serum concentrations of triiodothyronine (T3), thyroxine (T4), and free thyroxine (fT4) at rest, following thyroid-stimulating hormone (TSH) administration, and following phenylbutazone administration in healthy horses. This was done to determine which available laboratory test can best be used for diagnosis of hypothyroid conditions in horses. Serum T3, T4, and fT4 concentrations in serum samples obtained before and after TSH stimulation and following phenylbutazone administration for 7 days were determined. Baseline values ranged from 0.21 to 0.80 ng of T3/ml, 6.2 to 25.1 ng of T4/ml, and 0.07 to 0.47 ng of fT3/dl. After 5 IU of TSH was administered IV, serum T3 values increased to 6 times baseline values in 2 hours. Thyroxine values increased to 3 times baseline values at 4 hours and remained high at 6 hours. Free T4 values increased to 4 times baseline values at 4 hours and remained high at 6 hours. Administration of 4.4 mg of phenylbutazone/kg, every 12 hours for 7 days significantly decreased T4 and fT4 values, but did not significantly affect serum T3 concentrations, It was concluded that a TSH stimulation test should be performed when hypothyroidism is suspected. Measurement of serum fT4 concentrations, by the single-stage radioimmunoassay, does not provide any additional information about thyroid gland function over that gained by measuring T4 concentrations. Phenylbutazone given at a dosage of 4.4 mg/kg every 24 hours, for 7 days did significantly decrease resting T4 and fT4 concentrations, but did not significantly affect T3 concentrations in horses.

Concentrations of serum thyroxine (T4) and 3,5,3'-triiodothyronine (T3) were determined after the administration of freshly reconstituted thyrotropin-releasing hormone (TRH), reconstituted TRH that had been previously frozen, or thyrotropin (TSH) to 10 mature dogs (6 Greyhounds and 4 mixed-breed dogs). Thyrotropin-releasing hormone (0.1 mg/kg) or TSH (5 U/dog) was administered IV; venous blood samples were collected before and 6 hours after administration of TRH or TSH. Concentrations of the T4 and T3 were similar (P > 0.05) in serum after administration of freshly reconstituted or previously frozen TRH, indicating that TRH can be frozen at -20 C for at least 1 week without a loss in potency. Concentrations of T4, but not T3, were higher after the administration of TSH than they were after the administration of TRH (P < 0.01). Concentrations of T4 increased at least 3-fold in all 10 dogs given TSH, whereas a 3-fold increase occurred in 7 of 10 dogs given freshly reconstituted or previously frozen TRH. Concentrations of T4 did not double in 1 dog given freshly reconstituted TRH and in 1 dog given previously frozen TRH. Concentrations of T3 doubled in 5 of 10, 2 of 10, and 5 of 10 dogs given TSH, freshly reconstituted TRH, or previously frozen TRH, respectively. Results suggested that concentrations of serum T4 are higher 6 hours after the administration of TSH than after administration of TRH, using dosage regimens of 5 U of TSH/dog or 0.1 mg of TRH/kg. Additionally, results suggested that Greyhounds have lower concentrations of serum T4 than do mixed-breed dogs, but Greyhounds tend to have higher concentrations of serum T3.

Schirmer tear test (STT), intraocular pressure (IOP) measurement, slit-lamp biomicroscopy, and indirect ophthalmoscopy were performed on 8 dogs with (13)l-induced hypothyroidism and 4 euthyroid control dogs at weeks 0, 9, 13, 17, immediately prior to treatment with levothyroxine, after 5 weeks of levothyroxine administration (0.022 mg/kg of body weight, PO, q 12 h), and at euthanasia 7 weeks after discontinuation of replacement therapy. Although the control group had higher baseline STT values than the hypothyroid group after randomization of dogs into the 2 groups (P < 0.01), STT values remained unchanged from their respective baseline values at all time intervals for both groups. Hypothyroid and control dogs had significant (P < 0.05) reduction in IOP from baseline values at all subsequent time points, but differences were not observed when hypothroid dogs were compared with controls. Goblet cell indices determined from biopsy samples of the inferior-nasal conjunctival fornix obtained before induction of hypothyroidism (baseline), immediately prior to and at conclusion of levothyroxine therapy, and at euthanasia were not significantly different when values for hypothyroid dogs were compared with their own baseline values or with values for control dogs. Histologic examination of the globes and adnexa at euthanasia also failed to indicate consistent qualitative differences between hypothyroid and control dogs. Marked reduction in serum thyroid hormone concentrations had little effect on the eye and ocular adnexa over the course of the study.

Changes in platelet indices (platelet count and platelet size) and PCV associated with thyroid disease were studied in 7 dogs with hypothyroidism and 21 cats with hyperthyroidism that were admitted to the veterinary teaching hospital. Compared with control (euthyroid) dogs, dogs with hypothyroidism had higher platelet count (P = 0.003), smaller platelet size (P = 0.01), and lower PCV (P = 0.02). Comparison of the group of hyperthyroid cats with a group of similarly aged, clinically normal cats with normal thyroxine values indicated that the group of hyperthyroid cats had significantly (P = 0.03) higher mean platelet size than did control cats, but differences were not found in mean platelet count or PCV. Results of this investigation indicate that the changes in platelet size reported in human beings with thyroid endocrinopathies also are found in animals so-affected. Although the pathogenesis of platelet abnormalities in animals with thyroid derangement is unclear and likely is multifactorial, the observed relation between platelet and erythrocyte production in this group of dogs is consistent with reports of an inverse relation between thrombocytopoiesis and erythropoiesis in iatrogenically hyperthyroid mice and in mice exposed to hypoxia.