Effects of propylthiouracil and bromocryptine on serum concentrations of thyrotrophin and thyroid hormones in normal female horses

REASONS FOR PERFORMING STUDY: There exists a need for better diagnostic tests to characterise thyroid disease in horses. Currently available diagnostic tests fail to differentiate between thyroid gland disorders and thyroid abnormalities resulting from pituitary or hypothalamic problems. OBJECTIVES: To evaluate the effects of treatment with propylthiouracil (PTU) and bromocryptine (BROM) on serum concentrations of triiodothyronine (T3), thyroxine (T4), reverse T3 (rT3) and equine thyroid-stimulating hormone (e-TSH, thyrotrophin) in mature horses. METHODS: Healthy mature horses were treated using either PTU or BROM for 28 days. The effect of treatment on the thyroid axis was assessed by measuring T3, T4, rT3 and e-TSH before and at +14 and +28 days. The effect of PTU and BROM on the response of T3, T4, rT3 and e-TSH to thyrotrophin-release hormone (TRH) administration was also assessed before and at +14 and +28 days of treatment. RESULTS: Treatment with PTU led to a significant reduction in serum concentrations of T3, T4 and rT3 on Day 28 and increase of e-TSH on Day 28 (P < 0.05). Treatment with BROM did not cause any measurable effect on serum concentrations of T3, T4, rT3 or e-TSH. The percentage increment by which serum concentration of T4, T3 and e-TSH increased following stimulation with TRH was decreased by treatment with PTU for 28 days (P < 0.05) but were not affected by treatment with BROM for 28 days. CONCLUSIONS: These results suggest that 1) treatment with PTU may be used in horses as a model of primary hypothyroidism; 2) the use of BROM as a model of secondary hypothyroidism in horses is not supported; and 3) e-TSH assay deserves further investigation for the clinical diagnosis of thyroid axis dysfunction in horses. POTENTIAL RELEVANCE: Propylthiouracil effectively causes primary hypothyroidism. There is substantial variability between horses with respect to their sensitivity to this substance when administered orally. Further studies pertaining to the characterisation of equine thyroid disorders are warranted and the use of both PTU for the experimental induction of primary hypothyroidism and e-TSH for the diagnostic characterisation of thyroid disorders in horses should be considered.     

Association of the risk of development of hypothyroidism after iodine 131 treatment with the pretreatment pattern of sodium pertechnetate Tc 99m uptake in the thyroid gland in cats with hyperthyroidism: 165 cases (1990-2002)

OBJECTIVE: To assess whether the risk of development of hypothyroidism after treatment with iodine 131 (131I) was associated with the pattern of sodium pertechnetate Tc 99m activity in the thyroid gland detected via scintigraphy before treatment in cats with hyperthyroidism. DESIGN: Retrospective study. ANIMALS: 165 cats. PROCEDURE: Medical records of cats with hyperthyroidism that had been treated with 131I (from 1990 to 2002) and had undergone scintigraphy of the thyroid gland before treatment were reviewed; data regarding signalment, scintigraphic findings (classified as unilateral, bilateral-asymmetric, bilateral-symmetric, or multifocal patterns), serum total thyroxine (T4) concentrations before treatment and prior to hospital discharge, and 131I treatment were collected. A questionnaire was sent to each referring veterinarian to obtain additional data including whether the cats subsequently developed hypothyroidism (defined as serum total T4 concentration less than the lower reference limit > or = 3 months after treatment). RESULTS: 50 of 165 (30.3%) 131I-treated cats developed hypothyroidism. Hypothyroidism developed in 39 of 109 cats with bilateral, 10 of 50 cats with unilateral, and 1 of 6 cats with multifocal scintigraphic patterns of their thyroid glands. Cats with a bilateral scintigraphic pattern were approximately 2 times as likely to develop hypothyroidism after 131I treatment than were cats with a unilateral scintigraphic pattern (hazard ratio, 2.1; 95% confidence interval, 1.04 to 4.2). CONCLUSIONS AND CLINICAL RELEVANCE: Cats with hyperthyroidism that have a bilateral scintigraphic pattern in the thyroid gland before 131I treatment appear to have a significantly higher risk of subsequently developing hypothyroidism, compared with cats with a unilateral scintigraphic pattern.     

Immunohistochemical observations on TSH secreting cells in pituitary glands of goat kids with congenital goitre

Pituitary glands of normal-termed stillborn goat kids with congenital goitre and normal-termed stillborn goat kids without congenital goitre were examined macroscopically, histopathologically and immunohistochemically. Thyroid glands of these animals were also examined grossly and microscopically. The pituitary glands of kids with goitre were larger than those of normal kids, and on histopathological examination there was hyperplasia of the acidophil cells in the ventral part of the glands. However, it was impossible to distinguish thyroid stimulating hormone (TSH)-secreting cells from other acidophil cells in sections stained with haematoxylin and eosin (HE). Red granules were observed in the cytoplasm of these hyperplastic cells in periodic acid-Schiff (PAS)-stained sections. Sections were also immunostained with an antibody against TSH using the streptavidin-biotin peroxidase technique. Immunohistochemistry revealed TSH-secreting cells to have increased in number in the pituitary glands of kids with congenital goitre because of the extensive proliferation when compared with those of normal kids. The present study indicated that the presence of multiple fetuses (twins or triplets) may be a predisposing factor for congenital goitre.     

A case-control study of the congenital hypothyroidism and dysmaturity syndrome of foals.

A case-control study was conducted to identify risk factors for the congenital hypothyroidism and dysmaturity syndrome of foals. A questionnaire was used during personal interviews of foal owners and farm managers to collect information on animal signalment, farm environment, and mare management. Information on 39 foals with the congenital hypothyroidism and dysmaturity syndrome were compared with 39 control foals. Foals with the syndrome had a significantly (P < 0.0001) longer gestation (357.6 d) than control foals (338.9 d). Pregnant mares that were fed greenfeed, did not receive any supplemental mineral, left their "home farm" during gestation, or grazed irrigated pasture had 13.1 (P = 0.0068), 5.6 (P = 0.0472), 4.3 (P = 0.0076), and approximately 15.3 (P = 0.0245), respectively, greater odds of producing an affected foal than mares not experiencing these events. Greenfeed often contains high levels of nitrate (NO3-), which is known to impair thyroid gland function. In light of this, forage samples from participating farms were analyzed for nitrate levels. The odds of one or more congenitally hypothyroid and dysmature foals being born on a farm feeding forage with at least a trace of nitrate was 8.0 times greater (P = 0.0873) than the odds of the disease occurring on a farm that fed forage free of nitrate. Further, the odds of a mare producing an affected foal when fed forage containing at least a trace of nitrate were 5.9 times greater (P = 0.0007) than those of a mare fed nitrate free forage. This study suggests that congenital hypothyroidism and dysmaturity syndrome in foals may be the result of diets that contain nitrate or that are low in iodine being fed to pregnant mares.     

Congenital hypothyroidism in Scottish Deerhound puppies

Two Scottish Deerhound puppies had clinical and pathological features consistent with the diagnosis of congenital non-goitrous hypothyroidism. They were from separate litters, but were the progeny of the same sire and dam. The puppies were smaller, had shorter limbs and shorter, broader heads than their littermates. They also had histories of weakness, difficulty in walking and somnolence. A characteristic radiographic feature was the absence of epiphyseal growth centres. Both had depressed serum thyroxine (T4) levels and one did not respond to exogenous thyroid stimulating hormone. On necropsy, the thyroid glands were small, the follicles varied in size and contained little or no colloid. The adenohypophysis contained many cells with markedly vacuolated cytoplasm. It is suggested that the clinicopathological pattern is the result of a primary thyroid abnormality. Possible mechanisms include either primary thyroid hypoplasia or an unresponsiveness to thyroid stimulating hormone.     

Goitrogenic effects in offspring of swine fed sulfadimethoxine and ormetoprim in late gestation

Effects of feeding sulfadimethoxine and ormetoprim to sows and gilts in late gestation were evaluated. One sow and 2 gilts were randomly selected and were fed 1 of 3 rations: (1) a gestation ration from farm A, where congenital goiter in newborn pigs was a problem, (2) gestation ration from farm A containing 275 g of sulfadimethoxine and 55 g of ormetoprim/100 kg of ration, or (3) standard swine gestation ration containing 275 g of sulfadimethoxine and 55 g of ormetoprim/100 kg of ration. Sows and gilts were fed the appropriate ration for 22 to 58 days before farrowing. The numbers of stillborn or weak pigs did not increase in any group. However, congenital goiter was detected in all pigs from swine fed medicated rations 2 and 3. Congenital goiter was not present in pigs from swine given gestation ration 1.     

Fetal and neonatal goiter in cynomolgus monkeys following administration of the antithyroid drug thiamazole at high doses to dams during pregnancy

To evaluate morphologic alterations in the thyroid gland in the second generation in cynomolgus monkeys, pregnant dams were exposed to high doses of thiamazole. In Experiment A, dams received thiamazole intragastrically via a nasogastric catheter from gestation day (GD) 50 to GD 150 or on the day before delivery. Initially, the dose level was 20 mg/kg/day (10 mg/kg twice daily); however, the dose level was subsequently decreased to 5 mg/kg/day (2.5 mg/kg twice daily), since deteriorated general conditions were observed in two dams. Six out of seven neonates died on the day of birth. The cause of neonatal death was tracheal compression and suffocation from goiter. The transplacental exposure to thiamazole affected the fetal thyroid glands and induced goiter in all neonates. The surviving neonate was necropsied 767 days after discontinuation of thiamazole exposure and showed reversibility of the induced changes. In Experiment B, dams were intragastrically administered thiamazole at 5 mg/kg/day (2.5 mg/kg twice daily) for treatment periods from GDs 51 to 70, 71 to 90, 91 to 110, 111 to 130 and 131 to 150. All fetuses showed enlarged thyroid glands but were viable. Histopathologically, hypertrophy and/or hyperplastic appearance of the follicular epithelium of the thyroid gland was observed at the end of each treatment period. The most active appearance of the follicular epithelium, consisting of crowded pedunculated structure, was demonstrated at end of the treatment period from GD 131 to 150. This is the first report on the morphology of fetal and neonatal goiter in the cynomolgus monkey.     

Congenital hypothyroidism of dogs and cats: a review

Congenital hypothyroidism is a rare and underdiagnosed congenital endocrine disorder in dogs and cats and the true incidence is unknown. The disorder may cause a range of clinical signs depending on the primary defect, which affect production of thyroid hormones; some cases present when adult. Hallmark clinical signs of congenital hypothyroidism are mental impairment and skeletal developmental abnormalities, resulting in disproportionate dwarfism; goitre may or may not be present. Documented causes of congenital hypothyroidism in dogs include deficiency of, or unresponsiveness to, thyrotropin-releasing hormone (TRH) or thyroid-stimulating hormone (TSH), thyroid dysgenesis, dyshormonogenesis and iodine deficiency. In cats, TSH unresponsiveness, thyroid dysgenesis, dyshormonogenesis and iodine deficiency have been confirmed. Adequate replacement therapy results in a successful outcome in the majority of cases, especially when started early in life, as permanent developmental abnormalities can be prevented. This review describes reported cases in dogs and cats, diagnostic investigation, and recommendations for treatment.     

Responses in ovulation rate, embryonal survival, and litter traits in swine to 14 generations of selection to increase litter size

Eleven generations of selection for increased index of ovulation rate and embryonal survival rate, followed by three generations of selection for litter size, were practiced. Laparotomy was used to count corpora lutea and fetuses at 50 d of gestation. High-indexing gilts, approximately 30%, were farrowed. Sons of dams in the upper 10% of the distribution were selected. Selection from Generations 12 to 14 was for increased number of fully formed pigs; replacements were from the largest 25% of the litters. A randomly selected control line was maintained. Responses at Generation 11 were approximately 7.4 ova and 3.8 fetuses at 50 d of gestation (P < .01) and 2.3 fully formed pigs (P < .01) and 1.1 live pigs at birth (P < .05). Responses at Generation 14 were three fully formed pigs (P < .01) and 1.4 live pigs (P < .05) per litter. Number of pigs weaned declined (P < .05) in the index line. Total litter weight weaned did not change significantly. Ovulation rate and number of fetuses had positive genetic correlations with number of stillborn pigs per litter. Significantly greater rate of inbreeding and increased litter size at 50 d of gestation in the select line may have contributed to greater fetal losses in late gestation, greater number of stillborn pigs, and lighter pigs at birth, leading to lower preweaning viability. Heritabilities of traits were between 8 and 25%. Genetic improvement programs should emphasize live-born pigs and perhaps weight of live-born pigs because of undesirable genetic relationships of ovulation rate and number of fetuses with numbers of stillborn and mummified pigs and because birth weight decreased as litter size increased.     

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.     

Ultrastructural evidence that the negative feedback mechanism of the pituitary-thyroid axis can operate without the hypothalamus in fetal rats: observation of thyroid follicular cells

Hypothalamus-independent negative feedback mechanism of the pituitary-thyroid axis was studied by electron microscopic observation of thyroid follicular cells of encephalectomized or hypophysectomized fetal rats under hypothyroidism induced by propylthiouracil (PTU). Fetal hypophysectomy or encephalectomy was performed on day 19 of gestation. Mother rats were given either a daily amount of 40 mg PTU or saline alone on the day of operation and on the next day. On day 21, their fetuses were obtained. As a result, PTU induced marked goiters even in encephalectomized fetuses, the goiters being comparable in weight to those induced in littermate intact fetuses. Electron microscopically, the follicular lumen was narrowed, microvilli were lengthened with a marked increase in number, and rER was extremely expanded. Follicular cells often confined colloid droplets and lysosomes. Fetal hypophysectomy, even in PTU-treatment, caused a reduction in the thyroid weight, accompanied by flattening of follicular cells, shortening of microvilli, widening of follicular lumen, and shrinkage of rER. These findings would support the view that the negative feedback mechanism of the pituitary-thyroid axis can operate without the hypothalamus in fetal rats.     

Effect of methimazole-induced hypothyroidism on adrenal and gonadal functions in male Japanese quail (Coturnix japonica)

To investigate the effect of hypothyroidism on gonadal and adrenal functions in male Japanese quail (Coturnix japonica), hypothyroidism was induced in male adult Japanese quail by daily administration of 2-Mercapto-1-methylimidazole (methimazole) in their drinking water. Four weeks after methimazole treatment, the Japanese quail were sacrificed, and the plasma concentrations of free triiodothyronine (FT3), free thyroxine (FT4), total T3 (TT3), total T4 (TT4), corticosterone, testosterone, LH and immunoreactive (ir) inhibins were measured by radioimmunoassay, the testes and adrenal glands were removed and weighed and the thyroid glands and testes were fixed in 4% paraformaldehyde for histological observation. The results showed that the hypothyroidism induced by methimazole caused a significant decrease in body and testes weight; the plasma levels of FT3, FT4 and TT4 significantly decreased, and the hypothyroid quail possessed a greater number of small follicles and more follicular epithelial cells in the thyroid gland. In addition, hypothyroidism resulted in a significant decrease in the plasma concentrations of corticosterone, LH, testosterone and ir-inhibin. Furthermore, no spermatogenesis was found in the seminiferous tubules of the methimazole treatment groups. These results clearly demonstrate that hypothyroidism caused both gonadal and adrenal disturbances in the adult male Japanese quail.     

Tetraparesis due to vertebral physeal fracture in an adult dog with congenital hypothyroidism

A four-year-old male affenpinscher was referred for evaluation of hindlimb weakness that had progressed to tetraparesis over a period of four weeks. Neurological examination was suggestive of a cervical spinal cord lesion. Radiographic examination revealed diffuse skeletal immaturity with open physes and epiphyseal dysplasla in long bones and vertebrae, consistent with a diagnosis of congenital hypothyroidism. Total and free serum T4 concentrations were very low, indicative of hypothyroidism. Survey radiographs of the cervical spine revealed a dorsally displaced Salter-Harris type I fracture of the cranial portion of the fourth cervical vertebra with the endplate present in the vertebral canal. Although signs of transverse myelopathy are uncommon In dogs with congenital hypothyroidism, they may be associated with either intervertebral disc protrusion or endplate displacement into the vertebral canal secondary to the epiphyseal abnormalities associated with congenital hypothyroidism.     

Thyroid-stimulating hormone in adult euthyroid and hypothyroid horses

The purpose of this study was to validate a thyroid-stimulating hormone (TSH) assay in a model of equine hypothyroidism. Thyrotropin-releasing hormone (TRH) stimulation tests were performed in 12 healthy adult mares and geldings, aged 4 to greater than 20 years. before and during administration of the antithyroid drug propylthiouracil (PTU) for 6 weeks. Serum concentrations of equine TSH, total and free thyroxine (T4), and total and free triiodothyronine (T3) were measured. Before PTU administration, mean +/- standard deviation baseline concentrations of TSH were 0.40 +/- 0.29 ng/mL. TSH increased in response to TRH, reaching a peak concentration of 0.78 +/- 0.28 ng/mL at 45 minutes. Total and free T4 increased from 12.9 +/- 5.6 nmol/L and 12.2 +/- 3.5 pmol/L to 36.8 +/- 11.4 nmol/L and 23.1 +/- 5.9 pmol/L, respectively, peaking at 4-6 hours. Total and free T3 increased from 0.99 +/- 0.51 nmol/L and 2.07 +/- 1.14 pmol/L to 2.23 +/- 0.60 nmol/l and 5.78 +/- 1.94 pmol/L, respectively, peaking at 2-4 hours. Weekly measurements of baseline TSH and thyroid hormones during PTU administration showed that total and free T, concentrations fell abruptly and remained low throughout PTU administration. Total and free T4 concentrations did not decrease dramatically until weeks 5 and 4 of PTU administration, respectively. A steady increase in TSH concentration occurred throughout PTU administration, with TSH becoming markedly increased by weeks 5 and 6 (1.46 +/- 0.94 ng/mL at 6 weeks). During weeks 5 and 6 of PTU administration, TSH response to TRH was exaggerated, and thyroid hormone response was blunted. Results of this study show that measurement of equine TSH in conjunction with thyroid hormone measurement differentiated normal and hypothyroid horses in this model of equine hypothyroidism.     

Effects of the Glucosinolate Sinigrin in Combination With a Noniodine Supplemented Diet on Serum Iodine and Thyroid Hormone Concentrations in Nonpregnant Mares

Exposure to plants containing glucosinolates (GSLs) affects thyroid function in many species, in horses is implicated in the birth of foals with congenital hypothyroidism. The present study was performed to determine the effect of feeding a GSL (sinigrin) in combination with a low-iodine diet for 12 weeks on thyroid hormones and serum iodine concentrations in nonpregnant mares. Nineteen mares aged 2–14 years were divided into control (n = 6), low (20 mmol/day) (n = 7) and high GSL (35 mmol/day) (n = 6) groups. Thyrotropin-releasing hormone (TRH) stimulation tests and serum iodine measurements were performed at 0 and 12 weeks. Total triiodothyronine (TT3), total thyroxine (TT4), and thyroid-stimulating hormone (TSH) concentrations were measured at the baseline and in post-TRH samples. The post-TRH value minus the basal value (Delta Δ) and fold change (FC) were calculated for TSH, TT3, and TT4. Data were analyzed at P < .05. Highlights included Delta Δ and FC TT4 and TT3 concentrations having a group and week interaction (P < .001) with week 12 control mares having higher values than mares in week 12 low and high GSL groups. TT4 FC values had a group (P < .001) and group by week interaction (P < .001) with week 12 control concentrations higher (P < .006) than all groups. Iodine concentrations decreased (P < .002) over time in GSL mares. In conclusion, feeding mares a low-iodine diet with 20 and 35 mmol sinigrin/day resulted in lower serum iodine concentrations.     

Thyroid hormone levels in foals with congenital musculoskeletal lesions

Fourteen foals with congenital or neonatal musculoskeletal abnormalities are described. Ten of the fourteen foals had abnormally low total serum T₃ and/or T₄ concentrations suggesting hypothyroidism. Response to thyroid-stimulating hormone was determined in two foals and found to be poor. Seven of the foals were necropsied and six of these had histological evidence of thyroid hyperplasia. These findings suggest hypothyroidism as a cause of congenital musculoskeletal lesions.     

Diagnosis of congenital and adult-onset hypothyroidism in cats

Whereas hyperthyroidism is the most common endocrine disorder in the cat, hypothyroidism is the least common feline endocrine disorder. This is a the result of several factors including low index of suspicion, rarity of the naturally occurring hypothyroidism in cats, and a lack of species specific tests for endogenous TSH and antithyroglobulin antibodies. Nonetheless, hypothyroidism does occur in cats, especially in kittens and after radioactive treatment for hyperthyroidism. The clinician should become familiar with the common presentations of congenital and adult-onset hypothyroidism in cats. In addition, some of the tests specific to dogs (such as endogenous canine TSH) may be utilized to diagnose subclinical hypothyroidism in cats. Fortunately, the treatment of feline hypothyroidism with synthetic levothyroxine is both straightforward and effective.     

Etiopathologic findings of canine hypothyroidism.

The causes of canine hypothyroidism are varied, but most cases result from irreversible acquired thyroid pathologic changes and only a small proportion arise from congenital anomalies of the thyroid gland or pituitary. Of primary thyroid failure, at least half is the result of immune-mediated thyroiditis. Recent research has focused on the genetics and immunology of canine thyroid disease, adding to what is known from experimental and human studies. Epidemiologic and diagnostic laboratory studies continue to provide information on contributing factors and raise questions for future research directions. Serum antibodies against thyroid components are common in thyroid pathologic conditions and dysfunction, and understanding their properties and frequency is important in the interpretation of thyroid diagnostic test results.     

Juvenile-onset hypothyroidism in a dog

Juvenile-onset hypothyroidism was diagnosed in an adult mixed-breed dog examined because of quadraparesis. Unusual clinical signs attributable to juvenile-onset or congenital hypothyroidism included disproportionate dwarfism; enlarged, protruding tongue; mental dullness; and retention of a "puppy" coat, which was soft and fluffy, without guard hairs. Radiography of the vertebral column and long bones revealed multiple areas of delayed epiphyseal closure and epiphyseal dysgenesis. Myelography demonstrated several intervertebral disk protrusions in the cervical and lumbar regions. Hypothyroidism was confirmed on the basis of a low basal serum thyroxine concentration that failed to increase after the administration of thyroid stimulating hormone. Other laboratory abnormalities included nonregenerative, normocytic, normochromic anemia; mild hypercalcemia; and an impaired growth hormone (GH) secretory response after xylazine administration. At necropsy, the thyroid gland was small and weighed only 0.2g. Microscopic examination of the thyroid gland revealed a loss of glandular tissue, which was replaced by adipose tissue along its periphery. Gross or microscopic abnormalities were not noted in the pituitary gland, and immunohistochemical staining of the pituitary gland revealed a normal number of GH-containing acidophils. This suggests that primary hypothyroidism may result in an impaired secretion of growth hormone, and that pituitary dwarfism or GH deficiency may be difficult to differentiate from hypothyroid dwarfism on the basis of provocative GH testing alone.     

Effects of induced hypothyroidism or hyperthyroidism on growth and reproductive performance of Brahman heifers.

Prepubertal Brahman heifers (BW = 302 +/- 7.5 kg, body condition score [BCS] = 5.4 +/- .2, age = 498 +/- 3.4 d: SEM) were used to study the effects of thyroid function on growth and reproduction. Seven heifers were controls (C). Seven heifers were induced to become hypothyroid by ingestion of 4 mg/kg BW of 6-n-propyl-2-thiouracil (PTU). Seven heifers were induced to become hyperthyroid (T) by daily s.c. injections of triiodothyronine (T3, 1 mg/d). Treatments were administered for 84 d followed by an 84 d posttreatment period. Blood samples were obtained twice weekly via tail venipuncture for analysis of T3, thyroxine, and progesterone. The BW, BCS, and rectal temperature (RT) were recorded weekly. Estrus was monitored twice daily with the aid of a fertile bull equipped with a chin ball marker. Hyperthyroidism and hypothyroidism were successfully induced in T- and PTU- treated heifers, respectively. During the treatment period, PTU heifers gained the most BW and BCS (72.4 +/- 5.4 kg; .93 +/- .15 units), C heifers were intermediate (41.7 +/- 5.4 kg; .43 +/- .15 units), and T heifers gained the least (13.3 +/- 5.4 kg; -.36 +/- .15 units; P < .05). The RT also decreased (P < .05) in PTU heifers (-1.9 +/- .2 degrees C) compared with C (-1.2 +/- .2 degrees C) or T heifers (-.8 +/- .2 degrees C). No heifers exhibited estrus during the treatment period. During the posttreatment period, T heifers gained the most BW and BCS (93.9 +/- 6.1 kg; 1.14 +/- .13 units), C heifers were intermediate (67.0 +/- 6.1 kg; .86 +/-. 13 units), and PTU heifers gained the least (22.2 +/- 6.1 kg; -.14 +/- .13 units; P < .05). The reversal in BW and BCS gains during the posttreatment period corresponded to periods of transient hypo- and hyperthyroidism in T and PTU heifers, respectively. Age and BW at puberty and pregnancy were similar among all treatment groups. The BCS for T heifers was lower (5.7 +/- .2 units; P < .05) at puberty and pregnancy than for PTU heifers (6.6 +/- .2 units). Induction of hypothyroidism resulted in significant increases in BW and BCS during the treatment period, but these increases were not sufficient to dramatically affect reproductive performance of Brahman heifers.