PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PROPYLTHIOURACIL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources

Serum propylthiouracil concentration in patients with Graves' disease with various clinical course.

The serum levels of propylthiouracil (PTU) were determined by radioimmunoassay in 10 normal subjects and in 11 patients with Graves' disease after a single 100 or 200 mg oral dose of PTU. The serum half-life of PTU in the normal subjects and in hyperthyroid patients with uneventful clinical course was 75 +/- 19 min (mean +/- SD, n = 6) and 73 +/- 13 min (n = 7), respectively. Maximum serum PTU concentrations were usually attained within 1 h after a single 200 mg oral dose and at 1 h were 5.3 +/- 1.4 micrograms/ml (3.1 +/- 0.82 X 10(-5) M) in normal subjects (n = 6) and 4.8 +/- 2.4 micrograms/ml (2.8 +/- 1.4 X 10(-5) M) in hyperthyroid patients (n = 7). These between-group differences were not significant. Serum PTU concentrations were low in a pregnant hyperthyroid patient with a weak response to PTU treatment. In another patient, who appeared resistant to PTU therapy, the serum PTU level increased as expected at testing, and it was later confirmed that, during treatment, he had not taken the drug as prescribed. In a patient who developed agranulocytosis due to methimazole and subsequently fever due to PTU, the half-life of PTU was prolonged to about 130 min. These findings suggest that monitoring the serum PTU levels in patients with Graves' disease can be of clinical value in patients who do not respond to treatment. Furthermore, it may provide some clues as to the mechanism by which toxic reaction develops.

Administration, Oral↗

Effects of sodium ipodate and propylthiouracil in athyreotic human subjects, role of triiodothyronine and pituitary thyroxine monodeiodination in thyrotrophin regulation.

To investigate the respective role of triiodothyronine (T3) and thyroxine (T4) in the regulation of TSH secretion, we studied the action of sodium ipodate and propylthiouracil (PTU) in 11 athyreotic patients. The LT4 replacement dose was adjusted to obtain, in each patient, a normal basal TSH level and a normal TSH response to TRH. In the 5 ipodate-treated patients (single 6 g oral dose), the mean serum T3 level fell by 64% below the baseline value and serum rT3 rose 180% above the baseline. The free T4 index (FT4I) did not change whereas the mean serum TSH concentration increased 280% above baseline values. In the 6 PTU-treated patients (250 mg orally every 6 h for 10 days), serum T3 levels fell 33%, serum rT3 increased up to 82% and the FT4I did not change. The mean serum TSH concentration increased 68% above the baseline value. Thus, the mean percentage increase in serum TSH was less in PTU- than in ipodate-treated patients (68% vs 280%). Statistical analysis of the correlation between the serum T3 decrease (delta T3) and the serum TSH (delta TSH) increase demonstrated that for the same T3 diminution, the ipodate-treated group displayed higher increase of TSH than the PTU-treated patients. In the rat, PTU interferes with the 5'-deiodination of T4 in the liver and kidney but not in the pituitary, while ipodate appears to have the same effect in all tissues. If this holds true for human subjects, our data strongly suggest that circulating T4 (through its intrapituitary conversion to T3) shares with serum T3 the capacity to regulate TSH secretion in man.

Adult↗

A comparison of the effects of propylthiouracil and methimazol on circulating thyroid hormones and various measures of peripheral thyroid hormone effects in thyrotoxic patients.

Two groups of patients with newly diagnosed thyrotoxicosis were treated with propylthiouracil (PTU) 400 mg every 6 h for 4 days followed by methimazol (MMI) 40 mg every 6 h for 4 days or by MMI for 4 days followed by PTU for 4 days. The shift from MMI to PTU induced a considerable decrease in serum T3 while shift from PTU to MMI led to an increase in serum T3. Serum T4 decreased gradually during the whole treatment period. The opposite variations in serum T3 were accompanied by similar opposite variations in basal metabolic rate (BMR) (P less than 0.001). Hence the rapid variations in serum T3 which can be induced by PTU in thyrotoxic patients, are followed by rapid alterations in the thyrotoxic state as evaluated by BMR.

Achilles Tendon↗

Choice of breastfeeding and physicians' advice: a cohort study of women receiving propylthiouracil.

OBJECTIVE: To examine the gap between the current social/medical practice and the evidence-based recommendation in favor of breastfeeding during maternal propylthiouracil (PTU) therapy. DESIGN: Prospective, observational, cohort study. SUBJECTS: Women requiring PTU during pregnancy, and endocrinologists and family physicians in Ontario, Canada. INTERVENTIONS: Questionnaire. MAIN OUTCOME MEASURES: Women were interviewed postpartum regarding their choice of infant feeding method and relevant advice received from physicians. Physicians were questioned about their advice to nursing women receiving PTU. RESULTS: Of 78 women, 66 had live births. Thirty-six required PTU postpartum (group 1), and 30 did not (group 2). Thirty-six healthy women served as controls (group 3). Breastfeeding initiation rates for groups 1, 2, and 3 were 44%, 83%, and 83%, respectively. In group 1, 15 women who breastfed received advice from 22 physicians regarding breastfeeding (20 in favor, 1 against, and 1 equivocal). Eleven who formula fed received advice from 17 physicians (4 in favor, 12 against, and 1 equivocal). A logistic regression analysis of group 1 showed that physicians' advice was the only significant predictor of the woman's choice to breastfeed during PTU therapy (relative risk: 5.48; 95% confidence interval: 1.28-23.40). The physician survey showed that 44% of endocrinologists do not recommend breastfeeding during PTU therapy. CONCLUSIONS: A substantial proportion of the lactating patients on PTU still receive advice against breastfeeding from their physicians. Physicians' advice and attitudes toward breastfeeding during PTU therapy are a major factor in women's final decision to breastfeed. Physicians' compliance with evidence-based data will facilitate breastfeeding in this group.propylthiouracil, breastfeeding, decision-making.

Attitude of Health Personnel↗

[The effect of propylthiouracil on the efficacy of radioiodine (I-131) therapy in graves hyperthyroidism].

Aiming at evaluating the effect of antithyroid drugs on the efficacy of radioiodine treatment (RAI) we retrospectively analyzed 226 patients with Graves disease hyperthyroidism submitted to RAI between 1990 and 2001: 58 patients without any antithyroid drug (ATD) prior to RAI, 119 patients using propylthiouracil (PTU) and 49 patients using methimazole (MMI) prior to RAI. Clinical and laboratory parameters 1 year after RAI defined their clinical status (cured or not cured). High serum free T4 and 131-iodine uptake were negatively related with cure as well as lower RAI doses (mCi) and larger goiters (p< 0.05). The percentage of cured patients on PTU prior to RAI was 70.2% (84/119), while those on MMI was 85.7% (42/49), and 84.5% (49/58) of those without ATD prior to RAI (p= 0.034). On logistic regression analysis, free T4 > 4 ng/dl, large goiter, RAI dose < 10 mCi and PTU prior to RAI were related to lower cure rates. Compared to patients with no ATD prior to RAI, we concluded that the previous use of PTU implies in higher failure rates after RAI (OR= 3.13), an effect not observed in patients on MMI (OR= 1.28).

Adult↗

Propylthiouracil and peripheral neuropathy.

Peripheral neuropathy is a rare manifestation in hyperthyroidism. We describe the neurological manifestations of a 38 year old female with Graves' disease who developed peripheral neuropathy in the course of her treatment with propylthiouracil. After the drug was tapered off, the neurological signs disappeared. Therefore, we call attention for a possible toxic effect on peripheral nervous system caused by this drug.

Adult↗

Acute inhibitory effect of excess iodide on ornithine decarboxylase in the thyroid of propylthiouracil-treated rats.

Polyamines such as putrescine, spermidine and spermine have been thought to play an important role in thyroid growth induced by goitrogens. Reduced biosynthesis of these polyamines might play a role in the antigoitrogenic effects of excess iodide. This study was designed to examine the effect of potassium iodide (KI) on ornithine decarboxylase (ODC), a rate-limiting enzyme in the biosynthesis of polyamines. Thyroidal ODC activity, protein content and mRNA were increased in rats made hypothyroid by 10 days of propylthiouracil treatment. The increase in ODC activity was suppressed after subcutaneous injection of KI (13mg/kg body weight); the apparent half-life of ODC activity after the treatment was estimated to be 19 min and the maximum suppression (90%) was seen 60 min after the treatment. On the other hand, administration of iodine-containing compounds including L-thyroxine, L-di-iodotyrosine,amiodarone, iopanoic acid and erythrosine showed no significant effect on ODC activity. The inhibitory effect of excess iodide was not reversed by pretreatment with dibutyryl cAMP and theophylline. The amount of immunoreactive ODC protein was reduced by iodide treatment (40%). However, the decrease was not as great as the decrease in ODC activity (90%). No significant change in thyroidal ODC mRNA content was seen 1 and 3 h following KI treatment. These results suggest that excess iodide reduces ODC activity in the rat thyroid gland by a post-transcriptional mechanism.

Animals↗

Propylthiouracil-induced hypothyroidism is associated with increased tolerance of the isolated rat heart to ischaemia-reperfusion.

The present study investigated the response of the hypothyroid heart to ischaemia-reperfusion. Hypothyroidism was induced in Wistar rats by oral administration of propylthiouracil (0.05%) for 3 weeks (HYPO rats), while normal animals (NORM) served as controls. Isolated hearts from NORM and HYPO animals were perfused in Langendorff mode and subjected to zero-flow global ischaemia followed by reperfusion (I/R). Post-ischaemic recovery of left ventricular developed pressure was expressed as % of the initial value (LVDP%). Basal expression of protein kinase C epsilon (PKCepsilon) and PKCdelta and phosphorylation of p46 and p54 c-jun NH(2)-terminal kinases (JNKs) in response to I/R were assessed by Western blotting. LVDP% was found to be significantly higher in HYPO hearts than in NORM. At baseline, PKCepsilon expression was 1.4-fold more in HYPO than in NORM hearts, P<0.05, while PKCdelta was not changed. Furthermore, basal phospho-p54 and -p46 JNK levels were 2.2- and 2.6-fold more in HYPO than in NORM hearts, P<0.05. In response to I/R, in NORM hearts, phospho-p54 and -p46 JNK levels were 5.5- and 6.0-fold more as compared with the baseline values, P<0.05, while they were not significantly altered in HYPO hearts. HYPO hearts seem to display a phenotype of cardioprotection against ischaemia-reperfusion and this is associated with basal PKCepsilon overexpression and attenuated JNK activation after I/R.

Animals↗

Propylthiouracil-induced hypothyroidism protects ionizing radiation-induced multiple organ damage in rats.

The objective of this study was to examine the potential radioprotective properties of propylthiouracil (PTU)-induced hypothyroidism against oxidative organ damage induced by irradiation. Sprague-Dawley rats were pre-treated with saline or PTU (10 mg/kg i.p.) for 15 days, and were then exposed to whole-body irradiation (800 cGy). A group of rats were decapitated at 6 h after exposure to irradiation, while another group was followed for 72 h after irradiation, during which saline or PTU injections were repeated once daily. Lung, liver, kidney and ileum samples were obtained for the determination of malondialdehyde (MDA; an index of lipid peroxidation) and glutathione (GSH, an antioxidant) levels, myeloperoxidase activity (MPO; an index of tissue neutrophil accumulation) and collagen contents, while oxidant-induced DNA fragmentation was evaluated in the ileal tissues. All tissues were also examined microscopically and assayed for the production of reactive oxidants using chemiluminescence (CL). Lactate dehydrogenase (LDH), an indicator of tissue damage, and tumour necrosis factor-alpha (TNFalpha) were assayed in serum samples. Irradiation caused a significant decrease in GSH level, which was accompanied by significant increases in MDA levels, MPO activity, CL levels and collagen content of the tissues studied (P<0.05-0.001). Similarly, serum TNFalpha and LDH were elevated in the irradiated rats as compared with the control group. On the other hand, PTU treatment reversed all these biochemical indices, as well as histopathological alterations induced by irradiation. Our results suggested that PTU-induced hypothyroidism reduces oxidative damage in the lung, hepatic, renal and ileal tissues probably due to hypometabolism, which is associated with decreased production of reactive oxygen metabolites and enhancement of antioxidant mechanisms.

Animals↗

Propylthiouracil-induced diffuse proliferative lupus nephritis: review of immunological complications.

Propylthiouracil (PTU), used to treat Graves' disease, occasionally induces a lupus-like syndrome. A 39-year-old woman developed clinical manifestations of systemic lupus erythematosus with rash, serositis, myocarditis, and acute renal insufficiency, associated with serologies for lupus, after 3 wk of exposure to the drug. Renal biopsy revealed diffuse proliferative lupus nephritis. This article reviews the side effects of PTU and the literature on PTU-induced nephrotoxicity. Possible mechanisms and management of drug-induced lupus nephritis are also reviewed. To facilitate early and specific intervention, clinicians should be aware of the propensity of PTU to cause lupus-like syndromes with renal involvement.

Adult↗

The impact of propylthiouracil therapy on lipid peroxidation and antioxidant status parameters in hyperthyroid patients.

This study was performed on 17 hyperthyroid patients and 15 healthy controls. The patients were under propylthiouracil (PTU) therapy at a dosage of 3 x 100 mg/day for one month. Blood samples, taken at the beginning and on the 30th day of therapy, were analyzed for hormonal parameters (T3, T4, TSH), lipid peroxidation endproduct [thiobarbituric acid reactive substances (TBARS)] and antioxidant status parameters: glutathione (GSH), glutathione peroxidase (GSH-Px) and CuZn superoxide dismutase (CuZn SOD). Hyperthyroid patients were observed to have significantly higher TBARS, GSH and CuZn SOD levels than controls (P < 0.05, P < 0.001, P < 0.001, respectively). PTU therapy caused a relief in oxidative stress as reflected by significantly decreased TBARS levels (P < 0.001) and a selective modification in the antioxidant status parameters: significant decreases in GSH and CuZn SOD levels (P < 0.001) and a significant increase in GSH Px (P < 0.01) activity. Our findings suggest a selective modification of the antioxidative profile in hyperthyroidism. PTU should also be considered as an in vivo antioxidant, in addition to its antithyroid action.

Adult↗

Propylthiouracil-induced lupus-like syndrome developing in a Graves' patient with a sibling with systemic lupus erythematosus.

A 13-year-old girl with Graves' disease, whose younger sister had systemic lupus erythematosus, developed polyarthralgia, fever, neutropenia, hypergammaglobulinemia, and microscopic hematuria after treatment with propylthiouracil (PTU) for 2 years. Myeloperoxidase-anti-neutrophil cytoplasmic antibodies were strongly positive. Anti-single- and anti-double-stranded DNA antibodies were positive, whereas LE cells and anti-Sm antibodies were negative. PTU was discontinued and all symptoms subsided gradually. Two years later, the microscopic hematuria had disappeared completely. Both patients had the identical HLA-DR alleles (HLA-DR9). These present two cases in siblings suggest that both sisters had lupus diathesis, and that the elder sister developed a PTU-induced lupus-like syndrome.

Adolescent↗

A man with interstitial pneumonia due to propylthiouracil.

A 50-year-old Japanese man with Grave's disease had been taking propylthiouracil (PTU) for 10 years prior to the diagnosis of pneumonia. He noticed dyspnea on exertion and had a dry cough for at least 2 years and then suddenly developed high fever and dyspnea at rest. Clinical symptoms, chest radiographs, chest computed tomography and lung function revealed interstitial pneumonia. The symptoms were completely resolved after withdrawal of PTU, and consequently he was diagnosed with PTU-induced interstitial pneumonia. He also showed moderate myeloperoxidase (MPO)- antineutrophil cytoplasmic antibody (ANCA) positivity without any signs of vasculitis before as well as after PTU withdrawal. Although PTU-induced interstitial pneumonia is quite rare, with only 3 cases, including the present patient, so far reported, respiratory involvement should be considered in patients treated with PTU.

Antithyroid Agents↗

Propylthiouracil (PTU)-induced vasculitis associated with antineutrophil antibody against myeloperoxidase (MPO-ANCA).

A 54-year-old woman had been administered propylthiouracil (PTU) for Graves' disease for 4 years. Recently, she complained of hemoptysis due to pulmonary alveolar hemorrhage causing anemia, and also had microhematuria. Antineutrophil cytoplasmic antibody against myeloperoxidase (MPO-ANCA) was positive, and she was diagnosed with PTU-induced vasculitis. Cessation of PTU and the administration of corticosteroids ameliorated these manifestations.

Antibodies, Antineutrophil Cytoplasmic↗

[The effect of propylthiouracil on function of phagocytic peripheral blood cells in persons with thyroid hyperfunction].

INTRODUCTION: It is known that hyperthyroidism as well as thyrosuppressive therapy can influence the cells of immunological system. OBJECTIVE: To examine the function of phagocyte cells in persons with hyperthyroidism and to examine if propylthiouracil (PTU) influences this function. METHOD: The study included 15 patients with hyperthyroidism and 10 healthy persons. The parameters of phagocytic activity of mononuclear and polymorphonuclear leucocytes were tested by method of ingestion of particles of inactivated yeast labeled with neutral-red. RESULTS: It was demonstrated that patients with hyperthyroidism, before the onset of therapy as well as 14 days after introduction of PTU, had decreased number of leucocytes (before PTU: 6.7 +/- 3.2 x 10(9)/l, after PTU: 6.1 +/- 2.0 x 10(9)/l and control: 8.0 +/- 1.6 x 10(9)/l; p=0.039), PMN leucocytes (before PTU: 3.9 +/- 2,4 x 10(9)/l, after PTU: 3.5 +/- 1.6 x 10(9)/l and control: 4.8 +/- 0.9 x 10(9)/l; p=0.037) and number of phagocyte PMN cells (before PTU: 0.9 +/- 0.9 x 10(9)/l, after PTU: 0.9 +/- 0.7 x 10(9)/l and control: 1.3 +/- 0.6 x 10(9)/l; p<0,05), but they had increased index of phagocytosis (before PTU: 2.0 +/- 0.2, after PTU: 1.9 +/- 0.2 and control: 1.7 +/- 0.2; p=0.029), while capacity of phagocytosis remained unchanged (before PTU: 1.9 +/- 1.7 x 10(9)/l, after PTU: 1.6 +/- 1.9 x 10(9)/l and control: 2.4 +/- 1.4 x 10(9)/l; p>0.05). The number of mononuclear leucocytes and parameters of phagocytic activity of mononuclear phagocytes in persons with hyperthyroidism did not change significantly in comparison with the control group. CONCLUSION: Patients with hyperthyroidism had decreased number of leucocytes, PMN leucocytes and number of phagocyte PMN cells, and increased index of phagocytosis, while capacity of phagocytosis remained unchanged. The number and parameters of phagocytic activity of mononuclear leucocytes did not change. PTU therapy had no effect on the examined parameters.

Adult↗

Ovarian cyclicity in thyroid-suppressed ewes treated with propylthiouracil immediately before onset of seasonal anestrus.

Two experiments were conducted to determine if propylthiouracil (PTU)-induced thyroid suppression immediately before onset of anestrus would extend the breeding season in mature ewes. In Exp. 1, twice-weekly serum concentrations of progesterone indicated that all ewes were cyclic before initiation of treatment. Beginning on d 0 (January 17), ewes received 0 (n = 4), 20 (n = 5), or 40 (n = 5) mg of PTU x kg(-1) of body weight (BW) x (-1) for 35 d. Blood samples were collected regularly throughout the trial and serum thyroxine and progesterone were quantified. Ewe BW were similar (P > 0.90) among treatments before the experiment began (mean = 78.2 +/- 4.5 kg). Likewise, serum concentrations of thyroxine averaged 86.5 +/- 8.0 ng/mL on d 0. After 11 d of PTU treatment, serum thyroxine was 90.2,75.2, and 44.2 +/- 14.0 ng/mL in ewes receiving 0, 20, and 40 mg of PTU/kg BW, respectively (linear effect, P = 0.04). On d 20, thyroxine values in the three respective groups were 73.0, 51.1, and 16.1 +/- 12.9 ng/mL (linear effect, P < 0.01). Fourteen days after PTU treatment ended, serum thyroxine did not differ (P = 0.53) among the three respective groups (71.4,73.3, and 57.5 +/- 11.8 ng/mL). Ewes receiving PTU tended to weigh less on d 42 (84.2, 78.2, and 71.8 +/- 5.1 kg for ewes treated with 0, 20, and 40 mg PTU/kg, respectively; linear effect, P = 0.10). Day of onset of anestrus was designated as the day on which serum progesterone decreased and remained below 1 ng/mL. Ewes treated with 0, 20, or 40 mg of PTU/kg BW became anestrous on d 16,40, and 81 (+/- 12) of the experiment, respectively (linear effect, P < 0.01). At the time the 35-d treatment period ended, 25, 60, and 100% of ewes receiving 0, 20, or 40 mg of PTU/kg exhibited normal estrous cycles. In Exp. 2, ewes received 0, 20, or 40 mg of PTU/kg BW for 14 d. The dose was then decreased to 0, 10, and 20 mg of PTU/kg BW for the remaining 21 d. Serum thyroxine decreased to concentrations below 20 ng/mL by d 9 after initiation of PTU treatment. Ewe weights did not differ throughout the trial and no BW loss was observed. The average day that each group entered anestrus was similar to those in Exp 1. Large doses of PTU dramatically lower serum thyroxine and this effect appears to inhibit onset of anestrus in ewes.

Analysis of Variance↗

Changes in plasma concentrations of thyroxine and triiodothyronine in beef steers fed different levels of propylthiouracil.

Three Latin-square trials were conducted to determine the effects of feeding the thyroid depressant propylthiouracil (PTU) on plasma concentrations of thyroxine (T4) and triiodothyronine (T3) in feedlot steers. In trial 1, four steers were fed 0, 1, 2 or 4 mg PTU/kg body weight daily during five 35-d experimental periods. In trial 2, eight steers were fed 0, .5, 1 or 2 mg PTU/kg body weight daily during five 28-d periods. In trial 3, three steers were fed 0, 1 or 4 mg PTU/kg body weight daily during the first 3 d in each of three 28-d periods. In general, feeding PTU caused increases in plasma T4 concentrations that peaked 5 to 7 d after feeding started. Concurrently, T3 concentrations tended to decrease when PTU was fed. The effects of PTU on hormone concentrations were apparent within approximately 1 to 4 h after PTU feeding started. Furthermore, when PTU was not fed, T4 and T3 concentrations appeared to have rhythmic cycles of 90 and 111 min, respectively, and PTU treatment appeared to interrupt this cyclical pattern. After the initial PTU response, the dose response relationship between PTU level and plasma hormone concentration was not linear. Both 4 and 2 mg PTU appeared to depress both T4 and T3 concentrations, suggesting direct inhibition of the thyroid gland and, for the 1-mg PTU treatment, T4 tended to stabilize at concentrations significantly greater than for 0 mg PTU, while T3 concentrations for 1 mg PTU were slightly lower than for 0 mg PTU.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

In vitro studies of the effect of propylthiouracil and ronnel on thyroxine-5'-monodeiodinase activity in steers.

This study compares in vitro effects of propylthiouracil (PTU) and ronnel on the conversion of thyroxine (T4) to triiodothyronine (T3) in liver and kidney from Angus steers. Tissues were homogenized and incubated with T4 (1.3 microM) in the presence of 0 to 59 microM PTU or 0 to 49.7 microM ronnel. The T3 generated during a 30-min incubation was measured by radioimmunoassay. It was found that 1.47, 5.9 and 59 microM PTU decreased T4 to T3 conversion in liver and kidney by 62 and 88, 71 and 100, and 81 and 100%, respectively. The inhibition caused by 1.47 and 5.9 microM PTU was overcome by addition of 2 mM dithiothreitol (DTT). Ronnel in concentrations of 1.24, 6.22, 49.7 microM decreased T4 to T3 conversion in liver and kidney 46 and 45, 51 and 72, and 78 and 95%, respectively. However, with ronnel, the addition of DTT caused further inhibition. A Lineweaver-Burk plot of the data obtained using .32 to 6.43 microM T4 with 1.47 and 5.9 microM PTU or 6.22 and 12.44 microM ronnel indicated that PTU is an uncompetitive inhibitor (Ki = 1.67 microM) and ronnel is a noncompetitive (Ki = 15.5 microM) inhibitor of T4-5'-monodeiodination. The data suggest that decreased conversion of T4 to T3 by PTU or ronnel may be responsible for the increased plasma concentrations of T4 and slightly decreased plasma concentrations of T3 reported in steers treated with levels of both PTU and ronnel that are associated with growth stimulation.

Animals↗