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PURPOSE: To investigate the effect of pentoxifylline (PTX) in subjects with inactive Graves' ophthalmopathy (GO) through a specific quality of life (QOL) questionnaire and exophthalmometry readings. METHODS: Eighteen females were randomly divided in two groups. Group A (n=9) was treated with PTX 1200 mg orally/day for 6 months. Group B (n=9) received placebo during the initial 6 months and then PTX for another 6 months. Proptosis measurements were carried out every 3 months and a questionnaire graded from 0 to 10 according to the severity of the symptoms was performed at baseline and after placebo and PTX administration. RESULTS: At baseline, Group A questionnaire score values were 5.5 (median; range 3.5 to 8.0), and 5.0 after 6 months (3.0 to 6.0; p=0.01). In Group B, baseline values were not significantly different after 6 months of placebo: 6.0 (4.5 to 7.0) and 5.5 (4.5 to 7.0), respectively. However, a significant change was observed 6 months after PTX: 4.0 (2.0 to 5.0; p<0.001). Patients in Group A had a progressive improvement of proptosis during PTX: at baseline, 23 mm (median; range 20 to 32); after 3 months, 23 mm (18 to 30; p=0.02); and after 6 months, 23 mm (18 to 30; p=0.005). In Group B, proptosis remained stable during placebo: at baseline, 23 mm (21 to 25); after 3 months, 23 mm (20 to 25); and after 6 months, 23.5 mm (20 to 25). A significant change was observed after 3 and 6 months of PTX: 22 mm (19 to 24; p=0.0006) and 20.8 mm (17 to 25; p=0.0003), respectively. CONCLUSIONS: Pentoxifylline seems to improve the QOL of patients in the inactive phase of GO. The objective findings of the proptosis readings corroborate to suggest that PTX may be an effective and promising drug in the inactive phase of GO.

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INTRODUCTION: Thyroid hormones (TH) may affect bone metabolism and turnover, inducing a loss of bone mass among hyperthyroid and in hypothyroid patients under hormone replacement treatment. Thyroid dysfunction leads to changes in the dynamics of parathyroid hormone (PTH) and calcitonin (CT) secretion. OBJECTIVE: The objective of the study was to determine the usefulness of CT as adjuvant therapy in the prevention of bone loss during the treatment of hypothyroidism. MATERIAL AND METHODS: We studied 16 female patients with recently diagnosed primary hypothyroidism, divided into two groups: group G1 (n = 8) submitted to treatment with thyroxine (L-T4), and Group 2 (n = 8) that, in addition to being treated with L-T4, received a nasal CT spray. All patients were submitted to determination of TSH, free T4, bone mineral densitometry (BMD) and total bone calcium (TBC) at the time of diagnosis, after 6 to 9 months of treatment, and after 12 months of treatment. RESULTS: No statistical significant differences were detected in either group between the total BMD values obtained for the femur and lumbar spine before and after treatment. However, group G1 presented a statistical significant TBC loss after 12 months of treatment compared to initial values. In contrast, no TBC loss was observed in the group treated with LT-4 in combination with CT, a fact that may suggest that CT was responsible for the lower bone reabsorption during treatment of hypothyroidism.

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INTRODUCTION: Thyroid hormones (TH) may affect bone metabolism and turnover, inducing a loss of bone mass among hyperthyroid and in hypothyroid patients under hormone replacement treatment. Thyroid dysfunction leads to changes in the dynamics of parathyroid hormone (PTH) and calcitonin (CT) secretion. OBJECTIVE: The objective of the study was to determine the usefulness of CT as adjuvant therapy in the prevention of bone loss during the treatment of hypothyroidism. MATERIAL AND METHODS: We studied 16 female patients with recently diagnosed primary hypothyroidism, divided into two groups: group G1 (n=8) submitted to treatment with thyroxine (L-T4), and Group 2 (n=8) that, in addition to being treated with L-T4, received a nasal CT spray. All patients were submitted to determination of TSH, free T4, bone mineral densitometry (BMD) and total bone calcium (TBC) at the time of diagnosis, after 6 to 9 months of treatment, and after 12 months of treatment. RESULTS: No statistical significant differences were detected in either group between the total BMD values obtained for the femur and lumbar spine before and after treatment. However, group G1 presented a statistical significant TBC loss after 12 months of treatment compared to initial values. In contrast, no TBC loss was observed in the group treated with LT-4 in combination with CT, a fact that may suggest that CT was responsible for the lower bone reabsorption during treatment of hypothyroidism.

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OBJECTIVE: To propose a modified form of thyroid suppression test with use of a single oral dose of levothyroxine (35 mg/kg). METHODS: After a baseline scintigram, 23 patients with nodular goiter suspected of autonomous function (warm or hot nodules, subnormal or undetectable thyrotropin levels, or both findings) and 14 normal subjects underwent a repeated scintigram 4 days after administration of levothyroxine. We evaluated triiodothyronine (T(3)), free thyroxine, and thyrotropin before and on the first, second, third, fourth, and seventh days after administration of the individualized dose of levothyroxine. RESULTS: The 99th percentile of postsuppression uptake in normal subjects was determined, and an uptake >12.4%, a 131 I concentration restricted to the nodule, or both factors were adopted as the criteria for diagnosis of an autonomously functioning thyroid nodule. Twelve patients were considered to have autonomously functioning nodules, and 11 patients were considered to have nonautonomous nodules. Baseline thyrotropin levels in patients with autonomous nodules did not differ significantly from those in patients with nonautonomous nodules. No signs or symptoms of toxicity were detected during the test, but all study subjects had increased free thyroxine values, and seven had high levels of T(3). CONCLUSION: The thyroid suppression test with 35 mg/kg of levothyroxine is an effective method for the diagnosis of an autonomously functioning thyroid nodule, is nontoxic, and avoids the inaccurate use of the medication occasionally observed with T(3). Even sensitive methods of thyrotropin determination cannot replace this test in the evaluation of autonomous thyroid function.

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The effects of radioiodine (131I) therapy for hyperthyroidism on the ocular process of Graves' disease is controversial. In order to evaluate the outcome of ophthalmopathy after radioiodine therapy for thyrotoxicosis we studied prospectively 30 Graves' hyperthyroid patients, 22 submitted to radioiodine (131I) treatment (group A) and 8 treated with antithyroid drugs (group B). All patients were evaluated by clinical ophthalmologic examination, and ocular proptosis (OP) was measured with both a Hertel exophthalmometer (HE) and computed tomography (CT) before and 4 to 7 months after therapy. No statistical difference was obtained between pre- and post-treatment OP measurements in each eye in either group, and we did not observe worsening in the ophthalmopathy of patients treated with drugs or radioiodine. After therapy, there was an improvement in the clinical signs of ophthalmopathy in 59% of group A and in 37.5% of group B patients. We found a significant correlation between OP measured by HE and by CT. CT findings showed an increase in orbital fat and/or muscle thickening in all patients at baseline, proving to be a useful procedure for ophthalmologic diagnosis in doubtful cases. No patient in either group developed hypothyroidism or elevated TSH levels during the study period; this may explain our good results in the evolution of Graves' ophthalmopathy after treatment with 131I and antithyroid drugs. Euthyroidism seems to be an important factor in the outcome of ophthalmopathy after therapy, whatever the mode of treatment chosen to achieve it.

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PURPOSE: using bone densitometry, to evaluate bone loss of hyperthyroidism patients, and to study the possible contribution of parathyroid hormone (PTH) in the genesis of this osteopenia. TYPE: prospective study of patients with hyperthyroidism before and after treatment. PLACE: Division of Endocrinology, Escola Paulista de Medicina. São Paulo, SP. PATIENTS: 14 outpatients with clinical and laboratory diagnosis of toxic diffuse goiter (Basedow-Graves disease). Six of these patients were studied again after treatment, with at least 6 months of clinical and laboratory euthyroidism. METHOD: bone mineral content of the lumbar vertebral bodies was evaluated by dual-photon bone densitometry. Parathyroid hormone secretion was studied with an amino-terminal specific assay after EDTA-induced hypocalcemia; results were compared to those obtained from a group of 10 normal controls. RESULTS: there was a significant increase in bone mineral density after treatment (1.300 +/- 0.079 g/cm2) as compared to the pre-treatment condition (1.229 +/- 0.091 g/cm2, p less than 0.001). Decrement rate of serum calcium during EDTA infusion was significantly lower (p less than 0.001) in hyperthyroid (-0.698 x 10(-3) +/- 0.12 x 10(-5)) than in normal control individuals (-1.486 x 10(-3) +/- 9.33 x 10(-5)), and went back to normal after treatment. EDTA-induced calcium lowering was sufficient to induce a PTH plateau of maximum response. Maximum PTH response in hyperthyroidism patients (2.34 +/- 0.45pmol) was significantly lower (p less than 0.001) than that observed in normal controls (7.51 +/- 0.40), PTH response was normal after six months of euthyroidism. CONCLUSIONS: bone mineral density showed a significant increment in treated patients, suggesting that these patients had suffered some degree of bone loss during the course of thyrotoxicosis. The lower PTH secretory reserve found in untreated hyperthyroid patients suggests that hyperthyroid state-induced bone loss may be a consequence of a direct action of thyroid hormones. This conditions was reverted after 6 months of euthyroidism.

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Twelve euthyroid patients who had been treated with 131I for hyperthyroidism due to Graves' disease and six normal controls were submitted to an EDTA infusion test. Ionized calcium and parathyroid hormone were measured in serum samples collected every 10 min during the 2-h test. Basal values for calcium (1.22 +/- 0.03 vs 1.23 +/- 0.03 pmol/l, mean +/- SD, controls vs patients) and parathyroid hormone (3.3 +/- 0.65 vs 5.1 +/- 2.32 pmol/l) as well as maximum response during infusion (1.01 +/- 0.04 vs 1.01 +/- 0.05 for calcium and 12.0 +/- 2.2 vs 13.1 +/- 3.7 for parathyroid hormone) were not significantly different. We conclude that 131I treatment for hyperthyroidism due to Graves' disease had no effect on the parathyroid gland secretory reserve of the patients studied.

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Twelve euthyroid patients who had treated with I for hyperthyroidism due to Fraves' disease and six normal controls were submitted to an EDTA infusion test. Ionized calcium and parthyroid hormone were measured in serum samples collected every 10 min during the 2-h-test. Basal values for calcium (1.22 ñ 0.03 vs 1.23 ñ 0.03 pmol/l, mean ñ SD, controls vs patients) and parathyroid hormone (3.3 ñ 0.65 vs 5.5 ñ 2.32 pmol/l_ as well as maximum response during infusion (1.01 ñ 0.04 vs 1.01 ñ 0.05 for calcium and 12.0 ñ 2.2 vs 13.1 ñ 3.7 for parathyroid hormone) were not significantly different. We conclude that I treatment for hyperthyroidism due to Graves' disease had no effect on the parathyroid gland secretory reserve of the patients studied

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Twelve untreated hypothyroid patients were submitted to EDTA infusion and the parathyroid hormone response to the induced hypocalcemia was studied with an amino-terminal specific assay. Eight of these patients were retested 6 months after achieving clinical and laboratory euthyroidism. The PTH response in the pretreatment condition was significantly higher than that obtained in a group of 10 normal individuals; this increased response had not normalized after 6 months of euthyroidism. This persisting hyperresponsiveness can be a contributory factor to the bone hypersensitivity to thyroid hormone replacement seen in hypothyroid patients.

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1. Myrcia uniflora and Bauhinia forficata were compared with placebo for their hypoglycemic effect in randomized cross-over double-blind studies in 2 groups of normal subjects (10 subjects each) and 2 groups of Type II diabetic patients (18 in the M. uniflora group and 16 in the B. forficata group). The protocol with each plant lasted 56 days. 2. After the ingestion of infusions of 3 g leaves/day of M. uniflora and B. forficata leaves, no acute or chronic effects on plasma glucose levels or glycated hemoglobin were found in either group. However, plasma insulin levels in the diabetic group were lower after M. uniflora than after placebo. 3. Among other clinical parameters tested, a statistically significant difference was found only in the alkaline phosphatase level after placebo compared with that after M. uniflora in the normal group. 4. There were no differences in any clinical parameters after the use of placebo or of B. forficata. 5. We conclude that infusions prepared from the leaves of M. uniflora or B. forficata have no hypoglycemic effect on normal subjects or Type II diabetic patients.

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Foi desenvolvido um radioimunoensaio para a medida do sulfato de deidroepiandrosterona (DHA-S) no soro. Os valores normais para diferentes grupos etarios foram determinados em 146 individuos normais. Pacientes com diferentes doencas suprarrenais e hipofisarias tambem foram estudados e apresentados os dados sobre os niveis do DHA-S

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