[Parathyroid function in hyperthyroidism: implications for bone metabolism and effect of the treatment]. / Função paratiroidiana no hipertiroidismo: implicações no metabolismo ósseo e efeito do tratamento.

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.

Parathyroid hormone secretory reserve in patients submitted to 131-iodine therapy for hyperthyroidism.

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.

Parathyroid hormone secretory reserve in patients submitted to 131-iodine therapy for hyperthyroidism

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

Persistent hyperactivity of the parathyroid glands in treated hypothyroid patients.

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.

Clinical trial of Myrcia uniflora and Bauhinia forficata leaf extracts in normal and diabetic patients.

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.