PubMed Health⌕ Search

Biomedical subjects

M L Castro

Publications and source records attributed to M L Castro.

8 recordsLinked to original sources

Peak VO2 correction for fat-free mass estimated by anthropometry and DEXA.

PURPOSE: Anthropometric (ANTHRO) and dual-energy x-ray absorptiometric (DEXA) estimates of total body and leg fat-free masses (FFM) were obtained in 77 randomly selected sedentary men and women, aged 20-80: intermethod limits of agreement and their clinical significance, as inferred from the differences on peak VO2 corrected for FFMANTHRO and FFMDEXA, were determined. METHODS: Limits of agreement were calculated as mean bias +/- 95% confidence intervals: peak VO2 at maximum cycle ergometry was related to FFMANTHRO and FFMDEXA by using both standard (y x x(-1)) and power function ratios (allometry). RESULTS: Data distribution of the ANTHRO-DEXA differences presented significant heteroscedasticity in both sexes, i.e., differences were proportional to the mean (P < 0.05). After logarithmic transformation, the mean bias +/- 95% limits of agreement were expressed as ratios (ANTHRO x DEXA(-1) x// error ratio): these corresponded to 0.95 x// 1.11 or 0.99 x// 1.15 for total body FFM and 0.90 x// 1.10 or 1.02 x// 1.07 for leg FFM in men and women, respectively. In addition, we found different allometric exponents for FFMANTHRO and FFMDEXA: the intermethod differences, therefore, increased after power function expression (P < 0.05). CONCLUSION: Discrepancies between ANTHRO and DEXA measurements of FFM depend on the magnitude of the estimate: differences are typically within 10 to 15%. Importantly, FFM-corrected peak VO2 values can vary according to the method chosen for body composition assessment, especially when allometry is used for peak VO2 correction. These results demonstrate that ANTHRO-DEXA differences in FFM estimation do have relevant practical consequences for the analysis of maximum aerobic capacity in nontrained humans.

Absorptiometry, Photon↗

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.

Adolescent↗

[Monomeric plasmatic calcitonin and hypercalcemia in lung cancer patients].

BACKGROUND: Calcitonin (CT) is a peptidic hormone produced by the thyroid C cells and related to calcium metabolism. High plasmatic levels of this hormone are found in patients with medullary thyroid carcinoma, what makes it an excellent tumor marker for this disease. However, there are reports that showed an increase of plasmatic CT levels in patients with other tumors, mainly in lung cancer. PURPOSE: These data prompt us to investigate the validity of the CT level determinations as a potential tumor marker in different histologic lung cancer, and its correlation with hypercalcemia, a very common complication in these tumors. METHOD: Blood were sampled from 56 patients with malignant lung disease for the CT and ionized calcium determinations. Calcitonin was measured using a specific radioimmunoassay for the monomeric form of the molecule, in a previous silica extracted serum probe. RESULTS: We did not find elevated levels of monomeric CT in lung cancer. Only 3 patients had mild elevated levels, while in the others CT was normal or undetectable. Hypercalcemia was found in 21.4% of these patients, but only one with supranormal CT levels. CONCLUSION: Monomeric CT serum levels are normal in lung cancer, what makes the latter use an unreliable tumor marker.

Adenocarcinoma↗

[Parathyroid function in hyperthyroidism: implications for bone metabolism and effect of the treatment].

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.

Adolescent↗