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Biomedical subjects

G A Medeiros-Neto

Publications and source records attributed to G A Medeiros-Neto.

At least 37 records · Page 2Linked to original sources
PubMed1982

Thyroid function and chronic hepatosplenic schistosomiasis: peripheral conversion of thyroxine to 3,5,3'-triiodothyronine and pituitary-thyroid relationship.

The relationship between chronic hepatosplenic schistosomiaisis (CHES) and circulating thyroid hormones as well as the TSH response to TRH were investigated in 41 hospitalized CHES patients and compared to those in 11 patients with non-CHES cirrhosis with severe hepatic failure. CHES patients were subdivided into 3 groups depending on the severity of parenchymal dysfunction, based upon a composite clinical and laboratory index. Angiographic and hemodynamic studies of CHES patients revealed altered hepatic arteriograms, suggesting a decreased arterial blood flow associated with an increased venous blood flow from the portal system. A significantly reduced serum concentration of total T4 (but not free T4) was only found in the cirrhotic patients. Compared to CHES groups I and II, CHES group III patients and the non-CHES cirrhotics had significantly lower mean serum T3 levels of 80 +/- 12 and 52 +/- 8 ng/dl, respectively. The serum rT3 concentration was elevated (69 +/- 6.2 ng/dl) only in the cirrhotic patients. Both basal and peak TSH levels after TRH were within the normal range for all 4 groups of patients. The basal (40.7 +/- 8.3 ng/ml) and peak (85.5 +/- 13.7 ng/ml) serum PRL levels T4-binding globulin after TRH administration were only elevated in the cirrhotic group. Although the mean T4-binding globulin values were lower in CHES group III (17.5 +/- 3.2 micrograms/ml) and in the non-CHES cirrhotic group (18.3 +/- 2.1 micrograms/ml) compared to those in groups I (21.8 +/- 2.2 micrograms/ml) and II (20.4 +/- 2.3 micrograms/ml), the differences between groups were not statistically significant. It was concluded that hemodynamic changes without parenchymal failure have little, if any, effect on the hepatic T4 5'-monodeiodination to T3, and that the low T3 and high rT3 state does not modify the pituitary secretion of TSH, presumably by a local (at the thyrotroph level) normal conversion of T4 to T3, even at very low peripheral T3 concentrations.

Chronic Disease↗
PubMed1979

Congenital goitre and hypothyroidism with impaired iodide organification and high thyroid peroxidase concentration.

A sibship of thirteen subjects whose parents were first cousins was studied for a defect in thyroid hormone synthesis. Five sibs were goitrous and had congenital hypothyroidism. All but one showed a positive perchlorate discharge test (PDT). Three other subjects were goitrous and euthyroid (one with a positive PDT), and the remaining five sibs were euthyroid with a presumably normal thyroid. However, an abnormally exaggerated TSH response to TRH was observed not only in the hypothyroid patients but also in six of the other subjects, indicating a decreased thyroid feedback at the pituitary level in the presence of a normal serum concentration of thyroid hormones. In two hypothyroid patients a normal serum T3, low serum T4 and a low reverse T3 were observed. Microscopic studies of thyroid tissue from three of the sibs disclosed marked cellular hyperplasia with no lymphocytic infiltration anywhere in the tissue. Peroxidase activity was determined on tissue from three sibs by three different assay procedures. It was within the normal range in one patient and was significantly elevated in the other two. There was no evidence for a qualitatively defective peroxidase. The defect in thyroid function in this family does not appear to involve a peroxidase deficiency. Thyroglobulin isolated from the thyroid glands of two of the goitrous, hypothyroid subjects was poorly iodinated but was judged to be normal by immunoreactive and ultracentrifugation procedures. Although the nature of the thyroid metabolic defect in this family was not elucidated, the evidence suggests a genetic defect, probably involving a recessive gene.

Adolescent↗
PubMed1979

Imparied cyclic-AMP response to thyrotrophin in congenital hypothyroidism with thyroglobulin deficiency.

A 19 year old man had congenital hypothyroidism and severely retarded development. His thyroid gland was not enlarged and laboratory findings included low serum concentration of T4 (2.8 microgram/100 ml) and T3 (16 ng/100 ml) with a high level of TSH (52 microU/ml) that rose to 192 microU/ml after TRH. 131I uptake by the thyroid was normal (41.5% at 24 h) and did not show a normal increase after exogenous TSH administration (49.5% at 24 h). The perchlorate discharge test was negative and no antibodies against thyroid antigens were found. Studies on the biopsy specimen revealed low iodide trapping by the thyroid slices and no formation of cyclic AMP after TSH was added to the medium. The endogenous TSH of the patient was biologically active increasing cyclic adenosine monophosphate c-AMP concentration in normal thyroid slices. No thyroglobulin was found in the thyroid tissue either by immunological or ultracentrifugational methods. An increased proportion of iodoalbumin was present in the serum. We postulate that the fundamental defect in this gland is an impaired generation of c-AMP by the defective thyroid cell and deficiency of thyroglobulin formation resulting in inadequate thyroxine and triiodothyronine synthesis.

Adult↗
PubMed1978

Effects of iodides on the hypothalamic-pituitary-thyroid axis in neurological endemic cretinism: evidence for compensated thyroidal failure in adult life.

Thyroid function studies, performed after iodide administration to five patients with neurological endemic cretinism, were indicative of hypothyroidism. All five subjects had either a low serum thyroxine (T4) or a high basal thyrotrophin (TSH) level and a clearly exaggerated TSH response to thyrotrophin releasing hormone (TRH). These findings are in sharp contrast with those we have previously described in goitrous patients without cretinism from the same geographical area. One interpretation of our observations is that there is an underlying mild defect in thyroid hormone synthesis in endemic cretinism predisposing to iodine induced hypothyroidism.

Adult↗
PubMed1978

3,3',5'-triiodothyronine, thyroxine, triiodothyronine, and thyrotropin levels in maternal and cord blood sera from endemic goiter regions of Brazil.

T4, T3, rT3, and TSH were measured in cord blood of infants born in mild to severe endemic goiter areas and nonendemic urban areas in South and North America. A significantly high rT3 concentration was found in newborns living in the urban area of South America as compared to a Canadian newborn population. There were no differences among the various thyroid parameters in the groups of newborns studied. Blood from goitrous mothers showed significantly higher concentrations of T3 and TSH than nongoitrous mothers. However, these changes did not affect the concentrations of thyroid hormones, rT3, or TSH in the fetal circulation.

Brazil↗
PubMed1977

Familial goitre with partial iodine organification defect, lack of thyroglobulin, and high levels of thyroid peroxidase.

From a sibship of three sisters having congenital goitre and normal hearing, two had impairment of organification of iodine. S1 (4 years old) had goitre since birth, euthyroidism, and a negative perchlorate test. S2 (15 years old) and S3 (13 years old) were hypothyroid, and had radioiodide discharge after potassium perchlorate administration of 19.8% and 26.1%, respectively. Thyroid tissue was obtained at thyroidectomy. Peroxidase activity, in the thyroidal subcellular particles, was found to be qualitatively normal, but quantitatively increased. In the triiodide assay, the activity was: S1 6912 u, S2 2590 u, and S3 3844 u (normal values 900-1700 u). In the tyrosine-iodinase assay, the activities, expressed as nmoles of iodide incorporation per gram of tissue, were S1 1046, S2 471 (normal values 220-410). The activity of the thyroidal NADPH-cytochrome c reductase, an enzyme possibly involved in hydrogen peroxide generation, was: S1 0.084, S2 0.047, and S3 0.005 (normal values 0.018 muEq/min/mg). No thyroglobulin was detected by analytical ultracentrifugation, polyacrylamide gel electrophoresis, or double immunodiffusion in agar of the supernatant fractions. In patient S2, whose gland was labelled in vivo with 125I, 60% of the total radioactivity of the gland (pooled nodular and paranodular specimens) was in a particulate iodoprotein that was solublilized by trypsin, deoxycholate or digitonin. In the soluble fraction there were two iodoproteins: iodalbumin, and a second iodoprotein similar to the solubilized particulate iodoprotein. It is postulated that absence of the normal thyroidal receptor protein might be in some cases a cause of iodine organification defect.

Adolescent↗
PubMed1975

The effect of iodized oil on the TSH response to TRH in endemic goiter patients.

The TSH and T3 response to synthetic TRH was evaluated in 4 groups of patients: normal controls and goitrous subjects from the urban area of Sao Paulo (urinary iodine excretion: 172.2 +/- 48.3 mug I/g creatinine) and nongoitrous and goitrous subjects from the endemic areas of Sao Bento (urinary iodine excretion: 53.8 +/- 17.1 mug I/g). Plasma T4 and T3 were within our normal range in all groups of patients. The mean plasma TSH was significantly higher (5.2 +/- 3.3 muU/ml) in goitrous subjects living in Sao Bento as compared to normal control groups both in urban or endemic areas, and after TRH these patients had an exaggerated and sustained TSH response with a significantly higher peak level (21.1 +/- 7.9 muU/ml). T3 concentration rose in all subjects following TRH and all patients from the Sao Bento endemic areas had a significantly higher proportionate increase in plasma T3 at 120 min. After an injection of iodized oil basal plasma TSH returned to the normal range in the goitrous subjects from Sao Bento. The mean peak TSH response to TRH was 9.1 +/- 3.8 muU/ml at 3 months after the iodized oil injection, and only at 6 months after the iodized oil TSH response was significantly reduced (peak level: 6.1 +/- 2.4 muU/ml). It is confirmed that plasma TSH levels are increased in endemic goitrous patients but not in normal controls living in the same endemic area and it is suggested that the pituitary threshold for inhibition of secretion of TSH by T4 and T3 has been reset in these goitrous subjects to achieve a persistently higher secretion rate of TSH.

Brazil↗
PubMed1975

Effect of iodized oil on iodine content, thyroglobulin maturation and on biochemical constituents of endemic goitre in brazil.

The biochemical and morphological changes in thyroid glands were studied in 5 patients with endemic goitre in the region before and one year after the administration of iodized oil. Each patient received a tracer dose of 125-I 3-5 weeks before the biopsy and another tracer of 131-I 12 h before surgery. It was observed that: 1. Iodine deficient goitrous glands had more protein per gram of tissue and that this was corrected by iodination. 2. The goitrous glands exhibited a higher relative proportion of particulate iodoprotein that incorporates more labelled iodine in relation to time of labelling. This abnormal situation is reverted to normal by iodination. 3. A significantly higher proportion of T3 + T4 is synthetized by the glands treated with iodized oil. 4. The increased amount of 127-I per gram of tissue is followed by an increased iodination level of thyroglobulin. 5. The ultracentrifugal pattern of proteins observed for iodine deficient glands differed from the iodinated glands, indicating a failure of maturation of thyroglobulin and possibly a greater than normal degree of heterogeneity. 6. The shift in sedimentation pattern was clearly induced by the increased degree of iodination, as shown by the iodized oil injection. 7. The increased cellularity and the higher rate of protein synthesis in the goitrous glands are reverted to normal after the iodized oil injection.

Biopsy↗