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Serum thyroglobulin (Tg), T4, T3, FT4, FT3, TSH concentrations and TSH response to iv TRH (delta TSH) were measured in 56 consecutive patients with (multi) nodular goiter from a severely iodine-deficient endemic goiter area in Northeastern Sicily and in 11 non goitrous euthyroid individuals living in the same area. Serum Tg concentrations were sharply increased in goitrous subjects (453 +/- 476 ng/ml) and related to thyroid size and the presence of nodules (chi 2 = 43.5, p less than 0.0005). Serum TSH levels measured in goitrous patients (2.1 +/- 0.9 microU/ml) were significantly lower than those measured in nongoitrous iodine deficient subjects (3.1 +/- 0.9 microU/ml, p less than 0.001) and decreased with increasing goiter size and nodularity (chi 2 = 27.3, p less than 0.05). A similar pattern was shown by the analysis of the delta TSH (chi 2 = 43.1, p less than 0.0005). These results suggest that at least a part of the largest and multinodular goiters become autonomously functioning with duration and growing in size. In 13 goitrous patients with absent or impaired response to TRH, a significant direct relation was apparent between log-Tg and goiter size and nodularity (r = 0.64) with an inverse relationship between serum FT3 and delta TSH (r = 0.73). A computed program analysis based on the combination of different independent variables (x) including age, thyroid size and nodularity, serum TSH, log-Tg and FT3, indicated the existence of a significant negative relationship between these variables and the TSH response to TRH (r = 0.75, p = 0).(ABSTRACT TRUNCATED AT 250 WORDS)

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Gamma-glutamyltranspeptidase (GGT) and alkaline phosphatase (ALP) were assayed in the sera of 27 patients affected with Graves' disease prior to conventional (12-18 months) methimazole (30-5 mg/day) treatment, who were subsequently followed up over 36 +/- 1.5 months (m +/- SEM). Twelve patients underwent recurrence of thyrotoxicosis (relapsers) at variable intervals from withdrawal of treatment, whereas the remaining 12 remained euthyroid (nonrelapsers). In the study group as a whole, both GGT and ALP serum levels were significantly (p less than 0.001) increased with respect to 24 sex- and age-matched euthyroid controls (31.8 +/- 3.6 vs. 11.5 +/- 1.2 U/l and 203 +/- 13.8 vs. 110 +/- 7.3 U/l, m +/- SEM). Prevalence of GGT and ALP elevations was 56% (15/27) and 58% (15/26), respectively. Serum GGT activity was age dependent (r = 0.466, p less than 0.05) and inversely related to log2 microsomal antibody initial titer (r = 0.499, p less than 0.05) in the whole series. There was no difference in mean pretreatment thyroxine (T4) or triiodothyronine (T3) between the groups with supranormal enzyme and normal enzyme levels. However, in the group with enhanced enzyme levels, relapsed patients had higher initial T4 (20.3 +/- 0.8 vs. 17.1 +/- 0.7 micrograms/dl, p less than 0.01) and lower both initial T3 (452 +/- 31.1 vs. 551 +/- 57.8 ng/dl, p less than 0.02) than the nonrelapsed patients. Only in this group, initial T3:T4 ratio was a valuable indicator of the outcome of the disease, since it was below 30 in 7/7 (100%) relapsers vs. 2/8 (25%) nonrelapsers, but above 30 only in 6 subjects who remitted.

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In order to verify the hypothesis of the presence of IgM (or an IgM-like substance) capable of inhibiting thyroid hormone binding to serum proteins and, therefore, capable of enhancing serum free thyroid fractions in non-thyroid illnesses (NTI), we measured TBG and TBPA maximum binding capacities and TBG concentration by an immunoradiometric system in normal pooled sera (NPS) before and after enrichment with purified immunoglobulins (IgM and IgG) from euthyroid NTI sera (free T4, free T3 and TSH levels were normal). A known amount of TBG was diluted 1:2-1:6 with deionized water or with IgM from NPS or from each of 6 NTI sera; the measured values were not different from these expected on theoretical grounds. Likewise, IgM or IgG from normal or from each of 7 NTI sera failed to modify both TBG and TBPA capacities of different NPS, and NTI immunoglobulins showed no binding activity directed to [125I]T4, [125I]T3 or [125I]TBG. In addition, no inhibitory influence of TBG and TBPA capacities was observed when the whole euglobulin fraction obtained by precipitating the same 7 NTI sera by PEG was mixed with NPS. On the other hand, a significant IgM inhibitory effect on the binding of labelled T4 to TBG was found, only when IgM concentrations were experimentally rendered 41 times greater than that requested in the working mixtures. We conclude that no immunoglobulin inhibitor of thyroid hormone binding to transport proteins was evident in the NTI sera investigated.

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In 14 children affected by digestive diseases producing protein-calorie malnutrition T3 and rT3, T4, TSH serum levels and TBG and TBPA maximum binding capacity were measured at the moment of the hospitalisation and up to their clinical and biochemical amelioration. No changes in serum T4 and TSH levels and in TBGcap values were detected. TBPAcap was found to be persistently low. At the moment of the hospitalisation serum T3 and rT3 average values were found to be 65 +/- 25 ng/dl and 58 +/- 25 ng/dl respectively. Opposite changes in serum concentrations of the triiodothyronines were observed at the moment of the interruption of the study; T3 values were 200 +/- 64 ng/dl and rT3 value 25 +/- 16 ng/dl. T4 deiodination may be a homeostatic process and its preferential conversion to either activating (T3) or inactivating (rT3) pathways is related to the state of the organism.

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Serum concentrations of T4, T3, rT3, and TSH were measured by radioimmunoassay in 45 patients suffering from beta-thalassaemia. A TRH stimulation test was performed and the binding capacity of TBG and TBPA for T3 and T4 measured by reverse flow zone electrophoresis in a group of these patients. Mean T4 serum concentration was lower in thalassaemic patients than controls; T3, rT3, TSH levels, and the pituitary response to TRH were normal. TBPA binding capacity for thyroxine was greatly decreased, probably due to iron overload impairing the liver function. The decreased circulating total thyroxine might be explained by the reduced TBPA capacity, serum free thyroid hormone concentration total thyroxine might be explained by the reduced TBPA capacity, serum free thyroid hormone concentration values being normal. It is concluded that thalassaemic children are euthyroid, despite often having low-normal or subnormal thyroxine levels.

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