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Biomedical subjects

A Pinchera

Publications and source records attributed to A Pinchera.

At least 379 records · Page 21Linked to original sources
PubMed1979

Solubilization of human thyroid microsomal antigen.

The ability of detergents (Triton X-100 and deoxycholate), high ionic strength solution (3 M KC1), and proteolytic enzymes (papain and trypsin) to solubilize human thyroid microsomal antigen was studied. Antigenic activity released from thyroid microsomal preparation into the incubation mixture was separated by centrifugation at 143,000 x g for 90 min and measured using 125I-labeled human immunoglobulin G (IgG) with elevated antimicrosomal (anti-M) and undetectable anti-thyroglobulin antibodies (anti-M IgG). All solubilized materials were shown to bind [125I]anti-M IgG and to inhibit its binding to untreated thyroid microsomes. These effects were specific and dose related. Measurements of specific activity and total amount of solubilized antigen by an absorption technique showed that Triton X-100 was the most effective agent, followed by deoxycholate, papain, trypsin, and 3 M KC1 in decreasing order. Affinity chromatography with the deoxycholate-solubilized material coupled to Sepharose 4B resulted in a 15.6-fold purification of [125I]anti-M antibodies. The present results indicate that thyroid microsomal antigen may be solubilized by several agents and this can provide the basis for its identification and purification.

Antigens↗
PubMed1979

Thyrotropin secretion in patients with central hypothyroidism: evidence for reduced biological activity of immunoreactive thyrotropin.

TSH concentration was measured in plasma before and after TRH administration (200 micrograms, iv) in 89 patients with documented hypothyroidism consequent to various hypothalamic-pituitary disorders. Basal plasma TSH was less than 1.0 microI/ml in 34.8%, between 1.0-3.6 microU/ml in 40.5% and slightly elevated (3.7-9.7 microU/ml) in 24.7% of the cases. The plasma TSH response to TRH was absent in 13.5%, impaired in 16.8%, normal in 47.2%, and exaggerated in 22.5% of the cases, with delayed and/or prolonged pattern of response in 65% of the cases. The dilution curves of several plasmas drawn before and after TRH were parallel to those obtained with TSH standard preparation. After gel filtration, the elution pattern of TRH-stimulated plasmas from 4 patients did not show any major difference from that of pooled plasmas from normal subjects given TRH or from that of patients with primary hypothyroidism. Plasma TSH values determined by cytochemical bioassay on both basal and TRH-stimulated samples of 5 patients were markedly lower than those obtained by RIA. The serum T3 response to TRH was absent or low in 40 out of 53 patients in whom it was evaluated. The administration of T3 (100 micrograms/day for 3 days) or dexamethasone (3 mg/day for 5 days) respectively suppressed or reduced both basal and TRH-induced plasma TSH levels. Two patients became hypothyroid shortly after pituitary surgery in spite of basal and TRH-induced plasma TSH levels similar to or higher than those before surgery. Though thyroid atrophy due to chronic understimulation could explain the low T3 response to TRH in secondary hypothyroidism, it is difficult to reconcile thyroid understimulation with normal or increased plasma TSH unless the immunoreactive material has low biological activity. Present data suggest that several patients with hypothyroidism consequent to hypothalamic-pituitary diseases secrete a material which is immunologically similar to pituitary standard TSH and responds to stimulatory and suppressive agents in a manner similar to normal TSH but has low or absent biological activity. Thus, hypothyroidism due to insufficient TSH stimulation can be termed central hypothyroidism and can be due 1) to pituitary insufficiency (secondary hypothyroidism), 2) to a hypothalamic defect (tertiary hypothyroidism), or 3) to the secretion of biologically inactive TSH.

Biological Assay↗
PubMed1978

Comparison of radioassay and haemagglutination methods for anti-thyroid microsomal antibodies.

Parallel measurements of circulating anti-thyroid microsomal (anti-M) antibodies by radioassay and haemagglutination were performed on subjects with or without thyroid disorders. Three-quarters (75.4%) of control subjects had undetectable antibody levels (less than 10 u/ml) by radioassay and only 3.1% had concentrations of greater than or equal to 75 u/ml. Abnormally elevated levels (greater than or equal to 75 u/ml) were found in most of the patients with Hashimoto's thyroiditis (94.1%) or idiopathic myxoedema (86.7%), in the majority (75.0%) of those with Graves' disease and only in a minority of those with other thyroid disorders. The percentage of positive sera by haemagglutination was very similar in all groups to that of abnormal values observed in the radioassay. Direct comparison of parallel tests on a total of 631 sera revealed a highly significant correlation (r = 0.91, P less than 0.001) between the two methods, but elevated antibody titres by haemagglutination were found in some sera with negative radioassays. All these sera were from a single patient with thyroid carcinoma associated with Hashimoto's thyroiditis and had elevated levels of anti-thyroglobulin (anti-Tg) antibodies. Evidence that such discrepancies were due to anti-Tg antibodies reacting with microsomal-bound Tg was provided by the demonstration that the haemagglutination produced by these sera could be completely inhibited by the addition of Tg. A similar inhibition was observed with two rabbit antisera to human Tg, but not with sera from patients with thyroid autoimmune disorders containing high levels of anti-microsomal anti-bodies.

Adenoma↗
PubMed1976

Dissociation of responsiveness to thyrotropin-releasing hormone and thyroid suppressibility following antithyroid drug therapy of hyperthyroidism.

Responsiveness to synthetic thyrotropin-releasing hormone (TRH), thyroid suppressibility by triiodothyronine (T3) and the outcome of hyperthyroidism following prolonged therapy with thionamides were studied in a group of 35 patients with toxic diffuse goiter. TRH and T3 suppression tests were performed 10 days to 24 months (mean 4 months) after withdrawal of antithyroid drugs. Nineteen patients were euthyroid and had a normal thyrotropin (TSH) response to TRH, while 4 were recovering from mild hypothyroidism due to overtreatment and had an exaggerated response. No response was observed in 12 patients with recurrent hyperthyroidism. Positive T3 suppression tests were found only in 10 of the 30 cases examined. Peak and net 2 h secretion responses of TSH to TRH exhibited a significant inverse correlation with the levels of serum thyroxine and serum triiodothyronine, but were unrelated to the degree of thyroid suppressibility. Relapse or recurrence of thyrotoxicosis occurred in at least 9 of the 23 patients having no evidence of hyperthyroidism at the time of TRH test. Each of them was found to be responsive to TRH, while the T3 suppression test was negative in 8 and had to be discontinued in one because of thyrotoxic symptoms. The present data indicate that during the early period after completion of a prolonged course of antithyroid drug therapy responsiveness to TRH in toxic diffuse goiter is: a) correlated with circulating thyroid hormones, b) unrelated to the degree of thyroid suppressibility by T3 and c) of little value in predicting the long-term results of treatment.

Adult↗
PubMed1975

[Thyroxine and triiodothyronine].

The value of measurements of serum thyroxine (T4) and triiodothyronine (T3) concentrations in the clinical evaluation of thyroid function is well established. In the present report the properties of the methods currently available for the assessment of circulating thyroid hormones are examined. Recent data indicate that results of measurements of serum T4 by radioimmunoassay (RIA) or by displacement analysis are qualitatively and quantitatively similar. Evidence has been provided from this and other laboratories that elevated or subnormal serum levels of total tt4 may be observed in several euthyroid physiologicmal serum levels of total T4 may be observed in several euthyroid physiological or pathological conditions associated with altered capacity of the thyroxine-binding protein; in these cases a normal free thyroxine index is usually found indicating its importance in the evaluation of thyroid function. Several physiological observations and the recent recognition of clinical conditions associated with changes in the T4/T3 ratio, justify the present interest in the measurement of serum T3. The advantages of RIA methods with respect to displacement techniques in the determination of this hormone are well documented. The AA. report here their experience with a simple RIA method for total T3, using a single Sephadex G25 column for extraction of T3 from serum and for separation of bound from free hormone. The mean (+/-SD) values of serum T3 found in 78 normal, 23 hyperthyroid and 25 hypothyroid subjects were as follows:160+/37ng/dl, 604+/195ng/dl and 35+/23ng/dl respectively. High values were found in 19 pregnant women at delivery (236+/29ng/dl), but not in 5 subjects on contraceptives (156+/42ng/dl). A relatively large variability is noted when normal values reported from different laboratories are compared. This may be related at least in part to geographical and/or ethnical factors, but methodolgical differences may also be involved. The normal range of circulating T3 should be established in each individual laboratory.

Antibody Formation↗