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T Akamizu

Publications and source records attributed to T Akamizu.

97 records · Page 6Linked to original sources
PubMed1984

Abnormal thyrotropin-binding immunoglobulins in two patients with Graves' disease.

Among 154 patients with Graves' disease, 2 patients with serum TSH-binding immunoglobulins (Igs) of high affinity were detected by the TSH binding inhibitor Ig (TBII) assay. These IgGs bound 60% and 83% of radioactively labeled TSH, respectively, as determined by polyethylene glycol precipitation, higher than the maximal specific binding (33%) in the TBII assay. Such binding was detected even in the absence of TSH receptors. The addition of bovine TSH (bTSH) or human TSH (hTSH) resulted in dose-dependent reduction in polyethylene glycol-precipitable radioactivity, though hTSH was much less effective. Further, TBII IgGs of high titer or myxedema sera with elevated serum TSH levels did not inhibit the reaction. Scatchard analysis using bTSH revealed that the IgG of 1 patient had a dissociation constant of 4.0 X 10(-11) M and maximum specific binding of 1.6 X 10(-14) M/mg IgG. The 7S fraction was found to be a major binding component by gel filtration chromatography, and immunoelectrophoresis and subsequent autoradiography demonstrated the TSH-binding material to IgG with k-chain in both patients. Both of these patients possessed significant human thyroid stimulator activity and shared 6 of 8 loci in HLA studies. These patients are considered to have anti-TSH antibody, causing falsely increased binding of [125I]bTSH in the TBII assay. Such antibodies result in false TBII assay results and thus should be sought routinely in TBII assays.

Autoradiography↗
PubMed1983

[Usefulness of the TRH-T3 test in the diagnosis of central hypothyroidism].

TRH tests (500 micrograms, i.v. bolus) were performed in 15 patients with various hypothalamic or pituitary disorders and in 6 control subjects. TSH (highly sensitive RIA) and T3 were measured before and 30, 60, 90 and 120 min. after TRH. In 8 out of 15 patients, low circulating thyroid hormone levels were observed, but their basal TSH levels were all in the normal range or even higher (0.8 - 5.5 microU/ml). Further, their integrated TSH responses (38 +/- 21 microU/ml) did not differ significantly from those of control group (35 +/- 16 microU/ml). Except for 2 cases with hypothalamic hypothyroidism, T3 increments after TRH were found consistently lower than 5 ng/dl in these hypothyroid patients. One of them revealed significant elevations of T3, T4 and thyroid 99mTc-pertechnetate uptake after 5 I.U. x 2 i.m. bovine TSH. In 19 cases studied (2 cases with hypothalamic hypothyroidism were omitted), basal T3 levels were found to show quite a good correlation (r = 0.738) with T3 increments after TRH. Therefore, TSH values by radioimmunoassay in hypothalamo-pituitary disorders were considered not relevant to be the levels of a real thyroid stimulator, or they seemed to contain biologically inactive moieties. In conclusion, measurement of the TSH level and even the TRH-TSH test were found unreliable in diagnosing central hypothyroidism, and the TRH-T3 test appeared to give quite useful diagnostic information.

Adolescent↗
PubMedDate not supplied

Clinical significance of anti-TSH antibody in sera from patients with Graves' disease and other thyroid disorders.

In a survey of patients having anti-TSH antibody (TSH Ab), data from 167 subjects were collected from 8 Japanese Institutions. They were divided into a high TSH Ab group consisting of 63 cases; since the means of assay was via a subnormal thyrotropin binding inhibitor immunoglobulin (TBII) assay, this group had TBII values less than -20%. An additional low TSH Ab group was made up of 104 cases. Out of a total of 11,211 patients, the incidence of TSH Ab for the high and low groups were 0.57% and 13.4%, respectively. More than 95% of these TSH Ab carriers had Graves' disease or some other autoimmune thyroid disorder, and anti-thyroglobulin and anti-thyroid microsomal antibodies were detected similarly in both groups. It was significant that TSH receptor antibodies could also be detected in both groups, namely, thyroid stimulating antibody and long acting thyroid stimulator (LATS) in 4 of 9 patients in the high TSH Ab group and TBII in 55 of 104 in the low TSH Ab group, respectively. The high TSH Ab levels tended to persist, but 26% of cases showed disappearance or appearance of the antibody during the observation period. In one Graves' patient, a moderate TBII activity (64.2%) was followed by markedly elevated TSH Ab (TBII: -83.4%) within 2 months. The TSH Ab in the low TSH Ab group disappeared in most cases. Also, fluctuations in TSH Ab did not always parallel those seen for TBII and reciprocal fluctuation pattern (transient or otherwise) were observed in 33%. In conclusion, anti-TSH antibody is produced frequently in patients with either Graves' disease or some other autoimmune thyroid disorder.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Renal expression of two 'thyroid-specific' genes: thyrotropin receptor and thyroglobulin.

Numerous renal abnormalities accompany thyroid disease, most of which have been ascribed to the effects of thyroid hormone on renal metabolism. In the present report, we investigate the renal expression of the nominally thyroid-specific proteins, thyroid-stimulating hormone (TSH) receptor (TSHR) and thyroglobulin (Tg), as potential links between renal and thyroid function. The expression of TSHR has been identified in several extrathyroidal tissues, but its presence in the kidney remains controversial. We have used reverse-transcriptase polymerase chain reaction and DNA sequencing to demonstrate the presence of TSHR transcript in human and mouse kidney, in a primary culture of human kidney, and in a green monkey kidney epithelioid cell line. Furthermore, human kidney cells responded to TSH with a 2.5- fold increase in intracellular cyclic adenosine monophosphate, suggesting the presence of functional TSHR protein. Comparison of renal expression of TSHR in a bovine growth hormone transgenic mouse model of progressive glomerulosclerosis with control mice suggested increased TSHR transcript in the renal cortex of transgenic animals. TSHR transcript was also detected in mouse mesangial cells in vitro which responded to TSH with significant increases in the formation of three-dimensional hillhocks. Polymerase chain reaction also confirmed the presence of Tg transcript in human and mouse kidneys and in mouse mesangial cells, but no effect of either TSH or cyclic adenosine monophosphate on Tg transcript levels could be discerned. Immunofluorescent staining with a monoclonal anti-Tg antibody identified positive staining in the cytoplasm of mesangial cells. These data suggest that the kidney is capable of expressing the thyroid-specific genes, TSHR and Tg, which could conceivably mediate effects of thyroid disease in the kidney.

Animals↗