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Biomedical subjects

K Kasagi

Publications and source records attributed to K Kasagi.

At least 163 records · Page 9Linked to original sources
PubMed1978

Detection and properties of TSH-binding inhibitor immunoglobulins in patients with Graves' disease and Hashimoto's thyroiditis.

TSH-binding inhibitor immunoglobulins (TBII) have been detected in patients with Graves' disease and Hashimoto's thyroiditis by using the radioreceptor assay of TSH. In untreated Graves' patients, TBII levels correlated well with thyroidal 99mTc uptake at 30 min and the grade of epithelial hyperplasia of thyroid follicles. There were many Graves' patients whose sera contained high TBII levels but no detectable bioassayable thyroid-stimulating activity (LATS), and in these patients, close correlation was observed between serum levels of TBII and bioassayable LATS-protector activity. TBII were detectable in 2 (10%) of 20 patients with Hashimoto's thyroiditis, both of whom were clinically hypothyroid. The serum or IgG fraction from one of them, however, did not contain any significant LATS, LATS-protector, or human thyroid adenylate cyclase-stimulating activity and caused inhibition of adenylate cyclase stimulation by TSH. In that patient, TBII may be acting to block TSH binding to TSH receptors, thus causing TSH unresponsiveness and hypothyroidism.

Adolescent↗
PubMed1978

Anti-thyroxine and anti-triiodothyronine antibodies in three cases of Hashimotos thyroiditis.

Antibodies against thyroxine (T4) and/or triiodothyronine (T3) were detected in 3 patients with Hashimoto's thyroiditis. One of the patients had both anti-T4 and anti-T3 antibodies and the other 2 patients had only anti-T3 antibody. Serum T4 or T3 antibodies and the other 2 patients had only anti-T3 antibody. Serum T4 or T3 values measured by the single antibody radioimmunoassay (RIA), were low or nil in these patients. One patient was mildly hypothyroid. The other 2 patients were clinically euthyroid, but they were considered latent hypothyroid because of a slight elevation in serum TSH. On extraction of the sera with ethanol, high or normal values of T3 were obtained in all cases. Recovery of T4 or T3 added to the patients' sera determined by RIA was significantly low. The binding of [125I]T4 or [125I]T3 to the patients' sera was demonstrated by the polyethylene glycol method and by using RIA kits without adding the antibody provided. The binding activity was localized in the IgG fraction by column chromatography and by immunoprecipitation. T4- or T3-binding protein in two sera migrated in the gammaglobulin region on paper electrophoresis and was found in 7S fraction on Sephadex G-200 chromatography. In one serum containing both anti-T4 and anti-T3 antibodies, the association constants (Ka) for binding of T4 and T3 were 3.8 x 10(8) l/mol and 1.7 x 10(8) l/mol, respectively. The binding capacities in the serum were 8.2 microgram of T4 and 1.9 microgram of T3 per 100 ml of serum. For two sera containing anti-T3 antibody, Ka were 5.5 x 10(8) l/mol and 7.4 x 10(10) l/mol, and the binding capacities were 0.6 microgram/100 ml serum and 0.7 microgram/100 ml serum respectively. The clinical significance of these antibodies is discussed.

Adult↗
PubMed1976

Stimulation of growth hormone release by luteinizing hormone-releasing hormone in two males with isolated gonadotropin deficiency.

The pituitary functions were tested in two males with the typical clinical pictures of hypogonadism. The secretions of ACTH, TSH, GH and prolactin in these patients were maintained within normal limits, whereas they had markedly diminished LH and FSH levels in plasma. Plasma LH and FSH responses to the intravenous injection of 100 mug LH-RH were absent or limited. After 7-day treatment with intravenous infusion of 400 mug LH-RH, they showed normal or improved responses to the intravenous injection of 100 mug LH-RH. Thus, the diagnosis of isolated gonadotropin deficiency due to a hypothalamic lesion was established. Initially, the standard LH-RH test (100 mug intravenous injection) did not elicit a rise in plasma GH levels. However, it was of interest that after the repeated stimulation by 400 mug LH-RH, GH response to the intravenous injection of 100 mug LH-RH was observed in both patients.

Adult↗