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Biomedical subjects

T Piraphatdist

Publications and source records attributed to T Piraphatdist.

9 recordsLinked to original sources
PubMed1997

Primary thyroid carcinoma and thyrotoxicosis.

A 60-year-old man noticed rapid enlargement of a long-standing thyroid goitre, with dysphagia and difficulty in breathing. Thyrotoxicosis was diagnosed. Chest X-ray revealed multiple pulmonary metastases. He underwent near-total thyroidectomy. The histopathology revealed an undifferentiated thyroid carcinoma with some areas of papillary carcinoma and its follicular variant. Postoperative 131I total body scan showed residual thyroid tissue in the neck and one functioning metastasis in the right rib, posteriorly. The patient's condition deteriorated rapidly and he died from pneumonia. The autopsy showed widespread metastases of undifferentiated thyroid carcinoma. Only the right rib contained the follicular variant of papillary carcinoma.

Carcinoma, Papillary↗
PubMed1991

A synthetic oligopeptide derived from human thyrotropin receptor sequence binds to Graves' immunoglobulin and inhibits thyroid stimulating antibody activity but lacks interactions with TSH.

An 11-residue oligopeptide, P-195, was synthesized to match human thyrotropin (TSH) receptor structure from No. 333 to 343 of amino acid sequence. Preincubation of 5 Graves' IgGs with P-195 up to 10 micrograms resulted in dose-dependent reductions of thyroid stimulating antibody (TSAb) activity. [125I] labeled P-195 was found to bind Graves' IgG. The bound radioactivity correlated significantly with their TSAb activity (N = 25, r = 0.587, p less than 0.01). A peptide having a completely reverse sequence as P-195 did not show such biological activity. The peptide did not affect TSH and thyrotropin binding inhibitor immunoglobulin (TBII) on their receptor binding nor biological activities. P-195 was concluded to have a part of TSAb binding sites.

Amino Acid Sequence↗
PubMed1990

Possible binding site of thyrotropin binding inhibitor immunoglobulin (TBII) on the thyrotropin (TSH) receptor, which is different from TSH binding site.

A synthetic decapeptide, P-194, which has the sequence No. 103 to 111 of hTSH receptor structure with an additional N-terminal tyrosine, did not bind TSH nor affected its receptor binding and thyroid stimulating activity. Preincubation of P-194 with sera from thyroid patients caused a significant decrease in TBII activity in almost all 12 TBII positive sera and an increase of thyroid stimulating activity in 3 of 7 Graves' IgG studied. In addition, [125I] P-194 bound to serum IgG fraction from thyroid patients with a positive correlation with TBII (N = 35, r = 0.509, p less than 0.01). The P-194 portion may be, at least a part of, TBII binding site distinct from the TSH binding site on the TSH receptor.

Animals↗
PubMed1990

Sertoli-cell-only syndrome: a case report.

A 20-year-old male presented with a small hydrocoele in the left scrotal sac, bilateral small testes, and azoospermia with normal secondary sexual characteristics. Chromosome study revealed 46,XY. The results of hormonal and histopathological studies were consistent with Sertoli-cell-only syndrome.

Adult↗
PubMed1990

Complete heart block complicating hyperthyroidism: a case report.

Complete heart block developed in a 29-year-old man with hyperthyroidism and acute febrile illness. The definite cause of acute febrile illness was unknown. The results of bacteriological and viral studies were negative. Endomyocardial biopsy revealed no evidence of carditis which is the common cause of heart block. All the abnormalities resolved completely after the fever subsided and the patient was treated with an antithyroid drug. Available information indicates that a high degree of heart block can sometimes occur in hyperthyroidism in either the presence or absence of additional factors which can independently impair atrioventricular conduction. This course of events which occurred in this patient suggest that complete heartblock may have been the direct manifestation of the hyperthyroid state, however, the acute febrile illness may have been an aggravating factor in the development of abnormal atrioventricular conduction.

Adult↗