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Biomedical subjects

Makoto Iitaka

Publications and source records attributed to Makoto Iitaka.

5 recordsLinked to original sources
PubMed2002

Detection of low titre TBII in patients with Graves' disease using recombinant human TSH receptor.

OBJECTIVES: We evaluated thyrotropin-binding inhibitor immunoglobulin (TBII) in sera from patients with Graves' disease (GD) by using the new human recombinant TSH receptor (TSH-R) assay to determine if it is useful for the diagnosis and follow-up of GD. PATIENTS: Serum samples from 25 patients with untreated GD, 24 with relapsing GD, 15 with GD in remission and 197 treated GD patients were examined. TBII was also measured in sera from healthy individuals (n = 69). DESIGN AND MEASUREMENTS: TBII was retrospectively measured by using the conventional porcine TBII assay (pTBII) and the human recombinant TBII assay (hTBII). Specificity was adjusted at 97.5% for both assays by receiver-operating characteristic (ROC) plot analysis, resulting in cut-offs at 10.5% inhibition (hTBII) and 9.9% (pTBII). Sensitivity was 87% for hTBII compared to 52% for pTBII (P < 0.0001). RESULTS: Even in pTBII-positive patients, hTBII values (57.6 +/- 26.1%) were significantly (P < 0.0001) higher than pTBII values (34.2 +/- 27.6%). When 139 pTBII-negative serum samples from patients with treated GD were examined, 97 samples (69.8%) were positive for hTBII. hTBII values (23.9 +/- 17.0%) were significantly (P < 0.0001) higher than pTBII values (4.1 +/- 3.3%). hTBII was positive in 13 of 13 patients who were taking antithyroid drugs but had normal serum TSH levels. When 19 serum samples from pTBII-negative untreated patients with GD were examined, 15 out of 19 (79%) were positive for hTBII. We also examined 24 patients with relapsing GD. hTBII was positive in 16 (64%) patients, whereas seven (16%) were positive for pTBII (P < 0.01). Positivity of hTBII in these untreated or relapsing GD patients was significantly higher than that of thyroid stimulating antibodies. We then examined TBII levels in 15 patients with GD in remission who had normal serum TSH values. hTBII was positive in seven patients at the time of blood withdrawal, and GD subsequently relapsed in three hTBII-positive patients in 6 months. CONCLUSIONS: Low TBII titres can now be followed more accurately during the course of treatment, which will also allow better longitudinal studies on the importance of TBII for the diagnosis as well as the prognosis of GD with respect to remission or relapse.

Animals↗
PubMed2002

A case of primary mucoepidermoid carcinoma of the thyroid: molecular evidence of its origin.

Primary mucoepidermoid carcinoma (MEC) of the thyroid is very rare, and its origin has not been fully determined. We report a case of MEC, the origin of which was demonstrated by thyroid specific genes expressed in a metastatic lymph node. A 52-year-old male presented with chest pain, weight loss and diffuse goitre. Ultrasonography showed the thyroid to be diffusely enlarged with numerous small calcifications. The tumour was found to be infiltrating the thyroid, lung, lymph nodes and first thoracic vertebra. A variant type of papillary thyroid carcinoma was suspected by fine needle aspiration cytology of the thyroid. An open biopsy specimen from an axillary lymph node revealed the tumour to be composed of three distinct cell types: mucin-producing cells, intermediate cells and a small amount of epidermoid cells with scattered psammoma bodies. Immunohistochemical studies showed the tumour cells to be negative for thyroglobulin and calcitonin, but positive for CEA. To examine the primary origin of the tumour, the expression of thyroid specific genes in the lymph node specimen was examined by RT-PCR. TTF-1, TTF-2, Pax-8, Na-I symporter and thyroid peroxidase mRNA were detected. The presence of these thyroid-specific mRNAs indicates that this MEC originated from thyroid follicular epithelium. This is the first molecular evidence of dedifferentiation from thyroid follicular cells to MEC.

Carcinoma, Mucoepidermoid↗
PubMed2002

Preclinical Cushing's syndrome due to ACTH-independent bilateral macronodular adrenocortical hyperplasia with excessive secretion of 18-hydroxydeoxycorticosterone and corticosterone.

A 64-year-old woman developed hypertension and hypokalemia, due to ACTH-independent bilateral macronodular adrenocortical hyperplasia (AIMAH) with excessive secretion of 18-hydroxydeoxycorticosterone and corticosterone. Plasma cortisol did not show a diurnal rhythm, and was not suppressed by dexamethasone (8 mg). Plasma cortisol responded to ACTH and was increased by hypoglycemia without modifying ACTH levels. Radiological studies demonstrated that adrenal glands were enlarged with macronodules. Although the patient exhibited a low plasma renin activity and aldosterone levels, hypokalemia and hypertension were observed. Hormonal findings would support the hypothesis that the tumor of AIMAH originated from cells of the upper zona fasciculata.

18-Hydroxydesoxycorticosterone↗