Search PubMed⌕ Search

Biomedical subjects

Seiki Wada

Publications and source records attributed to Seiki Wada.

5 recordsLinked to original sources
PubMed2003

[Glucocorticoid-induced osteoporosis].

Glucocorticoid-induced osteoporosis is one of the major complications of long-term exposure to supraphysiological doses of glucocorticoid. It has been recognized that bone loss is rapid, particularly in the first 6 months of the therapy. The skeletal effects are both dose and duration dependent; daily glucocorticoid therapy at doses of 7.5 mg/day of prednisolone or above leads to decrease bone mass and increase risk of fractures. The mechanisms which glucocorticoid induces osteoporosis are suppression of bone formation and increase of bone resorption. Hypogonadism also contributes to this pathological condition via direct suppression of sex steroids and indirect suppression through decreased secretion of pituitary hormones. Estrogen, vitamin D and its active analogues, and calcitonin, have been therefore used to prevent glucocorticoid-induced osteoporosis; however, the effectiveness is somehow limited. Treatment with newly developed anti-resorptive amino-containing bisphosphonates such as alendronate and risedronate, showed significant increase of bone mineral density for both the prevention and the treatment of glucocorticoid-induced osteoporosis, as well as risk reduction of fractures in the patients. These bisphosphonates provide a better consequence for the treatment of glucocorticoid-induced osteoporosis.

Diphosphonates↗
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↗