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Biomedical subjects

Kanji Sato

Publications and source records attributed to Kanji Sato.

At least 19 recordsLinked to original sources
PubMed2006

Mild and short recurrence of type II amiodarone-induced thyrotoxicosis in three patients receiving amiodarone continuously for more than 10 years.

Although there are two types of amiodarone-induced thyrotoxicosis (AIT), only type II AIT has been seen at our institution in Japan so far. There have been few case reports of AIT recurrence, probably because of the fact that amiodarone is immediately discontinued once AIT has developed. Our own policy is not to discontinue amiodarone in all AIT patients, unless severe adverse effects such as pulmonary fibrosis develop. Among more than 50 patients with type II AIT we have encountered, three with arrhythmogenic right ventricular cardiomyopathy showed AIT recurrence. In these patients, the first episode of AIT developed 3, 4, and 2 years after the start of amiodarone administration, and recurrence was observed 5, 6, and 8 years after the first episode, respectively. The AIT resolved spontaneously in all cases while the patients continued to take amiodarone. In comparison with the first AIT episode, the second was milder and resolved within a shorter period. These three cases suggest that recurrence of type II AIT may not be rare in iodine-sufficient areas, and that it is relatively mild and may resolve spontaneously. Furthermore, at least in Japan, it may be possible for patients with recurrent type II AIT to continue taking amiodarone.

Aged↗
PubMed2006

Iodide inhibits vascular endothelial growth factor-A expression in cultured human thyroid follicles: a microarray search for effects of thyrotropin and iodide on angiogenesis factors.

OBJECTIVE: Excess iodide has been administered to hyperthyroid patients before thyroid surgery to reduce intraoperative bleeding and oozing. The purpose of this study was to elucidate the mechanism by which iodide reduces blood flow in the hypervascular thyroid gland. DESIGN: Human thyroid follicles were cultured in the presence or absence of thyrotropin (TSH), or in medium containing various concentrations of iodide, and TSH-or iodide-regulated gene expression was analyzed by cDNA microarray. MAIN OUTCOME: TSH stimulated the expression of thyroglobulin, peroxidase, sodium iodide symporter, vascular endothelial growth factor (VEGF)-A, VEGF-B, and placental growth factor (PGF) but decreased that of VEGF-C by half. When thyroid follicles were cultured in high-iodide (10(5) M) medium, TSH-induced expression of VEGF-A, VEGF-B, and PGF was decreased, accompanied by a reduction of VEGF-A release into the medium. Furthermore, expression of putative angiogenesis inhibitors such as urokinase-type plasminogen activator (PLAU) was increased. These findings were confirmed by real-time polymerase chain reaction (PCR) and Northern blot hybridization. CONCLUSIONS: We have demonstrated for the first time that iodide at high concentration decreases the expression of the angiogenic factors VEGF-A, VEGF-B, and PGF, accompanied by an increase in the expression of possible antiangiogenic factors such as PLAU. These proangiogenic and antiangiogenic factors may at least partly account for the iodide-induced decrease in thyroid blood flow.

Blotting, Northern↗
PubMed2006

[Drug-induced hypercalcemia].

Drug-induced hypercalcemia is caused by increased bone resorption (vitamin D and vitamin A intoxication), increased calcium absorption in the gastrointestinal tract (vitamin D intoxication, excessive intake of calcium) or increased calcium reabsorption in the renal tubules (thiazide diuretics). When vitamin D (D(2) or D(3)) intoxication develops, the hypercalcemia persists for more than several months. Therefore, short-acting active vitamin D (1alpha-OHD(3), 1,25- (OH) (2)D(3)) are clinically used. Recently, various analogs of 1,25- (OH) (2)D(3) with potent differentiation stimulating activity on keratinocytes but insufficient calcium-movilizing activity have been developed (tacalcitol, calcipotriol, 22-oxacalcitriol). However, severe hypercalcemia may develop when these ointments were abundantly applied to patients with psoriasis since the agents can be easily absorbed through the skin lesions.

Bone Resorption↗
PubMed2006

[Graves' disease and bone metabolism].

Thyroid hormone stimulates osteoclastic bone resorption, through increased expression of receptor activator of nuclear factor kappa B ligand (RANKL) in osteoblasts as well as via non-RANKL-mediated pathway. Therefore, in hyperthyroid patients with Graves' disease, bone resorption (urinary excretion of calcium, phosphate, deoxypyridinoline, N-terminal telopeptide of collagen type I) is increased. Due to accelerated bone remodeling, bone formation is also increased. However, the amount of bone formation is less than that of bone resorption, leading to a gradual decrease in bone mineral density (BMD). In young patients, the decreased BMD is reversible, but not in post-menopausal women. Therefore, in these patients with rapid bone looser, bisphosphonates may be beneficial treatment for prevention of osteoporosis and will prevent bone fractures in senile period.

Alkaline Phosphatase↗
PubMed2005

Rapid differential diagnosis of Graves' disease and painless thyroiditis using total T3/T4 ratio, TSH, and total alkaline phosphatase activity.

When thyrotoxic patients are first seen in an outpatient clinic, it is important to make a differential diagnosis of Graves' disease (GD) and painless thyroiditis (PT). Using the three parameters of total T3/T4 ratio, TSH and T-ALP activity, all of which can be obtained within one hour in our hospital, 173 untreated patients with thyrotoxicosis were evaluated for the ratio of each parameter. For GD vs. PT, total T3/T4 (ng/microg) ratio (>20), TSH (<0.005 microU/ml) and elevated T-ALP had a likelihood ratio of 2.14, 2.12 and 4.07, respectively. When a patient had all three positive parameters, the likelihood ratio increased to 5.81, which showed effective synergy. These data suggest that, in addition to total T3/T4 ratio and TSH value, T-ALP activity is a useful parameter for the rapid differentiation of GD. The lower T-ALP activity seen in PT is probably due to the fact that patients develop less severe thyrotoxicosis or visit hospital earlier than patients with GD. Therefore, the diagnostic accuracy for Graves' disease might be increased by using the three parameters in combination.

Adult↗
PubMed2005

[Referral of patients with parathyroid dysfunction to specialists--which patients should be referred to parathyroidologists?].

Although a diagnosis of primary hyperparathyroidism and hypothyroidism becomes very easy at the present time due to development of highly sensitive assay for parathyroid hormone, the diagnosis of hyper- and hypothyroidism should be made by excluding the loss and gain of function mutation of calcium sensing receptor, respectively. When a diagnosis of primary hyperparathyroidism is made but the localization of adenoma(s) is not identified, the patient should be referred to specialists for parathyroid surgery. Although patients with primary hypoparathyroidism can be followed by a general physician, they should be referred to specialists when they become pregnant, since active vitamin D is increased and decreased in the late pregnancy and in the postpartum period, respectively.

Female↗
PubMed2004

An assessment of bone mineral density in patients with Addison's disease and isolated ACTH deficiency treated with glucocorticoid.

Glucocorticoid replacement therapy needs to be tailored to individual patient's requirements in order to avoid risk of over or under medication. We measured bone mineral density (BMD) of lumbar spine using dual X-ray absorptiometory in 10 patients with Addison's disease and 5 patients with isolated ACTH deficiency receiving glucocorticoid replacement therapy. We also examined the effect of glucocorticoid replacement on BMD. Decreased %BMD (less than 80% of age-matched controls) was found in 2 female patients who had received hydrocortisone at a dose of 14.8 and 15.4 mg/m(2)/day. In contrast, no patient receiving a hydrocortisone dose of less than 12.4 mg/m (2)/day had decreased %BMD. There was no correlation between %BMD and hydrocortisone dose (mg/m(2)), duration of therapy, or cumulative hydrocortisone dose when treated with appropriate dose of hydrocortisone (<13.6 mg/m(2)). There was also no statistically significant difference in %BMD with age. We concluded that long-term glucocorticoid replacement therapy does not induce bone loss in patients with glucocorticoid deficiency unless an excessive dose of hydrocortisone is given.

Absorptiometry, Photon↗
PubMed2004

Hypercalcemia induced by excessive intake of calcium supplement, presenting similar findings of primary hyperparathyroidism.

A 31-year-old woman had ureterolithiasis related to hypercalcemia, and when she was admitted to our hospital ultrasonography and technetium-99 m sestamibi scintigraphy did not detect parathyroid abnormalities. Serum concentrations of calcium and intact parathyroid hormone were 9.7 mg/dl and 153 pg/ml, respectively, but subsequently increased to 13.5 mg/dl and decreased to 10 pg/ml, respectively. Diagnostic interview revealed that she had been taking excessive calcium supplements of 3,000 5,000 mg/day because she was worried about developing osteoporosis. Her hypercalcemia was cured after she stopped taking the supplements. The present case indicates that calcium supplementation of more than 2,500 mg/day elicits adverse effects on body mineral balance. Clear indications of the upper limits to supplements should be made known to the consumers.

Adult↗
PubMed2003

Stimulation of cellular prion protein expression by TSH in human thyrocytes.

The cellular isoform of prion protein (PrP(C)) is a cell-surface glycosyl-phosphatidylinositol-anchored protein which is ubiquitously expressed on the cell membrane. It may function as a cell receptor or as a cell adhesion molecule. Thyroid follicles, obtained from patients with Graves' disease at thyroidectomy, were cultured in F-12/RPMI-1640 medium supplemented with 0.5% fetal bovine serum and bovine thyroid stimulating hormone (bTSH). Northern blot analyses revealed that bTSH increased the steady-state expression levels of PrP mRNA in a time- and dose-dependent manner. This increase was reproduced by dibutyryl-cAMP and 12-decanoylphorbol-13-acetate. The mRNA expression was greater in thyroid follicles in suspension culture than in thyrocytes cultured in a monolayer. These findings suggest that TSH stimulates PrP mRNA expression in thyrocytes through the protein kinase A and C pathways. The greater mRNA expression in thyroid follicles than in monolayer cells suggests that PrP(C) may be involved in structure formation or maintenance of thyroid follicles.

Animals↗