يعرض 1 - 10 نتائج من 61 نتيجة بحث عن '"Manabu Taguchi"', وقت الاستعلام: 0.96s تنقيح النتائج
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    المصدر: Internal Medicine

    الوصف: A 77-year-old man was suspected of having tumor-induced osteomalacia (TIO) because of hypophosphatemia (1.9 mg/dL) and elevated serum fibroblast growth factor 23 (FGF23) level (186.9 pg/mL). We detected a tumor in his left parotid gland, and the FGF23 level in the left external jugular vein indicated that the tumor overproduced FGF23. After the removal of the tumor, the serum FGF23 level rapidly decreased, and the serum phosphate normalized. This is the first case of TIO caused by a tumor in a parotid gland. This case indicates that the responsible tumors for TIO can be quite diverse.

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    المصدر: Endocrine Research. 42:132-137

    الوصف: Fibroblast growth factor 23 (FGF23) is a hormone regulating phosphate metabolism. Excessive actions of FGF23 cause several types of FGF23-related hypophosphatemic rickets/osteomalacia. Recently, it was reported that FGF23 levels were independently correlated with left ventricular hypertrophy (LVH) in patients with chronic kidney disease (CKD). In addition, FGF23 was also shown to cause cardiac hypertrophy directly acting on cardiomyocytes. However, there is no study indicating the correlation between FGF23 and LVH in adult patients with FGF23-related hypophosphatemic rickets/osteomalacia. Therefore, we examined the existence of LVH in these patients.We recruited consecutive 24 patients with FGF23-related hypophosphatemic diseases. Their serum intact FGF23 levels and the parameters associated with LVH, including left ventricular mass index (LVMI), relative wall thickness (RWT), Sokolow-Lyon voltage, and Cornell product, were measured. The correlations between FGF23 and these parameters were examined.The participants did not show LVH on the whole. In addition, no significant correlation was observed by these examinations.It seems unlikely that FGF23 levels are the apparent determinant of the cardiac mass in patients with FGF23-related hypophosphatemic rickets/osteomalacia.

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    المصدر: Journal of Bone and Mineral Metabolism. 34:132-139

    الوصف: Fibroblast growth factor 23 (FGF23) has been shown to work as a phosphotropic hormone. Although FGF23 reduces the serum phosphate level, it has not been established that phosphate directly regulates FGF23 production. In this study, we investigated whether phosphate can enhance Fgf23 expression using the rat osteoblastic cell line UMR-106, which has been shown to express Fgf23 in response to 1,25-dihydroxyvitamin D [1,25(OH)2D]. Phosphate increased Fgf23 expression in a dose- and time-dependent manner in the presence of 1,25(OH)2D. Phosphate also increased Fgf23 promoter activity, but showed no effect on the half-life of Fgf23 messenger RNA. Phosphonoformic acid and PD98059, an inhibitor of MEK, inhibited the effects of phosphate on Fgf23 expression and promoter activity. In addition, phosphate enhanced production of reactive oxygen species (ROS) in UMR-106 cells, and hydrogen peroxide enhanced FGF23 production in a dose- and time-dependent manner. Hydrogen peroxide also enhanced Elk1 reporter activity, a target of the MEK-extracellular-signal-regulated kinase (ERK) pathway. Furthermore, the effect of phosphate on ROS production and Fgf23 expression was inhibited by apocynin, an inhibitor of NADPH oxidase. These results indicate that phosphate directly enhances Fgf23 transcription without affecting the stability of Fgf23 messenger RNA by stimulating NADPH-induced ROS production and the MEK-ERK pathway in UMR-106 cells.

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    المصدر: European Journal of Endocrinology. 167:165-172

    الوصف: ObjectiveX-linked hypophosphatemic rickets (XLHR) caused by mutations in the PHEX gene is considered to be the most frequent cause of fibroblast growth factor 23 (FGF23)-related congenital hypophosphatemic rickets. In previous studies, mutations in the PHEX gene were detected in 60–70% of patients with clinical diagnoses of XLHR. This leads to the question whether current screening methods for mutations in the PHEX gene are inadequate or whether there is a substantial number of patients with other genetic causes of hypophosphatemic rickets. We conducted a genetic analysis of patients with FGF23-related hypophosphatemic rickets to clarify their etiology and evaluate the prevalence of XLHR among this group.Design and methodsWe studied 27 patients with familial and sporadic congenital hypophosphatemic rickets in whom serum FGF23 was above 30 pg/ml using an assay for the full-length protein. Exons and exon–intron junctions of genomic DNA of causative genes for FGF23-related hypophosphatemic rickets were sequenced. PHEX mRNA from peripheral blood was analyzed in some patients.ResultsDirect sequencing of genomic DNA identified 11 novel and four known mutations in the PHEX gene. Additionally, there was a large PHEX gene deletion in one case and abnormal PHEX mRNA splicing in another. In summary, 26 patients (96%) had XLHR and one patient had autosomal recessive hypophosphatemic rickets 2.ConclusionsXLHR is by far the most prevalent cause of FGF23-related hypophosphatemic rickets. We propose that analysis of PHEX mRNA from peripheral blood would be appropriate for the first screening step in determining the etiology of FGF23-related hypophosphatemic rickets.

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    المصدر: Internal medicine (Tokyo, Japan). 54(17)

    الوصف: We describe a 30-year-old man with ectopic adrenocorticotropic hormone (ACTH) syndrome. Before the operation, there was no diurnal variation of ACTH, and ACTH did not respond to CRH or dexamethasone suppression tests. These abnormalities disappeared after the removal of a neuroendocrine tumor in the lung. In addition, plasma ACTH was measureable at as early as postoperative day 3 with ACTH levels increasing thereafter. Furthermore, an insulin tolerance test and inferior petrosal sinus sampling indicated that ACTH was secreted from the pituitary. This case indicates that the hypothalamic-pituitary function can recover within a couple of weeks after curative surgery for ectopic ACTH syndrome.