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Takehisa Yamamoto

Publications and source records attributed to Takehisa Yamamoto.

18 recordsLinked to original sources
PubMed2006

Prediction of non-responsiveness to standard high-dose gamma-globulin therapy in patients with acute Kawasaki disease before starting initial treatment.

Clinical, laboratory, and echocardiographic data were retrospectively analyzed in 112 patients with acute Kawasaki disease who received high-dose (2 g/kg) intravenous gamma-globulin (IVIG) treatment within 2 days and were compared for those who were responsive and non-responsive to initial IVIG treatment. Coronary arteries adjusted for body surface area (BSA) were evaluated quantitatively by comparison with the mean dimensions for 85 normal control subjects. The incidence of coronary abnormalities was higher in IVIG-non-responsive patients as compared to IVIG-responsive patients (71% versus 5%, p<0.0001). Univariate analysis of pre-IVIG data showed that the neutrophil count and serum levels of C-reactive protein (CRP), total bilirubin (TB), aspartate aminotransferase (AST), alanine aminotransferase, and lactate dehydrogenase (LDH) were significantly higher in IVIG-non-responsive versus responsive patients. Multivariate analysis selected CRP (p=0.009), TB (p<0.001), and AST (p=0.002) as independent predictors of non-responsiveness to initial IVIG treatment. By defining predictive values, patients with at least two of three predictors (CRP>or=7.0 mg, TB>or=0.9 mg, or AST>or=200 IU/L) are considered to be non-responsive to IVIG for acute Kawasaki disease. Alternatively, more intense initial therapy may be a promising therapeutic strategy for patients who are predicted to be IVIG-non-responsive.

Acute Disease↗
PubMed2006

A quantitative assessment of the risk of exposure to bovine spongiform encephalopathy via meat-and-bone meal in Japan.

The feeding of meat-and-bone meal (MBM) derived from cattle infected with bovine spongiform encephalopathy (BSE) is a major source of BSE infection. The risks of BSE infection via MBM in Japan were examined quantitatively to estimate infectivity to cattle via MBM derived from a single clinically infected animal being rendered. Three routes of exposure were modeled: (i) feeding cattle concentrates containing MBM as an ingredient, (ii) feeding cattle concentrates contaminated with MBM from non-ruminant feed at feed plants and (iii) directly feeding MBM in supplemental form to cattle on farms. The effectiveness of measures designed to restrict the feeding of ruminants with ruminant MBM (feed restriction) as well as differences in the risk of exposure among regions were examined using the model. The model revealed that the median total infectivity fed to dairy cattle via MBM derived from one infected animal was approximately 0.49 cattle oral ID(50) (5th percentile=0.43ID(50), 95th percentile=0.54ID(50)). This value was reduced by 55% after the addition of MBM to cattle concentrates was restricted in 1996. The risk of exposure in dairy cattle was twice that in beef cattle. Comparisons of regional differences in exposure risk indicated that the risk was highest in a region where 14 of the 20 BSE cases reported to date were born. Our model suggested that the routes of exposure via MBM were unlikely to result in increased propagation of BSE in Japan. Furthermore, despite some regional variation, the risk of exposure declined further after the feed restriction was imposed in 1996.

Animal Feed↗
PubMed2006

Two cases of hyponatremic-hypertensive syndrome in childhood with renovascular hypertension.

UNLABELLED: We report two children with renovascular hypertension and fibromuscular dysplasia. They initially presented with severe hyponatremia, hypokalemia, polyuria, and transient proteinuria. This combination of symptoms is known to occur in patients with renovascular and malignant hypertension, and is known as hyponatremic-hypertensive syndrome (HHS), although it is considered rare in children. Since in both of our patients, the renal arterial stenosis was very severely or almost totally occlusive, we could not perform percutaneous transluminal renal artery angioplasty, and therefore nephrectomy was the only option. A histological study showed partial or complete occlusion with intimal hyperplasia and medial fibroplasia of intrarenal arteries such as the interlobular arteries. CONCLUSION: Both patients showed rapidly progressive renovascular hypertension and loss of function of the affected kidney. In order to preserve renal function in such cases, early invasive intervention appears to be necessary.

Child, Preschool↗
PubMed2006

Clinical approach to clarifying the mechanism of abnormal bone metabolism in McCune-Albright syndrome.

Recent advances in our knowledge of the abnormal bone metabolism associated with McCune-Albright syndrome (MAS) is briefly reviewed. Polyostotic fibrous bone dysplasia and hypophosphatemia are well-known characteristics of MAS. To clarify the mechanism of bone dysplasia, an approach that uses human cells isolated from MAS patients was important. It is now clear that normal skeletal stromal cells without mutation of the Gsalpha protein are necessary for the presence of bone dysplasia and that exaggerated production of interleukin-6 by fibrous bone cells with mutation of the Gsalpha protein is linked to the increased number of osteoclasts in bone tissues. The observation of increased bone resorption by the increased osteoclasts is one of the reasons for using bisphosphonates to treat the bone lesions of MAS. The key observation of the mechanism of hypophosphatemia in MAS was in a clinical report, which suggested that the presence of some humoral factors regulate phosphate metabolism. Recently, the humoral factor that causes hypophosphatemia in MAS was clarified to be fibroblast-growth factor 23 (FGF-23), although the possibility of some other humoral factors was not excluded. This is because a humoral factor inhibiting intestinal phosphate transport is present in culture medium obtained from the cells derived from fibrous bone dysplasia. The abnormal vitamin D mechanism in response to hypophosphatemia in MAS patients also proved recently to be caused by the increased circulating FGF-23 levels. The lines of evidence described suggest that FGF-23 and other factors may coexist, causing hyperphosphaturia and impaired intestinal absorption of phosphate, respectively.

Bone and Bones↗
PubMed2006

Evaluation of bovine spongiform encephalopathy (BSE) infection risk of cattle via sewage sludge from wastewater treatment facilities in slaughterhouses in Japan.

Scattered SRM residues from BSE-infected cattle are possible to contaminate sewage during the slaughtering process in slaughterhouses. A proportion of the sludge discharged from wastewater treatment facilities at slaughterhouses has historically been processed into fertilizer. We therefore investigated the associated risk of BSE infection to cattle via sludge-derived fertilizer. Each stage of the process associated with BSE exposure was qualitatively evaluated and quantitative evaluations were subsequently performed using infectious dose as a unit of concern. Results of these qualitative evaluations indicated that installation of filter(s) at the drains to the wastewater treatment facilities has been undertaken by many slaughterhouses and has decreased the likelihood of SRM contamination of sewage. The level of sludge-derived fertilizer ingested by cattle was considered to be very low since the fertilizer is mixed with the ground soil, and the amount of soil ingested by cattle is likely to be small. Results from the quantitative analysis indicated the total infectious dose ingested by cattle in Japan from an infected cow has been estimated to be 5.5 x 10(-3) ID(50). Preventing scattering of SRM during the slaughtering process, installing filters to the drains with the removal of residues from the drain water and preventing the application of sludge-derived fertilizer to pasturelands would be effective to reduce the risk. Although the limited extent of available information, this study should provide useful indication for the development of an inclusive risk assessment for slaughterhouse sludge in the future.

Abattoirs↗
PubMed2006

[The role of AGEs for the pathogenesis of osteopenia in diabetes mellitus].

Osteopenia was reported in patients with type I diabetes mellitus (DM). Also, serum levels of advanced glycation endproducts (AGEs) were reported to be elevated in DM. In this review, we showed the effect of AGEs on primary human osteoblasts, the precursor of human osteoclast like cells and parathyroid cells in culture. AGEs were made from incubating bovine serum albumin with glucose 6 phosphate for 8 weeks (AGEs-BSA). AGEs-BSA (1,000 microg/mL) showed inhibitory effect for human osteoblasts in terms of the productions of procolagen c propeptide and osteocalcin, which were regarded as bone forming parameters. On the other hand, the same concentration of AGEs-BSA inhibited the increase in the parathyroid hormone secretion from the cultured human parathyroid cells induced by low calcium medium concentration. AGEs-BSA increased time dependently intracellular calcium levels of HEK 293 cells, which expressed the wild type human calcium-sensing receptor. Also, AGEs-BSA increased IL-6 synthesis by primary human osteoblast. Our preliminary data also showed that AGEs-BSA increased osteoclast-like cells formation in number from the osteoclast precursor rich bone marrow cells. These data suggested the important role of AGEs for the pathogenesis of osteopenia in patients with DM through decreased bone formation and increased bone resorption.

Bone Diseases, Metabolic↗
PubMed2005

The role of fibroblast growth factor 23 for hypophosphatemia and abnormal regulation of vitamin D metabolism in patients with McCune-Albright syndrome.

McCune-Albright syndrome (MAS) is sometimes complicated by hypophosphatemia and abnormally low levels of 1,25(OH)(2)D in the presence of hypophosphatemia. Recently, fibroblast growth factor 23 (FGF-23) was reported as a phosphaturic and a causal factor of abnormal vitamin D metabolism. This abnormal phosphate and vitamin D metabolism is well known to be found in oncogenic and X-linked hypophosphatemia. We furthermore reported increased circulating plasma FGF-23 levels in patients with oncogenic and X-linked hypophosphatemia. To determine whether FGF-23 may be involved in the pathogenesis of MAS, we measured plasma FGF-23 levels in six MAS patients. As a control for hypophosphatemia, we also investigated the plasma FGF-23 levels in two patients with hereditary hypophosphatemic rickets with hypercalciuria (HHRH). We also investigated the correlation of plasma FGF-23 levels with serum phosphate and 1,25(OH)(2)D levels after short-term pamidronate therapy in three MAS patients. Plasma FGF-23 levels were significantly increased in patients with MAS compared to normal controls, whereas they were not increased in HHRH patients. Serum phosphate levels of the MAS patients were significantly lower than those observed in normal controls. Plasma FGF-23 levels showed significant negative correlation with serum phosphate concentrations. In three MAS patients, pamidronate therapy decreased plasma FGF-23 levels, which showed significant negative correlation with serum 1,25(OH)(2)D concentrations. These data suggested that FGF-23 is a possible causal factor for hypophosphatemia and abnormal vitamin D metabolism in MAS.

Adolescent↗
PubMed2005

[Suspected case of pseudohypoparathyroidism type II].

We experienced a suspected case of pseudohypoparathyroidism type II. The patient came to our emergency room with no thermal convulsion. The Ellsworth-Howard test was applied to the patient to determine the type of PHP.

Biomarkers↗
PubMed2004

[Importance of calcium and vitamin D intake in the childhood for the prevention of osteoporosis].

Bone stored a large amount of calcium. It is well known to the people who are engaged in medicine that the maximal bone mineral density in female is achieved at the age of 16. However, this evidence is not so familiar to the healthy Japanese. In this article, I emphasize that calcium and vitamin D intake are very important nutrients for preventing osteoporosis. I also propose that bone survey of the female students, who are attending to the junior high school or high school, will be important to find out the high risk group of osteoporosis in future.

Adolescent↗
PubMed2003

Fibroblast growth factor 23 in oncogenic osteomalacia and X-linked hypophosphatemia.

BACKGROUND: Mutations in fibroblast growth factor 23 (FGF-23) cause autosomal dominant hypophosphatemic rickets. Clinical and laboratory findings in this disorder are similar to those in oncogenic osteomalacia, in which tumors abundantly express FGF-23 messenger RNA, and to those in X-linked hypophosphatemia, which is caused by inactivating mutations in a phosphate-regulating endopeptidase called PHEX. Recombinant FGF-23 induces phosphaturia and hypophosphatemia in vivo, suggesting that it has a role in phosphate regulation. To determine whether FGF-23 circulates in healthy persons and whether it is elevated in those with oncogenic osteomalacia or X-linked hypophosphatemia, an immunometric assay was developed to measure it. METHODS: Using affinity-purified, polyclonal antibodies against [Tyr223]FGF-23(206-222)amide and [Tyr224]FGF-23(225-244)amide, we developed a two-site enzyme-linked immunosorbent assay that detects equivalently recombinant human FGF-23, the mutant form in which glutamine is substituted for arginine at position 179 (R179Q), and synthetic human FGF-23(207-244)amide. Plasma or serum samples from 147 healthy adults (mean [+/-SD] age, 48.4+/-19.6 years) and 26 healthy children (mean age, 10.9+/-5.5 years) and from 17 patients with oncogenic osteomalacia (mean age, 43.0+/-13.3 years) and 21 patients with X-linked hypophosphatemia (mean age, 34.9+/-17.2 years) were studied. RESULTS: Mean FGF-23 concentrations in the healthy adults and children were 55+/-50 and 69+/-36 reference units (RU) per milliliter, respectively. Four patients with oncogenic osteomalacia had concentrations ranging from 426 to 7970 RU per milliliter, which normalized after tumor resection. FGF-23 concentrations were 481+/-528 RU per milliliter in those with suspected oncogenic osteomalacia and 353+/-510 RU per milliliter (range, 31 to 2335) in those with X-linked hypophosphatemia. CONCLUSIONS: FGF-23 is readily detectable in the plasma or serum of healthy persons and can be markedly elevated in those with oncogenic osteomalacia or X-linked hypophosphatemia, suggesting that this growth factor has a role in phosphate homeostasis. FGF-23 measurements might improve the management of phosphate-wasting disorders.

Adolescent↗
PubMed2003

[Not Available].

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Journal Article↗
PubMed2003

[Not Available].

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Journal Article↗
PubMed2003

[Infant bone quantity measurement by the ultrasonic].

It seems that the maximum bone quantity in the young people will influence osteoporosis development in the later age. This study is to clarify the age-related change in the adolescence and the relations between bone density and exercise habit or diet habit, ultrasonic-measured bone density, physical capacity test and questionnaire survey were used. The values of SOS tended to increase along with the increase of age in both sexes when they were in the primary and middle school, but a decreased tendency was observed when they were in the high school. And the peak values were found in 17 - 18-year-old boys and 16-year-old girls. SOS correlated significantly with weight, and showed greater value in the exercise group compared with the sedentary group. And finally, the questionnaire survey showed that the regular diets were beneficial to increase SOS.

English Abstract↗
PubMed2003

[Osteoporosis in osteogenesis imperfecta].

Osteogenesis imperfecta (OI) is a kind of genetic osteoporosis, whose clinical severities vary from patients to patients. In type I OI, some patients appear normal without investigating bone mineral density (BMD) by DXA. In severe OI children, pamidronate infusion therapy is effective, however it is still uncertain when to stop the pamidronate therapy without having the problems of bone fracture healing. Also, the appropriate therapy for adult and post-menopoause OI patients remains to be clarified in future.

English Abstract↗
PubMed2002

Marked hypercalcemia in a patient with hypocalciuric hypercalcemia without a mutation in the calcium-sensing receptor gene.

A 60-year-old man was admitted to our hospital with marked hypercalcemia. He had no symptoms that might be caused by hypercalcemia. Plasma concentrations of calcium and intact parathyroid hormone were 15.2 mg/dl and 103 pg/ml, respectively. Radiological examinations revealed no abnormal findings. His calcium-creatinine clearance ratio was calculated to be 0.004, thus he was diagnosed as having hypocalciuric hypercalcemia. Familial hypocalciuric hypercalcemia was a plausible diagnosis, however, gene analysis of his calcium-sensing receptor (CaSR) revealed no mutation. The patient was thought to be a case of hypocalciuric hypercalcemia without mutation in the CaSR gene.

Calcium↗