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Biomedical subjects

Hiroshi Shiraga

Publications and source records attributed to Hiroshi Shiraga.

7 recordsLinked to original sources
PubMed2005

An infant case of Graves' disease with ophthalmopathy.

Graves' disease is a rare disorder in children, particularly in infants. Ocular manifestations of Graves' disease in children are even more rare and are mild compared to adults. We report a 3-year-old girl with Graves' ophthalmopathy who visited our clinic because of lacrimation. Her family had also noticed exophthalmos, goiter, irritability and increased appetite for more than 3 months. The ophthalmologist noted bilateral proptosis, eyelid erythema, lacrimation, entropion of the lower eyelid, and superficial keratitis. Her serum concentrations of free thyroxine and free triiodothyronine were high, and thyroid-stimulating hormone (TSH) was low. Serum samples were markedly positive for antibodies to TSH receptor (TRAb) and thyroid-stimulating antibody (TSAb). Although hyperthyroidism was controlled with propylthiouracil within 3 weeks, her eye signs did not improve. We administered methylprednisolone pulse therapy for ophthalmopathy, but the effect was limited and the lacrimation due to entropion and superficial keratitis persisted. Titers of both TRAb and TSAb decreased slightly and transiently with the pulse therapy. One year later, both titers remained high and eye signs did not improve any more though she was clinically euthyroid. This might indicate that both TRAb and TSAb levels correlate with the clinical course. Therefore, TRAb or TSAb might be good indicators of progress of Graves' ophthalmopathy. Ocular manifestations of Graves' disease should be followed closely with measurements of both TRAb and TSAb even in infant cases.

Child, Preschool↗
PubMed2002

Kidney transplantation after liver transplantation from the same donor: four cases of successful steroid withdrawal.

BACKGROUND: Administration of corticosteroids to kidney recipients has hampered the complete clinical success of kidney transplantation. Because most organ transplantation in Japan is living-related, we had the experience of performing kidney transplantation (KT) after liver transplantation (LT) from the same donor in four patients and successfully withdrew corticosteroid administration. METHODS: Three pediatric and one adult patient received kidney allografts from 3 to 10 months after LT from the same donor. The immunosuppressive regimen consisted of a corticosteroid and tacrolimus. The steroid was withdrawn after KT in all four patients. After complete withdrawal of the steroid, DNA was extracted from two recipients and examined by polymerase chain reaction to detect microchimerism. A mixed lymphocyte reaction (MLR) and cell-mediated lymphocytotoxicity assay (CML) were performed to test for donor-specific hyporesponsiveness. RESULTS: Steroid withdrawal was successfully accomplished after KT in every patient. No steroid-withdrawal-associated complications were observed. In the three pediatric patients, remarkable catch-up growth was observed after steroid withdrawal. In the two patients tested, donor DNA was not detected by polymerase chain reaction, suggesting the absence of microchimerism. MLR and CML showed that recipient lymphocytes reacted against donor lymphocytes at the same level as against the third-party lymphocytes. CONCLUSION: Steroid withdrawal was successfully achieved in four kidney recipients who had received a liver allograft from the same donor. The MLR and CML findings indicated the absence of donor-specific hyporesponsiveness in vitro. Although the precise mechanism is not yet clear, KT after LT from the same donor should be considered as a method that allows steroids to be withdrawn from the immunosuppressive regimen of KT.

Adrenal Cortex Hormones↗
PubMed2002

A case of post-transplant hyperparathyroidism treated with ethanol injection.

A 15-year-old boy with chronic renal failure secondary to Alport's syndrome underwent living-related renal transplantation from his 48-year-old father. His primary immunosuppressive regimen was composed of tacrolimus, mizolibine, and methylprednisolone. The postoperative course was satisfactory with one episode of mild acute rejection, treated successfully with methylprednisolone pulse therapy. Two months later, hypercalcemia (11.8-13.2 mg/dl) and hypophosphatemia (2.5-3.0 mg/dl) were noted without any bone symptoms. The serum intact-parathyroid hormone (PTH) and serum alkaline phosphatase levels were 240 pg/ml and 2483 IU/l, respectively. Ultrasound studies revealed enlargement of the two parathyroid glands. Under the diagnosis of tertiary hyperparathyroidism, he underwent percutaneous ethanol injection (PEIT) into the left parathyroid gland. Although levels of serum calcium and phosphorus returned to normal ranges and the intact PTH level decreased to 95 pg/ml with the three injections, another injection was needed to normalize recurrent hypercalcemia 2 months later. The patient experienced only transient mild dysphonia and local pain after PEIT. Although PEIT is believed less effective than parathyroidectomy, it has some advantages such as applicability to high-risk patients, repeatability of treatment, low incidence and severity of side effects.

Administration, Cutaneous↗
PubMed2002

Successful treatment of Aspergillus peritonitis in a peritoneal dialysis patient.

Aspergillus peritonitis is a rare, potentially fatal complication of continuous ambulatory peritoneal dialysis (CAPD). We report the successful treatment of refractory fungal peritonitis in an 8-year-old girl treated by peritoneal dialysis for 3.3 years. This is the second report of Aspergillus thermomutatus(telemorph: Neosartorya pseudofischeri) in humans. Comprehensive treatment included early removal of the CAPD catheter, the use of liposomal amphotericin B, and the use of itraconazole.

Amphotericin B↗
PubMed2002

Age-dependent phosphate homeostasis is regulated by a circulating factor.

To evaluate the age-dependent phosphate homeostasis, we studied the serum inorganic phosphate (P(i)) concentration in 78 recipients, aged 5-25 years, a year after renal transplantation (RT). The significant age-dependent decline of the serum P(i) concentration was observed in recipients (p < 0.0001) as well as in normal children. Our study revealed that a circulating factor may play a central role in the age-dependent change of phosphate regulation in human.

Adolescent↗
PubMed2002

Urinary megalin deficiency implicates abnormal tubular endocytic function in Fanconi syndrome.

Normal reabsorption of glomerular filtrate proteins probably requires recycling of the endocytic receptors megalin (gp330) and cubilin. Both receptors are located on the luminal surface of the renal proximal tubule epithelium. Whether abnormal amounts of receptor are present in the urine of patients with Dent's disease, Lowe's syndrome, or autosomal dominant idiopathic Fanconi syndrome was explored. They are all forms of the renal Fanconi syndrome and are associated with tubular proteinuria. Urine samples of equal creatinine contents were dialyzed, lyophilized, and subjected to electrophoresis on nonreducing sodium dodecyl sulfate-5% polyacrylamide gels. Proteins were blotted and probed with anti-megalin IgG, anti-cubilin IgG, or receptor-associated protein. Megalin and cubilin levels detected by immunochemiluminescence were measured as integrated pixels and expressed as percentages of the normal mean values. A striking deficiency of urinary megalin, compared with normal individuals (n = 42), was observed for eight of nine families with Dent's disease (n = 10) and for the two families with Lowe's syndrome (n = 3). The family with autosomal dominant idiopathic Fanconi syndrome (n = 2) exhibited megalin levels within the normal range. The measured levels of cubilin were normal for all patients. These results are consistent with defective recycling of megalin to the apical cell surface of the proximal tubules and thus decreased loss into urine in Dent's disease and Lowe's syndrome. This defect would interfere with the normal endocytic function of megalin, result in losses of potential ligands into the urine, and produce tubular proteinuria.

Endocytosis↗