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Biomedical subjects

Y Amagasaki

Publications and source records attributed to Y Amagasaki.

At least 19 recordsLinked to original sources
PubMed1999

Vitamin A toxicity secondary to excessive intake of yellow-green vegetables, liver and laver.

We report a case of sudden onset of vitamin A poisoning. A 20-year-old Japanese woman had been eating pumpkin and only a very limited amount of other foods on a daily basis for 2 years. She was overly concerned about weight reduction. Aurantiasis cutis and abnormal liver function tests were noted by her family doctor in 1995 when she was 18 years old. At that time, she stopped eating pumpkin. However, she secretly continued an excessive intake of other beta-carotene-rich vegetables, liver and laver for about 2 years. Two and one-half years after being seen by her family physician, she experienced sudden onset of low-grade fever, limb edema, cheilitis, dry skin, and headache. These symptoms worsened daily. A liver needle biopsy was performed, and it showed a normal portal tract along with fat-laden Ito cells in the space of Disse. A final diagnosis of vitamin A poisoning and hepatic injury secondary to an eating disorder was made. Her symptoms and serum beta-carotene levels returned to normal with successful adjustment of her diet.

Adult↗
PubMed1998

A novel antibody directed against a three-dimensional configuration of a 95-kDa protein in patients with autoimmune hepatic diseases.

Sera from patients with primary biliary cirrhosis recognize various cellular components, such as mitochondria, centromere, nuclear envelope, and multiple nuclear dot antigens. There also appears to be a novel antibody reacting with a particular protein in these sera. The presence of this antibody was investigated by double immunodiffusion using rat liver cytoplasmic antigens, by immunoprecipitation of [35S]-methionine labelled HeLa cell extracts, and by immunoblot using disrupted HeLa cell extracts. Test sera were obtained from 491 patients with various liver diseases. Nine of the 491 sera were found to react with a 95-kDa protein as determined by immunoprecipitation of [35S]-methionine labelled HeLa cell extracts and by double immunodiffusion using a rat liver microsomal preparation. However, these same nine sera showed no reaction in the immunoblot assay. On the basis of its molecular mass and its presence in the cytoplasmic fraction, this antigen was named p95 C. This anti-p95 C antibody was detected in six of 50 (12%) sera from patients with primary biliary cirrhosis, and in three of 31 (9.7%) sera from patients with autoimmune hepatitis, but not in any of the remaining 410 sera obtained from patients with other hepatic diseases. It is concluded that anti-p95 C antibody reacts primarily with the native form of the 95-kDa protein, and represents another possible analyte for diagnosing autoimmune liver diseases.

Aged↗
PubMed1998

Dihydropyridine type calcium channel blocker-induced turbid dialysate in patients undergoing peritoneal dialysis.

We previously reported that manidipine, a new dihydropyridine type calcium channel blocker, produced chylous peritoneal dialysate being visually indistinguishable from infective peritonitis in 5 patients undergoing continuous ambulatory peritoneal dialysis (CAPD) [Yoshimoto et al. 1993]. To study whether such an adverse drug reaction would also be elicited by other commonly prescribed calcium channel blockers in CAPD patients, we have conducted postal inquiry to 15 collaborating hospitals and an institutional survey in International Medical Center of Japan as to the possible occurrence of calcium channel blocker-associated non-infective, turbid peritoneal dialysate in CAPD patients. Our diagnostic criteria for drug-induced turbidity of dialysate as a) it developed within 48 h after the administration of a newly introduced calcium channel blocker to the therapeutic regimen, b) absence of clinical symptoms of peritoneal inflammation (i.e., pyrexia, abdominal pain, nausea or vomiting), c) the fluid containing normal leukocyte counts and being negative for bacterial and fungal culture of the fluid, and d) it disappeared shortly after the withdrawal of the assumed causative agent. Results showed that 19 out of 251 CAPD patients given one of the calcium channel blockers developed non-infective turbid peritoneal dialysis that fulfilled all the above criteria. Four calcium channel blockers were suspected to be associated with the events: benidipine [2 out of 2 (100%) patients given the drug], manidipine [15 out of 36 (42%) patients], nisoldipine [1 out of 11 (9%) patients] and nifedipine [1 out of 159 (0.6%)] in descending order of frequency. None of the patients who received nicardipine, nilvadipine, nitrendipine, barnidipine and diltiazem (25, 7, 2, 1 and 8 patients, respectively) exhibited turbid dialysate. In conclusion, we consider that certain dihydropyridine type calcium channel blockers would cause turbid peritoneal dialysate being similar to that observed in patients developing infective peritonitis. To avoid unnecessary antibiotic therapy the possibility of this adverse reaction should be ruled out whenever a CAPD patient receiving a dihydropyridine type calcium channel blocker develops turbid dialysate.

Calcium Channel Blockers↗
PubMed1995

Angiotensin-converting enzyme polymorphism and development of diabetic nephropathy in non-insulin-dependent diabetes mellitus.

We determined the distribution frequency of angiotensin-converting enzyme insertion/deletion (I/D) polymorphism in 111 Japanese patients with non-insulin-dependent diabetes mellitus (NIDDM) of at least 10 years duration (80 patients with diabetic nephropathy and 31 patients without nephropathy) and 76 healthy Japanese controls. Patients with diabetic nephropathy showed an excess of the ID genotype compared with patients without nephropathy (p < 0.02) and less of the II genotype compared with healthy controls (p < 0.01) and patients without nephropathy (p < 0.01). NIDDM patients with the II genotype have a decreased risk for the development of diabetic nephropathy.

Adult↗
PubMed1993

A case of collagenofibrotic glomerulopathy associated with hepatic perisinusoidal fibrosis.

A patient with collagenofibrotic glomerulopathy associated with hepatic persinusoidal fibrosis is described. Renal biopsy revealed that the glomerular tufts contained homogeneous material that was proved by electron microscopy to be collagen fibers. The material was reactive to anti-type III collagen monoclonal antibody. Liver biopsy also showed an increase of type III collagen fibers in the perisinusoidal area. Since the serum procollagen III peptide level was elevated in this patient, fibrosis may have been simultaneously activated in kidney and liver by some unknown condition.

Biopsy↗
PubMed1992

Hypertension in unilateral atrophic kidney secondary to ureteropelvic junction obstruction.

A patient with atrophic unilateral hydronephrosis due to ureteropelvic junction obstruction associated with hypertension was successfully treated by nephrectomy. Preoperatively, plasma renin activity was elevated in both the peripheral vein and affected renal vein. Renin concentration in the resected kidney was high, and immunohistochemical localization of renin was observed along the afferent arterioles of the juxtaglomerular apparatus and in arterioles at some distance from the glomeruli.

Adult↗
PubMed1989

Significance of tubulointerstitial lesions in biopsy specimens of glomerulonephritic patients.

To evaluate the significance of tubulointerstitial lesions in the cortical area of renal biopsy specimens, clinicopathological studies were performed on 101 cases of IgA nephropathy, 31 cases of IgA-negative (non-IgA) proliferative glomerulonephritis and 75 cases of idiopathic membranous glomerulonephritis. The degree of tubulointerstitial lesions was assessed semiquantitatively by light microscopic observation and was correlated with the several histopathological and clinical parameters at biopsy, as well as with status at final follow-up (average follow-up period: 72 months). In these three types of glomerulonephritis, the degree of tubulointerstitial lesions in the cortical area was clearly correlated with the severity of glomerular injury, the prevalence of segmental sclerosis, global sclerosis, arteriolosclerosis, decreased renal function (GFR less than 70 ml/min) and hypertension (greater than 150/90 mm Hg) at the time of biopsy. The prevalence of stable renal function at final follow-up was statistically higher in the cases without tubulointerstitial lesions or with those whose lesions included less than 20% of the cortical area. From the above data, it was concluded that a semiquantitative evaluation of tubulointerstitial lesions in the cortex would reflect the severity of glomerular injury and also contribute to the assessment of prognosis in such primary glomerulonephritic patients.

Adult↗
PubMed1987

Thin basement membrane syndrome in adults.

Eight (two men, six women) cases of adult thin basement membrane syndrome were studied to clarify the clinicopathological characteristics of the disease. The average age at the time of biopsy was 40 years. All the patients had persistent microscopic haematuria, normal renal function, and normal blood pressure, with the exception of one who was hypotensive. Most of them had persistent or transient proteinuria. Renal symptoms were found in four families, although no relative had Alport's syndrome. Renal biopsy findings observed by light and immunofluorescence microscopy did not indicate any important abnormalities, but extensive diffuse thinning of the glomerular basement membrane, ranging from 153 to 213 nm, was a constant finding by electron microscopy. All the patients retained stable renal function at the time of final follow up, indicating a benign prognosis of the syndrome.

Adolescent↗
PubMed1986

Idiopathic membranous glomerulonephritis: aspects of geographical differences.

Clinicopathological studies of 89 cases of idiopathic membranous glomerulonephritis was carried out to investigate the clinical and histopathological characteristics of the disease. The results were compared with those of previous published reports to observe whether any difference between Japanese and caucasian patients exists. There were no obvious differences as to main clinical features, although an apparently better prognosis in our data was observed during long term follow up. In renal biopsy findings, especially glomerular capillary wall injuries, the prevalence of advanced electron microscopic stages (stages III and IV) was higher in the Japanese cases. A higher rate of clinical remission was observed in the treated group. It was concluded that Japanese cases had an obviously better prognosis despite having more advanced histological findings than the caucasian patients.

Adolescent↗
PubMed1985

The influence of antecedent renal disease on pregnancy.

The influence of antecedent renal disease on pregnancy was studied retrospectively in 72 women with various renal diseases that had been proved by biopsy. Among 105 pregnancies studied, normal deliveries were observed in 74 (71%), abnormal deliveries with live infants in 14 (13%), fetal or neonatal deaths in 11 (10%), and spontaneous abortions in six (6%). The incidence of normal delivery, as well as that of live births, was the highest in the cases of membranous glomerulonephritis, but there was no obvious difference in the incidence among IgA nephropathy and non-IgA proliferative glomerulonephritis. Cases in which there were tubulointerstitial changes of the cortical area or arteriosclerosis in biopsy specimens and cases that included hypertension (greater than 140/90 mm Hg) or decreased renal function (glomerular filtration rate, less than 70 ml/min) were clearly associated with an unfavorable outcome in delivery. It was concluded that assessment of the advisability of pregnancy in nephritic women should be made on the basis of a combination of the clinical and histologic parameters.

Abortion, Spontaneous↗
PubMed1984

Hypokalemia and prostaglandin overproduction in Bartter's syndrome.

In 2 adult patients with Bartter's syndrome, in whom chloride reabsorption at the diluting segment of the nephron was markedly reduced, serum potassium concentration could be improved with oral administration of a large amount of potassium chloride. In both cases, improvement of serum potassium levels with oral potassium load resulted in an increase in plasma renin activity (PRA) and plasma aldosterone concentration (PAC), a decrease in urinary excretion of prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha), and an improvement of pressor responsiveness to angiotensin II and norepinephrine. Treatment with indomethacin also improved the pressor responsiveness to angiotensin II and norepinephrine, but this occurred in association with a decrease in PRA, PAC and urinary excretion of PGE2 and PGF2 alpha. These results indicated that an event at the renal tubular level leading to potassium depletion is the most proximal pathogenetic defect in Bartter's syndrome, and that this in turn contributes to excessive prostaglandin production leading further to the decreased pressor responsiveness to vasoactive substances.

Aldosterone↗