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Biomedical subjects

K Nishiya

Publications and source records attributed to K Nishiya.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Parvovirus B19 infection-induced anemia and leukocytopenia after myomectomy].

A 38-year woman was hospitalized because of myoma uteri. She underwent myomectomy on September 30, 1997 with 2,000 ml blood loss. No blood transfusion was required, but she received a plasma protein product. On the 14th postoperative day, a complete blood count revealed anemia (Hb 9.3 g/dl) and leukocytopenia (1,600/ul). But it did not reveal anemia before the operation. Bone marrow smears showed erythroblastopenia with giant proerythroblasts. Anti-parvovirus B19 IgM antibody were positive in the serum and parvovirus B19 DNA was detected in the bone marrow cells by polymerase chain reaction. From the results, the patient was diagnosed as the anemia and leukocytopenia secondary to parvovirus B19 infection. Parvovirus B19 was not detected in the samples of the plasma protein product received on the myomectomy. The reticulocyte gradually decreased to 1/1000 on the 20th postoperative day. The anemia and leukocytopenia gradually improved. This case shows that parvovirus B19 infection could cause hematological disorders in the normal person under acute blood loss. This report warns that a careful observation is necessary for the patients who have received operations with acute blood loss.

Adult↗
PubMed1999

Additive triple DMARD combination therapy of a low dose of sulfhydryl compounds, sulfasalazine and methotrexate in the treatment of rheumatoid arthritis: a clinical trial.

To evaluate the efficacy and safety of additive triple disease modifying anti-rheumatic drug (DMARD) combination therapy of a low dose of sulfhydryl compounds ¿D-penicillamine, bucillamine or tiopronin¿, sulfasalazine (SSZ) and methotrexate (MTX) as a treatment for rheumatoid arthritis (RA) patients, we studied a total of 33 Japanese RA patients (6 males, 27 females). At 1 or 2 months after simultaneous administration of the 3 above-mentioned DMARDs was begun, significant improvements were seen in markers of joint inflammation, i.e., erythrocyte sedimentation rate and C-reactive protein in sera. At 6 months, clinical improvement judged by the physicians' overall assessment of joint symptoms and laboratory data was observed in 29 (88%) of the 33 RA patients. No marked effect was observed in the other 4 (12%) patients, however. We observed no significant adverse reaction to this therapy. This suggests that additive triple DMARD combination therapy of a low dose of sulfhydryl compounds, SSZ and MTX could be a useful drug therapy for the treatment of RA patients, even those who are refractory.

Adult↗
PubMed1999

Ferritin correlates with C-reactive protein and acute phase serum amyloid A in synovial fluid, but not in serum.

OBJECTIVE: To evaluate ferritin concentration in serum and synovial fluid (SF) as a marker of activity of arthritis in comparison with C-reactive protein (CRP) and acute-phase serum amyloid A protein (A-SAA). METHODS: We determined the concentrations of ferritin, CRP and A-SAA in paired serum and SF in 34 rheumatoid arthritis (RA) and 21 osteoarthritis (OA) patients. The erythrocyte sedimentation rate (ESR) was also measured. RESULTS: The serum concentrations of ferritin, CRP and A-SAA were 93 +/- 76 (mean +/- SD) ng/ml, 4 +/- 5 mg/ml, 8 +/- 4 mg/ml in OA and 140 +/- 227, 59 +/- 34, 289 +/- 223 in RA, respectively. There was no significant difference in serum ferritin levels between OA and RA, and serum ferritin did not correlate with ESR, CRP or A-SAA. Both serum CRP and A-SAA levels were significantly higher in RA than in OA (p < 0.0001, p < 0.0001), and correlated with ESR in all arthritis (r = 0.658, p < 0.0001, r = 0.404, p < 0.01), respectively. Serum CRP levels correlated with A-SAA levels in serum (r = 0.727, p < 0.0001). In SF, the concentrations of ferritin, CRP and A-SAA in RA (421 +/- 307, 25 +/- 20 and 39 +/- 41) were significantly higher (p < 0.01, p < 0.0001, p < 0.001) than those in OA (202 +/- 220, 2 +/- 2 and 2 +/- 2), respectively. There were significant correlations among SF ferritin, CRP and A-SAA. CONCLUSION: Ferritin levels in SF but not in serum are significantly elevated in RA more than in OA, and ferritin correlated with CRP or A-SAA in SF, but not in serum. Higher levels of SF ferritin, as well as SF CRP and SF A-SAA, seem to reflect greater degrees of joints inflammation in RA and OA.

Acute-Phase Reaction↗
PubMed1999

[Anti-myeloperoxidase and anti-lactoferrin antibodies in patients with IgA nephropathy and Henoch-Schönlein purpura].

Antineutrophil cytoplasmic antibodies (ANCA) for two antigens, i.e. myeloperoxidase (MPO) and lactoferrin (LF) in sera from 19 IgA nephropathy (IgAN), 3 adult Henoch-Schönlein purpura (HSP) and 8 child HSP patients were examined by enzyme-linked immunoabsorbent assay (ELISA) for immunoglobulin isotypes. All of child HSP patients showed negative ANCA. On the other hand, one IgAN patient and two adult HSP patients showed weak positivity for IgA class anti-MPO antibody. There was no patients who showed positivity for IgG and IgM class anti-MPO antibody. In anti-LF antibody, one IgAN and one adult HSP showed positivity in IgG class; 2 IgAN and 2 HSP in IgA class and 2 IgAN and one HSP in IgM class. These results indicate that adult HSP patients have higher prevalence of IgA class anti-MPO antibody and anti-LF antibody than IgAN or child HSP.

Adult↗
PubMed1999

[Detection of anti-IgA alloantibody in a case of non-hemolytic transfusion reaction].

A 59-year-old man with myelodysplastic syndrome exhibited unticaria, dyspnea, fever, and hypotension immediately after the start of platelet concentrate (PC) transfusion on the 15th day of hospitalization. On the 17th and 21st day of hospitalization, the patient exhibited severe unticaria resembling that of erythroderma after the start of PC transfusion. Anti-IgA IgG antibody was detected by enzyme-linked immunosorbent assay (ELISA) on the 28th day of hospitalization. Anti-IgA (purified from pooled human plasma) was detected by Western blotting. The patient's IgA level was normal. No antibodies against HLA or platelet-specific antigens were detected in serum. The patient had no reaction to administration of washed PC. These findings suggest that anti-IgA antibody might have been responsible for the nonhemolytic transfusion reaction in this patient.

Antibodies, Anti-Idiotypic↗
PubMed1999

[A case of secondary systemic amyloidosis associated with rheumatoid arthritis after 3-year disease duration].

A 63-year-old woman who started to have polyarthralgia in December 1993 has been diagnosed as rheumatoid arthritis (RA) and treated with muscular injection of gold sodium thiomalate. She began to have nausea, vomiting, anorexia and watery diarrhea in October 1995. A year later, she had to receive intravenous infusion on admission since more frequent watery diarrhea occurred more than ten times within a day. On admission in our hospital in December 1996, she had proteinuria in addition to gastrointestinal symptoms. The biopsy specimen from stomach, duodenum and kidney proved systemic amyloidosis associated with RA. In spite of steroid-pulse, dimethyl sulfoxide (DMSO) and colchicine therapy, profound proteinuria in nephrotic syndrome was continued in association with hypoproteinemia, anasarca and renal failure. She was treated on hemodialysis and intravenous hyperalimentation (IVH) until November 1997 when A-V shunt operation on left forearm was performed. However, the shunt was not available for HD and she suffered from septicemia and died on December 1997. This patient was a rare case of secondary systemic amyloidosis associated with RA in early clinical course.

Amyloidosis↗
PubMed1999

Neuropeptide Y Y1 receptor polymorphism as a prognostic predictor in Japanese patients with IgA nephropathy.

BACKGROUND: Neuropeptide Y exhibits a vasoconstricting action and regulates systemic blood pressure as well as noradrenalin. There are 5 types of NPY receptors, Y1 - Y5, which were introduced by pharmacological differences. Recently, a single point mutation in the first intron of the NPY Y1 receptor (NPYY1R) was reported. SUBJECTS AND METHODS: In this study, we investigated the relationship between NPYY1R gene polymorphism and clinical characteristics in patients with IgA nephropathy using polymerase chain reaction and restriction fragment length polymorphism analysis. RESULTS: Distribution of the NPYY1R genotypes which were defined as YY, Yy and yy genotypes, did not differ between 60 normal control subjects and 68 patients with IgA nephropathy (15 : 36 : 9 versus 21 : 40 : 7, respectively). In IgA nephropathy patients, the incidence of hypertension and the rate of urinary protein excretion were slightly higher in the non-YY genotype than in the YY genotype group (23% versus 5% and 1.1 +/- 1.2 versus 0.6 +/- 0.4 g/24 h, p = 0.09 and p = 0.05, respectively). The reciprocal of the serum creatinine level was estimated to determine the deterioration in renal function during follow-up after the renal biopsy. The level was lower in the non-YY genotype than in the YY genotype group (-0.002 +/- 0.064 vs 0.033 +/- 0.053/month, respectively, p < 0.01). Multiple regression analysis for the reciprocal of the serum creatinine level revealed that the NPYY1R genotype was an effective variable (p < 0.01). CONCLUSION: In conclusion, we propose that the NPYY1R gene polymorphism may be a novel prognostic predictor in patients with IgA nephropathy.

Adult↗
PubMed1999

[A case of systemic lupus erythematosus associated with severe acute pancreatitis].

A 22-year-old woman began to have the symptoms of anorexia, high fever, cough and general fatigue from June of 1997. She was admitted in our hospital on Aug. 8th, 1997 for the further detail examination because of pancytopenia and positive antinuclear antibody (ANA). Her laboratory findings and clinical symptoms were compatible with systemic lupus erythematosus (SLE) such as leukopenia, proteinuria, hypocomplementemia, positive ANA, elevated titer of autoantibodies including anti-DNA, anti-Sm, anti-RNP antibodies, polyarthralgia and photosensitivity. The administration of oral prednisolone (40 mg/day) was started on Aug. 15th, 1997 under the diagnosis of SLE. However, she had severe abdominal pain in epigastrium with elevated serum amylase, ascites and dull shape of pancreas tail by CT scan compatible with acute pancreatitis. On Aug. 18th, her general condition was worsening with fever, epigastralgia, abdominal distension, anemia, weak palpation of radial artery, hypotension, tachycardia, shallow breathing and cold sensation on both extremities as shock. In spite of steroid pulse therapy with nafamostat mesilate intraarterial infusion, her condition was not improved. The dose of 50 mg/day of cyclophosphamide was added to the regimen on Aug. 22nd. Then, gradually her condition started to be restored. Anemia, leukopenia, hypocomplementemia continued. Second steroid pulse therapy was done on Sep. 5th. After then, she became better in her clinical symptoms and laboratory data. The dose of PSL was tapered to 15 mg/day and 7.5 mg/day update of Oct. 1998 without the pseudcysts found after pancreatitis. She is a rare case who recovered from severe acute pancreatitis due to SLE itself.

Acute Disease↗
PubMed1999

[Correlation of serum IgA levels with serum IgG levels, erythrocyte sedimentation rate and platelet counts in 98 patients with rheumatoid arthritis].

Rheumatoid arthritis (RA) is an autoimmune disease with unknown etiology. Polyclonal B cell activation (PBA) is one of immunological abnormalities commonly found in RA patients. We examined serum IgG, IgA, IgM levels in 98 RA patients and compared 31 patients with high serum IgA levels (group B) with 67 patients with normal serum IgA levels (group A) in clinical background. Group B patients had significantly higher mean values of serum IgG levels, erythrocyte sedimentation rate (ESR), and platelet counts than group A. However, there was no correlation between serum IgA levels and X-ray stage, class of ADL or disease duration of RA. These results indicate that high serum IgA levels reflect for disease activity of RA. Serum IgA levels did not correlate with interleukin (IL)-6 levels in 53 RA patients studied. It is speculated that high serum IgA levels might be caused by the following evidences 1) that transforming growth factor (TGF) beta, a known cytokine to increase IgA production by human splenic B cells, gene expression is enhanced in mononuclear cells from synovial fluid and 2) that iron deposition is found in RA synovial and high serum IgA levels are found in iron overload like thalassemia intermedia.

Arthritis, Rheumatoid↗
PubMed1999

[B-cell, T-cell surface phenotypes and epitopes in autoimmune thyroid diseases].

Autoimmune thyroid diseases (AITD) are categorized as organ specific autoimmune diseases, including Graves' disease (GD), Hashimoto's thyroiditis and idiopathic myxoedema. In this article, B-, T-cell surface phenotypes and epitopes in AITD were reviewed. It has been reported that the proportion and absolute number of B and T lymphocyte subpopulation or CD4/8 ratio in peripheral blood from AITD was not different from normal subjects. Those of CD5+ B cells and gamma delta T cells known as autoreactive clones were, however, increased in peripheral blood from GD. In the thyroid tissue of AITD, B-cells with activated markers were predominantly infiltrated rather than T-cells. The CD4/8 ratio and the proportion of CD8+CD11b+ T (suppressor T) cells was decreased in contrast to the increase of CD8+CD11b- T (cytotoxic T) cells. The CD4+4B4+ T (helper/inducer) cells were more predominant than CD4+2H4+ T (suppressor/inducer) cells in thyroid tissue from GD. These abnormality might cause the cell destruction and the enhanced autoantibody production in the tissue of AITD. Thyroglobulin, thyroid peroxidase and thyroid stimulating hormone receptor are known as major autoantigens in AITD. Recently, B-cell and T-cell epitopes on these autoantigen molecules have been defined, using monoclonal antibodies, proteolytic or synthetic peptides with molecular gene engineering. These epitope analysis would be contributed to the autoimmune tolerance in AITD.

Autoimmune Diseases↗
PubMed1999

Effect of a polymorphism of endothelial nitric oxide synthase gene in Japanese patients with IgA nephropathy.

BACKGROUND: Nitric oxide (NO) is synthesized by endothelial cell NO synthase (ecNOS) on vascular endothelium, and it plays a key role in the regulation of blood flow and pressure. A polymorphism of the ecNOS gene was recently shown to be associated with the development of cardiovascular disease. PATIENTS AND METHODS: We investigated the ecNOS gene polymorphism in 68 Japanese patients with IgA nephropathy (IgAN) and 134 normal controls. RESULTS: The genotype distributions were not different between the normal controls and the IgAN patients (ecNOS4b/b: ecNOS4b/a: ecNOS4a/a = 106:27:1 and 50:18:0, respectively). There was no significant difference in the renal histopathological grading between the patients with ecNOS4b/a and ecNOS4b/b. However, among the subgroup of patients whose duration of illness was two or more years, the advanced histopathological grading was more frequent in the patients with the ecNOS4b/a genotype (than in those with the ecNOS4b/b (p = 0.04)). The incidence of hypertension was also higher in the patients with the ecNOS4b/a genotype (50% in ecNOS4b/a versus 12% in ecNOS4b/b, p = 0.04). CONCLUSION: These results suggest that the ecNOS4b/a genotype (or ecNOS4a allele) of the ecNOS gene polymorphism may be involved in the progression of IgAN.

Adult↗
PubMed1998

Biodegradation and tumorigenicity of implanted plates made from a copolymer of epsilon-caprolactone and L-lactide in rat.

Flat plates made from a copolymer of epsilon-caprolactone and L-lactide (P-CL-LA) [50:50 (w/w), molecular weight 1.62 x 10(5); 20 x 10 x 1 mm size] were subcutaneously implanted into 50 young, male Wistar rats (P-CL-LA group). After 24 months the plates had become a mass of small pieces, which were concentrated in an area of 3 x 2 x 1 mm. For comparison, 50 rats were implanted with medical-grade polyethylene plates (PE group) while another set of 50 rats was subjected to the same operation but without an implant (Sham Op group). Tumors arose in 25 rats from the P-CL-LA group: 24 were malignant mesenchymal tumors at the implant sites. In the PE group, tumors appeared in 16 rats (14 at the implant sites and two ectopically). The average tumor latency was 578+/-84 days in the P-CL-LA group and 452+/-102 days in the PE group. There was no difference in tumor incidence between the P-CL-LA and PE groups (p < 0.05). In the Sham Op group, two malignant tumors appeared over 2 years. Pathologically, these induced tumors arose from the inflammatory cells surrounding the degrading fragments of P-CL-LA within the tissue capsule. This indicates that relatively slowly degrading material can induce malignant tumors at a similarly high rate to nonabsorbable medical grade PE, at least in this animal model.

Abdominal Neoplasms↗
PubMed1998

Soluble thrombomodulin and antibodies to bovine glomerular endothelial cells in patients with Henoch-Schönlein purpura.

AIM: To evaluate the clinical significance of soluble thrombomodulin and antiendothelial cell antibodies (AECA) in children with Henoch-Schönlein purpura. METHODS: Binding of serum AECA to bovine glomerular endothelial cells was evaluated by enzyme linked immunosorbent assay, cytotoxicity against glomerular endothelial cells by spectrophotometric assay, and soluble thrombomodulin concentrations by sandwich enzyme immunoassay. RESULTS: IgA AECA were detected in seven of 15 patients with Henoch-Schönlein purpura and nephritis, but were not detected in patients without nephritis or in controls. Patients with Henoch-Schönlein nephritis had raised titres of IgA AECA and serum thrombomodulin; severe proteinuria and renal histological changes were associated with raised titres of IgA AECA and raised serum thrombomodulin. No subjects had complement dependent cytotoxicity against glomerular endothelial cells. CONCLUSIONS: High titres of IgA AECA and raised serum thrombomodulin may be clinically useful markers of renal involvement in patients with Henoch-Schönlein purpura.

Adolescent↗
PubMed1998

Down regulation by iron of prostaglandin E2 production by human synovial fibroblasts.

OBJECTIVE: To examine the effect of iron on the prostaglandin (PG) E2 production by human synovial fibroblasts in vitro. METHODS: Human synovial fibroblasts were isolated from synovial tissue of rheumatoid arthritis (RA) and osteoarthritis (OA) patients and cultured in medium. Synovial fibroblasts were stimulated by human recombinant interleukin (IL) 1 beta (0.1-10 ng/ml) with or without ferric citrate (Fe-citrate, 0.01-1 mM). The amount of PGE2 in the culture medium was measured by an enzyme linked immunosorbent assay. RESULTS: The production of PGE2 by the synovial fibroblasts was increased by stimulation with IL1 beta at all concentrations tested. Fe-citrate but not sodium citrate (Na-citrate) down regulated the production of PGE2 by the synovial fibroblasts, both with and without stimulation by IL1 beta. Fe-citrate inhibited the spontaneous PGE2 production by the cells in a dose dependent manner, and a maximum inhibition by Fe-citrate was observed at the concentration of 0.1 mM with IL1 beta stimulation. The down regulation by iron was reversed by the co-addition of desferrioxamine (100 micrograms/ml), an iron chelator. CONCLUSION: Iron down regulates the PGE2 production by synovial fibroblasts in vitro.

Aged↗
PubMed1998

Collagenofibrotic glomerulonephropathy associated with immune complex deposits.

A 66-year-old Japanese male, who suffered from persistent proteinuria and leg edema, underwent renal biopsy. Light microscopy revealed marked narrowing of the glomerular capillary lumen with a diffuse accumulation of weakly PAS-positive material. By electron microscopy, abundant abnormal collagen fibers were observed predominantly in the subendothelial space and occasionally in the mesangial matrix. The fibers had a periodicity of about 60 nm and were immunoreactive for anti-type III collagen. Subendothelial electron-dense deposits were also found in some of the capillary walls. The serum level of procollagen III peptides was elevated and changed in parallel with the amount of proteinuria during the patient's clinical course. On the basis of these findings, a diagnosis of the collagenofibrotic glomerulonephropathy was made. A review of the literature, including 29 similar or identical cases, failed to reveal the etiology and pathogenesis of this disease. We suggest that this disease may be divided into two different clinical subtypes, an adult-onset type and a pediatric type.

Aged↗
PubMed1998

Aldosterone-producing adrenocortical adenoma complicated by chronic renal failure. Case report and review of the literature.

A 61-year-old Japanese woman was hospitalized because of general malaise. The patient demonstrated hypertension, hypokalemia and chronic renal failure (CRF). Plasma aldosterone concentration and urinary excretion of aldosterone were elevated. Abdominal computed tomographic scan revealed right adrenal tumor and multiple cysts in both kidneys. Adrenal scintigram using 131I-adosterol disclosed uptake of the isotope in the area corresponding to the adrenal tumor. Plasma aldosterone concentration and renin activity (PRA) in an upright posture and daily variations in adrenocorticotropic hormone, cortisol, aldosterone levels and PRA were compatible with aldosterone-producing adrenocortical adenoma. After administration of spironolactone and manidipine hydrochloride, a calcium antagonist, general malaise disappeared, and blood pressure and serum potassium level returned to the normal range without adrenalectomy. Although adrenalectomy is known to be effective for the treatment of aldosterone-producing adrenocortical adenoma, several papers reporting cases of aldosterone-producing adrenocortical adenoma with CRF indicated that surgical therapy was not always optimal in terms of postoperative conditions. Taken together, the conservative therapy may be one of the choices considering the prognoses of hypertension and renal dysfunction in patients with aldosterone-producing adrenocortical adenoma with CRF.

Adrenal Cortex Neoplasms↗