[Rheumatoid factor].
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Arthritis, Rheumatoid↗
Biomedical subjects
S Yoshinoya
Publications and source records attributed to S Yoshinoya.
Clinical evaluation of pulmonary hypertension in systemic sclerosis and related disorders. A Doppler echocardiographic study of 135 Japanese patients.
BACKGROUND: Previous studies on pulmonary hypertension (PH) in systemic sclerosis and related disorders used differing patient populations, and defined PH according to different criteria. We have attempted to determine the prevalence and cause of PH in these disorders using a mainly noninvasive cardiopulmonary evaluation. PATIENTS AND METHODS: One-hundred thirty-five Japanese patients with systemic sclerosis and related disorders were divided into proximal and distal scleroderma groups, with or without overlapping features of systemic lupus erythematosus (SLE) and polymyositis. They underwent multiple cardiopulmonary tests, including chest radiography, pulmonary function tests, and echocardiography to screen for pulmonary fibrosis and PH. RESULTS: The pulmonary artery systolic pressure was estimated by Doppler echocardiography in 80 patients (59%). PH (systolic pressure > or = 40 mm Hg) was diagnosed in 28 patients by the Doppler method and in two patients by right heart catheterization (mean pressure > or = 20 mm Hg). Doppler-estimated pulmonary artery pressures were significantly higher in patients with proximal scleroderma (p < 0.05), and in those with an SLE/polymyositis overlap (p < 0.01). The FVC was significantly reduced in the proximal scleroderma group (p < 0.0005), but not in the overlap group. PH was attributable to pulmonary fibrosis in nine patients who had proximal scleroderma without overlap. Pulmonary arteriopathy was the probable cause of PH in seven patients with overlap and in four patients who had proximal scleroderma without overlap. CONCLUSIONS: These findings suggest that proximal scleroderma predisposes patients to PH mainly because of pulmonary fibrosis, but occasionally because of pulmonary arteriopathy. An overlap of SLE/polymyositis predisposes patients to PH due to the occurrence of arteriopathy.
Asian People↗
Annular erythema, dermatomyositis, and Sjögren's syndrome.
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Adult↗
[Standardization of quantitative measurement of rheumatoid factor].
Recently many automated methods have been developed for a quantitative measurement of rheumatoid factor (RF). As they are widely used, it has been claimed that estimated values of RF are quite different among institutions. Standardization of quantitative measurement of RF is, therefore, required. The subcommittee for standardization of RF of the Ministry of Health and Welfare of Japan, worked from 1988 to 1994 in order to obtain an appropriate national standard of RF and has reached the conclusion that murine monoclonal rheumatoid factor (mRF) would be recommended as a new national standard of RF, which allows new expression of RF value (microgram/ml equivalent to the mRF instead of unit/ml referred to the WHO standard). There are two types of methods widely used for the quantification of RF. The first type is a method of light scattering analysis which is based on interaction of RF with particle-coated or aggregated human IgG (Fc) in nepherometry or turbidimetry, RF being expressed as unit/ml referred to the WHO standard. The second is a radioimmunoassay or an enzyme immunoassay in which RF is expressed as index compared to arbitrary standard. The former expression of RF is recognized to indicate agglutination titer of RF and the latter expresses the concentration of RF. The subcommittee decided to target on the former type of methods because of rapid prevalence with large inter-laboratory variations. The mRF is able to agglutinate proportionally IgG-complex with various features in wide range (x x microgram/ml to more than 1 mg/ml). It can be measured by nepherometry and turbidimetry with sufficient stability. The mRF has no misgivings in present and future supply and in immutability after a century. One of the largest advantages of the use of mRF national standard is expected to be able to eliminate the inter-laboratory variations of RF values which are considered to be mainly derived from different methods of laboratory instruments as well as from biological properties of polyclonal RF. The use of microgram/ml equivalent to mRF instead of unit/ml referred to the WHO standard makes it possible to determine the exact RF value of test serum since the mRF preparation could be adjusted to the best concentration to be requested by any available method of instrument to measure agglutination titer of RF.
Animals↗
Association of HLA-B39 with HLA-B27-negative ankylosing spondylitis and pauciarticular juvenile rheumatoid arthritis in Japanese patients. Evidence for a role of the peptide-anchoring B pocket.
OBJECTIVE: To investigate the characteristics of HLA-B27 that render susceptibility to seronegative spondylarthropathies. METHODS: Serologic HLA class I typing of Japanese patients with ankylosing spondylitis (AS), juvenile rheumatoid arthritis (JRA), and healthy controls, was performed. HLA-B39 subtypes were determined by polymerase chain reaction-sequence-specific oligohybridization. RESULTS: HLA-B27 was present in 40 of 48 patients with AS (83%), and in only 1 of 210 healthy controls (0.5%). Three of 8 patients (37.5%) who were negative for HLA-B27 were positive for HLA-B39, which was significantly higher compared with the HLA-B27-negative controls (6.2%; P = 0.01). Significant association with HLA-B39 was also noted in the JRA patients (16.7%; P < 0.01), especially in those patients with pauciarticular-onset disease (33.3%; P < 0.01). Ten of 13 HLA-B39-positive patients had subtype B*3901 and 3 had B*3902. CONCLUSION: Because HLA-B27 and HLA-B39 share Glu at position 45 and Cys at position 67, both of which constitute components of the peptide-anchoring B pocket, and because they possess similar peptide-ligand motifs, our results may support either the role of the peptides presented by class I antigens or the importance of Cys at position 67, in the development of spondylarthropathies and pauciarticular-onset JRA.
Arthritis, Juvenile↗
[Proposals to revise the preliminary program of laboratory tests for diagnosis of collagen or autoimmune diseases].
There are several requests to complete the laboratory test program for initial diagnosis of collagen or autoimmune diseases. To make a definite diagnosis, certain criteria must be satisfied or proven to be present in a patient with collagen disease. One of the requests is that the revised program should point out the best laboratory test to satisfy the criteria. It should explain the specificity for diagnosis, usefulness and quantitative analysis for evaluation of disease activity on individual tests. Others concern the description of laboratory tests used for therapy guidance, inquiry of complications and differential diagnosis. Even if the initial aim of the program is limited to making a diagnosis, revision should be affirmatively made to meet these requests.
Autoimmune Diseases↗
[Immune complex and vasculitis].
In the early 1900s, von Pirquet first introduced the concept that antigen antibody complexes might cause disease. Since that time, systemic necrotizing vasculitis is believed to be a typical form of immune complex-mediated vasculitis and it may be found in many disorders associated with immunological abnormalities. In 1866, Kusmaul and Maier reported a case with multilesions of necrotizing vasculitis named as periarteritis nodosa which is now nominated as polyarteritis nodosa characterized by the presence of focal inflammatory lesions in small and medium-sized arteries. Besides polyarteritis nodosa, necrotizing vasculitis is frequently found in connective tissue diseases, especially in SLE and RA. Granulomatous vasculitis is a definitely different type of vasculitis from necrotizing vasculitis and known to be found in Wegener's granulomatosis. Whether or not granulomatous vasculitis is an immune complex-mediated disease is unknown, but it can be produced experimentally in several settings. In a experimental model of serum sickness, animals who are hyperimmune responders have widespread granulomatous lesions similar to Wegener's granulomatosis in histology. Intravenous injection of complete Freund's adjuvant in rabbits followed by intravenous administration of human IgM rheumatoid factor is capable of inducing a marked pulmonary granulomatous reaction. The relation of these observations to human Wegener's granulomatosis is uncertain, but the histology and location of the lesions are strikingly similar to human disease. Vasculitis involved in large and medium-sized arteries is seen in two different types of diseases known as temporal arteritis and Takayasu's arteritis. Circulating and tissue-bound immune complexes have been found in both conditions. Most common vasculitis in childhood is Schonlein-Henoch purpura in North America and Kawasaki disease in Japan.(ABSTRACT TRUNCATED AT 250 WORDS)
Antigen-Antibody Complex↗
Detection of glycosylation abnormality in rheumatoid IgG using N-acetylglucosamine-specific Psathyrella velutina lectin.
Although the galactose deficiency in the Asn297-linked sugar chains of serum IgG from patients with rheumatoid arthritis (RA) has been established, structural analysis of sugar chains has not been readily available. Psathyrella velutina lectin (PVL) preferentially interacts with the N-acetylglucosamine beta 1-->2Man group, exposed at the termini of sugar chains in agalacto IgG. Biotinylated PVL reacted strongly in Western blotting with H chains of IgG derived from patients with RA. An ELISA-based assay for the detection of agalacto IgG was developed using recombinant protein G and biotinylated PVL in combination, and the screening of patients' sera was performed. PVL binding of serum IgG significantly correlated with percentage of galactose-deficient IgG determined by the structural analysis. Age-related slight increase in PVL binding was observed among normal controls. Patients with RA showed significantly higher PVL binding (37.90 +/- 42.25 U/ml, n = 93) as compared with normal controls (5.75 +/- 2.92 U/ml, n = 112) (p = 0.0001). Patients with SLE showed lower but still significant PVL binding (17.86 +/- 5.18 U/ml, n = 10, p = 0.0001). PVL binding correlated with C-reactive protein level in serial analysis of individual RA patients, and was significantly higher in the synovial fluid compared with paired serum samples. PVL binding assay may provide an ideal tool for the simple and sensitive detection of agalacto IgG.
Acetylglucosamine↗
[New clinical tests in diagnosis of collagen diseases and allergic diseases].
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Antibodies, Anticardiolipin↗
Antibodies to human cytomegalovirus 65-kilodalton Fc binding protein in rheumatoid arthritis: idiotypic mimicry hypothesis of rheumatoid factor production.
We previously reported that rheumatoid factors (RFs) might bear the internal image of Fc gamma-binding proteins (FcBPs) of herpes family viruses, suggesting the possibility that some RFs may be produced as antiidiotypic antibodies to anti-viral FcBP antibodies. Since human cytomegalovirus (HCMV) has been implicated in the pathogenesis of RA, we made an attempt to detect antibodies to 65 KD major HCMV FcBP in sera and synovial fluid from patients with RA. Western blotting was performed using HCMV-infected MRC-5 cell lysate as the antigen. Eleven of 23 patients with RA possessed strong serum antibodies to HCMV-65 KD protein, whereas such antibodies were found in only 2 of 23 normal controls. In the synovial fluid, 10 of 19 RA patients showed anti-HCMV 65 KD reactivity. Pepsin-digested IgG retained anti-65 KD reactivity, indicating that false-positive reaction due to the presence of IgG Fc portion and/or RF was unlikely. 65 KD protein was shown to be different from human heat shock proteins (hsps) using monoclonal antibodies against human hsps. Patients' IgG F(ab')2 also reacted with the 65 KD protein of purified HCMV virion itself. These results support the possibility that some RFs could be produced as antiidiotypic antibodies to anti-viral FcBP antibodies.
Adolescent↗
[Basic and clinical evaluation of EIA (pin immuno assay, PIA) kit for antithyroglobulin antibody (TGAb) and antimicrosomal (antiperoxidase) antibody (TMAb)].
Newly developed enzyme immunoassay kit (Pin Immuno Assay, PIA) for quantitative determination of serum antithyroglobulin antibody (TGAb) and antimicrosomal (-peroxidase) antibody (TMAb) was evaluated. The method utilizes the Sandwich ELISA principle with a unique micropin as solid phase coated with antigen. Reproducibilities assessed by intra- and interassay variation were less than 6.9% (CV) and 7.2% for TGAb or 4.2% and 6.0% for TMAb respectively. Changes in the first or second incubation time did not affect both TGAb and TMAb values. Upper normal limits obtained from 47 healthy subjects were 150 IU/ml for TGAb and 25 IU/ml for TMAb. Positive results in TGAb were obtained 60.0% in patients with Graves' disease and 80.0% in chronic thyroiditis and in TMAb 77.8% in Graves' disease and 66.7% in chronic thyroiditis. Patients with other autoimmune diseases such as SLE, RA were also found high incidence of positive results, 48.3% for TGAb and 65.0% for TMAb respectively. These results indicate that the nonradioisotopic assay technique for thyroid autoantibodies are useful in diagnosis of autoimmune diseases especially thyroid diseases.
Autoantibodies↗
[Recent problems in laboratory tests for rheumatoid factor].
Conventional laboratory tests for detection of rheumatoid factor (RF) have changed because of the demands of recently-developed rheumatologic therapy. Quantitative analysis of the RA test by turbidimetry and nepherometry of latex agglutination or turbidity immunoassay (TIA) was recently introduced and popularized in Japan. Although the RF standards provided by WHO have become quite common, RF values obtained by quantitative analysis in various laboratories are not consistent with each other. We established a murine monoclonal rheumatoid factor (mRF) and recommend this as the national RF standard to replace the WHO standard. We believe that the RF titer of a clinical serum should be expressed as the corresponding concentration of mRF which agglutinates IgG-coated latex to the same degree as the serum in quantitative analysis. When possible, inconsistency of RF titers among various laboratories must be eliminated. Detection of IgG-RF has recently been included among tests available for medical insurance reimbursement. The test is very useful to diagnose malignant rheumatoid arthritis associated with vascular damage and extra-articular disorders.
Humans↗
[Detection of anticardiolipin antibody using the EIA kit prepared to eliminate interference of serum cofactor].
We studied sera from patients with various disorders including collagen diseases, Buerger's disease, deep vein thrombosis, repeated abortions and idiopathic thrombocytopenic purpura in order to measure anticardiolipin antibody (aCL) titers. In our assay system, we can detect aCL against bovine cardiolipin and the complex of cardiolipin and beta 2-glycoprotein I (beta 2-GPI). This was done with simultaneous assays using blank wells and bovine cardiolipin coated wells in the EIA method in which both wells were also coated with bovine serum albumin possibly containing beta 2-GPI, then aCL titers was given by subtraction of O.D. values of blank wells from those of cardiolipin coated wells. When the aCL was quantified by anti human immunoglobulin antibodies, collagen diseases showed positive aCL in 15 (11.5%) out of 130 sera with positive anti ENA antibodies, 3 (11.1%) out of 27 sera with positive anti DNA antibodies and 3 (5.2%) out of 58 sera with other positive ANA sera. The other hand, we found positive aCL in 2 (4.9%) out of 41 sera from patients with Buerger's disease, 4 (36.4%) out of 11 sera from patients with deep vein thrombosis, 1 (7.7%) out of 13 sera from patients with repeated abortions and 6 (14.6%) out of 41 sera from patients with idiopathic thrombocytopenic purpura. Twenty one (61.8%) out of these aCL positive sera had also positive IgG-aCL for the assay using anti human IgG antibody. Compared to previous reports, we thought, low incidence of aCL in our study was due to exclusion of anti beta 2-GPI antibody in our assay system.
Antibodies, Anticardiolipin↗
Endothelial cell destruction by polymorphonuclear leukocytes incubated with sera from patients with systemic lupus erythematosus (SLE).
When normal polymorphonuclear leukocytes (PMN) were incubated with sera from patients with active systemic lupus erythematosus (SLE), a significantly increased cytotoxicity against human cultured vascular endothelial cells (EC), compared with normal control sera, was demonstrated by the standard 51Cr release method. The degree of this cytotoxicity was correlated with the immune complex level in each serum. The cytotoxicity did not correlate with the presence of anti-EC antibody. An absorption study with C1q-Sepharose 4B further suggested that the immune complexes are the factor which induce cytotoxicity. A gel fractionation study, however, indicated the heterogenity of the cytotoxic activity, and suggested the possible contribution of other substances including anti-EC, at least in some of the patients. This type of cytotoxicity may initiate the inflammatory process including vascular damage of the disease.
Adult↗
Circulating immune complex levels measured by new ELISA kits utilizing monoclonal anti-C1q and anti-C3d antibodies correlate with clinical activities of SLE but not with those of RA.
The authors studied sera from both patients with SLE and from those with RA to evaluate clinical usefulness and significance of circulating immune complexes (CIC) detected with new ELISA kits utilizing monoclonal anti-C1q and anti-C3d antibodies. CIC values of patients with SLE significantly correlated to severity of disease activities evaluated by clinical symptoms and laboratory tests, especially for serum complement levels. Since substances detected with the ELISA kits were closely related to serum complement components, it was determined that a direct relationship exists between clinical activities and CIC values appearing in SLE patients with hypocomplementemia. In RA patients, CIC values did not correlate to clinical activities evaluated by Lansbury's index, anatomical bone damage with X-ray or functional assessment of activities of daily living, but did significantly correlate to levels of IgM-RF, serum IgG concentrations and some markers of systemic inflammation. Detection of IC after fractionation of RA sera revealed a broad range of molecular sizes detectable with the ELISA kits, which indicated that CIC in vivo were heterogenic and complicated in formation, degradation and interaction with serum complements.
Adult↗
[Immunological and serological tests useful for diagnosis of rheumatoid arthritis].
There are four areas of laboratory medicine engaged in the diagnosis of rheumatoid arthritis. They are serological tests for diagnosis of infection, tests for autoantibodies, analysis of serum proteins and lymphocyte function tests, including surface markers. In these areas except for diagnosis of infection, marked development has been achieved in the recent ten years. Enumerating roughly, I like to point out quantitative tests of rheumatoid factor, precise examinations for antinuclear antibodies, recent method for electrophoresis of serum protein and monoclonal antibodies for lymphocyte surface markers. Diagnosis of rheumatoid arthritis has became more precise and reliable by using these laboratory tests. In addition, effective tools are available to approach pathogenesis of rheumatoid arthritis through management of RA patients. An outline of these recent laboratory tests, useful for diagnosis of rheumatoid arthritis is presented.
Arthritis, Rheumatoid↗
[Assessment of test results in the diagnosis of collagen diseases].
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Antibodies, Antinuclear↗
[Cytoplasmic staining pattern characteristic for anti Jo-1 antibody in HEp-2 cells].
We wished to confirm the staining pattern of HEp-2 cells by the anti Jo-1 antibody, because we found antibodies in serum with positive anti Jo-1 antibody which showed either a fibrilar cytoplasmic staining or a nuclear speckled staining pattern in indirect immuno fluorescence+ examinations using HEp-2 cells. Sera available from eight patients with PM DM (polymyositis and/or dermatomyositis) showed positive anti Jo-1 antibody in the double immuno-diffusion technique but had various staining patterns of HEp-2 cells in the immunofluorescent examination. We examined these eight sera with the immuno-blotting method utilizing whole cell extract of HeLa cells, and found the 50 kDa band from all sera tested, to which Jo-1 antigen had been reported to move. We eluted the antibody which formed the 50 kDa band from the nitrocellulose membrane and applied it on HEp-2 cells. This maneuver gave us the fine granular cytoplasmic staining of anti Jo-1 antibody on HEp-2 cells. We therefore concluded that the anti Jo-1 antibody should have cytoplasmic staining on HEp-2 cells although observers might miss it due to other types of associated antinuclear antibodies.
Antibodies, Antinuclear↗