Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 2088651 | Agranulocytosis in a patient with primary Sjögren's syndrome. | 1990 Dec | The authors describe a case of primary Sjögren's syndrome, which was complicated with severe autoimmune agranulocytosis quite sensitive to immunosuppressive therapy. Agranulocytosis is a very rare complication of this autoimmune rheumatic disease as opposed to leucopenia. A remarkable feature of the presented case is the fact that correct diagnosis of primary Sjögren's syndrome has not been settled for almost 25 years. The disease has manifested only in the form of arthropathy imitating rheumatoid arthritis. | |
| 2696292 | [Plasma and tissue concentrations of biphenylacetic acid following 1 week oral fenbufen me | 1989 Nov | In an randomised study 30 patients were treated during one week before undergoing an elective surgery of the knee joint with 1 or 2 g respectively of 3% Felbinac gel (biphenylacetic acid gel) or oral 300 mg Fenbufen thrice daily. Biphenylacetic acid (BPAA) is the therapeutically active metabolite of the non-steroid anti-inflammatory drug Fenbufen. Plasma concentrations were measured before, during therapy and at the time of the operation. During the surgery of the knee joint specimens of synovial fluid and -membrane, of cartilage, muscle and tendons as well as of the skin and the subcutaneous fatty tissue were obtained and the BPAA concentrations measured. There was a large variance of the obtained values in all groups. It seems that mainly methodical problems are responsible for this. At the time of surgery, the plasma concentrations following oral administration were with 10,080 ng/ml 20 to 50 times higher than those after topical administration. The tissue concentrations reached 1/8 to 1/2 of the plasma concentrations. The relation of tissue concentrations to plasma concentrations of BPAA was smaller in patients treated with oral administration than in patients treated with topical administration. Therefore a partial direct penetration of Felbinac into the deeper tissue compartments can be assumed. There was no significant difference in plasma-, synovial- or tissue concentrations between the two groups treated with the topical administration. The tissue concentrations were 1 to 2 orders of magnitude lower than those after oral administration. Only in the skin the concentrations were with 9160 respectively 3830 ng/g higher than those obtained after oral application (2110 ng/g). | |
| 2835324 | Three Epstein-Barr virus (EBV)-determined nuclear antigens induced by the BamHI E region o | 1988 May 15 | In our previous study (Takada et al., 1986a), we showed that the BamHI E fragment of Epstein-Barr virus (EBV) DNA induces a nuclear antigen that is detected by human antisera against EBV-determined nuclear antigen (EBNA), when transfected into baby hamster kidney (BHK) cells. The present study shows that the sub-fragment containing the central open reading frame BERF2b of the BamHI E fragment (Baer et al., 1984) is responsible for nuclear antigen induction. In addition, 2 fragments corresponding to 2 other open reading frames of the BamHI E, BERFI and BERF4 also induce nuclear antigens upon transfection into BHK cells. These 3 antigens, designated RF2b, RFI and RF4 antigens, were serologically classified as EBNA and antigenically distinct. In immunoblotting analysis of latently EBV-infected BJ-B95-8 cells, 3 high-molecular-weight polypeptides (136, 142 and 147 kDa) were identified by anti-EBNA sera. Immunoblotting analysis of transfected BHK cells indicated that the RF2b antigen is 145 kDa in its native form and antigenically related to the 147-kDa protein of BJ-B95-8 cells. Although RFI and RF4 antigens were not detected by immunoblotting, reactivities of sera with RFI and RF4 antigens in the immunofluorescence test were correlated with those of sera with the 136- and 142-kDa polypeptides of BJ-B95-8 cells, respectively. The results suggest that 3 high-molecular-weight proteins of latently EBV-infected cells are encoded by 3 open reading frames of the BamHI E DNA fragment. | |
| 3118589 | [Interactions of non-steroidal antirheumatic drugs with oral antidiabetic agents: acemetac | 1987 Jul | In a double-blind cross-over trial on 20 diabetic patients of type IIb we investigated whether a drug interaction between glibenclamide and acemetacin may possibly occur. After hospitalization of all in-patients needing glibenclamide therapy, a one-week period of adaptation to clinical conditions with optimized diet, antidiabetic dosage of the drug and the beginning of a diabetes learning programme followed. Thereafter, in a randomized design, ten out of the 20 patients were treated concomitantly with either 60 mg acemetacin t.i.d. or placebo for 1 week. Furthermore, a cross-over period of one week's duration followed once more. Daily blood glucose profiles (four values) were measured every second day and suggested a continuous improvement of the severe diabetic state previously seen. Blood glucose levels reached an optimal steady-state condition after 1 week of adaptation. Concomitant treatment with acemetacin did not lead to a relevant alteration of the laboratory parameters used in type IIb diabetic patients. This could also be established due to HbA1 values. Contrary to other nonsteroidal anti-inflammatory drugs, interactions between acemetacin and the widely used oral antidiabetic glibenclamide could not be established. | |
| 3552347 | Secondary myelodysplastic syndromes and leukaemias. | 1986 Nov | Secondary MDS, or AL induced by the treatment of another primary disease, occurs at an average of 48-71 months after that treatment. A high percentage of the 2 MDS convert to AL. Survival of either is less than 1 year. A constellation of morphological abnormalities from all three cell lines produces a unique appearance. The 2 AL are difficult to classify by the FAB system. With the exception of cytogenetic analysis, the biology of 2 MDS/AL remains largely unexplored. Alterations of chromosomes 5 and 7 predominate, but other associated cytogenetical abnormalities are increasingly being recognized. A review of the development of 2 MDS/AL in a variety of primary diseases generates the following tentative conclusions: many of the commonly used alkylating agents, and the non-classical alkylating agent procarbazine, are leukaemogens; procarbazine is probably the important leukaemogen in the MOPP programme; cyclophosphamide appears to be a less potent leukaemogen than other alkylating agents; the method in which a drug is administered probably influences its leukaemogenic potential; the duration of therapy with a drug, or the total amount of drug delivered, is probably an important factor in leukaemogenesis; irradiation alone appears to be a weak leukaemogen; irradiation has little or no synergism with chemotherapy in leukaemogenesis; the older patient treated with leukaemogenic drugs is at substantial risk to develop a 2 MDS/AL; most studies show no plateau in the actuarial incidence of developing a 2 MDS/AL, despite lengthy follow-up. Benzene is the only chemical agent for which strong evidence of leukaemogenesis exists. Nonetheless, the similarities in the karyotypic alterations of leukaemic cells between those whose occupations expose them to chemical hazard and those who are exposed to cytotoxic agents lend support to the idea that more environmental leukaemogens have yet to be discovered. Aggressive therapy should be considered for a patient of any age with an adequate performance status and a diagnosis of secondary AL, especially if the karyotype in the malignant cell is predictive of a high response rate. The therapy of 2 MDS remains investigational. To mitigate the development of a leukaemic complication, maintenance therapy should be restricted to diseases in which its efficacy is established or to an investigational setting, and consideration of the leukaemogenic potential of equally effective regimens should be part of the therapeutic planning in the older patient. | |
| 3058116 | The precursor of a metalloendopeptidase from human rheumatoid synovial fibroblasts. Purifi | 1988 Sep 15 | Two active forms (Mr 45,000 and 28,000) of a metalloendopeptidase that digest proteoglycans and other extracellular matrix components of connective tissues have previously been purified from rheumatoid synovial cells and characterized [Okada, Nagase & Harris (1986) J. Biol. Chem. 261, 14245-14255]. To study the mechanisms of activation the precursor of this metalloendopeptidase has now been purified. The final products are homogeneous on SDS/polyacrylamide-gel electrophoresis and identified as a set of zymogens of Mr 57,000 and 59,000, in which the latter form is probably the product of post-translational glycosylation of the Mr 57,000 zymogen, as it binds to concanavalin A. The zymogen can be activated by trypsin, chymotrypsin, plasma kallikrein, plasmin and thermolysin, but not by thrombin. Although the activated metalloendopeptidase is further degraded by trypsin, plasma kallikrein and thermolysin during a prolonged incubation, it is relatively stable against plasmin and chymotrypsin. Activation with 4-aminophenylmercuric acetate is dependent on its concentration. It requires the reaction with the zymogen, possibly through thiol groups, and the continued presence of the agent. During this treatment the zymogen undergoes a sequential processing; first it becomes active without changing its apparent molecular mass, and then it is processed to low-Mr species of Mr 46,000, 45,000 (HMM) and 28,000 (LMM). The rate of conversion of the precursor into an initial intermediate of Mr 46,000 follows first-order kinetics (t1/2 2.0 h with 1.5 mM-4-amino-phenylmercuric acetate at 37 degrees C) and is independent of the initial concentration of the zymogen or the presence of up to a 676-fold molar excess of substrate, whereas the generation of HMM and LMM species is affected by these parameters. These results indicate that activation of the prometalloendopeptidase by an organomercurial compound is initiated by the molecular perturbation of the zymogen that results in conversion into the 46,000-Mr intermediate by an intramolecular action; the subsequent processing of this intermediate in HMM and LMM species is a bimolecular reaction. In vivo it is probable that the precursor of this metalloendopeptidase is activated either by direct limited proteolysis by tissue or plasma endopeptidases, or, alternatively, by factors that cause certain conformational changes in the zymogen molecule. | |
| 3006953 | Systemic lupus erythematosus sera antilymphocyte reactivity: detection of antibodies to Ta | 1986 Jan | Sera obtained from patients with systemic lupus erythematosus (SLE) were tested for their reactivity to cell lines derived from cutaneous T-cell lymphoma (CTCL), or adult T cell leukaemia (ATL), and with other cell lines, by indirect immunofluorescence method. Approximately one half of SLE sera reacted with the surface antigens of HUT-102 cells, a cell line from CTCL, which constitutively expresses Tac antigen. The titre tended to be higher in the active than in the inactive stage. These positive sera also reacted with other neoplastic or normal T cell lines having Tac antigen. SLE sera reacting with HUT-102 surface antigens were further examined for their reactivities to Tac antigen, the putative IL-2 receptor, using HUT-102 or ATL-2. Pretreatment with anti-Tac monoclonal antibody partially blocked the reactivities to HUT-102 surface antigens in nine of 15 SLE sera tested. The binding of 125I-labelled anti-Tac monoclonal antibody was displaced by the addition of sera from six of 15 SLE patients. In addition, nine of the 15 SLE sera could inhibit the binding of 125I-labelled IL-2 to ATL-2 cells. These results suggested that some of SLE sera contained antibodies against the IL-2 receptor. | |
| 2736833 | Statistical evaluation of different clinical and serological parameters for the diagnosis | 1989 Mar | The potential value for the diagnosis of Sjögren's syndrome (SS) of 28 clinical and 18 serological parameters was evaluated in 38 patients with primary (1 degree) SS, 29 with rheumatoid arthritis (RA), 30 with systemic lupus erythematosus (SLE), and 22 with mixed cryoglobulinemia (MC), by means of a stepwise discriminant analysis. Twelve patients with RA, 11 with SLE, and 8 with MC had evidence of sicca syndrome and were then classified as having a secondary (2 degree) SS. When comparing the various disease groups to each other, it was always possible to select different combinations of clinical and serological variables which defined highly significant discriminant functions. In addition, some parameters appeared to have a stronger discriminant power between different disease groups. For instance, 1 degree SS was well discriminated from RA by anti-Ro antibodies (Ab) and normal C-reactive protein (CRP) levels, from SLE by normal complement levels and the positivity of rheumatoid factor, from MC by the absence of liver involvement and normal complement levels. While anti-La Ab had the highest value in differentiating patients with 1 degree from those with 2 degrees SS, anti-Ro Ab and recurrent parotid swelling seem to be typical features of patients with SS with respect to those with other connective tissue disease but without sicca syndrome. | |
| 3255221 | [Intensive lymphoid hyperplasia of the peripancreatic ganglia and extrahepatic cholestasis | 1988 | The diagnostic triad of Sjögren's syndrome is keratoconjunctivitis sicca, xerostomia with o without salivary gland enlargement and the presence of a connective tissue disease usually rheumatoid arthritis). Is postulated an altered immune response of lymphocytes to ductal antigens glands and the result is an chronic inflammatory process with eventual fibrosis and hyposecretion of the affected glands. Lymphoproliferation is characteristic of the Sjögren's syndrome, the lungs, kidneys and salivary glands are the most affected: in this paper is presented the disease complex and not described of Sjögren's syndrome and intensive lymphoid hyperplasia of peripancreatic lymph nodes without chronic pancreatitis but with obstructive jaundice for involvement of the distal common bile duct. The percutaneous transhepatic cholangiography was suggestive of pancreatic disease and the surgery and the pathology certified the final diagnosis. A choledocho-enteric anastomosis was performed to remedy the extrahepatic cholestasis. | |
| 1881496 | Diagnostic and prognostic value of quantitative immunohistological examination of lip biop | 1991 Apr | Three patients are presented to illustrate the diagnostic and prognostic value of quantitative immunohistological examination of labial salivary gland biopsy in Sjögren's syndrome. In an obvious case of primary Sjögren's syndrome and in a case of rheumatoid arthritis without clinical and serological evidence of secondary Sjögren's syndrome, quantitative immunohistological examination of the labial salivary gland biopsy gave more appropriate information than the widely accepted lymphocytic focus score criterion for Sjögren's syndrome. In the third case quantitative immunohistological examination disclosed monoclonal B-cell expansion in the labial salivary gland biopsy six months before evidence of systemic monoclonal gammopathy appeared. | |
| 2782971 | Effect of indomethacin on swelling, lymphocyte influx, and cartilage proteoglycan depletio | 1989 Aug | The effects of indomethacin on antigen induced arthritis in rabbits have been investigated. Arthritis was induced in the knee joints of sensitised rabbits by intra-articular injection of antigen. Swelling of the joints was measured for 14 days after antigen challenge, and groups of animals were killed on days 1, 7, or 14 for collection of synovial fluids and tissues. Indomethacin (1 mg/kg, three times daily) reduced joint swelling and the prostaglandin E2 concentrations in synovial fluid. In addition, indomethacin increased the loss of proteoglycan from articular cartilage and the numbers of lymphocytes in the inflamed synovial lining. These findings suggest that the symptomatic benefits of indomethacin and related drugs in inflammatory arthritis may be achieved at the expense of significant adverse effects on joint tissues. | |
| 2174906 | Cytokines in chronic inflammatory arthritis. V. Mutual antagonism between interferon-gamma | 1990 Dec | The effects of a broad array of cytokines, individually and in combination, were determined on separate functions (proliferation, collagenase production, and granulocyte macrophage colony-stimulating factor [GM-CSF] production) and phenotype (expression of class II MHC antigens) of cultured fibroblast-like RA synoviocytes. The following recombinant cytokines were used: IL-1 beta, IL-2, IL-3, IL-4, IFN-gamma, tumor necrosis factor (TNF)-alpha, GM-CSF, and macrophage colony-stimulating factor (M-CSF). Only IFN-gamma induced HLA-DR (but not HLA-DQ) expression. TNF-alpha inhibited IFN-gamma-mediated HLA-DR expression (46.7 +/- 4.1% inhibition) and HLA-DR mRNA accumulation. This inhibitory effect was also observed in osteoarthritis synoviocytes. Only TNF-alpha and IL-1 increased synoviocyte proliferation (stimulation index 3.60 +/- 1.03 and 2.31 +/- 0.46, respectively). IFN-gamma (but none of the other cytokines) inhibited TNF-alpha-induced proliferation (70 +/- 14% inhibition) without affecting the activity of IL-1. Only IL-1 beta and TNF-alpha induced collagenase production (from less than 0.10 U/ml to 1.10 +/- 0.15 and 0.72 +/- 0.24, respectively). IFN-gamma decreased TNF-alpha-mediated collagenase production (69 +/- 19% inhibition) and GM-CSF production but had no effect on the action of IL-1. These data demonstrate mutual antagonism between IFN-gamma and TNF-alpha on fibroblast-like synoviocytes and suggest a novel homeostatic control mechanism that might be defective in RA where very little IFN-gamma is produced. | |
| 2419715 | Autoantibodies and their relation to rheumatic diseases. | 1986 Mar | The use of tissue culture substrates for immunofluorescence determinations of nuclear, cytoplasmic, and mitotic cell-related autoantibodies has resulted in the delineation of diverse new specificities, whose clinical correlates are now becoming apparent. This review details both major and minor autoantibody specificities, the status of knowledge regarding their target antigens, and the relation of these serologic systems to distinctive rheumatic disease syndromes. | |
| 3738584 | Spontaneous pyomyositis in a patient with Felty's syndrome: diagnosis using computerized t | 1986 Aug | Spontaneous pyomyositis, or so-called tropical pyomyositis, developed in the hamstring muscles of a 62-year-old man with rheumatoid arthritis and Felty's syndrome. The diagnosis was confirmed by computerized tomography, and the appropriate muscle compartment was surgically drained. | |
| 2153351 | Bronchoalveolar lavage fluid angiotensin-converting enzyme in interstitial lung diseases. | 1990 Jan | In this study we evaluated the disease specificity of bronchoalveolar lavage fluid angiotensin-converting enzyme (BALF-ACE), its correlation with cellular constituents of bronchoalveolar lavage fluid (BALF), and for sarcoidosis, with other proposed markers of disease activity. Furthermore, the question of the clinical value of BALF-ACE determinations in in interstitial lung diseases or any of its subgroups was addressed. The study population consisted of 222 patients, 69 with biopsy proven sarcoidosis, 3 with hypersensitivity pneumonitis, 4 with acute histoplasmosis, 27 with idiopathic pulmonary fibrosis (IPF), 4 with rheumatoid arthritis-related interstitial fibrosis, 9 with pulmonary drug toxicity, 16 with pulmonary malignancies, 26 with other parenchymal lung disease entities, and 30 in whom the final diagnosis remained indeterminate. Elevated BALF-ACE concentrations were seen in all diagnostic categories. In sarcoidosis BALF-ACE levels correlated well with lavage lymphocyte counts (r = 0.49; p less than 0.0001), in contrast to IPF where they correlated well with lavage neutrophil counts (r = 0.51; p less than 0.007). The correlation of BALF-ACE and serum-ACE was significant. In sarcoidosis the mean BALF-ACE level was lower for patients with Stage-I chest roentgenographic patterns (0.664 U/L), compared to those with Stage II (1.112 U/L) and Stage III (1.083 U/L). It was concluded that elevated BALF-ACE levels are not specific for sarcoidosis. The correlations of BALF-ACE levels with different cellular constituents of BALF suggest a different cellular origin of BALF-ACE. In sarcoidosis BALF-ACE levels correlate well with other proposed markers of disease activity and seem to reflect pulmonary activity better than serum ACE.(ABSTRACT TRUNCATED AT 250 WORDS) | |
| 3512617 | Current concepts in the treatment of rheumatoid arthritis. | 1986 Jan | The treatment of RA is complex and often frustrating. The pathologic process of RA is composed of acute inflammation, chronic immunologic phenomenon, and chronic connective tissue degradation. It is important to understand not only the pathophysiology of RA but also the mechanism of action of our therapeutic drugs so that treatment can be tailored to affect the important aspects of the process leading to end-organ damage. Despite the many drugs available, therapy is still unsatisfactory. Many drugs work in only certain patients. This could be secondary to variability in the disease state or to difference in drug metabolism. A better understanding of both disease and therapeutic agents may lead to better use of our present agents and development of new, more effective treatment modalities. | |
| 2838414 | Restriction fragment analysis of duplication of the fourth component of complement (C4A). | 1988 Jan | The two genes encoding the fourth component of complement (C4A and C4B) reside between HLA-B and HLA-DR on human chromosome 6. Two kilobases downstream from each C4 gene lies a 21-hydroxylase gene (CA21HA and CA21HB, respectively). Utilizing the method of Southern blotting and a 5'-end 2.4-kb BamHI/KpnI fragment of the C4 cDNA, we have analyzed TaqI-digested DNA from four pedigrees with one or more extended haplotypes containing a C4A duplication, as demonstrated by protein electrophoresis and segregation analysis. Two C4A protein duplications (C4A*2,A*3,C4B*QO and C4A*3,A*5,C4B*QO) segregated with two large TaqI DNA restriction fragments (7.0 and 6.0). In pedigree Fi, one individual homozygous for HLA-A3,B35,C4,DR1,DQ1,BFF,C2C,-C4A2,3,C4BQO had TaqI 7.0- and 6.0-kb restriction fragments with equal hybridization intensities as measured by two-dimensional densitometry (7.0/6.0 kb = 0.83, SD = 0.12, N = 7). A hybridization probe for the 21-hydroxylase gene also demonstrated equal gene dosage (CA21HA/CA21HB = 1.01). DNA from another individual (Ma I-2) with a different C4A gene duplication (C4A*3,A*5,C4B*QO) also had equal densitometry measurements (7.0/6.0 kb = 1.07). We conclude that two extended haplotypes from unrelated pedigrees have two C4 genes and both C4 genes encode separate C4A alleles. These findings are compatible with a gene conversion event of C4B to C4A. | |
| 2941021 | Decreased expression of the C3b/C4b receptor (CR1) and the C3d receptor (CR2) on B lymphoc | 1986 Jun | Decreased numbers of complement receptor type 1 (CR1) have been observed on erythrocytes of patients with systemic lupus erythematosus (SLE) and on glomerular podocytes of patients having proliferative nephritis of SLE. In the present study, the analysis of the cellular expression of CR1 has been extended to include leukocytes. In addition, expression by B lymphocytes of the C3d receptor (CR2), which also serves as the receptor for the Epstein-Barr virus, was assessed. Receptor expression was measured by 2-color fluorescent flow cytometry of peripheral blood B cells, identified by the presence of the B1 antigen, that had also been stained with anti-CR1 or anti-CR2. B cells from 17 patients with SLE exhibited a mean relative fluorescence for CR1 that was 61% of that found in 17 normal individuals (P less than 0.001). The expression of CR2 by the patients' B cells (n = 14) was 62% of that of the B cells from normal subjects (n = 17) (P less than 0.001). The expression of CR1 correlated with that of CR2 among patients (r = 0.63; P less than 0.01) but not with the expression of CR2 among normal individuals (r = 0.36; P greater than 0.1). The mean CR1 content of the patients' neutrophils was only 59% of the normal mean (P less than 0.001). Thus, abnormalities of complement receptor expression occur on the leukocytes of patients with SLE. These deficiencies may be secondary to interaction of the cells with the products of complement activation, or, in some individuals, the deficiencies may be familial. | |
| 3502561 | A possible haplotype association in Felty's syndrome. | 1986 Jun | The HLA-B7/DR association was examined in a normal British population and in seven HLA-B7-positive patients with Felty's syndrome. After the exclusion of the most frequent A3-B7-DR2 association, a significant A2-B7-DR4 association was evident. This was present in six of the seven HLA-B7-positive Felty's patients and might indicate that the A2-B7-DR4 haplotype is prevalent in some forms of rheumatoid arthritis. | |
| 2838572 | Characterization of the serological response in man to the latent membrane protein and the | 1988 Jun | A total of 116 sera from healthy individuals and from patients with Burkitt's lymphoma (BL), nasopharyngeal carcinoma (NPC) or rheumatoid arthritis (RA) were studied with respect to antibody responses to each of the seven known transformation-associated Epstein-Barr virus (EBV)-encoded antigens [latent membrane protein (LMP) and six nuclear proteins (EBNAs 1 to 6)]. The antibodies were detected using modified standard immunoblotting techniques. Antibodies to LMP were detected for the first time in sera from 6/27 (22%) healthy, EBV-immune individuals (seropositive for the viral capsid antigens). An increased incidence of anti-LMP antibodies was found in EBV-immune sera from patients with BL (17/24 positive; 71%), NPC (21/33; 64%), and RA (16/21; 76%). Antibodies to EBNA 1 were detected in all EBV-immune sera at a standard 1:20 dilution. Antibodies to the other EBNAs were detected in only a proportion of these sera (20 to 95%) at the same dilution. Only minor disease-associated differences in the incidence of these antibodies were observed, the most consistent being that RA sera had a higher incidence of antibodies to EBNAs 2 to 6 compared with healthy controls. Testing of the sera at a 1:100 dilution suggested that there were some disease-related differences in the titres of anti-EBNA antibodies. At this serum dilution, a reduced incidence of antibodies to EBNA 2 was seen in NPC (6/31) compared with RA (18/19) and healthy EBV-seropositives (16/26); antibodies to EBNA 3 were detected at an increased incidence in BL (8/15) and NPC (16/31) compared with control sera (7/26); antibodies to EBNA 4 were detected at increased incidence in BL (5/15) and RA (6/19) compared with control sera (1/26); and antibodies to EBNA 6 were detected at increased incidence in NPC (19/31) and RA (7/19) compared with control sera (3/26). |