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W J Koopman

Publications and source records attributed to W J Koopman.

At least 145 records · Page 8Linked to original sources
PubMed1987

Airways disease in rheumatoid arthritis patients. One element of a general exocrine dysfunction.

Airflow limitation is a frequent finding in patients with rheumatic diseases. We have previously suggested that it is associated with autoimmune exocrinopathy in Sjögren's syndrome. To compare clinical features of patients with and without airways dysfunction and to further test the hypothesis of a link between airways disease and exocrinopathy, we prospectively studied 2 groups of 15 lifetime nonsmoker female patients with seropositive rheumatoid arthritis (RA). The 2 groups were similar in their clinical and immunologic features, but differed in terms of airways function. Salivary, lacrimal, and sweat gland dysfunction were significantly more prevalent or severe in the group with airways disease. Antinuclear antibodies were also more prominent in the patients with airways disease, but antibodies against RNP, SS-A, SS-B, and double-stranded DNA were not present in these patients. HLA-DR4 was found in 80% of the RA patients with airways disease and in 57% of those without airways disease. HLA-B8 and DR3 were equivalently distributed in both groups. This prospective study further documents the existence of small airways disease in RA and supports the view that autoimmune exocrinopathy predisposes to its expression.

Adult↗
PubMed1987

Association of a 9.2-kilobase Pvu II class I major histocompatibility complex restriction fragment length polymorphism with ankylosing spondylitis.

We analyzed DNA restriction fragment length polymorphism (RFLP) in 53 white ankylosing spondylitis (AS) patients and 92 healthy controls, utilizing a full-length HLA-B7 complementary DNA probe. A 9.2-kilobase (kb) Pvu II fragment was found to be significantly increased in frequency in B27 positive AS patients compared with the B27 positive control group (P = 0.00085, relative risk = 7.2). The presence of both B27 and the 9.2-kb RFLP in an individual conferred a relative risk for AS of 297, compared with a relative risk of 119 in those who had B27 alone. The 9.2-kb RFLP appears to be a marker for AS which, with HLA-B27, contributes further to susceptibility to the disease. Our findings indicate that this fragment and HLA-B27 segregate independently in familial studies of AS.

Genetic Techniques↗
PubMed1987

A low molecular weight, heat-labile factor enhances neutrophil Fc receptor-mediated lysosomal enzyme release and phagocytosis.

When exposed to solid-phase immune complexes, polymorphonuclear neutrophils (PMN) degranulate and release proteases capable of degrading the major structural macromolecules of the joint. Evidence indicates that the PMN response to such activators may be modified by factors present at the sites of inflammation. We have evaluated the effects of a low molecular weight factor present in synovial fluid from rheumatoid arthritis (RA) patients on Fc receptor-mediated PMN degranulation and phagocytosis. Synovial fluid samples from 11 RA patients were studied; 10 of them contained factor(s) which augmented phagocytosis and degranulation mediated through the Fc receptor. This factor(s) alone, however, did not initiate neutrophil degranulation: its MW is less than 10,000 daltons and it is unstable when heated to 56 degrees C. We also examined supernatants that were produced by coculturing adherent human mononuclear cells stimulated by IgG-coated sheep red blood cells with autologous nonadherent mononuclear cells. A factor(s) with properties similar to those found in the synovial fluids (i.e., heat-labile at 56 degrees C and capable of augmenting Fc receptor-mediated degranulation and phagocytosis) was found in the stimulated human mononuclear cell culture supernatants. Filtration studies indicated that the MW of this factor(s) is between 2,000 and 10,000 daltons. No such activity was detected in culture supernatants of unstimulated mononuclear cells. Production of the cytokine was blocked by cycloheximide, indicating that protein synthesis was necessary. This factor(s), by enhancing PMN degranulation, may augment PMN-mediated tissue destruction in diseases such as RA.

Adult↗
PubMed1987

Analyses of HLA linkage in white families with multiple cases of seropositive rheumatoid arthritis.

Families with multiple cases of seropositive rheumatoid arthritis (RA), identified through 2 probands with the disease, were analyzed for genetic linkage between an autosomal susceptibility gene for RA and the HLA loci. These analyses were carried out over a wide range of penetrances (0.1-0.4), with prevalence for the disease fixed at 0.01 or 0.04. In some models, a sporadic frequency of 20% was assumed. Close linkage to the HLA loci was ruled out for all models where the gene was autosomal dominant, except for those with low penetrance and with prevalence set at 0.04. The models in which the gene was autosomal recessive produced results similar to those in models where it was autosomal dominant when prevalence was set at 0.01, and close linkage was ruled out, except at very low penetrances. With prevalence set at 0.04, the autosomal recessive gene model produced log odds scores which were all negative (-2.6 to -0.3). Therefore, the evidence in these families does not support close linkage with HLA, even though a significant DR4 RA population association exists. The data suggest that non-major histocompatibility complex (MHC) genes may contribute to the development of RA and, therefore, disease susceptibility may involve the genetic interaction of one or more MHC genes and non-MHC genes, in addition to environmental agents.

Arthritis, Rheumatoid↗
PubMed1987

Enhanced in vitro IgM rheumatoid factor synthesis in seropositive rheumatoid arthritis families.

We studied the patterns of in vitro IgM RF production by peripheral blood mononuclear leukocytes (MNL) in first- and second-degree relatives and non-blood relatives of 14 RA patients. In all these included 25 individuals with RA (14 probands, 11 other affected members), 88 non-affected first- and second-degree relatives and 15 non-affected non-blood relatives. In vitro production of IgM RF and IgM by MNL from RA patients was similar to what we and others have previously described. Spontaneous production of IgM RF was demonstrated by MNL from some RA patients and the ratio of IgM RF to total IgM was higher for patients than controls. The non-blood relatives failed to demonstrate spontaneous in vitro IgM RF production. In contrast, MNL from approximately 16% of non-affected blood relatives spontaneously produced IgM RF. Spontaneous IgM RF production in this group did not correlate with HLA-DR3 or HLA-DR4 and was found in Caucasoids. American blacks, simplex (one affected individual), and multiplex (more than one affected individual) families. Linkage analysis using either a recessive or dominant model of inheritance failed to detect linkage among affected and non-affected family members.

Arthritis, Rheumatoid↗
PubMed1987

Humoral sensitivity to native collagen types I-VI in the arthritis of MRL/l mice.

The presence of immune reactivity to collagen in patients with rheumatoid arthritis as well as recent interest in the type II collagen-induced arthritis model have suggested a role for autoimmunity to collagen as a major disease mechanism. However, data concerning the occurrence of antibodies (AB) against the different types of collagen during a spontaneously occurring, histologically well-defined arthritis have been lacking. Sera from 48 MRL/l mice aged 5 to 25 weeks with spontaneously occurring hindlimb arthritis were obtained. Sera were tested for auto-AB against collagens utilizing highly purified native collage types I-VI. Significant levels of circulating AB against native collagen types I, III, and VI could not be detected in any age group. The greatest elevation of antibodies directed against type II collagen was found in 13- to 15-week-old mice. AB against type IV collagen were detected in slightly elevated levels with a maximum at 9-10 weeks. Most strikingly, AB against type V were markedly elevated after 19 weeks. The occurrence of high levels of AB against type V collagen, largely found in the pericellular matrix of smooth muscle cells, is associated with the late stage of disease characterized by histologically documented vasculitis. The results suggest that AB to collagen occur as a consequence of tissue destruction and that evidence for a pathogenetic role of AB in MRL/l arthritis is lacking.

Animals↗
PubMed1987

Striking elevation of serum IgA, IgA-containing immune complexes, and IgA rheumatoid factor in clinically silent dermatitis herpetiformis.

We describe a patient with dermatitis herpetiformis with immunoglobulin A (IgA)-containing circulating immune complexes and IgA rheumatoid factor who presented with acute renal insufficiency; a renal biopsy specimen showed IgA nephropathy. The renal function and proteinuria spontaneously returned to normal despite markedly elevated levels of IgA-containing circulating immune complexes, IgA rheumatoid factor, and IgA antibodies to some environmental antigens. IgA1 was the predominant subclass. IgA2-containing immune complexes and IgM rheumatoid factor were not detected. Cultures of peripheral blood mononuclear cells produced increased quantities of IgA and IgA rheumatoid factor spontaneously and after pokeweed mitogen stimulation. These data indicate that renal function can improve and remain normal despite the presence of increased levels of IgA-containing circulating immune complexes and IgA rheumatoid factor.

Acute Kidney Injury↗
PubMed1987

Analysis of restriction fragment length polymorphisms in rheumatic diseases.

Considerable evidence indicates that genes residing within the major histocompatibility complex (MHC) influence susceptibility to certain rheumatic diseases, such as ankylosing spondylitis (AS) and rheumatoid arthritis (RA). However, it has not yet been possible to precisely identify the gene(s) responsible for conferring enhanced susceptibility to these diseases. The availability of recombinant DNA technology should accelerate progress in obtaining this goal. A particularly promising method in this regard is restriction fragment length polymorphism (RFLP) analysis using appropriate class I and class II MHC gene probes. In preliminary studies, RFLPs have been identified for AS and RA which associate with susceptibility to the disease. Further studies using this approach should permit localization and precise identification of the disease susceptibility gene(s) for these diseases.

Arthritis, Rheumatoid↗
PubMed1987

Toxicity of methotrexate in rheumatoid arthritis.

Seventy-two patients with rheumatoid arthritis had been treated with pulse weekly oral methotrexate with a mean followup of one year. Minor side effects (oral ulcers, transient elevation of liver enzymes, nausea, vomiting) were present in 46 patients (63.8%), whereas major side effects (severe infection, cytopenia, respiratory failure, seizures, gastrointestinal bleeding) were present in 7 (9.7%), 2 of whom died. Patients with major side effects had shorter disease duration and increased frequency of extraarticular manifestations as compared to those with no side effects. No association between a particular clinical or genetic variable and occurrence of side effects to methotrexate was found.

Administration, Oral↗
PubMed1987

Development of clinical criteria for osteoarthritis.

Clinical criteria for the classification of osteoarthritis (OA) in the knee have been developed and the use of algorithms has been proposed. Criteria for the classification of OA in the hand and hip are still being developed.

Hand↗
PubMed1986

VH gene expression is restricted in anti-IgG antibodies from MRL autoimmune mice.

Antibodies directed against IgG and DNA are found in the sera of autoimmune MRL/Mp lpr/lpr mice. Little is known of the molecular mechanisms underlying expression of such autoantibodies. We have investigated the binding diversity and pattern of VH gene expression in a panel of murine anti-IgG antibodies. We constructed eight hybridoma clones secreting IgM antibodies that bound to mouse IgG by using spleen cells from MRL/Mp lpr/lpr mice varying in age from 4 to 15 wk; one clone was derived from a 32-wk-old MRL +/+ mouse. The monoclonal IgM products exhibited varying binding specificities for intact mouse IgG, fragments of mouse IgG [Fc, Fab, (Fab')2], and heterologous IgG. Two of these antibodies crossreacted with B and/or Z DNA. Probes from seven of eight identified mouse VH gene families (7183, S107, Q52, J558, J606, 36-60, and 3609) were hybridized under high-stringency conditions with cytoplasmic RNA blots from each clone. Six clones hybridized only with the probe from the five-member 36-60 family. The remaining three clones crosshybridized with the 36-60 probe and the probe from the 60 member J558 family, perhaps reflecting somatic mutation from the original germline VH gene resulting in recognition by a probe from another family, in addition to the probe from the original germline family. Our results indicate that spontaneous MRL lpr/lpr anti-IgG antibodies are encoded predominantly by the 36-60 VH gene family and imply a nonrandom selection of this VH gene family in the production of these antibodies.

Animals↗
PubMed1986

Molecular forms of IgA rheumatoid factor in serum and synovial fluid of patients with rheumatoid arthritis.

The distribution of molecular forms of serum IgA rheumatoid factor (IgA-RF) in 42 patients with rheumatoid arthritis was examined by solid-phase radioimmunoassay following fractionation by gel chromatography or ultracentrifugation in acidic buffer. Analysis of the fractions using phosphate buffered saline indicated that the IgA-RF in each serum was mainly polymeric. However, monomeric IgA-RF was detected in sera from approximately two-thirds of the patients, after dilution of chromatographic or ultracentrifugal fractions in diluent containing mouse monoclonal anti-human alpha chain antibody. The levels of monomeric IgA-RF (mean +/- SD 38 +/- 86 micrograms/ml) and the ratios of monomeric to polymeric IgA-RF (mean +/- SD 0.29 +/- 0.41) varied over a wide range. Paired synovial fluids from 9 of the patients were also examined. Monomeric IgA-RF was detected in each, although 2 samples demonstrated only minimal quantities. Neither form of IgA-RF was detected in serum from healthy adults when analyzed under the same conditions. Thus, both monomeric and polymeric IgA-RF can occur in serum and synovial fluid from patients with rheumatoid arthritis, and their proportions vary widely among patients.

Arthritis, Rheumatoid↗
PubMed1986

HLA antigens and gold toxicity in American blacks with rheumatoid arthritis.

An increase in the frequency of DR3 in rheumatoid arthritis (RA) patients exhibiting toxic reactions to gold salt (GS) therapy has been observed in several studies of Caucasoid patients. Likewise, the association of B35 with gold-induced mucocutaneous reactions has also been reported in Caucasoid RA patients. Similar studies in other ethnic groups have not been previously documented. The present study was performed in American black RA patients receiving GS to determine if there were similar HLA associations with toxic reactions as those reported in Caucasoids. Eight-two seropositive and 18 seronegative American black RA patients were studied. Forty-one of the seropositive (50.0%) and six of the seronegative (33.3%) developed a toxic manifestation. No significant differences in the frequency distribution of HLA-B8, HLA-B35, DR, or DQw antigens were observed between the patients who had a toxic reaction and those who did not in either the seropositive or the seronegative RA patients. In particular, DR3 was not increased in patients with renal toxicity and B35 was not increased in patients with mucocutaneous reaction. Our study demonstrates that American black RA patients exhibiting GS toxicity do not have the same HLA associations as Caucasoids. The possibility that other genetic factor(s) may account for the occurrence of gold salt toxicity in American blacks requires further investigation.

Black or African American↗