Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 20 de 93
Filter
1.
Lupus ; 9(7): 515-20, 2000.
Article in English | MEDLINE | ID: mdl-11035417

ABSTRACT

Annexin XI, a calcyclin-associated protein, has been shown to be identical to a 56,000 Da antigen recognized by antibodies found in sera from patients suffering from systemic autoimmune diseases. In this work hexahistidine-tagged recombinant annexin XI (His6- rAnn XI) was used as antigen in ELISA experiments for determination of autoantibodies to annexin XI in sera of patients with systemic rheumatic autoimmune diseases. Immunoblotting with HeLa cell extract and with His6-rAnn XI as antigen was used for confirmation of positive ELISA results. We found eleven anti-annexin XI positive sera (3.9%) out of 282 sera from patients with systemic rheumatic diseases. The highest number of annexin XI positive sera were found in primary antiphospholipid syndrome (3/17), and in subacute lupus erythematosus (1/6), while lower frequencies of positive sera were found in patients with systemic sclerosis (5/137), rheumatoid arthritis (1/21), and systemic lupus erythematosus (1/58). Sera from healthy donors and patients with chronic infections were negative, except for one Salmonella typhimurium antibody positive serum. Autoantibodies to annexin XI were found to relate to thrombosis, but not to other clinical or laboratory features. A relation between antibodies to annexins and thrombosis has so far only been known for annexin V.


Subject(s)
Annexins/immunology , Autoantibodies/blood , Autoimmune Diseases/immunology , Adult , Aged , Antiphospholipid Syndrome/blood , Antiphospholipid Syndrome/immunology , Arthritis, Rheumatoid/blood , Arthritis, Rheumatoid/immunology , Autoimmune Diseases/blood , Enzyme-Linked Immunosorbent Assay , Female , HeLa Cells , Humans , Lupus Erythematosus, Systemic/blood , Lupus Erythematosus, Systemic/immunology , Male , Middle Aged , Recombinant Proteins/immunology , Reproducibility of Results , Scleroderma, Systemic/blood , Scleroderma, Systemic/immunology
2.
Ann Rheum Dis ; 58(8): 488-92, 1999 Aug.
Article in English | MEDLINE | ID: mdl-10419867

ABSTRACT

OBJECTIVE: Urokinase type plasminogen activator (uPA) catalyses the formation of the proteolytic enzyme plasmin, which is involved in matrix degradation in the processes of tissue remodelling. Because of a surface bound uPA receptor (uPAR), expressed by some cell types (for example, macrophages, malignant cells and inflammatory activated synoviocytes), the action of uPA can be localised and intensified. uPAR seems to have a role in the mechanisms leading to invasive growth of malignant tissue and the rheumatoid pannus. uPAR may become cleaved at its cell surface anchor, thus forming a free soluble receptor (suPAR). suPAR is detectable in low but constant values in plasma of healthy people, while increased concentrations are found in patients with disseminated malignant disease, so that suPAR may be an indicator of invasive growth and tissue remodelling. suPAR concentrations in plasma have not previously been measured in rheumatic patients. A controlled cross sectional measurement was performed of suPAR in plasma of patients with various inflammatory rheumatic disorders with special reference to rheumatoid arthritis (RA). METHODS: suPAR in plasma was measured by ELISA technique in patients with RA (n=51), reactive arthritis (ReA) (n=23), primary Sjögren's syndrome (PSS) (n=42) and sex and age matched healthy controls (n=53). RESULTS: In the control group suPAR (median) was 0. 91 (range 0.56-1.94) microg/l. Median suPAR value in RA was 1.47 (range 0.65-6.62) microgram/l; in ReA 0.68 microgram/l (range 0.52-1.48) and in PSS 1.12 microgram/l (range 0.76-1.92); p versus controls <0.001 in all patient groups. suPAR values in RA were also significantly increased compared with ReA (p<0.001) and PSS (p=0.004) groups. suPAR in RA was positively correlated to C reactive protein (CRP) (p<0.01) and erythrocyte sedimentation rate (p<0.05) and number of swollen joints (p<0.05). The ReA group had the highest CRP values of all groups, but at the same time the lowest suPAR concentrations in plasma. CONCLUSIONS: Increased suPAR concentrations were found in plasma in RA, and to a smaller extent also in PSS, but not in ReA. In RA suPAR is related to disease activity. suPAR seems though not merely to be an acute phase reactant like CRP. Increased suPAR values might reflect erosive activity in RA.


Subject(s)
Arthritis, Rheumatoid/blood , Plasminogen Activators/blood , Receptors, Cell Surface/blood , Adult , Aged , Arthritis, Reactive/blood , Cross-Sectional Studies , Enzyme Precursors/blood , Female , Humans , Male , Middle Aged , Prohibitins , Receptors, Urokinase Plasminogen Activator , Sjogren's Syndrome/blood , Solubility , Urokinase-Type Plasminogen Activator/blood
3.
Scand J Rheumatol ; 28(3): 180-3, 1999.
Article in English | MEDLINE | ID: mdl-10380841

ABSTRACT

The purpose of this study was to explore the clinical and pathogenic significance of vitamin D metabolites in primary Sjögren's syndrome (primary SS). We measured blood concentrations of 25-hydroxyvitamin D (25 OH D) and calcitriol (1,25(OH)2D)vc in 41 patients and correlated the results with blood levels of various immune activation products, as well as with patients' clinical status. Levels of 25 OH D were slightly decreased as compared to normal controls and the reduced levels of 25 OH D were stable over the observed period of 2 years. Levels of 25 OH D correlated inversely with levels of soluble interleukin-2 receptor, status indices for global disease, total exocrine disease, surface exocrine disease, internal organ exocrine disease, and mediator-induced disease. Levels of 1,25(OH)2D varied considerably and compared to normal control values. Levels of 1,25(OH)2D did not correlate with clinical/immunopathological status. In conclusion the inverse correlations found between levels of 25 OH D and measures of clinical and immunoinflammatory status support the notion that vitamin D metabolism may be involved in the pathogenesis of primary SS.


Subject(s)
Sjogren's Syndrome/blood , Vitamin D/analogs & derivatives , Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Vitamin D/blood
4.
Article in English | MEDLINE | ID: mdl-9849649

ABSTRACT

In 41 primary Sjögren's syndrome patients we compared fatty acid levels within erythrocyte phospholipids, plasma phospholipids, plasma triglycerides and plasma cholesterol esters, with the immunopathological and clinical disease status. Docosahexaenoic acid was the essential fatty acid (EFA), the levels of which correlated (inversely) most closely with the clinical disease status (r=-0.33 to -0.50). Levels of dihomogammalinolenic acid and eicosapentaenoic acid correlated inversely to levels of IgM rheumatoid factors (r=-0.33) and anti-SSA/Ro antibodies (r=-0.40) respectively. Moreover, levels of anti-SSA/Ro antibodies (r=-0.34-0.40) correlated with levels of the proinflammatory arachidonic acid. Sigma n-3 EFA/sigma n-6 EFA ratios correlated significantly to the quantitative estimates of immunopathological and clinical disease status. Our data are in agreement with current understanding of pro- and anti-immunoinflammatory roles within EFA metabolism, and support the rationale for intervention studies.


Subject(s)
Fatty Acids, Essential/blood , Sjogren's Syndrome/classification , 8,11,14-Eicosatrienoic Acid/metabolism , Adult , Aged , Autoantibodies/blood , Cholesterol Esters/blood , Docosahexaenoic Acids/metabolism , Erythrocytes/chemistry , Female , Health Status , Humans , Male , Middle Aged , Phospholipids/blood , Sjogren's Syndrome/immunology , Sjogren's Syndrome/pathology , Triglycerides/blood
5.
Drugs ; 56(3): 345-53, 1998 Sep.
Article in English | MEDLINE | ID: mdl-9777311

ABSTRACT

The aetiology of Sjögren's syndrome (SS) is unknown, and consequently curative treatments are not available. The immunopathogenesis of SS is partly clarified and immune-regulating drugs (IR) may therefore be of therapeutic value. However, the present understanding of SS is still too unclear to allow an exact and evidence-based algorithm for therapeutic decision making. Rational drug recommendations for the therapy of SS must, therefore, rely mostly on empirical data. Several IR drugs have been shown to be able to downregulate the immunopathological activity of primary SS, but it is not certain whether the diagnostic and cardinal manifestations from the eyes and mouth can be improved. In primary SS the disease-modifying qualities of IR and cytotoxic drugs, therefore, largely apply to the treatment of severe internal organ involvement, inflammatory vascular disease and malignant B lymphocyte disease. In secondary SS the IR therapy is directed against the basic immunoinflammatory connective tissue disease. Symptom-modifying therapies include drugs to stimulate and substitute for exocrine functions, and drugs to treat complications of the exocrine disease manifestations and to improve the various nonexocrine disease manifestations. The main drugs available for increasing lacrimal and salivary gland output are bromhexine and pilocarpine, respectively. However, exocrine substitutes, and in particular eye drops, are still the most important means of alleviating the sicca symptoms. They are also indispensable local treatment measures which may help to prevent mucosal complications.


Subject(s)
Adjuvants, Immunologic/therapeutic use , Sjogren's Syndrome/drug therapy , Humans , Sjogren's Syndrome/physiopathology
7.
Med Hypotheses ; 50(6): 483-92, 1998 Jun.
Article in English | MEDLINE | ID: mdl-9710321

ABSTRACT

Primary Sjögren's syndrome (pSS) is increasingly acknowledged as a disease entity with consistent pathogenesis and clinical presentation. This has encouraged proposals for uniform nomenclature, as well as for classification of disease subsets and clinical disease manifestations. The purpose of this literature survey is to analyse present pathogenetic and clinical data on pSS from the viewpoint of their usability for developing criteria for activity and damage. It appears that the routinely used tests for evaluating clinical disease manifestations in pSS probably measure both activity and damage. Moreover, no immunopathogenic marker has been shown to adequately represent all aspects of disease activity in pSS. The survey demonstrates the need for longitudinal studies in which potential markers of disease activity and damage are validated.


Subject(s)
Sjogren's Syndrome/physiopathology , Biomarkers , Humans , Sjogren's Syndrome/classification , Terminology as Topic
9.
Scand J Rheumatol ; 26(3): 197-205, 1997.
Article in English | MEDLINE | ID: mdl-9225875

ABSTRACT

Quantitative and qualitative assessment of the clinical disease manifestations in 41 primary Sjögren's syndrome (pSS) patients was performed according to a new classification model. Frequencies of subgrouped disease manifestations were as follows: 1) surface exocrine disease: 100%, 2) internal organ exocrine disease: 63%, 3) monoclonal B lymphocyte disease: 5%, 4) inflammatory vascular disease: 71%, 5) non-inflammatory vascular disease: 59%, 6) mediator induced disease: 98%. Summary scores for severity of surface exocrine disease correlated to the summary scores of all other disease manifestations (p = 0.02), to the summary scores of internal organ exocrine disease (p = 0.003), and to the summary scores of mediator induced disease (p = 0.03). Blood leucocyte counts showed significant negative correlations to levels of plasma IgG, serum IgA-RF, IgM-RF, anti-SSA/SSB antibodies, IL-6, and IL-1Ra. We conclude that the model made detailed analysis of the clinical presentation of pSS possible, and thus may assist in elucidating important pathobiological aspect of the disease.


Subject(s)
Severity of Illness Index , Sjogren's Syndrome/diagnosis , Adult , Aged , Aged, 80 and over , Autoantibodies/blood , Blood Proteins/analysis , Cross-Sectional Studies , Cytokines/blood , Female , Humans , Immune System/immunology , Interleukins/blood , Male , Middle Aged , Sjogren's Syndrome/blood , Sjogren's Syndrome/classification
10.
J Intern Med ; 239(6): 475-82, 1996 Jun.
Article in English | MEDLINE | ID: mdl-8656140

ABSTRACT

OBJECTIVES: The clinical features of 80 patients with primary Sjögren's syndrome (PSS) were revised in order to evaluate the descriptive and analytical facilities of a newly proposed model for classification of the exocrine and nonexocrine disease manifestations in PSS. DESIGN: Retrospective, long-term (median 7.5 years follow-up) observational, clinical study. SETTING: Patients were recruited from our Department, which is a tertiary referral centre for PSS patients. SUBJECTS: Eighty patients fulfilling the Copenhagen criteria for keratoconjunctivitis sicca and/or xerostomia and followed between 1972 and 1991 were studied. RESULTS: All patients had 'surface exocrine disease' and in 31% this was the only disease manifestation. 'Internal organ exocrine disease' was found in 25% of the patients, whilst 2.5% developed 'monoclonal B lymphocyte disease' (non-Hodgkin's lymphoma). 28% displayed 'inflammatory vascular disease', 25% 'noninflammatory vascular disease', 41% "mediator-induced disease' and 2.5% 'autoimmune endocrine disease' (thyroiditis). In patients with 'internal organ exocrine disease' the frequencies of "mediator-induced disease' (70%; P < 0.01) and 'inflammatory vascular disease, (50%; P < 0.03) were significantly higher than expected by chance. The level of immunoinflammatory activity (assessed by plasma IgG, serum ANA and focus scoring of minor labial salivary gland biopsies) correlated with the extent of clinical disease as assessed by the model. CONCLUSIONS: We conclude that this theoretically based model for classification of disease manifestations in PSS contains descriptive and analytic powers which may assist the clinical handling of these patients.


Subject(s)
Sjogren's Syndrome/classification , Aged , Autoimmunity , Biomarkers/blood , Diagnosis, Differential , Exocrine Glands , Female , Humans , Inflammation , Male , Middle Aged , Models, Biological , Retrospective Studies , Sjogren's Syndrome/blood , Sjogren's Syndrome/immunology , Sjogren's Syndrome/pathology , Sjogren's Syndrome/physiopathology
11.
J Intern Med ; 239(6): 467-74, 1996 Jun.
Article in English | MEDLINE | ID: mdl-8656139

ABSTRACT

A new model for classifying the clinical disease manifestations of primary Sjögren's syndrome is introduced. Three "exocrine' and four "nonexocrine' subgroups of disease manifestations are defined. Accordingly, "surface exocrine disease' includes the diagnostic features from eyes, mouth, and the manifestations from the upper airways, skin and genital tract. Involvement of the excretory parenchyma of the lungs, hepatobiliary system, pancreas, gastrointestinal tract and kidneys is designated "internal organ exocrine disease'. We suggest "monoclonal B lymphocyte disease' to be an exocrine disease manifestation because it originates mostly from the immunoinflammatory foci of the autoimmune exocrinopathy. The nonexocrine manifestations are subgrouped into "inflammatory vascular disease'. "noninflammatory vascular disease', "mediator-induced disease' and "autoimmune endocrine disease'.


Subject(s)
Sjogren's Syndrome/classification , Autoimmunity , Exocrine Glands , Humans , Inflammation , Models, Biological , Sjogren's Syndrome/immunology , Sjogren's Syndrome/pathology , Sjogren's Syndrome/physiopathology
12.
Clin Exp Rheumatol ; 13(6): 693-6, 1995.
Article in English | MEDLINE | ID: mdl-8835240

ABSTRACT

In spite of our continuously improved pathobiological understanding, there is still no consensus on terminology and disease criteria in Sjögren's syndrome (SS). This survey points out discrepencies in the current description of the syndrome, and argues for a new classification model. We suggest that the present nomenclatures for the global disease (Sjögren's disease) and disease subsets (primary and secondary SS) be retained until additional pathobiological insights give rise to new and descriptive terms. We do find evidence, however, to support a new terminology and classification of the main immunoinflammatory manifestations of primary SS. Accordingly, three "exocrine" and four "non-exocrine" subgroups of disease manifestations are here defined. The usefulness of the proposed model should be evaluated in clinical studies and in a debate engaging all of the medical specialities involved.


Subject(s)
Sjogren's Syndrome/classification , Terminology as Topic , Autoimmune Diseases/classification , Autoimmune Diseases/pathology , Autoimmune Diseases/physiopathology , Exocrine Glands/pathology , Exocrine Glands/physiopathology , Humans , Sjogren's Syndrome/pathology , Sjogren's Syndrome/physiopathology
13.
Clin Rheumatol ; 14 Suppl 1: 3-7, 1995 Jul.
Article in English | MEDLINE | ID: mdl-7493452

ABSTRACT

Establishing a model for classification of the clinical disease manifestations in primary Sjögren's syndrome is a challenge with important implications for handling individual patients and for describing and analyzing patient materials. Based on the pathobiology of primary SS we define three (1-3) "exocrine" and four (4-7) "nonexocrine" subgroups of disease manifestations. Accordingly, 1) "surface exocrine disease" includes the diagnostic features from eyes (keratoconjunctivitis sicca) and mouth (xerostomia), and the manifestations from upper airways (rhinitis sicca, xerotracheitis) and skin (xeroderma). Involvement of the excretory parenchyma of the lungs, hepatobiliary system, pancreas, intestinal tract and kidneys is designated 2) "internal organ exocrine disease". These manifestations are potentially severe, do not lead to subjective dryness, and none of them are diagnostic for the disease. We suggest 3) "monoclonal B-lymphocyte disease" (lymphoma) to be an exocrine disease manifestation because it originates mostly from the immunoinflammatory foci of the autoimmune exocrinopathy. The nonexocrine manifestations are subgrouped into: 4) "inflammatory vascular disease" (vasculitis and perivasculitis), 5) "noninflammatory vascular disease" (Raynaud), 6) "mediator-induced disease" (hematologic cytopenia, fever and fatigue) and 7) "autoimmune endocrine disease". Subdividing the seven subgroups leads to a third order of classification in which single and separate manifestations are placed. The descriptive and analytic power of the proposed model for classification of disease manifestations in primary Sjögren's syndrome should be evaluated in clinical studies.


Subject(s)
Sjogren's Syndrome/classification , Eye Diseases/etiology , Eye Diseases/pathology , Eye Diseases/physiopathology , Humans , Mouth Diseases/etiology , Mouth Diseases/pathology , Mouth Diseases/physiopathology , Sjogren's Syndrome/pathology , Sjogren's Syndrome/physiopathology , Skin Diseases/etiology , Skin Diseases/pathology , Skin Diseases/physiopathology
15.
Rheumatol Int ; 14(3): 115-8, 1994.
Article in English | MEDLINE | ID: mdl-7839071

ABSTRACT

To evaluate longitudinal alterations in pulmonary function, 63 patients suffering from rheumatoid arthritis (RA) with previously reported reduced pulmonary diffusing capacity were re-examined in an 8-year follow-up study. Cross-sectional examination revealed normal values for vital capacity (VC), forced expiratory volume in 1 s (FEV1) and diffusing capacity per litre alveolar volume (KCO). Total diffusing capacity (DLCO; P < 0.0001), maximal expiratory flow at 75% of expired VC (MEF75; P < 0.0001) and MEF50 (P < 0.01) were decreased. Longitudinal evaluation revealed unchanged MEF50, MEF75 and FEV1, whereas increases in DLCO (P < 0.0001) and KCO (P < 0.0001) and a decrease in VC (P < 0.05) were found. The longitudinal changes in diffusing capacity were unrelated to patient age, disease duration, disease activity in the study period or pulmonary function at the first examination. Thus, in patients suffering from RA, the most prominent functional pulmonary abnormality, decreased diffusing capacity, appeared to improve in the course of time, despite a slight decrease in VC and continued articular disease activity.


Subject(s)
Arthritis, Rheumatoid/physiopathology , Pulmonary Diffusing Capacity , Vital Capacity , Adult , Aged , Aged, 80 and over , Arthritis, Rheumatoid/complications , Cross-Sectional Studies , Female , Follow-Up Studies , Forced Expiratory Volume , Humans , Male , Middle Aged , Prognosis , Respiratory Function Tests
16.
Semin Arthritis Rheum ; 22(2): 114-26, 1992 Oct.
Article in English | MEDLINE | ID: mdl-1439843

ABSTRACT

Primary Sjögren's syndrome is a chronic autoimmune disorder of the lacrimal and salivary glands, reflecting general involvement of the exocrine tissues and leading to functional impairment. This polyglandular disease is often associated with systemic extraglandular manifestations, and laboratory tests usually indicate polyclonal B-lymphocyte hyperactivity. Clinical and laboratory markers monitoring the disease processes are needed for improved management of primary Sjögren's syndrome. However, incomplete knowledge of the long-term course of inflammation as well as of clinical manifestations makes precise and simple directions for monitoring disease activity in primary Sjögren's syndrome difficult. This review describes potential primary (eg, salivary gland histopathology, autoantibodies, soluble interleukin-2 receptors, and beta 2-microglobulin) and secondary disease activity markers (clinical and laboratory signs of glandular and extraglandular organ damage) and their known associations. The importance of genetic characteristics, patient age, and symptom duration for the disease activity markers is indicated. The systematic use of primary and secondary disease activity markers will improve our understanding of primary Sjögren's syndrome and help create better guidelines for monitoring the disease.


Subject(s)
Sjogren's Syndrome/physiopathology , Aging , Biomarkers , Genetic Predisposition to Disease , Humans , Sex Characteristics , Sjogren's Syndrome/classification , Sjogren's Syndrome/pathology , Terminology as Topic , Time Factors
17.
Clin Exp Rheumatol ; 10(3): 229-34, 1992.
Article in English | MEDLINE | ID: mdl-1582067

ABSTRACT

To examine whether abnormalities in essential fatty acid (EFA) metabolism are associated with the impaired natural killer (NK) cell functions in primary Sjögren's syndrome, we measured the levels of phospholipid fatty acids in blood mononuclear cells with (MD) and without monocyte depletion (MC), and NK cell activity before and after indomethacin-boosting. We found MD levels of 20:3n6 (dihommo-gamma-linolenic acid), and basal and indomethacin-enhanced NK cell activity significantly reduced, in 10 primary Sjögren's syndrome patients as compared with 10 healthy controls. In the controls the relative (%) increase in indomethacin-enhanced NK cell activity correlated with the level of MD 18:2n6 (linoleic acid) (r = 0.97, p less than 0.001). In the patients the relative (%) indomethacin-enhanced NK cell activity correlated with the 20:4n6 (arachidonic acid)/20:3n6 ratio in the MC (r = 0.90, p less than 0.001). This ratio has been assumed to be an important determinant for the production of prostaglandin 1 and 2. The present data suggest that in healthy persons, as opposed to primary Sjögren's syndrome patients, the level of MD 18:2n6 is a determinant for the sensitivity of NK cells to monocyte-derived prostaglandins. Furthermore, in patients with primary Sjögren's syndrome the MC levels of 20:3n6 and 20:4n6 may be regulating factors for the production of NK cell suppressing prostaglandins.


Subject(s)
Fatty Acids, Essential/analysis , Killer Cells, Natural/physiology , Leukocytes, Mononuclear/chemistry , Membrane Lipids/analysis , Sjogren's Syndrome/blood , Adult , Aged , Female , Humans , Indomethacin/pharmacology , Killer Cells, Natural/drug effects , Middle Aged
18.
Autoimmunity ; 12(3): 185-91, 1992.
Article in English | MEDLINE | ID: mdl-1343766

ABSTRACT

The presence and distribution of 7 cytokines was examined immunohistologically in labial salivary gland (LSG) specimens from patients with primary Sjögren's syndrome (SS) and control subjects. The cytokines interleukin (IL)-1 beta IL-6, tumor necrosis factor (TNF) alpha and interferon (IFN) gamma were identified in defined parts of LSG from patients but not in the corresponding parts of control glands: (a) LSG acinar epithelium expressed IL-1 beta, (b) blood vessels located in both normal LSG stroma and within lymphocytic infiltrates expressed IL-1 beta, IL-6 and IFN gamma, and (c) lymphocytic infiltrates expressed IL-1 beta, IL-6 and TNF alpha. All four cytokines were expressed by salivary ducts within both patient and control specimens, but with generally greater intensity in patients. IL-1 alpha, IL-4 and TNF beta (lymphotoxin) could not be detected in any of the specimens from patients or controls. The locations of cytokines in LSG suggests possible mechanisms of immunologically mediated parenchymal damage in primary SS.


Subject(s)
Cytokines/analysis , Salivary Glands/metabolism , Sjogren's Syndrome/metabolism , Adult , Aged , Cytokines/immunology , Cytokines/metabolism , Female , Humans , Middle Aged , Recombinant Proteins/metabolism
19.
Dis Markers ; 9(5): 289-96, 1991.
Article in English | MEDLINE | ID: mdl-1686751

ABSTRACT

We investigated the DNA restriction fragment length polymorphism (RFLP) of the Major Histocompatability Complex (MHC) class II genes: HLA-DRB, -DQA, -DQB, DPA, and -DFB in 24 patients with rheumatoid arthritis (RA), in 19 patients with primary Sjögren's syndrome (primary SS), and healthy Danes. The frequencies of DNA fragments associated with the following HLA class II genes were increased in RA when compared to normal controls: DRB1*04 (DR4) (relative risk, RR = 7.4, P less than 10(-3), DRB4*0101 (DRw53) (RR = 9.6, P less than 10(-3), DQA1*0301 (RR = 9.6, P less than 10(-3), DQB1*0301 (DQw7) (RR = 2.8, P less than 0.05, 'corrected' P greater than 0.05), and DQB1*0302 (DQw8) (RR = 4.5, P less than 10(-2). Negative associations were found between RA and DRB1*1501 (DR2/DRw15) (RR = 0.2, P less than 10(-2) and DQB1*0602 (DQw6) (RR = 0.2, P less than 10(-2), 'corrected' P greater than 0.05). The frequencies in RA of other HLA class II associated DNA fragments including DPA and DPB and the antigens DPw1-w6 defined by primed lymphocyte stimulation, did not differ significantly from those in controls. In primary SS, the frequency of HLA-B8 was significantly increased (RR = 9.0, P less than 10(-3). Positive associations were found between primary SS and DNA fragments associated with DRB1*03/13 (RR = 6.8, P less than 10(-3), DRB3*0101 (DRw52) (RR = 5.7, P less than 10(-2), DQA1*0501 (RR = 6.8, P less than 10(-3), DQB1*0201 (DQw2) (RR = 11.6, P less than 10(-5), and DQB1*0602 (DQw6) (RR = 2.7, P less than 0.05, 'corrected' P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)


Subject(s)
Arthritis, Rheumatoid/genetics , Genes, MHC Class II/genetics , Sjogren's Syndrome/genetics , Arthritis, Rheumatoid/immunology , Genetic Markers , Humans , Polymorphism, Restriction Fragment Length , Sjogren's Syndrome/immunology
SELECTION OF CITATIONS
SEARCH DETAIL
...