Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A group of patients has been identified with cutaneous necrotizing venulitis (vasculitis). These patients, some with concomitant connective tissue disorders, have skin lesions that separate them from the arteritis commonly described as rheumatoid vasculitis. HLA typing has been performed on 31 of these unrelated patients with cutaneous necrotizing venulitis, including 19 with associated chronic disorders. The antigen pair A11, BW35 was found in 5 of these 19 patients and in 11 of 346 controls. This difference in frequency is statistically significant. Because HLA genes appear to be linked to immune response genes, these data suggest that such genes may exist in patients with this form of cutaneous necrotizing venulitis with associated connective tissue disease.
Arthritis Rheum
PMID:Association between HLA and cutaneous necrotizing venulitis. 0 96

Juvenile rheumatoid arthritis or, more correctly, juvenile chronic polyarthritis with its many clinical manifestations can be separated into the Still-syndrome with acute beginning, high fever and a high percentage of extra-articulalar, i.e. visceral symptoms, and the chronic polyarthritis in the more strict sense with non-visceral symptoms. The subsepsis allergica should be regarded as a subseptic first stage of the Still syndrome. The Still-syndrome implies a systemic disease mainly of the reticulo-endothelial system, with carditis, nephropathy, recurrent erythemas, and a progressing polyarthritis. Later symptoms are amyloidosis, chronic nephritis, myo- and pericarditis, and artheriitis necroticans. Predominanly the involvement of the kidneys is the reasons for the high mortality rate of 13%. Chronic polyarthritis in the strict sense is similar in children and adults, though in children rheumatic factors are rarely detected. The exsudative form of arthritis tends to cause early deterioration. Joint symptoms are distributed asymmetrically and show locally inflammed growth otherwise less common in Still-syndrome. Spondylitis cervicalis rapidly causes ankylosis. Atlanto-axial-arthritis with consequent atlanto-axial dislocation can be the reason for neurological disturbances. Juvenile mono- or oligo-arthritis often turns into polyarthritis; but for joints the prognosis is more favourable. In contrast, rheumatoid iridocyclitis as found in 22% of the cases causes unfavourable complications because symptoms are not noticed in time so that treatment is often too late. Juvenile spondylitis ankylosans begins with a peripheral arthritic stage which is not easily distinguished from chronic polyarthritis. The male sex, mono- or oligoarthritis of the outer extremities, pain in the heel, atlanto-axial-arthritis, iridocyclitis, and a positive HLA of 27 give a diagnostic clue. -- Characteristics of the therapy will be discussed.
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PMID:[Juvenile rheumatoid arthritis and related collagen diseases. Clinical aspects (author's transl)]. 1 66

Lymphocytotoxic antibodies (LCTAB) were sought in sera of patients with rheumatic diseases and in family members. Patients with SLE and cutaneous necrotizing venulitis and family members of JRA patients had an increased frequency of LCTAB; JRA patients and family members of SLE patients did not. The only association between LCTAB and the HLA phenotype of persons with LCTAB was a decreased frequency of LCTAB in individuals with HLA-B27.
Arthritis Rheum 1977 May
PMID:Lymphocytotoxic antibodies. HLA antigen associations, disease associations, and family studies. 1 18

To study the role of genetically determined immune responsiveness in the pathogenesis of systemic amyloidosis complicating rheumatoid arthritis the HLA antigens were identified in 26 patients with rheumatoid arthritis complicated by secondary amyloidosis, in 44 patients with rheumatoid arthritis, and in 11 patients with secondary amyloidosis of non-rheumatoid origin. Subjects with ankylosing spondylitis, sacroiliitis without peripheral polyarthritis, Reiter's disease, reactive arthritis, erosive osteoarthritis, psoriatic arthropathy, systemic lupus erythematosus or arthritis associated with a gastrointestinal involvement were excluded from the study. Patients with amyloidosis secondary to rheumatoid arthritis had a high frequency of the HLA specificity B27 and of the haplotype likely to bear A2, B27. The association with B27 was closest in the group of male patients with amyloidosis whose rheumatoid arthritis had begun at an early age and who lacked demonstrable rheumatoid factor in serum. These patients may represent a genetically determined subentity of rheumatoid arthritis.
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PMID:HLA-B27 in rheumatoid arthritis and amyloidosis. 6 5

HL-A typing was performed on 97 patients with pustular psoriasis. HLA-B27 was found increased for the combined three subgroups: localized psoriasis of palms and soles, acrodermatitis continua and generalized pustular psoriasis, who were associated with a high incidence of arthritis. These subgroups have this in common with Reiter's disease indicating a link between the entities. In persistent palmo-plantar pustulosis an increased incidence of HLA-Bw35 was found. HLA-B13, HLA-B17 and HLA-Bw37 which are found markedly increased in psoriasis vulgaris were in acrodermatitis continua, generalized pustular psoriasis and persistent palmo-plantar pustulosis either absent or not increased as compared with the control population. 7 of 30 patients with localized psoriasis of palms and soles had one of these antigens. Our findings confirm that psoriasis vulgaris and pustular psoriasis as such, seem to be different aetiological entities. Some patients with localized psoriasis of palms and soles may be true psoriatics which besides their psoriasis have a tendency to develop a pustular reaction in their palms and soles similar to persistent palmo-plantar pustulosis.
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PMID:HL-A antigens in pustular psoriasis. 6 58

The Ia alloantigens as measures of different alleles of loci in the major histocompatibility complex were determined in patients with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA). The Ia specificities of reagents used were defined by their pattern of reaction with lymphoblastoid lines derived from normal donors homozygous for HLA-D determinants. The reagent specificities included those associated with a single Dw type as well as those reacting with a single specificity shared by several Dw types. Patients with RA had a marked elevation in the frequency of alloantigens detected by reagent sera that recognize various determinants shared by cell lines from HLA-Dw4, Dw7, or Dw10 individuals (Ia 4-7-10). The frequency of mixed lymphocyte culture alleles Dw4 and Dw10 was found to be increased; however this elevation did not approach the higher frequency for the serologically determined antigens of the Ia 4-7-10 group. In contrast, patients with SLE had an increased frequency of reactions with the reagent alloantisera defined by reactions with either HLA-Dw2 or Dw3 positive cell lines. The data suggest that immunogenetic factors are relevant to both groups of patients, but that these are entirely distinct for each disease.
Arthritis Rheum 1978 Jun
PMID:Contrasting patterns of newer histocompatibility determinants in patients with rheumatoid arthritis and systemic lupus erythematosus. 7 11

This family consists of forty-eight subjects, all of whom have been examined with regard to the presence of psoriasis and nearly all for the presence of arthritic lesions (sacroiliitis and peripheral arthritis). All the members have been tissue-typed not only for HLA-A, B and C locus products but also for D locus products. This has enabled us to study the entire HLA chromosomal region. In the family concerned we have found that those subjects haploidentical with the proband have, to a very large degree, either one or all clinical manifestations, which demonstrates a close genetic relationship between joint (especially sacroiliitis) and cutaneous manifestations. These findings prompt us to repeat our previously made proposal about different phenotypic expressions of the same genotype. In this family study the disease-associated haplotypes did not contain the genes for B13, 17 or 37 antigens which are known to occur frequently in psoriatic patients. However, not all psoriasis patients have these antigens. Despite that, we believe that the gene(s) which increase the likelihood of developing psoriasis are identical in all patients and therefore family studies where the proband does not carry the particular psoriasis associated B-alleles are equally illuminating as to the inheritance pattern of disease.
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PMID:Psoriasis and arthritic lesions in relation to the inheritance of HLA genotypes: a family study. 8 75

There appears to be an association between deficiencies of a number of complement components, particularly of the second component (C2), and rheumatic diseases, especially lupus. The meaning of this association is not clear, but the linkage of deficiency of C2 with HLA, especially HLA-A10, B18, Dw2, as well as with BfS, suggests a possible linkage to immune response genes.
Arthritis Rheum 1978 Jun
PMID:Genetics of complement deficiencies associated with lupus-like syndromes. 9 43

The serum of a 29-year old woman with a recent episode of disseminated gonococcal infection and a history of meningococcal meningitis and arthritis as a child was found to lack serum hemolytic complement activity. The seventh component of complement (C7) was not detected by functional or immunochemical assays, whereas other components were normal by hemolytic and immunochemical assessment. Her fresh serum lacked complement-mediated bactericidal activity against Neisseria gonorrhoeae, but the addition of fresh normal serum or purified C7 restored bactericidal activity as well as hemolytic activity. The absence of functional C7 activity could not be accounted for on the basis of an inhibitor. Opsonization and generation of chemotactic activity functioned normally. Complete absence of C7 was also found in one sibling who had the clinical syndrome of meningococcal meningitis and arthritis as a child and in this sibling's clinically well eight-year-old son. HLA histocompatibility typing of the family members did not demonstrate evidence for genetic linkage of C7 deficiency with the major histocompatibility loci. This report represents the first cases of C7 deficiency associated with infectious complications and suggests that bactericidal activity may be important in host defense against bacteremic neisseria infections.
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PMID:Familial deficiency of the seventh component of complement associated with recurrent bacteremic infections due to Neisseria. 10 May 62

One hundred and twenty-eight of 145 patients with ankylosing spondylitis (AS) were found to be HLA B27 positive. Five patients had evidence of a sero-negative peripheral arthritis resembling peripheral psoriatic arthritis and 3 of these were B27 negative. One further B27 negative patients had a sister with ankylosing spondylitis and ulcerative colitis and a mother with ulcerative colitis. There was evidence of a somewhat later age of onset of symptoms in B27 negative patients. These findings are interpreted as suggesting some degree of clinical and genetic heterogeneity in ankylosing spondylitis with genes for psoriasis and inflammatory bowel disease being important in some individuals, particularly those who are B27 negative. Twenty-five first-degree relatives with ankylosing spondylitis were all B27 positive. The only instance of disassociation of B27 and spondylitis in a family was where the proband had ulcerative colitis as well as spondylitis. Of 13 B27 positive fathers 3 could be diagnosed as having definite ankylosing spondylitis (23%). These findings are thought to provide evidence against the concept that the gene for ankylosing spondylitis is not B27 but a closely linked gene and favour the occurrence of an environmental event affecting approximately one-fifth of B27 positive males to result in disease.
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PMID:HLA B27 and the genetics of ankylosing spondylitis. 10 68


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