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)

We measured the level of serum haptoglobin, transferrin, alfa-I antitrypsin, orosomucoid, beta-2-microglobulin, ferritin in the case of 30 children (aged 11-16 years) with juvenile chronic arthritis. We divided the patients into two groups. In the first group there were 15 patients with active disease under continuous treatment and in clinical remission (We 20 mm/hour). In the second group there were 15 patients without active disease and they were not given continuous treatment for two Years. These groups were studied, by a control one. If we measure more phase-proteins together, they are suitable for the demonstration of the inflammatory activity in juvenile chronic arthritis. We made a points system for the evaluation of activity.
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PMID:Measurement of the inflammatory activity by the help of serum acute-phase proteins in juvenile chronic arthritis. 172 74

Basic facts are presented of the recently identified and yet clinically very significant complication of chronic artificial kidney treatment -- haemodialysis amyloidosis. The manifestations include the carpal tunnel syndrome, humeroscapular periarthritis, and other types of arthritis, destructive spondyloarthropathy, bone cysts as well as, very probably, visceral involvement. Fully developed, the disease may cause invalidism. The presence of amyloid with beta-2-microglobulin as the main component was proved in articular structures and other localizations. The precise mechanism of the build-up of this amyloid is not known, though a massive and chronic increase in beta-2-microglobulin in the blood of haemodialyzed patients is thought to be mainly responsible. Since beta-2-microglobulin is not normally removed in routine cuprophane haemodialysis, its blood values keep increasing. This phenomenon is reported to be connected with the biocompatibility of the dialysis membrane and, of late, with serum osmolality changes in the course of haemodialysis. While the highly previous membranes used for haemofiltration and haemodiafiltration do remove beta-2-microglobulin the serum levels are never completely normalized. Current research centers on the problem of whether the incidence of dialysis amyloidosis can be reduce by a wider use of on-line haemofiltration.
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PMID:[Dialysis amyloidosis and beta-2-microglobulin]. 265 13

The object of this study was to determine whether levels of beta-2-microglobulin and of rheumatoid factor measured by an enzyme-immunoassay allowed good discrimination between inflammatory and degenerative arthropathies. A multiparametric study of synovial fluid was performed on 85 specimens from patients with rheumatoid arthritis, chondrocalcinosis, mechanical arthritis and traumatic arthopathies. A beta-2-microglobulin level of less than 4 mg/l is a result very mich in favor of a non-inflammatory arthropathy (48/49 cases). The quantification of intra-articular rheumatoid factor allows for reclassification in the context of sero-negative rheumatoid arthritis.
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PMID:[Beta-2-microglobulin and rheumatoid factor levels in the synovial fluid (author's transl)]. 616 49

Serum beta-2-microglobulin (beta 2m) levels, incidence and levels of anti-beta 2m autoantibodies, and quantity of circulating macromolecular complexes containing beta 2m were studied in patients with Felty's syndrome (FS), joint-restricted rheumatoid arthritis (RA), and healthy controls. The serum beta 2m concentrations detected in the FS group (6.95 +/- 2.9 mg/liter) greatly exceeded those of the RA group (3.4 +/- 1.2 mg/liter) and the control group (1.42 +/- 0.69 mg/liter). Autoantibodies to beta 2m were frequent in the FS group. Circulating complexes containing beta 2m, prepared by precipitation in 3% polyethylene glycol, were detected in 65% of FS and 35% of RA patients. In the majority of these cases the solid-phase C1q purified immune complexes also contained beta 2m. Detection of anti-beta 2m antibodies in a significant part of complexes containing beta 2m suggests the presence of specific immune complexes in this fraction of FS and RA patients.
Arthritis Rheum 1983 Jun
PMID:High serum beta-2-microglobulin levels and circulating immune complexes containing beta 2m and anti-beta 2m antibodies in Felty's syndrome. 619 Apr 86

Dialysis-related amyloidosis secondary to beta-2-microglobulin (beta 2m) deposits is a common complication of long-term dialysis patients and is responsible for significant morbidity with potential mortality. Beta 2m amyloid has a propensity to deposit in the osteoarticular tissues, particularly in large bones close to the joint spaces, and in synovial membranes and carpal tunnel tissue. Older age at the onset of dialysis and the duration of dialysis are two important risk factors for development of this disease. The high-flux, more biocompatible membranes have been shown to remove and adsorb beta 2m more efficiently than the cellulosic membranes. This study presents the case of a chronic dialysis patient who developed recurrent arthritis of the left knee, followed by carpal tunnel syndrome; biopsy of the patient's knee showed very large aggregates of beta 2m amyloid deposits in the tendon sheets. A brief review of the literature on this subject is also presented.
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PMID:Beta 2-microglobulin amyloidosis in chronic dialysis patients: a case report and review of the literature. 907 20

Genetic linkage analyses, genome-wide association studies of single nucleotide polymorphisms, copy number variation surveys, and mutation screenings found the human chromosomal 12q24 locus, with the genes SH2B3 and ATXN2 in its core, to be associated with an exceptionally wide spectrum of disease susceptibilities. Hematopoietic traits of red and white blood cells (like erythrocytosis and myeloproliferative disease), autoimmune disorders (like type 1 diabetes, coeliac disease, juvenile idiopathic arthritis, rheumatoid arthritis, thrombotic antiphospholipid syndrome, lupus erythematosus, multiple sclerosis, hypothyroidism and vitiligo), also vascular pathology (like kidney glomerular filtration rate deficits, serum urate levels, plasma beta-2-microglobulin levels, retinal microcirculation problems, diastolic and systolic blood pressure and hypertension, cardiovascular infarction), furthermore obesity, neurodegenerative conditions (like the polyglutamine-expansion disorder spinocerebellar ataxia type 2, Parkinson's disease, the motor-neuron disease amyotrophic lateral sclerosis, and progressive supranuclear palsy), and finally longevity were reported. Now it is important to clarify, in which ways the loss or gain of function of the locally encoded proteins SH2B3/LNK and ataxin-2, respectively, contribute to these polygenic health problems. SH2B3/LNK is known to repress the JAK2/ABL1 dependent proliferation of white blood cells. Its null mutations in human and mouse are triggers of autoimmune traits and leukemia (acute lymphoblastic leukemia or chronic myeloid leukemia-like), while missense mutations were found in erythrocytosis-1 patients. Ataxin-2 is known to act on RNA-processing and trophic receptor internalization. While its polyglutamine-expansion mediated gain-of-function causes neuronal atrophy in human and mouse, its deletion leads to obesity and insulin resistance in mice. Thus, it is conceivable that the polygenic pathogenesis of type 1 diabetes is enhanced by an SH2B3-dysregulation-mediated predisposition to autoimmune diseases that conspires with an ATXN2-deficiency-mediated predisposition to lipid and glucose metabolism pathology.
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PMID:12q24 locus association with type 1 diabetes: SH2B3 or ATXN2? 2493 53