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At least 1,135 records · Page 63Linked to original sources
PubMed1976

Ophthalmic screening of patients receiving ketoprofen or flurbiprofen medication for inflammatory and degenerative joint diseases.

Twenty-seven patients with inflammatory and degenerative arthritis, who had been treated with either ketoprofen and flurbiprofen, for a period of up to twenty-four months, were examined for evidence of ocular toxicity. A practical method for examining the ocular structures and assessing visual function is described. A number of ophthalmic abnormalities were noted but these were related to previous or present eye disease or degeneration. It was considered that no ocular toxic sideeffects could be attributed to either drug during the period of treatment.

Adult↗
PubMed1991

Serum concentrations of hyaluronan and proteoglycan in joint disease. Lack of association.

Circulating hyaluronan originating from the synovial membrane and circulating proteoglycan released from cartilage were determined by specific assays in patients with osteoarthritis (OA), rheumatoid arthritis (RA), reactive arthritis or juvenile chronic arthritis (JCA). Elevated hyaluronan concentrations were found in OA and RA, suggesting proliferation of the synovial membrane in both diseases. The proteoglycan concentrations were highest in OA and polyarticular JCA indicating increased turnover of cartilage matrix. The concentrations of the macromolecules did not correlate except in the group with JCA. Serum concentrations of hyaluronan and proteoglycan thus differ between disease groups and may reflect different aspects of the arthritic process.

Adolescent↗
PubMed1986

Magnetic resonance imaging of joint disease.

MRI is capable of demonstrating superb anatomic detail of the appendicular skeleton and articulations. Disorders of subcortical bone, cartilage, ligaments, and synovium are being evaluated by MRI. MRI should become an increasingly important diagnostic tool in a variety of articular disorders as technical improvements are made and clinical experience accumulates.

Arthrography↗
PubMed1996

Presence of antibodies to native G1 domain of aggrecan core protein in synovial fluids from patients with various joint diseases.

OBJECTIVE: To investigate the occurrence of IgG antibodies to aggrecan in synovial fluids (SF) from patients with arthritis and various articular diseases, and to determine the nature of epitopes present within aggrecan that react with these antibodies. METHODS: SF samples were reacted with native aggrecan, reduced and alkylated aggrecan, chondroitin sulfate, and keratan sulfate, using dot-blots and a novel enzyme-linked immunosorbent assay (ELISA). The nature of the epitopes present on aggrecan was elucidated using Western blots and a competitive inhibition ELISA. RESULTS: IgG antibodies to aggrecan were found in > 50% of the SF samples tested. No IgG antibody reactivity was observed in serum from the same patients. The antibodies appeared to react predominantly with native aggrecan, and there was no disease specificity. It was shown that the epitopes to these antibodies were located within the N-terminal region of the core protein. CONCLUSION: This study demonstrates the frequent occurrence of IgG antibodies to aggrecan in human SF. The major epitope is located in the G1 domain of the aggrecan core protein. These IgG antibodies appear to be produced locally within the synovial cavity, probably in response to various articular diseases, resulting in the loss of native aggrecan from articular cartilage.

Adult↗
PubMed2005

Bone and joint disease associated with primary immune deficiencies.

Primary immune deficiencies (PIDs) are characterized by functional and/or quantitative abnormalities of one or more immune system components. Several bone and joint abnormalities can occur in patients with PID, with arthritis being the most common. Joint manifestations, of which arthritis is the most common, occur chiefly in humoral PIDs (agammaglobulinemia, common variable immunodeficiency, hyper-IgM syndromes, and IgA deficiency) and occasionally in other PIDs (chronic granulomatous disease and Wiskott-Aldrich syndrome). Monoarthritis or oligoarthritis is the usual pattern, although polyarthritis may occur, occasionally with nodules suggesting rheumatoid arthritis. Arthritis in patients with PID is usually infectious in nature, the most common causative organism being Mycoplasma, followed by Staphylococcus, Streptococcus, and Haemophilus. These bacteria can induce not only synovial infections, but also aseptic arthritogenic inflammatory responses. Arthritis having no demonstrable relation to chronic infection has been reported also and ascribed to dysimmunity-driven mechanisms that exhibit a number of specific features. Bone lesions are far less common and usually due to infections complicating humoral PID. Distinctive bone manifestations occur in a number of rare PIDs (e.g., hyper-IgE syndrome and Di George syndrome) and in syndromes characterized by spondyloepiphyseal dysplasia. Familiarity with PID syndromes both enhances the diagnostic capabilities of physicians and provides insight into the pathophysiology of bone and joint abnormalities associated with immune dysfunction. In children and occasionally in adults, a combination of bone and/or joint manifestations and hypogammaglobulinemia may indicate PID. When there is no evidence of lymphoproliferative disease, infection, or iatrogenic complications, investigations for PID should be obtained. PID-related arthritis is a unique model for studying the pathogenesis of presumably postinfectious arthritis and of inflammatory joint diseases including rheumatoid arthritis.

Agammaglobulinemia↗
PubMed2005

Patients with antinuclear antibody-positive juvenile idiopathic arthritis constitute a homogeneous subgroup irrespective of the course of joint disease.

OBJECTIVE: We recently hypothesized that in the International League of Associations for Rheumatology (ILAR) classification of juvenile idiopathic arthritis (JIA), the presumably homogeneous patient group characterized by early onset of disease, a female predilection, the presence of antinuclear antibodies (ANA), asymmetric arthritis, and the risk for iridocyclitis is classified into different categories. We sought to investigate whether ANA-positive patients belonging to the ILAR categories of oligoarthritis and rheumatoid factor (RF)-negative polyarthritis share homogeneous features and to compare these features with those of ANA-negative patients with JIA in the same categories. METHODS: We identified patients who were followed up during a 15-year period. All patients had JIA according to the ILAR criteria, with oligoarticular or polyarticular onset. ANA positivity was defined as 2 or more positive results at a titer of >or=1:160. Demographic and clinical features, including the number of joints involved over time and measures of JIA severity at the last followup visit, were recorded retrospectively. RESULTS: A total of 256 patients were included: 190 were ANA positive (109 had persistent oligoarthritis, 48 had extended oligoarthritis, and 33 had RF-negative polyarthritis), and 66 were ANA negative (35 had RF-negative polyarthritis, and 31 had oligoarthritis). All patients who were positive for ANA were similar in terms of age at disease presentation, female-to-male ratio, and frequency of symmetric arthritis and iridocyclitis. Compared with ANA-positive patients with polyarticular disease, ANA-negative patients with polyarticular arthritis were older at disease presentation and had a lower frequency of iridocyclitis, a higher frequency of symmetric arthritis, a greater cumulative number of joints affected over time, and a different pattern of joint disease, with a greater frequency of shoulder and hip involvement. The strong relationship between the presence of ANA and younger age at disease presentation, asymmetric arthritis, and development of iridocyclitis was confirmed by multivariate regression analysis. CONCLUSION: Our results support the hypothesis that patients with similar characteristics are currently classified into different JIA categories. The value of ANA positivity as a possible modifier of the current classification system deserves consideration.

Antibodies, Antinuclear↗
PubMedDate not supplied

[Roentgenologic determination of degenerative joint diseases in a new animal experiment arthrosis model].

Our previous experiments have shown that intraarticular injections of sodium iodoacetate or phenylbutazone into the knee joint of animals (hens) induce degeneration of the articular tissues. This method proved to be a useful model for experimental osteoarthrosis. After autopsy degenerative processes in the joint can be evaluated by macroscopical, histological and biochemical techniques, and show good correlations with osteoarthrosis in humans. To study the onset and progress of experimentally induced osteoarthrosis in living animals we developed a new X-ray method using special mammography-film (Kodak Definix Medical). By this technique also changes of the joint space can be measured quantitatively. Comparison between the degenerative lesions of cartilage as seen macroscopically during autopsy and the data obtained from the living animal by X-ray techniques show excellent correlations. By using X-ray mammography film in our studies of experimental model it is possible to observe the pathological alterations of the knee joint of the living animals and to investigate the effect of pharmacologically active compounds for the treatment of osteoarthrosis.

Animals↗
PubMed1981

[Joint diseases as the early clinical symptom of hemochromatosis].

In three patients arthropathy was the earliest symptom of hemochromatosis. Two of these patients had a precirrhotic stage of hemochromatosis. The liver histology of the third patient showed a beginning cirrhosis. The serum iron ranged from 212 to 260 micrograms/dl. The transferrin saturation was 95-100%. Serum iron and transferrin should be determined in all patients with arthralgias, since arthropathy may be the first clinical sign of hemochromatosis.

Diagnosis, Differential↗
PubMed1987

Unruptured abdominal aortic aneurysm mimicking hip joint disease.

A 66-year-old man with an 8-month history of progressive left hip pain was found to have a large unruptured infrarenal aortic aneurysm. The hip pain abated after aneurysm repair. His clinical picture suggested that the hip pain was caused by aneurysmal sac encroachment upon a nerve branch of the lumbar plexus. We report this previously unrecognized association to heighten awareness of this atypical but potentially life threatening cause of hip pain.

Aged↗
PubMed1987

Effect of iron chelation on inflammatory joint disease.

Mild iron deficiency induced by treatment with the iron chelator desferrioxamine reduced the incidence and severity of joint inflammation associated with adjuvant disease in rats but did not alter the local primary inflammatory response or the systemic sequelae. Both rats treated with desferrioxamine and control rats showed increased levels of alpha 1 acid glycoprotein, characteristic pathological changes in the liver and inguinal lymph nodes, and the primary inflammatory response at the site of injection. Histology, microfocal radiography, and gross assessment of the joints, however, showed a suppression or reduction in soft tissue swelling and bone erosion in the rats treated with desferrioxamine. This is a novel observation suggesting an apparently selective influence of iron on joint mediated inflammation.

Animals↗
PubMed1983

Prognosis of inflammatory joint diseases. A three-year follow-up study.

The prognosis 3 years after the onset of the disease was studied in 107 patients with definite rheumatoid arthritis, 161 with probable RA or non-specific arthritis, 84 with either ankylosing spondylitis, Reiter's disease or reactive arthritis, 14 with psoriatic arthritis and 10 with a systemic connective tissue disease. Prognosis was measured by clinical involvement of joints, radiological erosions in joints, deterioration in joint function, ESR, and working ability. A total of 44% of all patients were symptomless after 3 years. The prognosis was best in patients with an "HLA B 27-associated" disease and non-specific arthritis, and worst in RA. Two patients died during the follow-up of systemic connective tissue disease and one committed suicide with an overdose of hydroxychloroquine. Two HLA B27-positive patients developed systemic amyloidosis.

Arthritis↗
PubMed1994

[The test of the synovial fluid in microcrystalline joint diseases].

The search for crystals in the synovial fluid must be carried out promptly and is very helpful in the diagnosis of microcrystalline arthropathy. If at light microscopy the fluid is negative for crystals and negative or weakly positive for alizarin red, and if the diagnosis is nevertheless suspected, analysis of the centrifuged fluid sediment facilitates the identification of crystals and increases the specificity of alizarin red (the specific stain for crystals) in the identification of apatite crystal deposits. Electronmicroscopy can the be used to confirm the presence or absence of crystals.

Apatites↗
PubMed1998

Immunohistochemical localization of metallothionein in synovial tissue of patients with chronic inflammatory and degenerative joint disease.

Metallothioneins (MTs) are low-molecular-weight cytosolic proteins, which are thought to participate in metal homeostasis and protection against metal toxicity and oxidative stress. MT synthesis can be induced by a variety of inflammatory mediators and antirheumatic drugs, and high levels of MT have been implicated in resistance of cells to some antirheumatic drugs. We studied the expression and localization of MT in synovial tissue samples from patients with rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis or osteoarthritis (OA) by quantitative immunohistochemistry. Immunostaining for MT was detected in a large number of intimal lining cells in most of the investigated synovial tissue samples (75%). In a smaller proportion of samples (42%), some of the fibroblast-like cells of the subsynovial layer were also MT positive. Immunostaining and double-staining experiments with antibodies against monocyte-, macrophage- and leucocyte-associated antigens suggested that most of the MT-positive cells were intimal fibroblast-like cells and subsynovial fibroblasts. However, there were no statistically significant differences in the intensity of staining for MT between the rheumatic diseases and OA at the single-cell level. Thus, MT is expressed in synovial tissue and may participate in homeostatic and protective functions. The interindividual variability in the expression of MT in synovial tissue may be related to the therapeutic efficacy of the gold compounds and chemotherapeutic antirheumatic drugs sequestered by MT.

Adolescent↗
PubMed1975

Immunopathological changes in rheumatoid arthritis and other joint diseases.

A comparative study of the distribution of immunoglobulins G, M, and A and C3 in the synovium and inside synovial fluid leucocytes and of the relative levels of IgG, IgM, AND C3 in paired samples of serum and synovial fluid from both seropositive and seronegative patients with rheumatoid arthritis and other types of non-infective synovitis shows that although there is no distinctive immunopathological feature of rheumatoid arthritis, the incidence of immune complexes containing IgG and IgM with and without detectable C3 in the affected synovium or inside synovial fluid granulocytes is higher in rheumatoid arthritis and especially so in seropositive cases. The mean level of C3 in synovial fluid from patients with rheumatoid arthritis is lower than that from the group without rheumatoid arthritis. In contrast to previous reports, extracellular clumps of IgA could be detected in the affected synovium of a number of affected patients. Aggretated human IgG could be bound by some of the synovial biopsies and synovial fluid leucocytes from both seropositive and seronegative rheumatoid arthritis patients. Antinuclear factor and rheumatoid factor could be detected in the synovial fluid but not in the serum of several patients suggesting either selective sequestration or local synthesis of antinuclear and rheumatoid factors in the affected joints.

Antibodies, Antinuclear↗