Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence favoring genetic predisposition to each of the major classes of rheumatic diseases is reviewed, including juvenile-onset rheumatoid arthritis, rheumatic fever, ankylosing spondylitis and other syndromes associated with spondylitis, adult-onset rheumatoid arthritis, gout and pseudogout, and systemic lupus erythematosus. In addition, simply inherited genetic diseases that may present with arthritis are noted for purposes of differential diagnosis. The importance of heterogeneous causes and mechanisms within each major class of disease is emphasized, both for patient care and for clinical investigation.
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PMID:Genetics of rheumatic diseases. 40 Aug 31

Ten patients with inflammatory disease (rheumatoid arthritis, ankylosing spondylitis, Reiter's disease) or metabolic disease (gout, pseudogout, tendinous xanthomatosis) affecting the Achilles tendons are presented and discussed. Radiological lateral views of heel were obtained with xeroradiographic techniques, which permitted the recording on the same image of details of both bone and soft tissue and the evaluation and quantification of the changes in the Achilles tendons. Xeroradiography seems to be a very suitable radiological technique for routine use in the evaluation and follow up of rheumatic diseases of the foot.
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PMID:Xeroradiographic techniques applied to assessment of Achilles tendon in inflammatory or metabolic diseases. 122 36

Although in higher age degenerative diseases of the spine and joints preponderate, the portion of inflammatory rheumatic diseases is relatively high, and may raise difficult diagnostic problems. Prevalence of rheumatic fever, ankylosing spondylitis, gout and some connective tissue diseases starting in higher age is low and their course is more benign and milder than in earlier age groups. Chondrocalcinosis (pseudogout) and polymyalgia rheumatica are typical rheumatic diseases of higher age. Rheumatoid arthritis with first onset in higher age is also not rare. This disease may start explosively and may run a progressive course. Very hig blood sedimentation rate, early arthritis of shoulder joints and symptoms of a severe general disease often are the leading symptoms. Diagnostic similitarities with other diseases like malignant tumors or with paraneoplastic arthritis may mislead in diagnosis of senile rheumatoid arthritis.
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PMID:[Inflammatory rheumatic diseases in old age]. 704 94

Serum beta-endorphin levels have been determined in patients with a wide variety of rheumatic disorders as well as a group of healthy men and women controls. Normal levels of endorphin have been found in patients with juvenile rheumatoid arthritis. Patients with rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, gout, ankylosing spondylitis, pseudogout and psoriatic arthritis have diminished levels of endorphins. Speculation is offered to explain these changes. Perturbations in endorphins are postulated to be part of the organism's protective mechanism in inflammatory arthritis.
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PMID:Serum beta-endorphin in rheumatic disorders. 716 73

The integrin LFA-1 (CD11a/CD18) is a cell surface adhesion molecule required for leukocyte extravasation and subsequent immune and inflammatory responses. Rapid transition between nonadherent and adherent states of LFA-1 is of key importance to Ag-specific recognition of T lymphocytes. In this paper, LFA-1-mediated adhesiveness of peripheral blood (PB) and synovial fluid (SF) T lymphocytes to affinity-purified ICAM-1-coated plates was studied in patients with rheumatoid arthritis (RA) and in patients with non-RA panels, including osteoarthritis, ankylosing spondylitis, erythema nodosum, pseudogout, and pustulosis. LFA-1-mediated adhesiveness of SF T lymphocytes was not observed in any of the 10 non-RA patients studied, although cross-linking of the TCR on lymphocytes from these patients rapidly converted LFA-1 to an adhesive state. In contrast, SF T lymphocytes from 10 of 12 RA patients exhibited LFA-1-mediated adhesiveness without a requirement for cross-linking of the TCR. No difference was seen in the cell surface density of LFA-1 between non-RA and RA T lymphocytes, suggesting that the difference in adhesiveness was due to a high avidity state of LFA-1 on SF T lymphocytes in RA. Furthermore, exposure of PB T lymphocytes, which showed a low avidity state of LFA-1, to whole SF from RA patients that was depleted of T lymphocytes could induce a high avidity state of LFA-1 in vitro. Cellfree SF from RA patients also could stimulate adhesiveness, although to a lesser extent. These data suggest the existence of a LFA-1-activating environment that is selectively found in SF from RA patients.
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PMID:High avidity state of leukocyte function-associated antigen-1 on rheumatoid synovial fluid T lymphocytes. 756 Nov 25

The objective of this study was to detect strengths and weaknesses in the diagnosis of rheumatic diseases by general practitioners in order to set up post-graduate training accordingly and to assess whether open-ended questions give results comparable with multiple choice-type questions. Fifty-one general practitioners were given eight written cases: rheumatoid arthritis (RA), ankylosing spondylitis (AS), reactive arthritis, psoriatic arthritis (PsA), systemic lupus erythematosus (SLE), gout, polymyalgia rheumatica and pseudogout. Only signs and symptoms were provided. All cases were derived from real patients with a definite diagnosis. Each case was presented in both types of question formats. The cases were also presented to 23 rheumatologists. We found that in the open-ended question format 57.1% of the general practitioners gave the correct answers. Cases of RA, AS, gout and PsA were correctly diagnosed by > 70% of the general practitioners. Cases of polymyalgia rheumatica and reactive arthritis were correctly diagnosed by 55 and 39% of the general practitioners, respectively. The cases of pseudogout and SLE were correctly diagnosed by less than 11% of the general practitioners. Fifty-two per cent of the general practitioners gave the correct answers to the multiple choice-type questions. There was no statistical difference in the correct answers between the open-ended questions and the multiple choice-type questions. We concluded that assuming generalization of the results, training of general practitioners should include polymyalgia rheumatica, reactive arthritis, SLE and pseudogout.
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PMID:Assessing clinical competence: recognition of case descriptions of rheumatic diseases by general practitioners. 778 55

The nucleotide-binding domain, leucine-rich repeat containing family (NLR) network has provided pivotal genetic and molecular insights into diseases that were hitherto regarded as autoimmune. The NLR-related disorders include rare monogenic autoinflammatory diseases collectively termed cryopyrin-associated periodic syndromes, Crohn's disease which is a common polygenic disease and also an association at the mechanistic level with gout and pseudogout. Unlike the classical autoimmune diseases where disease immunopathogenesis is played out primarily in the primary and secondary lymphoid organs, the immunopathogenesis of the NLR-related disorders is played out in the tissues where inflammation arises. As the genetic mutations or molecular cascades associated with the NLR-related disorders have a widespread cellular distribution, it has been somewhat enigmatic why these disorders attack certain territories, but not others. This implies that tissue-specific factors in the target organs themselves contribute to disease expression. Such examples include the high abundance of NOD2 expressing cells in the part of the gut most typically afflicted by Crohn's disease and the preferential deposition of crystals in the joints to where inflammation localises in gout and pseudogout. The NLR network is associated principally with increases in TNF or IL-1 production, both of which are key players in innate immunity. Therefore, the NLR network identifies at the genetic and molecular level a robust paradigm for innate immune activation against self. This tissue-specific-factor-associated inflammation is the diametric opposite of classical autoimmunity. Of note, the MHC class-I-associated diseases including psoriasis (HLA-Cw6) and ankylosing spondylitis (HLA-B27) show striking clinical overlaps with Crohn's disease and also some rare monogenic diseases. Thus, the NLR innate immune pathway allows the full spectrum of inflammation against self to be viewed along an immunological disease continuum with autoantibody-associated disease at one end, innate immune diseases at the other and MHC class-1-related disorders as an intermediate.
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PMID:The NLR network and the immunological disease continuum of adaptive and innate immune-mediated inflammation against self. 1780 42

Most individuals seeking consultation at sports medicine clinics are young, healthy athletes with injuries related to a specific activity. However, these athletes may have other systemic pathologies, such as rheumatic diseases, that may initially mimic sports-related injuries. As rheumatic diseases often affect the musculoskeletal system, they may masquerade as traumatic or mechanical conditions. A systematic review of the literature found numerous case reports of athletes who presented with apparent mechanical low back pain, sciatica pain, hip pain, meniscal tear, ankle sprain, rotator cuff syndrome and stress fractures and who, on further investigation, were found to have manifestations of rheumatic diseases. Common systemic, inflammatory causes of these musculoskeletal complaints include ankylosing spondylitis (AS), gout, chondrocalcinosis, psoriatic enthesopathy and early rheumatoid arthritis (RA). Low back pain is often mechanical among athletes, but cases have been described where spondyloarthritis, especially AS, has been diagnosed. Neck pain, another common mechanical symptom in athletes, can be an atypical presentation of AS or early RA. Hip or groin pain is frequently related to injuries in the hip joint and its surrounding structures. However, differential diagnosis should be made with AS, RA, gout, psudeogout, and less often with haemochromatosis and synovial chondochromatosis. In athletes presenting with peripheral arthropathy, it is mandatory to investigate autoimmune arthritis (AS, RA, juvenile idiopathic arthritis and systemic lupus erythematosus), crystal-induced arthritis, Lyme disease and pigmented villonodular synovitis. Musculoskeletal soft tissue disorders (bursitis, tendinopathies, enthesitis and carpal tunnel syndrome) are a frequent cause of pain and disability in both competitive and recreational athletes, and are related to acute injuries or overuse. However, these disorders may occasionally be a manifestation of RA, spondyloarthritis, gout and pseudogout. Effective management of athletes presenting with musculoskeletal complaints requires a structured history, physical examination, and definitive diagnosis to distinguish soft tissue problems from joint problems and an inflammatory syndrome from a non-inflammatory syndrome. Clues to a systemic inflammatory aetiology may include constitutional symptoms, morning stiffness, elevated acute-phase reactants and progressive symptoms despite modification of physical activity. The mechanism of injury or lack thereof is also a clue to any underlying disease. In these circumstances, more complete workup is reasonable, including radiographs, magnetic resonance imaging and laboratory testing for autoantibodies.
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PMID:Rheumatic diseases presenting as sports-related injuries. 1893 22

The interleukin 1 family is composed by the interleukin 1 (IL-1) and its natural occurring inhibitor, the interleukin 1 receptor antagonist (IL-1Ra). The role of both molecules in rheumatoid arthritis has been widely established, and in this sense new molecules blocking IL-1 actions are under investigation. Anakinra is the recombinant form of IL-1Ra, and has proven to be well tolerated and indicated in the treatment of rheumatoid arthritis. Nevertheless, other molecules such as mAb anti-IL-1 and IL-1 Trap are being developed. Moreover, the recent relation of IL-1 in the inflammasome and pathways of innate immunity has lead to new indications of anti-IL-1 molecules, especially in the autoinflammatory syndromes as well as in other inflammatory diseases. Herein we have performed a review of the literature, limited to English language journals (PUBMED search: combination of descriptors IL-1 and anakinra, systemic juvenile idiopathic arthritis, adult's onset Still's disease, autoinflammatory syndromes, gout, pseudogout, ankylosing spondylitis, and systemic lupus erythematosus from January 1985-December 2008) emphasizing the possible new indications. Although sufficient data is not yet available to fully assess the efficacy and safety of anti-IL-1 molecules in patients with inflammatory disorders other than rheumatoid arthritis, new data is promising.
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PMID:Anti-IL-1 molecules: new comers and new indications. 2004 71

Patients with parathyroid disease can have important musculoskeletal problems.Hypoparathyroidism can cause subcutaneous calcifications, tetany, muscle cramps,and paresthesias, but also myopathies and an ankylosing spondylitis-like back disease. Hypoparathyroidism can occur in SLE caused by antiparathyroid antibodies.Patients with hyperparathyroidism can develop bone disease with cysts, erosions,and deformities. They can also develop pseudogout, gout, myopathies, and tendon ruptures.
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PMID:Parathyroid disease. 2109 44


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