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)

We, in this study, report a 72-year-old woman presenting with premature osteoarthritis of the spine, the hips, the knees and the shoulders symptomatic since the age of 50 years. The initial presentation of backache led to a mistaken diagnosis of ankylosing spondylitis. Subsequent manifestation of characteristic discoloration of her sclera and overnight dark urine led to the correct diagnosis of ochronosis.
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PMID:Premature arthritis in an elderly woman. 1685 58

The present study surveys the problems of diagnostics of early ankylosing spondylitis (AS) and axial spondylarthritis (SpA). Epidemiologic studies repeatedly identified seven- to nine-year delay of diagnosis of AS from its development to its first manifestations. Delayed diagnostics is caused both by unfamiliarity of rheumatologists with the disease and the inappropriateness of New York classification criteria for early stages of AS. In this study, we suggest diagnostic algorithms allowing high probability diagnosis of AS/axial in X-ray silent stage (the so-called pre X-ray stage). Spondylarthritis represents approximately 5% of a total number of chronic low back pain (CLBP) cases. The probability grows up to 15% with the presence of inflammatory character of back pain. The presence of HLA B 27 increases the probability to 59% and the occurrence of other 1 or 2 clinical signs raises the probability up to 90%. Probability reaches 95% with positive MRI. The overall concept requires verification of new samples in a prospective study. After certification of such study, it will be possible to use biological medications for much more efficient therapy of patients in early AS stages.
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PMID:[Early diagnosis of ankylosing spondylitis]. 1696 15

The term 'spondyloarthritis', which is preferred to 'spondyloarthropathy', refers to a group of similar diseases with distinct clinical features and a common genetic predisposition, rather than one disease with different clinical presentations. Mainly for clinical purposes, five disease subtypes are recognized: ankylosing spondylitis (AS), psoriatic spondyloarthritis, reactive spondyloarthritis, spondyloarthritis associated with inflammatory bowel disease, and undifferentiated spondyloarthritis. Irrespective of the disease subtype, the main clinical manifestations of spondyloarthritides are inflammatory back pain, peripheral arthritis, enthesitis and anterior uveitis, while other organ manifestations are rare. The need for a standardized, evidence-based approach to disease classification led to the development of the European Spondyloarthropathy Study Group preliminary criteria for spondyloarthritis in 1991, which confirmed the unifying concept of this group of diseases. In the past 10 years, the work of the European Spondyloarthropathy Study Group has been taken over by the Assessments in AS working group. There is still a considerable delay in diagnosis of AS and, because of the well-documented efficacy of anti-tumor-necrosis-factor therapy for all spondyloarthritis subtypes, diagnostic criteria (especially for early forms of spondyloarthritis) are needed. Diagnosis can be achieved by determination of the predominant clinical manifestation, and by the inclusion of sensitive diagnostic tools for early disease (such as HLA-B27 genotype and MRI) in the criteria set. In addition, because of the high incidence of back pain in affected individuals, the development of practical screening parameters that facilitate referral to the rheumatologist is important.
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PMID:Early diagnosis of spondyloarthritis. 1701 79

Research that explores being a parent or grandparent with musculoskeletal problems has been fairly limited to date. The aim of this study was to describe the experience of parenting in the context of back pain (BP), ankylosing spondylitis (AS) and rheumatoid arthritis (RA), with a particular focus on the extent and nature of childcare experiences and to compare these experiences across the three groups. In addition, the possible reasons for these reported experiences, the availability of advice and support and the development of strategies for coping were explored using a cross-sectional descriptive survey. A total of 448 participants was recruited from relevant charitable organizations and the National Health Service (280 with BP, 106 with AS and 62 with RA). A combination of opportunistic and random sampling was used. Quantitative data were analysed with appropriate descriptive and inferential statistics using Statistical Package for the Social Sciences (SPSS version 10). Qualitative data were analysed using content analysis. Results indicate that a high proportion of all groups experienced a wide range of difficulties with parenting (81% BP, 77% AS, 97% RA). The most prevalent problems were similar for all three groups: lifting baby/child from the floor or cot, encouraging children/grandchildren to help with domestic chores and keeping up (in terms of energy) with children/grandchildren. However, the RA group reported having greater difficulties than the other two groups. Very little advice was offered to participants with parenting difficulties which may indicate a gap in service provision. However, a wide range of strategies for coping were described by respondents. The study highlighted a need for healthcare professionals to develop a greater awareness of parenting issues and to provide opportunities for these issues to be addressed.
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PMID:Being a parent or grandparent with back pain, ankylosing spondylitis or rheumatoid arthritis: a descriptive postal survey. 1704 65

Back pain is a frequent complaint seen in neurological practice. In evaluating back pain, neurologists are asked to evaluate patients for radiculopathy, determine whether they may benefit from surgery, and help guide management. Although disc herniation is the most common etiology of compressive radiculopathy, there are many other causes, including genetic disorders. This article is a discussion of genetic disorders that cause or contribute to radiculopathies. These genetic disorders include neurofibromatosis, Paget's disease of bone, and ankylosing spondylitis. Numerous genetic disorders can also lead to deformities of the spine, including spinal muscular atrophy, Friedreich's ataxia, Charcot-Marie-Tooth disease, familial dysautonomia, idiopathic torsional dystonia, Marfan's syndrome, and Ehlers-Danlos syndrome. However, the extent of radiculopathy caused by spine deformities is essentially absent from the literature. Finally, recent investigation into the heritability of disc degeneration and lumbar disc herniation suggests a significant genetic component in the etiology of lumbar disc disease.
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PMID:Genetic disorders producing compressive radiculopathy. 1704 53

Ankylosing spondylitis is a common inflammatory rheumatic disease that affects the axial skeleton, causing characteristic inflammatory back pain, which can lead to structural and functional impairments and a decrease in quality of life. New imaging techniques and therapies have substantially changed the management of this disease in the past decade. Whether inhibition of radiographic progression and structural damage can be reached with available drugs is as yet unclear. Furthermore, treatment with non-steroidal anti-inflammatory agents and physiotherapy remains an important approach to long-term management of patients with ankylosing spondylitis. The new treatment options with tumour necrosis factor blockers seems a breakthrough for patients refractory to conventional treatment.
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PMID:Ankylosing spondylitis. 1761 67

Low back pain (LBP) is a common medical problem. Interaction between genetic and environmental factors predisposes individuals to LBP even at an early age. Inflammatory back pain or spondylarthropathies include ankylosing spondylitis (AS), psoriatic arthritis (PSA), reactive arthritis enteropathic and undifferentiated arthropathies. Angiotensin-converting enzyme (ACE) plays an important role in circulatory homeostasis, physiology of vasculature and inflammation. The insertion-deletion (I/D) polymorphism of the ACE gene has been shown to determine the plasma and tissue levels of ACE especially in the synovial fluid. The aim of this study was to investigate an association between ACE gene I/D polymorphism and inflammatory back pain (spondylarthropathies) secondary to ankylosing spondylitis (AS), psoriatic arthritis, inflammatory bowel disease and undifferentiated spondylarthropathies. The prevalence of ACE gene I/D polymorphism genotypes was determined in 63 patients with inflammatory back pain by polymerase chain reaction (PCR) and compared with that in 111 healthy controls. Of the 63 patients studied, 45 (71.4%) were with AS, 13 (20.6%) were with PSA, 4 (6.3%) were with reactive arthropathy and 1 (1.6%) manifested undifferentiated arthropathy. There were 43 males and 20 females. Mean age of patients was 39.0+/-11.36 years, age at onset of spondylarthropathy was 27.7+/-7.49 years and disease duration was 10.3+/-7.74 months. The controls were selected to match with the patients group in terms of gender ratio, age and ethnicity. The ACE gene polymorphism showed an overall significant difference between patients and controls (p=0.050). When the ID and II genotype frequency was combined and compared with that for DD genotype amongst patient and control groups, a considerably higher incidence was detected for ID and II genotypes than the DD genotype in spondylarthropathy patients compared to that in the controls (p=0.036). This study showed a significant association of the I-allele of ACE gene I/D polymorphism with spondylarthropathy in Kuwaiti Arabs.
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PMID:Association of angiotensin-converting enzyme (ACE) gene insertion-deletion polymorphism with spondylarthropathies. 1771 61

Diagnosis of ankylosing spondylitis is still delayed by many years. Several efforts have been made in the past few years to shorten this delay. A new set of criteria for inflammatory back pain has performed better than previous sets. MRI has evolved to become the standard imaging modality for the detection of sacroiliitis during early disease, and it clearly outperforms quantitative scintigraphy, which was the standard screening test for many years. Promising new developments such as whole body MRI and ultrasound (sonography) for the detection of enthesitis or sacroiliitis deserve further evaluation. Serum antibodies directed against a 28-kD Drosophila antigen may provide additional diagnostic information. A recently proposed diagnostic algorithm in patients with suspected early ankylosing spondylitis may help physicians confidently diagnose patients before definite radiographic sacroiliitis is detectable. Finally, referral strategies for patients seen by primary care physicians seem to work well and are currently under further valuation.
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PMID:Diagnosing early ankylosing spondylitis. 1791 92

Low back pain is a frequent symptom to consult the general practioner or the osteo-articular specialist. It is important to identify patients with inflammatory back pain (5 to 10 %) because the management and the treatment are different. Spondylarthropathies, especially ankylosing spondylitis (AS) are the most frequently encountered. The inflammatory characteristics of pain give clues for the diagnosis and allow to make appropriate management. Biological tests and imaging from X rays to MRI are used. As therapy is primarily based on NSAID use, in case of unsatifactory response in peripheral arthritis, disease modyfing drugs such as salazopyrine and methotexate (MTX) are used. Anti TNF are used in AS patients unresponsive to previous therapy (infliximab, etanercept, adalimumab) with a response in 50% of the patients. Etanercept is however not indicated in patients with uveitis.
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PMID:[Inflammatory low back pain]. 1795 23

A guideline on pelvic girdle pain (PGP) was developed by "Working Group 4" within the framework of the COST ACTION B13 "Low back pain: guidelines for its management", issued by the European Commission, Research Directorate-General, Department of Policy, Coordination and Strategy. To ensure an evidence-based approach, three subgroups were formed to explore: (a) basic information, (b) diagnostics and epidemiology, and (c) therapeutical interventions. The progress of the subgroups was discussed at each meeting and the final report is based on group consensus. A grading system was used to denote the strength of the evidence, based on the AHCPR Guidelines (1994) and levels of evidence recommended in the method guidelines of the Cochrane Back Review group. It is concluded that PGP is a specific form of low back pain (LBP) that can occur separately or in conjunction with LBP. PGP generally arises in relation to pregnancy, trauma, arthritis and/or osteoarthritis. Uniform definitions are proposed for PGP as well as for joint stability. The point prevalence of pregnant women suffering from PGP is about 20%. Risk factors for developing PGP during pregnancy are most probably a history of previous LBP, and previous trauma to the pelvis. There is agreement that non risk factors are: contraceptive pills, time interval since last pregnancy, height, weight, smoking, and most probably age. PGP can be diagnosed by pain provocation tests (P4/thigh thrust, Patrick's Faber, Gaenslen's test, and modified Trendelenburg's test) and pain palpation tests (long dorsal ligament test and palpation of the symphysis). As a functional test, the active straight leg raise (ASLR) test is recommended. Mobility (palpation) tests, X-rays, CT, scintigraphy, diagnostic injections and diagnostic external pelvic fixation are not recommended. MRI may be used to exclude ankylosing spondylitis and in the case of positive red flags. The recommended treatment includes adequate information and reassurance of the patient, individualized exercises for pregnant women and an individualized multifactorial treatment program for other patients. We recommend medication (excluding pregnant women), if necessary, for pain relief. Recommendations are made for future research on PGP.
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PMID:European guidelines for the diagnosis and treatment of pelvic girdle pain. 1838 93


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