Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-term treatment with oral carotenoids in 57 patients suffering from a variety of photodermatoses and disorders associated with cutaneous light sensitivity was evaluated. All patients were treated for two or more 6-month periods in separate years. Best therapeutic results were seen in PMLE patients, a good to excellent therapeutic response was noted for 65% of all patients, increasing to 81% of those assigned to skin types III and IV, and decreasing to 47% of those with skin types I and II. The therapeutic effect observed in disorders characterized by other mechanisms than provocation by solar radiation per se was less conspicuous, viz. for light-sensitive psoriasis and lupus erythematosus. Even here, therapeutic failure seems to be more common in individuals with skin types I and II than for skin types III and IV. Photodermatoses such as persistent light reaction, actinic reticuloid and solar urticaria did not respond to any significant degree to carotenoid treatment. Our findings would appear to justify further treatment with oral carotenoids in selected cases of PMLE, and a higher dosage level may be tried for non-responding individuals with light-sensitive psoriasis and DLE or SLE. Serious side effects have not been observed in spite of long-term therapy lasting several years.
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PMID:Carotenoid treatment for light sensitivity: a reappraisal and six years' experience. 615 29

Vasculitis due to immunological mechanisms is caused by attachment of immune-complexes to the wall of vessels. This occurs in capillaries causing dysfunction and damage or organs or in other vessels causing isolated vasculitis. Regularly, also serositis can be seen. Best known examples are systemic lupus erythematosus and serum-sickness. Diagnosis refers to the detection of antigen and antibody or of immune-complexes. Steroids and antiinflammatory as well as immunosuppressive drugs are used for therapy. During the acute phase also plasmapheresis is of benefit.
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PMID:[Immunological vasculopathies]. 714 66

The aim of this study was to measure the urinary excretion of the pyridinium cross-links of collagen and to determine their usefulness as markers of reduced bone mineral density in systemic lupus erythematosus (SLE). All female SLE patients managed at a single centre were invited to participate in a cross-sectional study of urinary pyridinium cross-links excretion (HPLC), bone mineral density (DXA), and SLE-related variables. Ninety-one women with SLE were studied, 35 of whom were postmenopausal. Pyridinoline/Creatinine (Pyd/Cr) and deoxypyridinoline/Cr (Dpd/Cr) levels in postmenopausal women were significantly increased compared with premenopausal values (p = 0.010 and p = 0.004, respectively). Univariate linear regression analysis revealed a significant association of Dpd/Cr with reduced femoral neck and lumbar spine BMD (p = 0.001, p<0.001), and of Pyd/Cr with reduced femoral neck BMD (p = 0.020). In addition, the association of Pyd/Cr with reduced lumbar spine BMD approached significance (p = 0.055). Stepwise multiple linear regression analysis adjusting for other variables confirmed a significant association of Dpd/Cr with reduced lumbar spine BMD (p = 0.006), and a significant association of both Pyd/Cr and Dpd/Cr with postmenopausal status (p = 0.003, p<0.001). It was concluded that in this SLE population, the urinary excretion of Dpd/Cr was a useful marker of reduced BMD at the lumbar spine. Menopausal status was a major predictor of cross-links excretion in SLE.
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PMID:Urinary excretion of the pyridinium cross-links of collagen in systemic lupus erythematosus. 977 7

Recent studies have shown that systemic lupus erythematosus (SLE) is associated with a loss of trabecular bone. However, these changes have not been not described in patients with SLE at the time of diagnosis. To investigate the markers of bone metabolism 20 female patients with a recently manifested clinical picture of SLE were selected. All patients included in this study met the ARA criteria (for classification) of SLE. For comparison, 35 female patients with SLE, which had previously manifested itself and which had been treated with glucocorticoids, were included in a second group. A control group (III) consisting of 20 healthy individuals of the same age was formed to compare the results obtained. Test parameters comprised both serum levels of osteocalcin (OC) as the marker for bone formation and crosslinks excretion (CE) in urine as a specific marker for bone resorption. The bone density (BMD) was examined by dual energy X-ray absorption (DEXA) of the vertebral column (L2-L4), femoral neck, Ward's triangle and trochanter. The patients under study received either no medication or nonsteroidal antirheumatic drugs. The BMD of the vertebral column was significantly lower than expected in SLE-afflicted subjects of group II when compared with the age-matched normal female controls. The reduction of BMD in female patients with SLE was related to the significantly increased excretion of urinary pyridinoline, to hypoparathyroidism, and to the decrease in serum OC. Bone loss in women with fresh manifestation of SLE (I) increases to a degree similar to that of patients in group II. Lowered BMD predicts an increased risk for bone fractures. Therefore, female premenopausal SLE patients should be monitored for osteoporosis.
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PMID:Bone metabolism and bone mineral density of systemic lupus erythematosus at the time of diagnosis. 1022 Aug 33

Patients whose symptoms include widespread, diffuse musculoskeletal pain are commonly referred for rheumatological evaluation, even when the underlying cause may lie out with the remit of rheumatology. A diagnosis of fibromyalgia may seem highly probable even from the referral letter, or after a few leading questions during the consultation. However, the lack of specificity of the many symptoms associated with widespread pain means that other diagnoses have to be considered. The history and examination must bear in mind alternative and concomitant musculoskeletal disorders, such as mild systemic lupus erythematosus, polyarticular osteoarthritis, rheumatoid arthritis, polymyalgia rheumatica, hypermobility syndromes and even osteomalacia. Non-rheumatological diseases may also have symptomatic similarities to fibromyalgia, including neoplastic and neurological diseases, hypothyroidism and other endocrine disorders, chronic infections, as well as a variety of psychiatric conditions. A rational approach to investigation will usually allow other diagnostic possibilities to be excluded without reinforcing the abnormal illness behaviour so common in chronic pain states.
Baillieres Best Pract Res Clin Rheumatol 1999 Sep
PMID:The differential diagnosis of generalized pain. 1056 69

The clinically relevant antiphospholipid antibodies (APA) include anticardiolipin antibodies and lupus anticoagulant. Most autoimmune APA require the presence of a cofactor for phospholipid binding, and the growing list of candidate cofactors has prompted redefinition of APA to 'antiphospholipid protein antibodies'. Current evidence favours beta2-glycoprotein I (beta2GPI) and prothrombin as the primary antigens for anticardiolipin antibodies and lupus anticoagulant respectively. Patients with APA show a predisposition for venous and arterial thromboembolism, recurrent fetal loss, thrombocytopenia and a number of neurological syndromes and miscellaneous conditions. The association between APA and thrombosis has been well documented, but a definite mechanism remains to be clarified. Proposed mechanisms have included disruption of endothelial regulatory processes, impairment of fibrinolysis, augmented platelet activation and/or adhesion, inhibition of antithrombin activity and negation of the anticoagulant effects of beta2GPI and annexin V. In this review we describe recent insights into the role of beta2GPI as a natural anticoagulant, the procoagulant effects of APA on the Protein C system, the interactions between APA and prothrombin resulting in augmentation of thrombin generation, and cellular expression of Tissue Factor in patients with APA. Cellular immunity to beta2GPI is also discussed. Elucidation of these pathophysiological mechanisms may shed further light on the association between APA and thrombosis.
Baillieres Best Pract Res Clin Haematol 1999 Sep
PMID:Recent insights into antiphospholipid antibody-mediated thrombosis. 1085 78

Since the original description of mixed connective tissue disease (MCTD) as an apparently unique syndrome by Sharp and co-workers, the concept of MCTD has been highly controversial. In this chapter, a quarter of a decade later, we examine the evidence that MCTD is a distinctive entity rather than a haphazard association of clinical and serological features and that the presence of high titres of autoantibodies to UIRNP influences the expression of connective tissue disease in ways that are relevant to prognosis and treatment. Results of longterm clinical studies are presented, which show that the clinical phenotype of MCTD is robust and can be defined by classification criteria that show reasonable sensitivity and specificity. In addition, the chapter addresses the results of immunogenetic and serological studies that demonstrate that MCTD is quite distinctive from systemic lupus erythematosus and systemic sclerosis. Indeed, there is good evidence that the clinical and serological features of MCTD are not just a haphazard association but that these patients represent a distinctive subset of connective tissue disease in which the specific autoimmune response is relevant to clinical expression and to understanding the underlying pathogenesis.
Baillieres Best Pract Res Clin Rheumatol 2000 Mar
PMID:Mixed connective tissue disease: overlap syndromes. 1088 17

The association of thromboses and/or cytopenias with anti-phospholipid antibodies (aPL), the anti-phospholipid syndrome (APS), is well recognized. The syndrome may be primary or occur within systemic lupus erythematosus (SLE). The notion of the syndrome occurring within SLE is important since patients found to have aPL may be at risk for developing APS manifestations, those who develop some manifestations may be at risk for developing others and, finally, SLE patients with this syndrome may need special treatment. There are subtle differences between the primary and the secondary forms, mostly due to the frequently higher and more persistent autoantibody levels in the primary and the influence of lupus in the secondary. These syndromes may be related to various antigen/antibody systems in which phospholipids participate either directly or through their effect on the proteins that bind them. Similar clinical manifestations also occur in patients who have serum antibodies to such proteins (e.g. beta2-glycoprotein-I) in the absence of phospholipid. Some of these antibodies may even be more important pathogenically than the antibodies against cardiolipin that were originally described. Testing for the latter is, however, still the first choice when suspecting an antiphospholipid syndrome. If this is negative in this situation, a search for the other autoantibodies is indicated.
Baillieres Best Pract Res Clin Rheumatol 2000 Mar
PMID:The anti-phospholipid antibody syndrome: clinical and serological aspects. 1088 19

Malignant neoplasms are associated with a wide variety of paraneoplastic rheumatological syndromes. Among these, hypertrophic osteoarthropathy, carcinoma polyarthritis, dermatomyositis/polymyositis, and paraneoplastic vasculitis are the most frequently recognized. Other less known associations are based upon a smaller number of reported patients, and include fasciitis, panniculitis, erythema nodosum, Raynaud's syndrome, digital gangrene, erythromelalgia and lupus-like syndromes. Musculoskeletal manifestations of malignancy may coincide, follow or antedate the diagnosis of cancer, or herald its recurrence. The clinical course generally parallels that of the primary tumour, and treatment of the underlying malignancy often results in regression of the rheumatic disorder. Awareness that cancer can cause certain non-metastatic symptoms is important for early diagnosis and treatment of an occult neoplasm. Rheumatic manifestations suggesting a hidden cancer include: rapid onset of an unusual inflammatory arthritis clubbing or diffuse bone pains in a patient 50 years of age or older, chronic unexplained vasculitis, refractory fasciitis, Raynaud's syndrome unresponsive to vasodilator therapy, rapidly progressive digital gangrene or Lambert-Eaton myasthenic syndrome. Management consists of control of the underlying cancer and symptomatic treatment of the rheumatic syndrome with non-steroidal anti-inflammatory drugs or corticosteroids.
Baillieres Best Pract Res Clin Rheumatol 2000 Sep
PMID:Paraneoplastic rheumatic syndromes. 1098 84

The prevalence and disability rate of rheumatic diseases are increasing. It seems that non-medical causes play an important role in the morbidity, disability and mortality of these patients. Efforts to reduce their impact are extremely important. Patient education is thought to be one way to limit disability in rheumatic diseases and to achieve an improvement in quality of life. In this chapter, we review the influence of non-medical causes of morbidity on disease outcome, some basic aspects of education and the evidence of the effectiveness of patient education in diseases such as ankylosing spondylitis, systemic lupus erythematosus, rheumatoid arthritis and fibromyalgia syndrome.
Baillieres Best Pract Res Clin Rheumatol 2000 Dec
PMID:How important is patient education? 1109 96


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