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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nineteen patients with different clinical subsets of cutaneous lupus erythematosus (LE) were treated with the aromatic retinoid etretinate. In 11 of them excellent or good treatment results were obtained within two to six weeks. Best response to etretinate therapy was seen in male patients with discoid lupus erythematosus. Etretinate should prove a valuable drug in LE therapy.
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PMID:Treatment of cutaneous lupus erythematosus with etretinate. 241 87

Twenty-four in- or out-patients (12 males and 12 females) with chronic cutaneous (CCLE) (n = 19) or subacute cutaneous (SCLE) (n = 5) lupus erythematosus have been treated with oral isotretinoin. The initial dose 0.15 mg/kg/day was progressively increased to a maximum of 0.50 mg/kg/day; the total treatment period was 16 weeks. One female patient with SCLE stopped the therapy for sudden fever. None of the other known side effects induced interruption of treatment. In 20 subjects (86.9%) isotretinoin therapy was associated with clearing or improvement of clinical lesions and histopathologic changes. Best responses with isotretinoin therapy was seen in patients with CCLE. No changes were observed in the laboratory parameters before, during, and at the end of the study. In the light of these results, isotretinoin can be considered as an effective and well-tolerated drug in the treatment of cutaneous lupus erythematosus.
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PMID:[Use of oral isotretinoin in the treatment of cutaneous lupus erythematosus]. 263 Apr 41

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

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

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

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease, as yet of unknown aetiology, with diverse clinical manifestations and a variable course and prognosis. The diagnosis is based on recognizing the overall pattern of clinical and laboratory abnormalities. However, even today, there is often a significant delay between onset of symptoms and diagnosis. Over the last two decades there has been great progress in identifying the profile of antinuclear antibodies that characterizes SLE, and in this chapter we describe how serological techniques can be important tools for the clinician in the early diagnosis of this disorder. Also described is the lupus band test, which has rather fallen out of favour as a diagnostic tool but which can still provide valuable evidence for the diagnosis in patients in whom the clinical and serological features are inconclusive. Nevertheless, because the presentation of lupus is protean, and the early manifestations are often non-specific, SLE can still be easily confused with a wide range of other conditions. Here, we describe some of the common clinical conundrums encountered in patients referred to the Lupus Clinic to 'rule out lupus', providing a framework for diagnosis. Finally, the chapter considers the major problem that clinicians who treat patients with SLE frequently face in distinguishing between a flare of lupus and infection. Diagnosis of SLE is still a great clinical challenge, and while it is important to recognize patients with potentially aggressive disease and treat them appropriately at an early stage it is also important to be able to recognize patients with potentially benign disease and avoid over-treatment.
Best Pract Res Clin Rheumatol 2002 Apr
PMID:Is it SLE? 1204 47

Systemic lupus erythematosus (SLE) is a multisystem autoimmune rheumatic disease (ARD) characterized by flares and remissions. SLE has protean and often complex manifestations, necessitating careful clinical assessment. However, it is important to remember that not all clinical problems reported by a lupus patient are due to the disease. Some may be a consequence of therapy and others may be unrelated to lupus. Therefore it is important to understand the totality of the effect of the disease on the patient. In order to do this measures are needed which distinguish current, potentially reversible disease activity, permanent organ damage and the effect of the disease on the patients' health status. Several measures are in current use in clinical trials, but not all are suitable for use in the routine clinical setting. This chapter discusses the current measures available to assess disease activity and damage in SLE.
Best Pract Res Clin Rheumatol 2002 Apr
PMID:How does one assess and monitor patients with systemic lupus erythematosus in daily clinical practice? 1204 48

The clinical and renal biopsy predictors of assistance in determining therapy are reviewed. While pulse cyclophosphamide remains the most effective treatment for proliferative nephritis, there is increasing interest in other agents, such as azathioprine, particularly to maintain remission. While lupus membranous nephropathy has attracted limited study, preliminary work suggests a role for cyclophosphamide. Newer therapies, including cyclosporine A, mycophenolate mofetil, immunoadsorption, intravenous immune globulin, LJP-394, high-dose immunoablation and nucleoside analogues require further study but offer hope for those failing conventional treatments.
Best Pract Res Clin Rheumatol 2002 Apr
PMID:How to manage patients with lupus nephritis. 1204 49

Systemic lupus erythematosus (SLE) is a connective tissue disease characterized by the formation of autoantibodies and immune complexes. The heart and lungs are among the organ systems commonly affected in SLE. Pericarditis, premature coronary atherosclerosis, pleuritis and pulmonary infections are the most prevalent cardiopulmonary manifestations. Other rare associations include myocarditis, coronary arteritis, acute lupus pneumonitis/pulmonary haemorrhage, acute reversible hypoxaemia and 'shrinking lung' syndrome. Current imaging modalities may provide earlier detection of subclinical disease, which may aid in preventing these potentially fatal complications. The response to treatment varies, depending on the presentation of disease. In this chapter we address the frequency, diagnosis and monitoring, and treatment regimens of cardiac and pulmonary involvement in patients with SLE.
Best Pract Res Clin Rheumatol 2002 Apr
PMID:How to manage patients with cardiopulmonary disease? 1204 50


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