Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A computer analysis was made of the data from a prospective study of the clinical course of systemic lupus erythematosus (SLE) in 234 patients followed for an average of 46 months. All fulfilled four ARA criteria for the diagnosis of SLE. Sixteen of the 234 patients were aged 51 or older. They were compared with the 218 younger SLE patients to determine the influence of age on the signs and symptoms of the disease, the organ systems involved, the laboratory data, amount and duration of corticosteroid or azathioprine therapy, and the prognosis. The older group showed more discoid lupus, photosensitivity and pulmonary fibrosis than did the younger group, but a similar incidence of malar rash, alopecia, arthritis, arthralgia, myalgia and serositis, and a lower incidence of oral ulcers, Raynaud's phenomenon, cutaneous vasculitis, neuropsychiatric manifestations, leukopenia, hypocomplementemia and profus proteinuria. The older patients needed a lower dosage of corticosteroids, and a shorter course of azathioprine therapy. These findings suggest a milder form of SLE with better response to therapy in the older group.
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PMID:Systemic lupus erythematosus in the older age group: computer analysis. 76 67

The iatrogenic L-tryptophan-induced eosinophilia-myalgia syndrome, often considered to be a "new" disease, has proven to be a remarkable mimic of the classic sclerosing rheumatologic disorders. Although subacute cutaneous lupus erythematosus remains a clinically defined entity, supportive histologic and immunopathologic findings have recently been proposed. Rheumatoid neutrophilic dermatitis needs to be added to our usual differential diagnosis of a neutrophilic dermatosis without leukocytoclastic vasculitis. The antiphospholipid syndrome is associated with noninflammatory vascular thrombosis and often has recognizable cutaneous findings. Finally, ANCA are a valuable adjunct in the systemic evaluation of patients with vasculitis syndromes and suggest a common pathogenesis for several of the systemic vasculitides.
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PMID:Collagen vascular disease. 173 Jan 64

Autoantibodies against neutrophil cytoplasmic antigens (ANCA) produce two major immunofluorescence (IF) patterns on ethanol-fixed granulocytes: the "classical" (centrally accentuated) C-ANCA, associated with Wegener's granulomatosis (WG), and P-ANCA (perinuclear), which mainly occur in renal vasculitis. Rheumatic manifestations are an important clinical finding in systemic vasculitis, often preceding a fulminant course and sometimes imitating various rheumatic disorders. We analyzed the incidence of ANCA in rheumatic patients and looked for the frequency of rheumatic symptoms in systemic vasculitis. In WG (n = 186), we found rheumatic symptoms in 55% (myalgia, 45%; arthritis, 21%); in 90%, rheumatic complaints were associated with active vasculitis. In 730 patients with various rheumatic conditions (eg, 268 rheumatoid arthritis, 130 systemic lupus erythematosis [SLE], 32 sharp-S, 50 ankylosing spondylitis, 43 systemic sclerosis) no C-ANCA were found. On the contrary, the P-ANCA pattern was seen in seven of 62 giant cell arteritis, five of 27 Felty's/Still's syndrome, and four of 130 SLE patients in addition to renal vasculitis (21/74). We demonstrated that 95% of C-ANCA-positive sera react with proteinase 3 (PR3 or myeloblastin). Using monoclonal antibodies, we showed that PR3 is expressed on the plasma membrane of neutrophil granulocytes and monocytes; thus, PR3 autoantigens are accessible for circulating antibodies. The detection of ANCA in sera from vasculitis and other rheumatic diseases is of immunodiagnostic value and provides new insight in the pathogenesis of systemic vasculitides.
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PMID:Antineutrophil cytoplasmic autoantibody-associated diseases: a rheumatologist's perspective. 186 75

Early in the course of studies of the Spanish toxic oil syndrome it was recognized that vascular lesions were a major problem, most logically attributable to endothelial damage by the toxic oil. However, most clinical attention has been directed to the pulmonary complications and the evolution into a scleroderma-like illness later. In this study of 11 victims of the toxic oil syndrome careful postmortem studies of the coronary arteries and conduction system and neural structures of the heart demonstrated major injury to all those components of the heart. Obliterative fibrosis of the sinus node in four cases resembled findings in fatal scleroderma heart disease, and in eight the cardiac lesions resembled those of lupus erythematosus. The more impressive pathologic features involved the coronary arteries and neural structures, which were abnormal in every heart. The arterial disease included widespread focal fibromuscular dysplasia, but there was also an unusual myointimal proliferative degeneration of both small and large coronary arteries in five patients, four of whom were young women. In two hearts, portions of the inner wall of the sinus node artery had actually detached and embolized downstream. Coronary arteritis was rarely found. Inflammatory and noninflammatory degeneration of cardiac nerves was widespread. Fatty infiltration, fibrosis and degeneration were present in the coronary chemoreceptor. In most respects these cardiac abnormalities resemble those described in the eosinophilia-myalgia syndrome caused by an altered form of L-tryptophan. In both diseases there is good reason to anticipate more clinical cardiac difficulties than have so far been reported, and even more basis for future concern, especially relative to coronary disease and cardiac electrical instability.
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PMID:Cardiac abnormalities in the toxic oil syndrome, with comparative observations on the eosinophilia-myalgia syndrome. 191 15

15 cases of subacute cutaneous lupus erythematosus are reported. The diagnosis was based on the presence of the typical clinical features, on the histologic and immunpathologic examination of lesional skin and on the characteristic laboratory findings. 8 patients had annular type, 4 patients had papulosquamosus type of the characteristic skin signs of subacute cutaneous lupus erythematosus. In 3 patients both types of lesions existed simultaneously. 5 patients fulfilled the American Rheumatism Association criteria for systemic lupus erythematosus, however the systemic symptoms (arthritis, arthralgia, fever, myalgia, photosensitivity) were mild. 4 patients had positive ANA test, anti-Ro/SSA antibodies were determined in 5 patients, anti-RNP antibodies were detected in 8 patients. Anti-dsDNA antibodies were not detected. Subacute cutaneous lupus erythematosus is an intermediate subset in severity between discoid lupus erythematosus and severe systemic lupus erythematosus, therefore a milder form of therapy should be chosen.
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PMID:[Subacute cutaneous lupus erythematosus based on a study of 15 cases]. 268 50

A young woman had a history of subcutaneous nodules, migratory arthralgia, myalgia, and lymphadenopathy. Histopathologic characteristics of the nodular subcutaneous lesion showed a massive lobular panniculitis characteristic of lupus erythematosus (LE) panniculitis. The diagnosis of LE panniculitis was established by demonstration of a positive linear basement membrane zone stain of the involved skin by direct immunofluorescence microscopy. Initial serologic findings showed negative antinuclear antibody (ANA) and anti-DNA antibody test results and a negative LE cell preparation. Subsequently, a positive ANA test result developed. The test result for extractable nuclear antigen was strongly positive, although initial test results for antibodies to ribonucleoprotein and Sm antigens were negative.
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PMID:Lupus erythematosus panniculitis. 618 92

A patient with Graves' disease who experienced various allergic reactions to both PTU and MMI is reported. She developed fever, skin rash, lymphadenopathy, liver damage and moderate leukopenia during PTU administration. Furthermore, she developed an MMI-induced lupus-like syndrome characterized by generalized lymphadenopathy, migrating, polyarthritis and myalgia, and results of tests for anti-DNA antibody and anti-nuclear antibody, and LE were positive. All these abnormalities reverted to normal upon discontinuation of medication after subtotal thyroidectomy.
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PMID:Lupus-like syndrome--a rare complication in thionamide treatment for Graves' disease. 689 90

Drug-induced lupus is a syndrome resembling mild systemic lupus erythematosus which can complicate treatment with certain apparently unrelated therapies. The most common individual agents are procainamide and hydralazine. Drugs less frequently associated with the disease are chlorpromazine, isoniazid, methyldopa, penicillamine, quinidine and sulfasalazine. Whole drug groups have also been implicated, such as the anticonvulsants, beta-blockers, sulfonamides and some of the newer 'biological' agents. The syndrome is characterised by arthralgia, myalgia, pleurisy, rashes and fever in association with antinuclear antibodies in the serum. More serious features of idiopathic lupus such as nephritis and cerebral disease are rare in drug-induced disease. The pathogenesis is unknown but in some cases is thought to be due to interactions between the drug and DNA or histones, rendering them immunogenic. For the biological agents, including interferons and antibodies to tumour necrosis factor-alpha, it has been suggested that it is due to disruption of the cytokine network. Although extremely rare, recognition of drug-induced lupus is important because it reverts within a few weeks of stopping the drug. It is possible that understanding its pathogenesis may shed light on its more serious relative, systemic lupus erythematosus.
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PMID:Drug-induced lupus. 764 27

Patients with systemic lupus erythematosis (SLE) often manifest features of other autoimmune diseases. In this review, we provide a detailed compendium of features of SLE that overlap with other conditions. This compendium is important because a critical feature in our understanding of autoimmunity has been the clustering of coexisting/different autoimmune diseases both within an affected patient and within a pedigree. Indeed, autoimmune disorders share a variety of similar clinical and serological defects. For example, all autoimmune disorders are associated with the elaboration of autoantibodies and/or the production of self-reactive mononuclear cell populations; many have high levels of immune complexes and defects in cell-mediated immunity. Several diseases share similar genetic backgrounds, as reflected by study of loci within the major histocompatibility complex. In part the coassociation is due to common genetic tendencies with different environmental precipitating agents (trigger mechanisms). It is likely that many factors can modulate the immune system to autoimmunity in the presence of an appropriate genetic background, eg, drugs, viral infections, UV irradiation, and toxins, ie, toxic oil syndrome and L-tryptophan-induced eosinophilic myalgia. The coexistence of SLE with other autoimmune diseases is an excellent venue to understand these events, and we believe that the presence of other autoimmune diseases in patients with SLE can be called the kaleidoscope of autoimmunity.
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PMID:The coexistence of systemic lupus erythematosus with other autoimmune diseases: the kaleidoscope of autoimmunity. 783 52

A 52-year-old woman was admitted to our hospital because of a skin rash, high fever and myalgia. She had been diagnosed ten years ago by a dermatologist as having MCTD (mixed connective tissue disease). At the time of admission a diagnosis of active SLE was made by fulfilling four of the 1982 ARA criteria together with increasing levels of anti-DNA antibody and low levels of complements. Prednisolone (PSL) given orally in an initial dosage of 60 mg/day was effective during the first 6 weeks. Then a high fever, skin rash and pancytopenia appeared without active findings of SLE. Infection caused by bacteria, fungus or virus was suspected, but no infectious agent was present in cultures derived from blood or other sources. Antimicrobic drugs used were not effective at all. The clinical picture was suggestive of a drug allergy, but no causative drug was found. A diagnosis of hemophagocytic syndrome (HPS) was made because of the increased number of unusual hemophagocytic cells in the bone marrow. High levels of serum ferritin and neopterin, which are known to reflect macrophage activation, supported the diagnosis of HPS. HPS is characterized by activated phagocytosis presumably induced by hypersecretion of cytokines. Malignant lymphoma and infection are the two representative diseases which may cause HPS. Recently, an acute lupus HPS was reported in patients with active SLE. Here we reported a case of reactive HPS observed in a patient with SLE who had been receiving high dose PSL. Symptoms and findings of the patient gradually disappeared in several weeks after rapid reduction of the PSL dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemophagocytic syndrome observed in a patient with systemic lupus erythematosus]. 797 30


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