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)

Skin affected by a burn cancer is scarred, ulcerated, and often appears as erythema ab igne clinically in adjacent skin. The latent period in burn scar malignancy is much longer for SCC than BCC. Malignant melanoma and various sarcomas are reported to arise in burn scars, too. The other extreme on the temperature scale can less often result in enough permanent acral damage that poor wound healing may eventually result in cancer, usually SCC. About 1% of patients with chronic osteomyelitis develop cancer, usually SCC in sinus tracts. As with tumors arising in burn scars and chronic leg ulcers of varied etiology, black patients are disproportionately overrepresented in osteomyelitic malignancy. In nearly all of the patients with radiation-induced skin cancer, concomitant radiodermatitis is present. As with burn scar and osteomyelitic cancer, x-ray related cancer has a long latent period. Similar to burn scar cancer, SCC predominates in osteomyelitis and occurs on the extremities. BCC, when it arises, is more common on the face and neck in burn- and radiation-induced tumors. Multiple tumors are frequent as is recurrence in x-ray malignancy. Mortality is high: one out of three to four patients with burn scar, osteomyelitic, and radiation cancer die of dermatosis-related malignancy. Recently, radioactivity-contaminated gold rings have been implicated in causing SCC. Carcinoma tends to occur in irradiated benign dermatoses whereas sarcomas tend to complicate irradiated malignancies. Stasis ulceration and anogenital fistulae may rarely lead to cancer, SCC in the former and adenocarcinoma in the latter. SCC can rarely develop in four related conditions (acne conglobata, dissecting perifolliculitis of the scalp, hidradenitis suppurativa, and pilonidal sinus) after a lengthy latent period; prognosis is poor with a high metastatic rate. A whole host of chronic cutaneous infections can lead to malignancy occasionally; these include lupus vulgaris, lymphogranuloma veverum, granuloma inguinale, leprosy, actinomycosis, and candidiasis. BCC more than SCC is known to complicate smallpox vaccination sites. Certain erosive and/or scarring dermatoses other than those mentioned above can be unusually affected by secondary malignancy. Discoid lupus erythematosus lesions often subjected to the carcinogenic effects of sunlight can degenerate into SCC in patients with either light or dark skin. In acrodermatis chronica atrophicans, a condition not often seen in the United States, the involved skin, particularly of the lower extremities, is susceptible to SCC, lymphoma, and BCC. Epidermolysis bullosa, especially the recessive dystrophic variant, can be complicated by SCC on affected mucous membrane and acral skin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cancer complicating chronic ulcerative and scarifying mucocutaneous disorders. 307 55

Two patients with the lupus anticoagulant exhibited unusual cutaneous manifestations. They both fulfilled four criteria for systemic lupus erythematosus and had experienced deep venous thrombosis. The first patient suffered from a leg ulcer that resembled a pyoderma gangrenosum. The second patient presented erythematous and purplish macules on the fingertips. The histologic studies showed only microthrombosis in the dermal vessels without vasculitis, although such lesions in systemic lupus erythematosus are usually attributed to vasculitis. The association of these cutaneous lesions with lupus anticoagulant has never been reported. It is likely that this association is not fortuitous. After a review of the literature, it seems possible to individualize a new syndrome characterized by the presence of a subgroup of antiphospholipid antibodies. Thrombosis, spontaneous abortions, neurologic manifestations, pulmonary hypertension, positive results of a Coombs' test, and thrombocytopenia can be included in this syndrome, which overlaps with systemic lupus erythematosus. Certain cutaneous symptoms are associated with the presence of lupus anticoagulant or other antiphospholipid antibodies: leg ulcers, distal cutaneous ischemia, widespread cutaneous necrosis, and livedo. They can be considered as the dermatologic manifestations of this syndrome.
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PMID:Cutaneous manifestations associated with the presence of the lupus anticoagulant. A report of two cases and a review of the literature. 309 56

The immunoglobulin classes/complement fixation of anti-dsDNA were studied in sera obtained from 17 systemic lupus erythematosus (SLE) patients with digital ulcers and/or gangrene (Group A); 13 SLE patients with leg ulcer, peripheral neuropathy or livedo (Group B); 24 SLE patients with Raynaud's phenomenon (Group C); and 18 SLE patients with active lupus nephritis (Group D). Antibodies to dsDNA of IgG and IgA classes were commonly present (often in high titers) in Groups A and D. However, complement fixation of anti-dsDNA was more common in Group D than in any of the other 3 groups.
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PMID:Digital ulcers/gangrene and immunoglobulin classes/complement fixation of anti-dsDNA in systemic lupus erythematosus patients. 660 40

Annexins/lipocortins are a group of structurally related calcium and lipid binding proteins which have been implicated as mediators of the anti-inflammatory action of corticosteroids. Autoantibodies against annexin-1 have been reported in association with autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis and their presence has been hypothesized as the reason for the steroid resistance phenomenon. In this study we investigated IgG- and IgM-autoantibodies against annexin-1,-2,-3,-4,-5 and -6 in sera of 221 patients with skin disorders and 114 healthy blood donors with newly established ELISAs. Patients were clustered into 5 groups according to their diagnosis: autoimmune diseases, psoriasis, leg ulcer, malignant melanoma, and miscellaneous diseases. Autoantibodies directed against each annexin were detectable in all investigated groups, in the control group as well as in the disease groups, without displaying any significant correlation to any of the disease states. The homogenous distribution of annexin-autoantibodies throughout the control group and all the disease groups studied, do not support the implication of annexin-autoantibodies in pathophysiological states and make them an unlikely candidate for use as a diagnostic marker.
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PMID:Autoantibodies to annexins: a diagnostic marker for cutaneous disorders? 786 77

The occurrence of cardiac manifestations and their relationship with the lupus anticoagulant (LA) in SLE was studied in 74 patients who were followed up for 22 years (median), of which 16 years were after the initial LA testing. Pericarditis was the most common cardiac event occurring in 16 (22%) patients but it did not correlate with LA. Valvular heart disease, coronary artery disease, left ventricular failure and/or cor pulmonale were observed in 16 (22%) patients. Taken together, their occurrence was associated with a history of leg ulcers (odds 3.8, P = 0.028) but not with LA or other common clinical manifestations of the antiphospholipid syndrome. Valvular heart disease in five patients was significantly associated with LA (P = 0.05). Cor pulmonale due to chronic pulmonary embolism was present in two patients with LA. Myocardial infarctions in five patients occurred late in the course of disease but in relatively young patients (mean 43 years). Fatal myocardial infarction in the absence of atherosclerosis in two LA-positive patients supports a pathogenetic role for LA in these cases. In conclusion, of the various cardiac complications in SLE, valvular heart disease and cor pulmonale appear to be connected with the antiphospholipid syndrome. Both conditions should be actively sought in patients with LA to decrease possible adverse events (arterial emboli and right ventricular failure) affecting the patients' prognosis.
Lupus 1994 Jun
PMID:Lupus anticoagulant and cardiac manifestations in systemic lupus erythematosus. 795 2

The objective of this study was to determine the prevalence and clinical significance of elevated antiphospholipid antibodies (APA) in a large series of patients admitted to a department of Internal Medicine. At the end of entry phase, 1014 patients were tested (488 males-526 females, mean age: 66.7 years, range 18-97). Seventy-two (7.1%) patients were found APA positive at least once: 44 males and 28 females, mean age 69 years, range 23 to 94. Twenty fulfilled the criteria of Primary Antiphospholipid Antibody Syndrome: 10 patients were referred for deep vein thrombosis, 3 had history of deep vein thrombosis, 1 had both arterial thrombosis and a history of venous thrombosis; 2 had thrombocytopenia; 3 had stroke, 1 had a history of a stroke. One patient had SLE according to ARA classification. The most frequent associated disease was cancer: 14 patients, 9 had evolutive malignant disease, 5 were in clinical remission of neoplasia. Other clinical conditions included chronic and/or acute alcoholic intoxication (n = 8), severe atherosclerosis (n = 4), leg ulcer (n = 4). Insufficient data are available about the evolution, but 7 patients died in the year following diagnosis. Eight patients had fluctuations in APA detection: 2 initially APA positive became negative, 5 initially negative became positive and 1 patient was alternatively positive, negative and positive without steroid treatment. Thus, as expected, APA occur in a variety of clinical disorders. The association with cancer or alcoholic intoxication deserves further investigations.
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PMID:A prospective epidemiological study on the occurrence of antiphospholipid antibody: the Montpellier Antiphospholipid (MAP) Study. 798 47

Recent evidence suggests that lupus anticoagulants are immunologically distinct from the anticardiolipin antibodies. Nevertheless, the associated clinical complications exhibited by the two groups of antibodies are similar. They have been shown to have a strong association with a history of arterial and venous thrombosis, thrombocytopenia and neurological disease in patients with SLE or lupus-like disorders. The association between antiphospholipid antibodies and recurrent fetal loss is suggested by the currently available data but is not firmly established. Patients with lupus and antiphospholipid antibodies and an established history of recurrent fetal wastage are at high risk for experiencing subsequent fetal loss, but it is not yet known whether the same is true for patients without a history of fetal loss. The association of thrombosis, neurological disease, thrombocytopenia, and fetal loss in patients with non-SLE disorders has not been as extensively studied. Only recently have investigators such as Ginsberg and colleagues begun to show in prospective studies that there may, in fact, be a statistically significant risk of thrombotic events in otherwise healthy individuals with antiphospholipid antibodies. Many of the diverse minor manifestations reported in individual patients, case series, or cross-sectional studies such as livedo reticularis, leg ulcers, and hemolytic anemia may, alternatively, be due to coincidence or chance. Efforts to elucidate the mechanisms of thrombosis in patients with antiphospholipid antibodies is an area of active research. Most efforts have been based on the effects of these antibodies on endothelial cell and platelet function as well as on the fibrinolytic system. In addition, it has recently been shown that binding of antiphospholipid antibodies to phospholipids requires the serum "co-factor" beta 2-glycoprotein I. In patients with SLE selected for the presence of the lupus anticoagulant, thrombosis, or fetal loss, Viard and associates found that 17 of 47 (36%) patients had anti-beta 2-glycoprotein I antibodies. They were able to show, in their small retrospective study, that there was an association between the presence of these antibodies and anticardiolipin activity, lupus anticoagulant activity, and thrombotic events, but not with spontaneous abortion. Of patients with SLE and thrombosis (9 of 47) eight of nine were positive for anti-beta 2-glycoprotein I antibodies, seven of nine were positive for anticardiolipin antibodies, and eight of nine were positive for the lupus anticoagulant. The known inhibitory effect of beta 2-glycoprotein I on platelet aggregation, on platelet prothrombinase activity, and on the intrinsic pathway of coagulation supports the hypothesis that implicates beta 2-glycoprotein I in the pathogenesis of unwanted thrombotic events.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical syndromes associated with lupus anticoagulants. 805 30

A 24-year-old woman with Graves' disease treated with methimazole for 4 years, developed recalcitrant ulcers on the lower legs. Histological studies demonstrated vasculitis in deep dermal vessels accompanied by C3 deposition. Laboratory investigation revealed lupus-like abnormalities (leucocytopenia, positive antinuclear and antidouble strand (ds) DNA antibodies, and positive ANCA). The leg ulcers dramatically improved after methimazole was withdrawn. In addition, leucocytopenia and the immunological abnormalities soon faded. Although lupus-like syndrome is well known to be induced by antithyroid drugs, vasculitis is a rare complication. To the best of our knowledge, this is the first report describing ANCA-associated vasculitis caused by methimazole.
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PMID:ANCA-associated vasculitis and lupus-like syndrome caused by methimazole. 854 97

The non-healing leg ulcer is examined by discussing three disease processes: peripheral vascular occlusive disease (PVOD), chronic venous insufficiency (CVI), and vasculitis. For PVOD, management decisions are based on risk factors and disease history. Comprehensive management includes the discontinuation of smoking, exercise conditioning and regulation of diabetes, hyperlipidemia, hypertension, and the appropriate application of anticoagulant/antiplatelet drugs. Methods of surgical management include bypass with autogenous or synthetic material in addition to reconstructive surgery with patch angioplasty or extra-anatomic bypass, amputation, percutaneous transluminal angioplasty/stents, thrombolytic infusion, atherectomy, intraluminal ultrasound, and angioscopy. The optimal healing environment for all ulcers prevents contamination, pain, and fluid loss. In CVI, higher venous pressure in the veins of the lower limb during exercise results in ambulatory venous hypertension and ulceration. Various theories are associated with the disease and ulceration process; the classic treatment of elevation, ambulation, and compression for venous disease remains unchallenged. Diagnosis is based on history, physical examination, invasive venography, and/or non-invasive studies. Two groups of vasculitic disorders that share varying degrees of vascular inflammation and necrosis are arteritis (lupus, erythematosus, periarteritis nodosa, dermatomyositis) and blood dyscrasias (sickle cell disease, thalassemia). Leg ulcers associated with vasculitis are due to inadequate tissue oxygenation at the local level, are typically chronic, slow to heal, and commonly recur.
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PMID:The non-healing leg ulcer: peripheral vascular disease, chronic venous insufficiency, and ischemic vasculitis. 939 80

Infection with marine bacteria is uncommon. A patient with systemic lupus erythematosus who developed concurrent infection with Shewanella putrefaciens and Mycobacterium marinum (M. marinum) is described. After bathing leg ulcers in sea water, severe cellulitis of the left leg with necrotic areas and extensive bullae developed. Infection due to S. putrefaciens was confirmed and a long course of hospitalization, oral ciprofloxacin and skin grafting was required. During hospitalization subcutaneous nodules developed on the other leg. Biopsy revealed acid-fast bacilli and culture grew M. marinum. These lesions responded to rifampicin and cotrimoxazole. Patients with leg ulcers, peripheral vascular disease, diabetes, or receiving immunosuppressive drugs may acquire unusual infections after salt water exposure.
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PMID:Concurrent infection due to Shewanella putrefaciens and Mycobacterium marinum acquired at the beach. 961 78


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