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)

A woman with hypertension had been treated with hydralazine and propranolol for the past 6 years. Leg ulcers and mild joint involvement had been observed for 3 years. When oral zinc therapy was started, multisystemic manifestations of a lupus erythematosus-like syndrome developed within one week. The possible implication of zinc in drug-induced lupus is discussed.
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PMID:Drug-induced lupus erythematosus aggravated by oral zinc therapy. 9 57

Livedoid vasculitis, a hyalinizing vasculopathy, is characterized by extensive formation of microthrombi and deposition of fibrin in the middermal vessels, which result in epidermal infarction, ulceration, and formation of stellate scars. In a prospective study of nonhealing ulcers in patients with livedoid vasculitis, we found a high incidence of anticardiolipin antibodies, lupus anticoagulants, increased levels of plasminogen activator inhibitor, and low levels of endogenous tissue plasminogen activator (t-PA) activity. This procoagulant tendency and decreased fibrinolysis may provide an explanation for the occlusive vasculopathy often noted in biopsy specimens from these patients. On the basis of these findings, we proposed that fibrinolysis with recombinant t-PA would lyse microvascular thrombi, restore circulation, and promote wound healing. In six patients who had nonhealing ulcers caused by livedoid vasculitis and in whom numerous conventional therapies had failed, low-dose t-PA (10 mg) was administered intravenously during a 4-hour period daily for 14 days. Five of the six patients had dramatic improvement; almost complete healing of the ulcers occurred during hospitalization, and tissue oxygenation, as measured by transcutaneous oximetry, increased. The one treatment failure was due to rethrombosis of the microvasculature; this patient was subsequently re-treated but with concurrent anticoagulation, and her leg ulcers healed. We conclude that daily administration of a low dose of t-PA is safe and effective treatment for nonhealing ulcers due to occlusive vasculopathy.
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PMID:Tissue plasminogen activator for treatment of livedoid vasculitis. 143 47

We describe a 60-year-old man with ankylosing spondylitis (AS), hospitalized for leg ulcers. Laboratory investigations revealed the presence of the lupus anticoagulant. We found no such an association by a computer assisted search of the literature published from 1975 to 1989. The relationship between the AS, the lupus anticoagulant and leg ulcers is discussed.
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PMID:Lupus anticoagulant and leg ulcers associated with ankylosing spondylitis. 823 46

Skin manifestations were described in lupus anticoagulant (LA) positive and in LA negative SLE patients. Necrotic ulcers appearing at the beginning of the disease process characterized the 33 LA positive patients. Thirteen patients had a "peripheral vascular syndrome"; small leg ulcers of livedoid vasculitis type following deep venous thromboses, in 3 patients developing into pyoderma gangrenosum like ulcers and in 2 patients into pseudo-sarcoma Kaposi. The lesions were histologically characterized by capillary angiogenesis with extravasated red blood cells, sparse inflammatory cell infiltrates and microthromboses. Three patients had ulcers clinically and histologically resembling those seen in Degos' disease. Five patients had anetoderma showing elastic tissue depletion and microthromboses histologically. A different pattern of skin changes was seen in the LA negative patients. Our findings suggest that antiphospholipid antibodies play a pathogenetic role in the described skin manifestations of LA positive SLE patients.
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PMID:Lupus anticoagulant and the skin. A longterm follow-up study of SLE patients with special reference to histopathological findings. 168 71

Recently, the association between anti-phospholipid antibodies (false positive VDRL, lupus anticoagulant or anti-cardiolipin antibody) and diverse clinical manifestations has been termed antiphospholipid syndrome. We report 6 female patients with "primary" antiphospholipid syndrome, not related to connective tissue disorders. Their age ranged from 23 to 66 years and they were followed from 1 to 27 years (mean 9.2). Venous occlusion developed in 4, arterial occlusion in 4 (TIA, convulsive episode and cutaneous thrombotic microangiopathy). Three of 5 had fetal loss and 3/6 developed thrombocytopenia. Leg ulcer, migraine and mitral valvulopathy and peripheral facial paralysis were isolated manifestations in different patients. High titers for type IgG anticardiolipin antibodies were present in all patients. Low titers for IgM antibodies were present in 2. The pathogenesis of this syndrome is discussed.
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PMID:[Primary antiphospholipid syndrome: clinical experience of 6 patients]. 184 92

Leg ulcers are associated with antiphospholipid antibodies in patients with systemic lupus erythematosus. They may also occur in patients with primary antiphospholipid syndrome(PAPS). Histopathologic findings at the edges of the ulcers may give insight into their pathogenesis. In a patient with PAPS and a leg ulcer, a biopsy of the ulcer's edge revealed a peculiar small vessel nodular proliferation in the upper and lower dermis. There was mild mixed inflammatory infiltrate in the surrounding connective tissue, a few vessels with fibrin thrombi, and some with fibrin deposition within their walls. A review of the literature revealed similar findings in other skin ulcers associated with lupus anticoagulants. This suggests peculiar pathogenetic mechanisms that may be akin to those responsible for antiphospholipid arterial vasculopathy.
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PMID:Leg ulcers in the primary antiphospholipid syndrome. Report of a case with a peculiar proliferative small vessel vasculopathy. 190 10

The antiphospholipid syndrome (characterized by the presence of circulating lupus anticoagulants or anticardiolipin antibodies) was first recognized in patients with systemic lupus erythematosus (SLE), but the syndrome can also exist in the absence of SLE. The clinical features include arterial or venous thrombosis, recurrent abortion, neurological problems, and various cutaneous disorders including thrombophlebitis, livedo reticularis, atrophie blanche, leg ulcers, and gangrene. In some cases, antiphospholipid antibodies may play a role with other recognized syndromes characterized by vascular occlusion, such as Sneddon's syndrome (livedo reticularis with cerebrovascular occlusion) and Degos' disease.
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PMID:Antiphospholipid syndrome and cutaneous vasoocclusive disorders. 193 63

The case of a woman with systemic lupus erythematosus with unusual clinical, cutaneous and biologic features and lupus anticoagulant is presented. According to the literature this association is not fortuitous: a new syndrome characterized by the presence of a subgroup of antiphospholipid antibodies has been recognized. The cutaneous symptoms of this syndrome include: leg ulcers, livedo reticularis, widespread cutaneous necrosis and distal cutaneous ischemia. In our patient a nearly complete picture of the clinical and biologic features of this syndrome, including a characteristic retinal vein thrombosis is present.
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PMID:[Clinical manifestations associated with the presence of lupus anticoagulant]. 250 30

An antiphospholipid antibody (APLA) syndrome has been proposed for those patients with systemic lupus erythematosus (SLE) or with other connective tissue diseases who have APLA and manifestations that seem related to their effect (venous thrombosis, arterial occlusions, thrombocytopenia, hemolytic anemia, recurrent fetal loss, leg ulcers, and livedo reticularis). Occurrence of a primary antiphospholipid syndrome has also been mentioned but not defined. We present 9 young patients who had at least 2 of the clinical manifestations that have been related to high titers of APLA, but had neither SLE nor other recognizable connective tissue disease. We propose criteria for diagnosis of such a primary antiphospholipid syndrome and discuss the possible mechanisms whereby a single autoantibody can cause systemic disease.
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PMID:Primary antiphospholipid syndrome. 274 88

Five hundred consecutive patients with systemic lupus erythematosus (SLE) were entered into a prospective study of anticardiolipin antibodies (ACLA) in their 3 major immunoglobulin isotypes and followed thereafter with repeated testing for a mean period of nearly 8 months. Manifestations of SLE that were strongly associated with ACLA included venous thrombosis (particularly when recurrent), thrombocytopenia, hemolytic anemia, recurrent fetal loss, and leg ulcers. Other manifestations found to be associated with ACLA were arterial occlusions, transverse myelitis, and pulmonary hypertension. Conversely, we found no relationship between ACLA and migraine, convulsions, transient ischemic attacks, psychoses, or avascular necrosis of bone. No relationship was found between the presence of ACLA and that of anti-DNA antibodies studied in the same serum sample. Association with ACLA grew stronger and titers became higher in patients with several of the associated manifestations. Statistical analyses revealed the existence of a syndrome, the antiphospholipid syndrome, comprising 2 or more manifestations in conjunction with ACLA titers 5 standard deviations above the mean of normal control subjects, particularly if ACLA had been positive on at least 2 occasions. We propose that such criteria could be applied to the definition of the antiphospholipid syndrome. The presence and the titers of these antibodies related to disease activity and titer decreased by treatment, particularly when they were of the IgM isotype. Patients in whom a thrombotic episode occurred during the course of the study were observed to have a coincident decrease in ACLA titers, a finding that might indicate consumption of the antibody during the event. Treatment and the resulting inactivation of disease appear to have independent effects on ACLA titers. Physicians should therefore be cautious in prescribing high doses of corticosteroids or immunosuppressants to patients with SLE solely because they have high titers of ACLA.
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PMID:Antiphospholipid antibodies and the antiphospholipid syndrome in systemic lupus erythematosus. A prospective analysis of 500 consecutive patients. 281 61


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