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 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

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


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