Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasculitis can be a systemic manifestation of hypersensitivity to many drugs, among them anticonvulsants. The clinical manifestations include rash and renal, hepatic, and pulmonary involvement. Diagnosis is based upon clinical findings and a characteristic biopsy showing granulocytic and sometimes eosinophilic infiltrates around small blood vessels, especially venules. A severe form of hypersensitivity vasculitis, with extensive visceral involvement and poor prognosis, has been encountered very rarely following phenytoin and in isolated cases following carbamazepine and trimethadione administration. Drug-induced systemic lupus erythematosus is much more frequent, with distinct clinical and laboratory abnormalities. The syndrome was described following treatment with most anticonvulsants in clinical use--phenytoin, carbamazepine, ethosuximide, trimethadione, primidone, and valproate, but not phenobarbital or benzodiazepines. The early recognition of these syndromes as being related to drugs is important, because they usually remit upon withdrawal of the offending agent.
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PMID:Hypersensitivity vasculitis and systemic lupus erythematosus induced by anticonvulsants. 842 54

Drug-induced lupus erythematosus (DILE) is defined as an entity characterized by clinical manifestations and immunopathological serum findings similar to those of idiopathic lupus but which is temporally related to continuous drug exposure and resolves after discontinuation of the offending drug. Similar to idiopathic lupus, DILE can be divided into systemic lupus erythematosus (SLE), subacute cutaneous lupus erythematosus (SCLE) and chronic cutaneous lupus erythematosus (CCLE). Based on the literature review and retrospective analysis of our case series, we focused on the dermatological aspects of DILE. The cutaneous features of drug-induced SLE are protean, including particularly purpura, erythema nodosum and photosensitivity as well as the skin lesions characterizing both urticarial and necrotizing vasculitis. The typical laboratory profile of systemic DILE consists of positive antinuclear antibodies (ANA) and antihistone antibodies, the latter being regarded as the serum marker of this subset. The drugs most frequently implicated in the development of systemic DILE are hydralazine, procainamide, isoniazid and minocycline. Drug-induced SCLE usually presents with annular polycyclic or papulosquamous cutaneous manifestations as in the idiopathic form, but blisters or targetoid lesions mimicking erythema multiforme cannot rarely be associated. The clinical presentation is often generalized, with involvement of the lower legs that are usually spared in idiopathic SCLE. ANA and anti-Ro/SSA antibodies are usually present, whereas antihistone antibodies are uncommonly found. Drugs associated with SCLE include particularly calcium channel blockers, angiotensin-converting enzyme inhibitors, thiazide diuretics, terbinafine and the recently reported tumour necrosis factor (TNF)-alpha antagonists. Drug-induced CCLE is very rarely described in the literature and usually refers to fluorouracile agents or TNF-alpha antagonists. The picture is characterized by the occurrence of classic discoid lesions, but aspects of lupus tumidus can occasionally develop. ANA are demonstrated in around two-thirds of the cases. Management of DILE is based on the withdrawal of the offending drug. Topical and/or systemic corticosteroids and other immunosuppressive agents should be reserved for resistant cases.
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PMID:Drug-induced lupus: an update on its dermatologic aspects. 1976 93

Drug-induced lupus erythematosus differs in its manifestation from drug-induced vasculitis. The former is associated with characteristic symptoms that improve following discontinuation, whereas the latter is predominantly an antineutrophil cytoplasmic antibody (ANCA) positive small vessel vasculitis involving the kidneys, skin, and lungs. We present a case of advanced disease in an elderly Caucasian woman requiring corticosteroids, and immunosuppressive therapy, who was on hydralazine for >2 years.
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PMID:Hydralazine-induced pulmonary-renal syndrome: a case report. 2072 11