Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stevens-Johnson syndrome is a rare immunologic reaction that may involve skin or various mucosal surfaces. The etiology may range from multiple pharmacologic agents to viral infections. Associated findings can range from minimal skin and mucosal involvement to extensive dermal exfoliation, nephritis, lymphadenopathy, hepatitis, and multiple serologic abnormalities. We report a 36 year-old caucasian male who developed a pruritic, raised maculopapular eruption on Day 17 of intravenous vancomycin for treatment of probable bacterial endocarditis. The vancomycin was discontinued. The patient had received a prosthetic aortic valve subsequent to acute rheumatic valve disease 20 years earlier, but had been well until development of endocarditis. The rash became more extensive to involve the torso, abdomen, legs, and arms. His fever persisted, and he developed neutropenia and eosinophilia. Axillary and inguinal lymphadenopathy, pharyngeal irritation, lip swelling, conjunctival injection, and elevated liver function studies also developed following cessation of the vancomycin. Eight days after eruption and fever began, corticosteroid therapy was instituted, with subsequent improvement of symptoms in less than 24 hours. Allergic reactions to vancomycin have included Stevens-Johnson syndrome rarely, and only one other case of adenopathy has been recorded. Most reactions have been in patients with severe renal insufficiency. We believe this patient is the first case of vancomycin-induced Stevens-Johnson syndrome in a previously healthy patient to be complicated by lymphadenopathy, hepatitis, and multiple serologic abnormalities.
Allergy Asthma Proc
PMID:Vancomycin-induced Stevens-Johnson syndrome. 893 97

Autoimmune carditis is associated with many human rheumatic conditions, including rheumatic fever, systemic lupus erythematosus, and rheumatoid arthritis. The immune mechanisms that mediate the cardiovascular pathology connected to these diseases are poorly defined. Several animal models are used to recapitulate human pathophysiology in order to better characterize the immunopathogenic mechanisms driving autoimmune endocardial inflammation. These animal models point toward common mechanisms mediating autoimmune endocarditis; in particular, CD4+ T cells and pro-inflammatory macrophages play critical roles in directing the disease process. The goals of this review are to discuss the prevailing animal models of autoimmune endocarditis and their underlying immunologic mechanisms and to provide insight regarding potential therapeutic targets in humans.
Curr Allergy Asthma Rep 2015 Jan
PMID:Autoimmune valvular carditis. 2543 Sep 52