Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Drug-induced uveitis is a relatively rare occurrence. For example, the patient database at the tertiary referral Uveitis Clinic at the Casey Eye Institute, Oregon Health Sciences University records an incidence of less than 0.5%. Despite this, the frequency of uveitis secondary to rifabutin therapy in AIDS patients has brought greater recognition to the potential role of medications as a cause of intraocular inflammation. A brief review of uveitis including its classification, causes, symptoms and signs is presented along with a review of systemic medications associated with uveitis. These medications include cidofovir, cobalt, diethylcarbamazepine, pamidronic acid (disodium pamidronate), interleukin-3 and interleukin-6, oral contraceptives, quinidine, rifabutin, streptokinase and sulfonamides. Other systemic medications may cause uveitis. Topical ocular medications such as beta-blockers and corticosteroids as well as other topical ocular medications have been associated with uveitis. Cidofovir, pamidronic acid, sulfonamides, rifabutin and topical metipranolol can 'probably' cause uveitis. The remainder of the medications discussed have a 'possible' cause-and-effect relationship with uveitis. Treatment begins with recognition of a drug-related event and usually subsequent avoidance of the drug. Therapy depends on the severity and likelihood of the reaction. Drug-induced uveitis is almost always reversible within weeks of discontinuation of the drug and treatment of the inflammation.
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PMID:Drug-induced uveitis. Incidence, prevention and treatment. 930 54

The causes of death from intranasal cowpox virus infections in mice remain unclear. Hypotheses include severe pneumonitis, hepatitis and/or hyperproduction of cytokines and chemokines. This work explores these hypotheses by studying the influence of low- and high-volume virus inocula on viral pathogenesis. BALB/c mice were infected intranasally with a syncytium-forming variant of cowpox virus in 5 microL or 50 microL volumes containing the same infectious virus challenge dose. The 50 microL infection produced a more rapidly lethal disease associated with severe pneumonitis, high lung and nasal virus titres and increased cytokine and chemokine levels in the lungs and nasal tissue, whilst liver infection was minimal. The 5 microL inoculum infection was also lethal, but the infection was primarily confined to the upper respiratory tract and included elevated nasal cytokine and chemokine levels. Levels of the pro-inflammatory cytokine interleukin-6 were particularly high in both infections. Treatment of the infections with cidofovir (100mg/kg/day for 2 days starting 24h after virus exposure) led to survival and suppression of tissue virus titres. Treatment reduced pneumonitis in the 50 microL infection and lessened cytokine hyperproduction in both infections. We conclude that a 5 microL volume inoculum of cowpox virus causes a lethal upper respiratory tract infection, whilst the 50 microL inoculum targets both upper and lower respiratory tracts, with excessive release of systemic pro-inflammatory factors. Cidofovir effectively treated both infections and slowed viral replication sufficiently to subdue the exaggerated release of pro-inflammatory mediators.
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PMID:Differential pathogenesis of cowpox virus intranasal infections in mice induced by low and high inoculum volumes and effects of cidofovir treatment. 1820 53