Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tetracyclines are active in vitro against most urinary tract pathogens, Chlamydia, Mycoplasma pneumoniae, Brucella, rickettsiae, and Nocardia. Chloramphenicol is used primarily for anaerobic infections, Haemophilus influenzae meningitis, and infections due to Salmonella typhi. Erythromycin is active in vitro against M. pneumoniae, Streptococcus pneumoniae, and group A beta-hemolytic streptococci. Erythromycin may be used as prophylactic therapy for subacute bacterial endocarditis and for recurrence of acute rheumatic fever in patients who are allergic to penicillin. Clindamycin should be used only for the treatment of anaerobic infections. Tetracycline may cause gastrointestinal upset; phototoxic dermatitis; hepatitis, especially in pregnant females; discoloration of teeth and bone dysplasia in the human fetus and children; and suprainfections, especially oral and anogenital candidiasis. Tetracycline should be used with caution in patients with renal insufficiency. The most important toxic effect of chloramphenicol is bone marrow suppression, which is dose related and idiosyncratic. The incidence of undesirable side effects associated with the use of erythromycin is low. Gastrointestinal irritation is the most common; cholestatic hepatitis may occur with erythromycin estolate. Pseudomembranous colitis is the most important toxic effect associated with clindamycin.
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PMID:Tetracyclines, chloramphenicol, erythromycin, and clindamycin. 90 15

1. In animal studies, TPTA was found to be neurotoxic. In humans, variable CNS pictures have been described with or without significant EEG findings. Brain CT does not usually reveal any abnormalities. 2. Our patient presented with intermittent unique spontaneous involuntary movement of hands, facial twitching, silly smile and crying. Diplopia, drowsiness, giddiness, vertigo, bidirectional nystagmus, impairment of calculation ability, as well as disorientation to time, people and place also developed. EEG showed mild cortical dysfunction without seizures. MRI and Tc-99m HMPAO brain SPECT revealed no significant findings. TPTA may cause cellular dysfunction of brain without structural damage, which results in variable CNS clinical presentations. 3. Nadir of leucopenia was noted on the sixth day after consumption of TPTA. Liver impairment occurred on the ninth day. Borderline demyelinated neuropathy developed on the fifty-third day. CNS abnormalities, delayed peripheral neuropathy, hepatitis and leucopenia deserve monitoring for a prolonged period, even when the victim initially presents with GI upset only after consumption of TPTA.
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PMID:Unique cerebral dysfunction following triphenyltin acetate poisoning. 972 37