Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149514 (bronchitis)
6,902 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two prospective randomized, double-blind, parallel studies were carried out in Europe to compare cefaclor advanced formulation (cefaclor AF) with cefaclor in the treatment of acute bronchitis caused by susceptible pathogens. A total of 1,321 patients suffering from acute bronchitis confirmed by clinical data and a negative chest X-ray were randomized for treatment in the two multicentre trials. Three doses of cefaclor AF were tested: 375 mg twice daily and 500 mg twice daily were compared with cefaclor 250 mg three times daily; and cefaclor AF 750 mg twice daily was compared with cefaclor 500 mg three times daily. Duration of therapy was seven days. Assessments (complete history, physical examination, sputum specimens for culture and Gram's stain, plus clinical and laboratory evaluations of safety) were carried out within 24 hours before the first dose, during therapy, within 72 hours after therapy completion and, in the 375 mg and 500 mg dose groups, 1-2 weeks after the end of therapy. There were no significant differences between the total evaluable cefaclor AF population and the total evaluable cefaclor population with regard to favourable post-therapy responses. Most favourable clinical and bacteriological response rates in the 375 and 500 mg doses were 80% or above. In the higher dose group, there was a favourable post-therapy symptomatic response in 100% of evaluable patients, with favourable bacteriological responses in 93.3% patients receiving cefaclor AF and 96.8% receiving cefaclor (no significant difference). Only one serious drug-related adverse event was reported (anaphylactic reaction). Adverse events related to the digestive system were reported by 4.7% of the cefaclor AF-treated patients and 4.5% of the cefaclor-treated patients during the entire study period. Cefaclor AF, at all three dose levels studies, was seen to be as safe as cefaclor in the treatment of acute bronchitis caused by Streptococcus pneumoniae, Haemophilus influenzae and Moraxella (Branhamella) catarrhalis.
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PMID:A multicentre trial of cefaclor advanced formulation versus cefaclor in the treatment of acute bronchitis. 128 14

A 54-year-old female with bronchial asthma and PIE syndrome induced by disodium cromoglycate (DSCG) was reported. She was referred to our hospital for further examination of the abnormal chest shadows and eosinophilia. She had been treated with DSCG, Cefaclor. Bromhexine and bronchodilator for bronchial asthma and bronchitis. Withdrawal of the drugs except for the bronchodilators alleviated her symptoms. Therefore, drug induced lymphocytes stimulation tests (DLST) were performed for those three drugs. Only DLST for DSCG showed a positive result. She had been asthmatic for ten years and treated by the drug for 18 months prior to admission. The skin test for the drug was negative and a precipitating antibody for the drug could not be found. To obtain a definite diagnosis, bronchial challenge by DSCG was performed, after her symptoms were under control. Severe asthmatic responses were provoked in 6 and 24 hours after the inhalation of DSCG. Bronchoalveolar lavage, performed 8 days after the provocation, revealed increased eosinophils and lymphocytes in BAL fluid. Although several cases of PIE syndrome induced by DSCG have been reported, this seems to be the first report of late and delayed type bronchial response and pulmonary infiltration with eosinophilia provoked by DSCG. The bronchial response to the drug was a late and delayed type reaction and sustained for a long period. This might indicate that PIE syndrome induced by the drug may be caused by a same mechanism as the provoked asthmatic response.
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PMID:[A case of bronchial asthma and PIE Syndrome induced by disodium cromoglycate]. 250 49

Cefaclor and tetracycline were compared in a single-blind study designed to treat patients with acute bacterial bronchitis and acute exacerbations of chronic bronchitis. Twenty-five pathogens (including 19 of Haemophilus influenzae and four of Streptococcus pneumoniae) were obtained from sputum samples of 48 patients. No pathogen could be cultured from the sputum of 23 patients. All of these pathogens were susceptible to cefaclor, while 12 (63%) of the 19 H influenzae isolates and three of the four S pneumoniae isolates were resistant to tetracycline. When the susceptibility of the 25 isolates to other commonly used antibacterials was tested, 18 isolates of H influenzae were resistant to erythromycin and one was resistant to ampicillin. (One H influenzae isolate was not tested for erythromycin susceptibility.) The four isolates of S pneumoniae were susceptible to erythromycin and ampicillin. Satisfactory results were achieved in 21 of the 23 patients receiving cefaclor. After four to six days of cefaclor therapy, the other two patients were diagnosed as having bronchopneumonia, and parenteral antibiotic therapy was instituted. Of the 25 patients assigned to the tetracycline regimen, three with resistant H influenzae had unsatisfactory clinical responses and required parenteral antibiotic therapy for recovery. Although patients were randomly assigned to therapy, only three of the 16 patients infected with tetracycline-resistant organisms were assigned to the tetracycline group, and all three failed to respond to treatment. Had the patients been more evenly distributed according to susceptibilities, it is possible that more treatment failures would have occurred in the group receiving tetracycline.
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PMID:A comparison of cefaclor and tetracycline in the treatment of bacterial bronchitis. 623 Nov 4