• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2012.10a
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• pp.991-993
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• 2012

We analyzed RNA polymerase beta subunit gene (rpoB) mutation of rifampin-resistant Mycobacteria through analysis of nucleotide sequence of rpoB DNA (351 bp) containing rifampin resistant region, $rif^r$. For this study, we collected rifampin-resistant Mycobacteria that were identified by conventional culture methods from Masan National Hospital and The Korean Institute of Tuberculosis. We performed sequencing of DNA nucleotides and analyzed rpoB gene of those rifampin-resistant Mycobacteria. From this analysis, we invcestigated diverse mutations of rpoB gene included rifampin-resistant gene, which were not reported, from those rifampin-resistant Mycobacteria.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2012.05a
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• pp.913-915
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• 2012

RNA polymerase beta subunit gene (rpoB) mutation of rifampin-resistant Mycobacteria was analyzed using nucleotide sequence of rpoB DNA (351 bp) containing rifampin resistant region, $rif^r$. For this purpose, we collected rifampin-resistant Mycobacteria that were identified by conventional culture method from Masan National Hospital and The Korean Institute of Tuberculosis and performed analysis of nucleotide sequence of rpoB of them. We found various mutations of rpoB linked rifampin resistant gene from rifampin-resistant Mycobacteria. From this study, we identified mutations of different codons from codons that have been reported recently.

• Tuberculosis and Respiratory Diseases
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• v.47 no.6
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• pp.768-774
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• 1999

Background: It is well known that rifampin decreases the hypoprothrombinemic effect of warfarin by induction of cytochrome P-450 enzyme in healthy volunteer. However, in patients the dosage schedule of warfarin during rifampin therapy is not established. Therefore, patients taking both rifampin and warfarin were reviewed to find out the adequate dosage schedule of warfarin in addition to side effects by interaction of two drugs. Method: Patients taking both rifampin and warfarin were retrieved from patients who were admitted due to heart disease and tuberculosis at Boochun Sejong Hospital from January of 1995 to August of 1999. To decide the adequate dosage of warfarin, the dosage of warfarin before, during, and after rifampin was evaluated in patients who kept adequate hypoprothrombinemic effect of warfarin during rifampin. To decide the adequate dosage schedule of warfarin, the time interval from the beginning of rifampin to normalization of prothrombin time(INR$\geq$1.1) was evaluated. And, the side effects by interaction of two drugs were reviewed. Results: All 12 patients taking both rifampin and warfarin were retrieved. Among them only 6 kept adequate hypoprothrombinemic effect of warfarin during rifampin. The dosage of warfarin during rifampin was $2.4{\pm}0.6$(mean$\pm$standard deviation) times as much as that before rifampin but the dosage after rifampin was the same as that before rifampin. The time interval from the beginning of rifampin to normalization of prothrombin time was $5.8{\pm}2.9$(mean${\pm}$standard deviation) days. 2 out of 12 had complication related to the interaction of rifampin and warfarin, one cerebral embolism just after the beginning of rifampin and the other cerebral hemorrhage just after the discontinuation of rifampin. Conclusion: When both rifampin and warfarin are prescribed, it would be a possible method to be confirmed by prospective study that warfarin be gradually increased about 2 times more than that without rifampin over 1 week or so after the beginning of rifampin and be tapered to the same dosage as that before rifampin when rifampin is discontinued. And, it would be prudent that prothrombin time be monitored frequently during rifampin and warfarin therapy, especially the beginning or discontinuation of rifampin.

• Journal of Yeungnam Medical Science
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• v.15 no.1
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• pp.173-181
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• 1998

Rifampin is common drug to treat tuberculosis. Rifampin induced acute renal failure, hemolytic anemia and thrombocytopenia is rare and severe complication. We have experienced a case of rifampin induced acute renal failure, hemolytic anemia and thrombocytopenia. Forty-six years old male was suffered from reactivation of pulmonary tuberculosis, and had to medicate antituberculosis drugs including rifampin(600mg/day). Seven years ago, antituberdulosis medication were successfully administered to treat pulmonary tuberculosis without any side effects of drugs. But eight days after readministration of rifampin, fever, abdominal pain, vomiting, oliguria, elevated BUN and creatinine were developed. And thrombocytopenia was also identified after administration of rifampin. The patient was recovered slowly after discontinuation of rifampin & intensive medical care. The renal function was normalized at 55 days after cessation of rifampin. The renal pathologic findings were interstitial nephritis and acute tubular necrosis. And, the rifampin dependent antibodies were identified by indirect antiglobulin test in the presence of rifampin. So we report this case with a brief review of literature.

• Pediatric Infection and Vaccine
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• v.7 no.2
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• pp.240-244
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• 2000

Rifampin is a bactericidal antibiotic used primarily in the treatment of tuberculosis. The adverse effects of rifampin, though few, include dermatologic, gastrointestinal, and hepatic manifestations. Occasionally it produces a flu-like syndrome, interstitial nephritis, hemolytic anemia, and thrombocytopenia. These manifestations usually appear in patients who take the drug intermittently. We experienced a 13 year-old girl who developed thrombocytopenia during rifampin administration of daily dosage, therefore we report a brief review with the related literatures.

• The Journal of the Korean Society for Microbiology
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• v.21 no.2
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• pp.271-276
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• 1986

Amphotericin B and rifampin or 5-fluorocytosine were tested for synergism against Candida albicans in a synthetic mdium. The test was based on viability studies in which fungicidal activity was determined during the incubation hours of drug exposure. Concentration of amphotericin B(0.2ug per ml and 0.4ug per ml) in combination with inactive concentration of rifampin(12.5ug per ml) or 5-fluorocytosine(25ug per ml) resulted in rapid decrease of colony froming unit(CFU). On the basis of these and earlier studies, it is concluded that amphotericin Band rifampin or 5-fluorocytosine are synergistic against various yeasts and yeast-like fungi under widely differing experimental conditions.

• Journal of Microbiology and Biotechnology
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• v.11 no.2
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• pp.287-293
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• 2001

A fast and easy PCR-SSCP method was developed and assessed for the early detection of rifampin-resistant Mycobacterium leprae in skin biopsy samples from Korean leprosy patients. The 190 bp of the rpoB gene, in which mutation is known to cause resistance to rifampin, was amplified by PCR and then analyzed by SSCP and DNA sequencing, All PCR products showing mobility shift on PCR-SSCP contained mutations, demonstrating that this method can be used for an early diagnositic method to detect a putative rifampin-resistant M. leprae strain. DNA sequence analysis revealed that 19 of 34 patient samples contained M. leprae strains with missense mutations in the rpoB gene: five were the same mutations previously reported to cause rifampin resistance and eight were the new type of mutatios that likely cause rifampin resistance. These newly identified dmutations, whose all five cytosine bases of four amino acids were substitued with thymine, were found at different sites from those reported in Mycobacterium tuberculosis or M. leprae. Therefore, they may provide additional clues to understand the molecular biological basis on the rifampin resistance of M. leprae.

• Journal of the Korea Institute of Information and Communication Engineering
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• v.17 no.4
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• pp.1005-1009
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• 2013

Using DNA sequencing method, we analyzed mutations of rpoB (RNA polymerase beta subunit) rifampin-resistant Mycobaterium tuberculosis strains which were identified by conventional test at Masan National Hospital and The Korean Institute of Tuberculosis. Though it has been reported different mutations of rpoB region of rifampin-resistant M. tuberculosis strains in the south of Korea, it is not confirmed whether these mutations of rpoB region actually express rifampin resistance through experiment. We confirmed experimentally these mutations of rpoB region of M. tuberculosis strains induced rifampin-resistance through ampified rpoB by polymerase chain reaction (PCR) and cloning of mutant rpoB into rifampin sensitive-M. tuberculosis strain.

• Tuberculosis and Respiratory Diseases
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• v.44 no.4
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• pp.930-934
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• 1997

Drug-induced thrombocytopenia and purpura have been developed by many various agents. Rifampin and Pyrazinamide have been known as bactericidal antituberculous drugs, but, the above side effects have been a problem. Especially, hematologic side effects are fatal to patients occasionally. Rifampin-induced thrombocytopenia and purpura have been well known, also, pyrazinamide-induced thrombocytopenia have been reported. A new quilonone agent, Ciprofloxacin, has been commonly used in clinics now, but it's side effects are not known well. So, we report a case of a 23-year-old female with thrombocytopenia and purpura after taking Rifampin, Pyrazinamide, and Ciprofloxacin as antituberculous agents.

• Tuberculosis and Respiratory Diseases
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• v.65 no.2
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• pp.116-120
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• 2008

Rifampin is one of the first line drugs for treating tuberculosis, but it might be associated with serious adverse effects, including renal failure. We report here on a case of a 57-year-old patient who developed Henoch-$Sh{\ddot{o}}nlein$ purpura during antituberculosis therapy that included rifampin. The patient converted to negative on the AFB smear for tuberculosis two weeks after the initial administration of antituberculosis medication. After treatment for 60 days, this patient was diagnosed with Henoch-$Sh{\ddot{o}}nlein$ purpura by the purpura lesion on the lower legs, the leukocytoclastic vasculitis, the renal impairment and the pathological examination. After stopping rifampin, the skin lesions disappeared in about 10 days and his renal function gradually improved. This case study showed that Henoch-$Sh{\ddot{o}}nlein$ purpura can be caused by rifampin during antituberculosis therapy and we recommend that the use of rifampin should be restrained when clinical symptoms of Henoch-$Sh{\ddot{o}}nlein$ purpura are observed.