Rifabutin
MATERIALS AND METHODS Isolates. Twenty-six clinical isolates of Aspergillus A. fumigatus, n 16; A. flavus, n 10 ; and 25 clinical isolates of Fusarium F. solani, n 11; F. moniliforme, n 5; F. semitectum, n 5; F. proliferatum, n 4 ; were obtained from the Clinical Microbiology Laboratory at the Shands Teaching Hospital at the University of Florida, Gainesville, or the Fungus Testing Laboratory, University of Texas Health Sciences Center, San Antonio. Paecilomyces variotii ATCC 22319 was incorporated into each set of experiments as a quality control isolate. Antimicrobial agents. A stock solution of amphotericin B Bristol-Myers Squibb, Princeton, N.J. ; at a concentration of 1, 600 g ml was prepared in sterile water and was stored at 70C in 0.5-ml aliquots. Amphotericin B stock solutions were used within 2 months of initial preparation. A stock solution of rifabutin Pharmacia-Upjohn, Kalamazoo, Mich. ; at a concentration of 1, 600 g ml in methanol was prepared fresh from powder for each experiment. Susceptibility testing. A two-dimensional macrodilution checkerboard technique was used for susceptibility testing. Details of the procedure have been described elsewhere 23 ; . Briefly, testing was performed in RPMI 1640 medium American Biorganics, Inc., Niagara Falls, N.Y. ; with L-glutamine but without bicarbonate, and the RPMI 1640 medium was buffered to pH 7.0 with 0.165 M morpholinepropanesulfonic acid MOPS ; . Aliquots of 50 l each drug at concentrations 20 times the final concentrations were dispensed into polystyrene tubes 12 by 75 the case of single-drug controls, 50 l of sterile water was dispensed along with 50 l of drug. Final test concentrations ranged from 0.03 to 16 g for amphotericin B and 0.06 to 32 g for rifabutin. In addition, tubes containing methanol at concentrations similar to those present in the rifabutin control tubes were prepared to ascertain that methanol at these concentrations did not affect fungal growth. In total, 132 tubes were used to test each isolate. Isolates were subcultured onto potato dextrose agar at 35C for 7 to 10 days. Plates containing sporulated Aspergillus or Fusarium were overlaid with 5 ml of sterile water, the surface was scraped with a sterile inoculating loop, and the resulting suspension was transferred to a glass tube with a sterile transfer pipette. The suspension was vortexed and diluted 1: 100 with sterile water, and the number of conidia was counted with a hemacytometer. The suspension was adjusted to a concentration of 1 105 to 5 105 CFU ml and was diluted 1: 10.
REFERENCES 1. Acocella, G. 1978. Clinical pharmacokinetics of rifampicin. Clin. Pharmacokinet. 3: 108127. 2. Adkins, J. C., and D. Faulds. 1998. Amprenavir. Drugs 55: 837842. 3. Brophy, D. F., D. S. Israel, A. Pastor, C. Gillotin, G. E. Chittick, W. T. Symonds, Y. Lou, B. M. Sadler, and R. E. Polk. 2000. Pharmacokinetic interaction between amprenavir and clarithromycin in healthy male volunteers. Antimicrob. Agents Chemother. 44: 978984. 4. Burman, W. J., K. Gallicano, and C. Peloquin. 1999. Therapeutic implications of drug interactions in the treatment of human immunodeficiency virus-related tuberculosis. Clin. Infect. Dis. 28: 419430. 5. Cato, A., III, J. Cavanaugh, H. Shi, A. Hsu, J. Leonard, and R. Granneman. 1998. The effect of multiple doses of ritonavir on the pharmacokinetics of rifabutin. Clin. Pharmacol. Ther. 63: 414421. 6. Centers for Disease Control and Prevention. 2000. Updated guidelines for the use of rifabutin or rifampin for the treatment and prevention of tuberculosis among HIV-infected patients taking protease inhibitors or nonnucleoside reverse transcriptase inhibitors. Morb. Mortal. Wkly. Rep. 48: 185189. 7. Danner, S., A. Carr, J. M. Leonard L. M. Lehman, F. Gudiol, J. Gonzales, A. Raventos, R. Rubio, E. Bouza, and V. Pintado. 1995. A short-term study of the safety, pharmacokinetics, and efficacy of ritonavir, an inhibitor of HIV-1 protease. N. Engl. J. Med. 7: 15281533. 8. Decker, C. J., L. M. Laitinen, G. W. Bridson, S. A. Raybuck, R. D. Tung, and P. R. Chaturvedi. 1998. Metabolism of amprenavir in liver microsomes: role of CYP3A4 inhibition for drug interactions. J. Pharm. Sci. 87: 803807. 9. Fitzsimmons, M. E., and J. M. Collins. 1997. Selective biotransformation of the human immunodeficiency virus protease inhibitor saquinavir by human small-intestinal cytochrome P4503A4: potential contribution to high firstpass metabolism. Drug Metab. Dispos. 25: 256266. 10. Flexner, C. 1998. HIV-protease inhibitors. N. Engl. J. Med. 338: 12811292. 11. Garaibeh, M. N., L. P. Gillen, B. Osborne, J. I. Schwartz, and S. A. Waldman. 1998. Effect of multiple doses of rifampin on the [14C N-methyl] erythromycin breath test in healthy male volunteers. J. Clin. Pharmacol. 38: 492495. 12. Griffith, D. E., D. A. Brown, W. M. Girard, and R. J. Wallace. 1995. Adverse events associated with high-dose rifabutin in macrolide-containing regimens for the treatment of Mycobacterium avium complex lung disease. Clin. Infect. Dis. 21: 594598. 13. Hafner, R., J. Bethel, M. Power, B. Landry, M. Banach, L. Mole, H. C. Standiford, S. Follansbee, P. Kumar, R. Raasch, and G. Drusano. 1998. Tolerance and pharmacokinetic interactions of rifabutin and clarithromycin in human immunodeficiency virus-infected volunteers. Antimicrob. Agents Chemother. 42: 631639. 14. Hall, S. D., K. E. Thummel, P. B. Watkins, K. S. Lown, L. Z. Benet, M. F. Paine, R. R. Mayo, D. K. Turgeon, D. G. Bailey, R. J. Fontana, and S. A. Wrighton. 1999. Molecular and physical mechanisms of first-pass extraction. Drug Metab. Dispos. 27: 16116. 15. Iatsimirskaia, E., S. Tulebaev, E. Storozhuk, I. Utkin, D. Smith, N. Gerber, and T. Koudriakova. 1997. Metabolism of rifabutin in human enterocyte and liver microsomes: kinetic parameters, identification of enzyme systems, and drug interactions with macrolides and antifungal agents. Clin. Pharmacol. Ther. 61: 554562. 16. Jamis-Dow, C. A., A. G. Katki, J. M. Collins, and R. W. Klecker. 1997. Rifampin and rifabutin and their metabolism by human liver esterases. Xenobiotica 27: 10151024. 17. Kim, R. B., M. F. Fromm, C. Wandel, B. Leake, A. J. J. Wood, D. M. Roden, and G. R. Wilkinson. 1998. The drug transporter P-glycoprotein limits oral absorption and brain entry of HIV-1 protease inhibitors. J. Clin. Investig. 101: 289294!
Concomitant administration of rifampin or rifabutin is known to reduce atovaquone levels by approximately 50% and 34%, respectively.
Rifampin, rifabutin ; andstrong inhibitors e, g.
Patients 34, 47, 51, and 53 had abnormalities in Ph cells; the karyotype reflects the most recent evaluation. MUD indicates matched unrelated donor; and TBI, total body irradiation. Other abbreviations are explained in the text and Table 1.
Rifabutin is known to increase the metabolism of other drugs metabolized by the cytochrome P.450 system. The interaction between rifabutin and cyclosporine has not been studied. Care should be exercised when these two drugs are administered concomitantly. Other Drug lnteractions: Reduced dearance of prednisolone, digoxin, and lovastatin has been observed when these drugs are administered with cyclosporine. In addition, a decrease in the apparent volume of distribution ofdigoxin has been reported after cyclosporine administration. Severe digitalis toxicity has been seen within days ofstarting cyclosporine in several patients taking digoxin. Cyclosporine should not be used with potassium-sparing diuretics because hyperkalemia can occur. During treatment with cyclosporine, vaccination may be less effective. The use oflive vaccines should be avoided. Myositis has occurred with concomitant lovastatin, frequent gingival hyperplasia with nifedipine. and convulsions with high dose methylprednisolone. Further information on drugs that have been reported to interact with cyclosporine is available from Sandoz Pharmaceuticals Corporation. Carcinogenesis, Mutugenesis, and Impairment of Fertility: Cyclosporine gave no evidence of mutagenic or teratogenic effects in appropriate test systems. Only at dose levels toxic to dams, were adverse effects seen in reproduction studies in rats. See Pregnancy ; Carcinogenicity studies were carried out in male and female rats and mice. In the 78-week mouse study, evidence ofa statistically significant trend was found for Iymphocytic Iymphomas in females, and the incidence ofhepatocellular carcinomas in mid-dose males significantly exceeded the control value. In the 24-month rat study. pancreatic islet cell adenomas significantly exceeded the control rate in the low dose level. Doses used in the mouse and rat studies were 0.01 to 0.16 times the clinical maintenance dose. The hepatocellular carcinomas and pancreatic islet cell adenomas were not dose related. No impairment in fertility was demonstrated in studies in male and female rats. Cydosporine has not been found to be mutagenic genotoxic in the Ames Test, the V79-HGPRT Test, the micronucleus test in mice and Chinese hamsters, the chromosome-aberration tests in Chinese hamster bone-marrow, the mouse dominant lethal assay. and the DNA-repair test in sperm from treated mice. A recent study analyzing sister chromatid exchange SCE ; induction by cyclosporine using human lymphocytes in vitro gave indication ofa positive effect i.e. induction ofSCE ; , at high concentrations in this system. An increased incidence of malignancy is a recognized complication of immunosuppression in recipients oforgan transplants. The most common forms ofneoplasms are non-Hodgkin's lymphoma and carcinomas of the skin. The risk of malignancies in cyclosporine recipients is hipher than in the normal, healthy population but similar to that in patients receiving other immunosuppressive therapies. Reduction or discontinuance of immunosuppression may cause the lesions to regress. Pregnancy: Pregnancy Category C. Cyclosporine has been shown to be embryo- and fetotoxic in rats and rabbits following oral administration at maternally toxic doses. Fetal toxicity was noted in rats at 0.8 and rabbits at 5.4 times the human maintenance dose of6.O mg kg. where dose corrections are based on body surface area. Cyclosporine was embryo- and fetotoxic as indicated by increased pre. and postnatal mortality and reduced fetal weight together with related skeletal retardations. There are no adequate and well'controlled studies in pregnant women. Neoral5 should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. The following data represent the during pregnancy, 90% ofwhom throughout the entire gestational birth gestational period of28 to occurred. Most of the pregnancies reported outcomes ofll6 pregnancies in women receiving cyclosporine were transplant patients, and most ofwhom received cyclosporine period. The only consistent patterns of abnormality were premature 36 weeks ; and low birth weight for gestational age. Sixteen fetal losses 85 of 100 ; were complicated by disorders, including pre-eclampsia and rifadin.
Quantification of BCR-ABL transcripts in Ph ALL has been used to assess treatment response and to detect residual leukemia prior to overt hematologic relapse.15, 25-28 Radich et al25 studied 36 adults with Ph ALL and found that patients who were PCR positive after SCT have a significantly higher probability of relapse than PCR-negative patients. Recently, Scheuring et al29 reported on the usefulness of MRD analysis, using RQ-PCR in patients with relapsed or refractory Ph ALL treated with imatinib monotherapy as a salvage treatment. They found that 40 71% ; of the 56 patients achieved a good response with a significant decrease in MRD 1.37 logs in BM, 2.64 logs in PB ; , and that the BCR-ABL levels in BM and PB after 2 weeks of imatinib treatment and in BM after 4 weeks had a predictive relevance to response and progression-free survival. On the basis of these results, we investigated the MRD-based role of imatinib as a first-line interim therapy in newly diagnosed Ph ALL. Using RQ-PCR, we found that median BCR-ABL ABL ratios reduced by 0.77 log in 25 responders 86.2% ; after the first imatinib cycle, compared with levels after induction. After the second imatinib cycle, median BCR-ABL ABL ratios decreased by 0.34 log, compared with levels after consolidation. Furthermore, imatinib interim therapy possibly induced molecular CR in 7 patients. Indeed, 28 of the 29 enrolled patients underwent allogeneic SCT as scheduled after the completion of imatinib interim therapy. Of these, which included 7 patients with molecular CR, 25 were in first CR at the time of SCT. Patients receiving imatinib interim therapy showed a lower incidence of relapse during the consolidation phase and a higher rate of proceeding to SCT in first CR than the historical patients. A possibility of effect of different induction regimen or CNS prophylaxis on the pretransplantation disease status may be excluded in this study because CR rates after induction chemotherapy and incidence of CNS leukemia were similar between the 2 groups Table 1 ; . Several potential factors could account for the increased success of performing allogeneic SCT in first CR, including increased availability of HLA-matched unrelated donors and development of supportive care. Nevertheless, considering the similar presenting features and the same postinduction chemotherapy protocol, it is unlikely that these results were caused merely by selection biases. Rather, these results likely reflect an effect of imatinib on improving the quality of response and further reducing leukemia burden before SCT. Shimoni et al30 also reported on the substantial activity of pretransplantation imatinib monotherapy for patients with chronic myeloid leukemia in blastic crisis n 10 ; and Ph ALL n 5 ; . their study, 11 of the 15 patients received transplants in the chronic phase or in CR. Therefore, first-line imatinib interim therapy allowed SCT to be conducted in a more favorable status in association with a low MRD level in patients with Ph ALL.
REFERENCES 1. Barditch-Crovo, P., S. G. Deeks, A. Collier, S. Safrin, D. F. Coakley, M. Miller, B. P. Kearney, R. L. Coleman, P. D. Lamy, J. O. Kahn, I. McGowan, and P. S. Lietman. 2001. Phase I II trial of the pharmacokinetics, safety, and antiretroviral activity of tenofovir disoproxil fumarate in human immunodeficiency virus-infected adults. Antimicrob. Agents Chemother. 45: 27332739. 2. Borin, M. T., J. H. Chambers, B. J. Carel, S. Gagnon, and W. W. Freimuth. 1997. Pharmacokinetic study of the interaction between rifampin and delavirdine mesylate. Clin. Pharmacol. Ther. 61: 544553. 3. Bowen, E. F., P. S. Rice, N. T. Cooke, R. J. Whitfield, and C. F. Rayner. 2000. HIV seroprevalence by anonymous testing in patients with Mycobacterium tuberculosis and in tuberculosis contacts. Lancet 356: 14881489. 4. Burman, W. J., K. Gallicano, and C. Peloquin. 2001. Comparative pharmacokinetics and pharmacodynamics of the rifamycin antibacterials. Clin. Pharmacokinet. 40: 327341. 5. Cundy, K. C., C. Sueoka, G. R. Lynch, L. Griffin, W. A. Lee, and J. P. Shaw. 1998. Pharmacokinetics and bioavailability of the anti-human immunodeficiency virus nucleotide analog 9-[ R ; -2- phosphonomethoxy ; propyl]adenine PMPA ; in dogs. Antimicrob. Agents Chemother. 42: 687690. 6. Deeks, S. G., P. Barditch-Crovo, P. S. Lietman, F. Hwang, K. C. Cundy, J. F. Rooney, N. S. Hellmann, S. Safrin, and J. O. Kahn. 1998. Safety, pharmacokinetics, and antiretroviral activity of intravenous 9-[2- R ; - phosphonomethoxy ; propyl]adenine, a novel anti-human immunodeficiency virus HIV ; therapy, in HIV-infected adults. Antimicrob. Agents Chemother. 42: 2380 2384. Douglas, J. G., and M. J. McLeod. 1999. Pharmacokinetic factors in the modern drug treatment of tuberculosis. Clin. Pharmacokinet. 37: 127146. 8. Finch, C. K., C. R. Chrisman, A. M. Baciewicz, and T. H. Self. 2002. Rifampin and rifabutin drug interactions: an update. Arch. Intern. Med. 162: 985992. 9. Greiner, B., M. Eichelbaum, P. Fritz, H. P. Kreichgauer, O. von Richter, J. Zundler, and H. K. Kroemer. 1999. The role of intestinal P-glycoprotein in the interaction of digoxin and rifampin. J. Clin. Investig. 104: 147153. 10. Justesen, U. S., A. B. Andersen, N. A. Klitgaard, K. Brosen, J. Gerstoft, and C. Pedersen. 2004. Pharmacokinetic interaction between rifampin and the combination of indinavir and low-dose ritonavir in HIV-infected patients. Clin. Infect. Dis. 38: 426429. 11. Kearney, B. P., J. F. Flaherty, and J. Shah. 2004. Tenofovir disoproxil fumarate: clinical pharmacology and pharmacokinetics. Clin. Pharmacokinet. 43: 595612. 12. la Porte, C. J., E. P. Colbers, R. Bertz, D. S. Voncken, K. Wikstrom, M. J. Boeree, P. P. Koopmans, Y. A. Hekster, and D. M. Burger. 2004. Pharmacokinetics of adjusted-dose lopinavir-ritonavir combined with rifampin in healthy volunteers. Antimicrob. Agents Chemother. 48: 15531560. 13. Lopez-Cortes, L. F., R. Ruiz-Valderas, P. Viciana, A. Alarcon-Gonzalez, J. Gomez-Mateos, E. Leon-Jimenez, M. Sarasanacenta, Y. Lopez-Pua, and J. Pachon. 2002. Pharmacokinetic interactions between efavirenz and rifampicin in HIV-infected patients with tuberculosis. Clin. Pharmacokinet. 41: 681 690. Msamanga, G. I., and W. W. Fawzi. 1997. The double burden of HIV infection and tuberculosis in sub-Saharan Africa. N. Engl. J. Med. 337: 849 851. Peloquin, C. A., R. Namdar, M. D. Singleton, and D. E. Nix. 1999. Pharmacokinetics of rifampin under fasting conditions, with food, and with antacids. Chest 115: 1218. 16. Polk, R. E., D. F. Brophy, D. S. Israel, R. Patron, B. M. Sadler, G. E. Chittick, W. S. Symonds, Y. Lou, D. Kristoff, and D. S. Stein. 2001. Pharmacokinetic interaction between amprenavir and rifabutin or rifampin in healthy males. Antimicrob. Agents Chemother. 45: 502508 and rifapentine.
Conflicts of interests Joan-Carles Arce, Lisbeth Helmgaard and Per Srensen are employees of Ferring Pharmaceuticals. Sren Ziebe, Kersti 2148.
REFERENCES 1. Alder, J., M. Mitten, N. Shipkowitz, L. Hernandez, Y. Hui, K. Marsh, and J. Clement. 1994. Treatment of experimental Pneumocystis carinii infection by combination of clarithromycin and sulphamethoxazole. J. Antimicrob. Chemother. 33: 253263. 2. Araujo, F. G., T. Slifer, and J. S. Remington. 1994. Rifabutin is active in murine models of toxoplasmosis. Antimicrob. Agents Chemother. 38: 570 575. Bartlett, M., S. Queener, M. Shaw, J. Richardson, and J. Smith. 1994. Pneumocystis carinii is resistant to imidazole antifungal agents. Antimicrob. Agents Chemother. 38: 18591861. 4. Black, J. R., J. Feinberg, R. F. Murphy, R. J. Fass, J. Carey, and F. R. Sattler. 1991. Clindamycin and primaquine as primary treatment for mild and moderately severe Pneumocystis carinii in patients with AIDS. Eur. J. Clin. Microbiol. Infect. Dis. 10: 204207. 5. Brun-Pascaue, M., F. Chau, L. Garry, D. Jacobus, F. Derouin, and M. Girard. 1996. Combination of PS-15, epiroprim, or pyrimethamine with dapsone in prophylaxis of Toxoplasma gondii and Pneumocystis carinii dual infection in a rat model. Antimicrob. Agents Chemother. 40: 20672070. 6. Centers for Disease Control and Prevention. 1995. USPHS IDSA guidelines for the prevention of opportunistic infections in persons infected with human immunodeficiency virus: a summary. Morbid. Mortal. Weekly Rep. 44: 134. 7. Clarkson, A., S. Muhamed, and R. Grady. 1990. Deferoxamine and eflornithine DL difluoromethylornithine ; in a rat model of Pneumocystis carinii pneumonia. Antimicrob. Agents Chemother. 34: 18331835. 8. Comley, J. C. W., and A. M. Sterling. 1995. Effect of atovaquone and atovaquone drug combinations on prophylaxis of Pneumocystis carinii pneumonia in SCID mice. Antimicrob. Agents Chemother. 39: 806811. 9. Crampton, S., J. C. Craft, G. Notaro, and D. Henry. 1996. Prevention of Pneumocystis carinii pneumonia in AIDS patients by clarithromycin prophylaxis for Mycobacterium avium complex MAC ; . In Abstracts of the Third International Conference on Macrolides, Azalides, and Streptogramins. 10. Frenkel, J. K., J. T. Good, and J. A. Schultz. 1966. Latent Pneumocystis infection of rats, relapse, and chemotherapy. Lab. Invest. 15: 15591577. 11. Gonzalez-Ruiz, A., S. Haworth, A. O'Neil, and D. Warhurst. 1991. Dapsone in low doses prevents Pneumocystis carinii pneumonia in the rat model. J. Infect. 22: 143152. 12. Greco, W. R., G. Bravo, and J. C. Parsons. 1995. The search for synergy: a critical review from a response surface perspective. Pharmacol. Rev. 47: 331 385. Guay, D. R. P., D. R. Patterson, N. Seipman, and J. C. Craft. 1993. Overview of the tolerability profile of clarithromycin in preclinical and clinical trials. Drug Safety 18: 350364. 14. Guo-Zhong, C., L. Foster, and J. Bennett. 1990. Antischistosomal action of mevinolin: evidence that 3-hydroxy-methylglutaryl-coenzyme a reductase activity in Schistosoma mansoni is vital for parasite survival. Arch Pharmacol. 342: 477482. 15. Hughes, W. T., J. Killmar, and H. Oz. 1994. Relative potency of 10 drugs with anti-Pneumocystis carinii activity in an animal model. J. Infect. Dis. 170: 906911. 16. Hughes, W. T., and B. L. Smith. 1984. Efficacy of diaminodiphenyl-sulfone and other drugs in murine Pneumocystis carinii pneumonitis. Antimicrob. Agents Chemother. 26: 436440. 17. Kaneshiro, E., J. Ellis, H. Zhou, H. Rudney, A. Gupta, K. Jayasimhulu, K. Setchell, and D. Beach. 1994. Isoprenoid metabolism in Pneumocystis carinii. J. Eukaryot. Microbiol. 41 Suppl. ; : 93. 18. Kaneshiro, E. S., J. E. Ellis, K. Jayasimhulu, and D. E. Beach. 1994. Evidence of "metabolic sterols" in Pneumocystis: identification and initial characterization of Pneumocystis carinii sterols. J. Eukaryot. Microbiol. 41: 78 85. Kim, C. K., J. M. Foy, M. T. Cushion, D. Stanforth, M. J. Linke, H. L. Hendrix, and P. D. Walzer. 1987. Comparison of histologic and quantitative and rifaximin.
This work was supported by National Institutes of Health Grants CA76643 to M.R.K. ; , NS38506 to M.R.K. ; , R43 CA83507 to M.R.K. ; , P01-CA75426 to M.R.K., D.A.W. ; , and Department of Defense-Congressionally Directed Medical Research Programs Predoctoral Fellowship BC991226 to M.L.-F.
Pathognomonic ; of papillary carcinoma of the thyroid. 101: 1448-50 and riluzole.
Centers for Disease Control and Prevention. Prevention and treatment of tuberculosis among patients infected with human immunodeficiency virus: principles of therapy and revised recommendations. MMWR Morb Mortal Wkly Rep 1998; 47 : 1-25. British HIV Association. BHIVA treatment guidelines for TB HIV infection September 2004; p. 1-32. Available at : bhiva accessed on January 5, 2005 ; . World Health Organization. Fact sheets on antiretroviral drugs. New Delhi: WHO, SEARO; 2002 p. 11. SEAAIDS-134. World Health Organization. Scaling up antiretroviral therapy in resource-limited settings: treatment guidelines for a public health approach. 2003 revision. Geneva: World Health Organization; 2004 p. 40-2. Dean GL, Edwards SG, Ives NJ, Matthews G, Fox EF, Navaratne L, et al. Treatment of tuberculosis in HIVinfected persons in the era of highly active antiretroviral therapy. AIDS 2002; 16 : 75-83. Sun E, Heath-Chiozzi M, Cameron DW. Concurrent ritonavir and rifabutin increases risk of rifabutin-associated adverse events [Abstract]. In Program and abstracts of the XI International Conference on AIDS. Vancouver, British Columbia; 1996: Mo.B.171. El-Sadr WM, Perlman DC, Denning E, Matts JP, Cohn DL. A review of efficacy studies of 6-month short course therapy for tuberculosis among patients infected with human immunodeficiency virus: differences in study outcomes. Clin Infect Dis 2001; 32 : 623-32. Korenromp EL, Scano F, Williams BG, Dye C, Nunn P. Effects of human immunodeficiency virus infection on recurrence of tuberculosis after rifampicin-based treatment: an analytical review. Clin Infect Dis 2003; 37 : 101-12. Perriens JH, St Louis ME, Mukadi YB, Brown C, Prignot J, Pouthier F, et al. Pulmonary tuberculosis in HIV-infected patients in Zaire. A controlled trial of treatment for either 6 or 12 months. N Engl J Med 1995; 332 : 779-84. Fitzgerald DW, Desvarieux M, Severe P, Joseph P, Johnson WD Jr, Pape JW. Effect of post-treatment isoniazid on prevention of recurrent tuberculosis in HIV-1-infected individuals: a randomised trial. Lancet 2000; 356 : 1470-4. Dooley DP, Carpenter JL, Rademacher S. Adjunctive corticosteroid therapy for tuberculosis: a critical reappraisal of the literature. Clin Infect Dis 1997; 25 : 872-87. Hakim JG, Ternouth I, Mushangi E, Siziya S, Robertson V, Malin A. Double blind randomised placebo controlled trial of adjunctive prednisolone in the treatment of effusive.
These studies were successful in standardising various factors such as type of drug, dose and exercise levels, and in excluding patients with premorbid psychiatric disorders and or substance abuse. Thus, at least to some extent, these studies evaluated the effects of steroids in isolation. As a result, they did not explore the effects of a multitude of issues that occur in regular practice, such as use of steroids at extremely supratherapeutic doses, stacking of multiple steroids simultaneously, the presence of preexisting psychiatric disorders and the effects of other high-risk behaviours that may accompany steroid use and rimantadine.
ACTIONS Calcium chloride increases the force of myocardial contraction; calcium may either increase or decrease systemic vascular resistance. In normal hearts, calcium's positive inotropic and vasoconstricting effects produce a predictable rise in systemic arterial pressure. INDICATIONS Calcium chloride is indicated during resuscitation for the treatment of hypocalcemia and calcium channel blocker toxicity e.g. Verapamil or Cardizem overdose ; and magnesium sulfate overdose. It also protects the heart from hyperkalemia as may occur in patients with end-stage renal disease. CONTRAINDICATIONS Cardiopulmonary arrest not associated with calcium channel blocker toxicity, hypocalcemia, or hyperkalemia. ADVERSE REACTIONS AND SIDE EFFECTS If the heart is beating, rapid administration of calcium can produce slowing of cardiac rate. WARNINGS Calcium chloride should not be administered in the same infusion with sodium bicarbonate, since calcium will combine with sodium bicarbonate to form an insoluble precipitate calcium carbonate ; . Calcium chloride should be given with extreme caution, and in reduced dosage, to persons taking digitalis because it increases ventricular irritability and may precipitate digitalis toxicity. DOSAGE Adult: For hypotension following administration of calcium channel blockers e.g. Cardizem, Verapamil ; : 4 mg kg IV, slowly. If patient is taking digitalis, 2 mg kg IV, slowly. Repeat every 10 min. PRN. For calcium channel blocker overdose and hyperkalemia: 8-16 mg kg IV, slowly. Ped: 5 mg kg. or 0.2 ml kg IV, slowly, every 10 min. PRN For calcium channel blocker overdose and hyperkalemia: 20 mg kg IV, slowly.
INTRODUCTION: Interactions between rifamycins and anti-HIV drugs complicates the management of both tuberculosis TB ; and HIV infection. This study compares rifabutin and rifampin in the treatment of HIV-associated TB in terms of clinical efficacy and impact on anti-HIV therapy. METHODS: Retrospective review of all medical records from HIV positive patients with tuberculosis admitted to AIDS Unit, St. Pierre Hospital Brussels, Belgium ; , from January 1998 to December 2004. Demographic data, HAART regimen, adverse events, CD4 cell count, plasma HIV RNA VL ; and TB outcomes were extracted. The data were analyzed by Mantel-Haenszel method. RESULTS: 122 patients were evaluated rifabutin: 57, rifampin: 65 ; . Clinical cure was obtained in 51 57 89, % ; vs 53 65 82, ; . Among the 6 remaining rifabutin patients, 2 presented disease relapse, 3 were lost to follow-up during the treatment and 1 died notrelated to TB ; . Whereas in the 12 remaining rifampin patients, 10 were lost to follow-up and 2 died from tuberculosis. 44 patients were on HAART at TB diagnosis.10 patients never started HAART. Among the 68 remaining patients, time to initiation of HAART was 3 months in 37 patients 22 in the rifabutin group and 15 in the rifampin group ; and 3 months in 31 patients 14 in the rifabutin group and 17 in the rifampin group ; . Response to antiretroviral therapy was comparable in both groups despite the fact that rifabutin patients had a higher VL at baseline 367332 vs 178177 ; . CONCLUSIONS: Clinical outcome of TB was comparable in rifabutin and rifampin patients. Patients on rifabutin tended to be treated earlier and showed a similar response to HAART compared to rifampin patients, despite higher viral load at baseline and ritonavir.
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18.5.1. Rifamycins The rifamycins are metabolized mainly in the liver, and to a lesser extent in the intestine wall, where they induce several pathways involving isoenzymes of the cytochrome P450 system, such as the isoenzyme CYP3A4 Yew 2002 ; . The extent of the induction of the isoenzyme CYP3A4 depends on the particular rifamycin drug that is being used, and so, RIF is the most potent inducer, whereas rifapentine is a moderate inducer and rifabutin is the least potent inducer of the isoenzyme CYP3A4. Rifabutin, but not RIF or rifapentine, is also a substrate of CYP3A4. Then, other drugs that share or interact with the cytochrome P450 system may have significant levels of interaction with the rifamycins and rifabutin.
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Buscail, R., Schrimm, M. and Adjeroud, M. 1998 ; Variability of sedimentary organic matter in an insular coral reef ecosystem: bay, lagoon and external slope Moorea, French Polynesia ; . Int. Soc. Reef Stud., Perpignan pp. 37 and rituxan.
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