Hostname: page-component-cd9895bd7-gbm5v Total loading time: 0 Render date: 2024-12-26T21:38:37.316Z Has data issue: false hasContentIssue false
  • English
  • Français

Antimalarial interaction of quinine and quinidine with clarithromycin

Published online by Cambridge University Press:  09 November 2012

SWAROOP KUMAR PANDEY ,
HEMLATA DWIVEDI ,
SARIKA SINGH ,
WASEEM AHMAD SIDDIQUI  and
RENU TRIPATHI
SWAROOP KUMAR PANDEY
Affiliation:
Division of Parasitology, CSIR-CDRI, Lucknow, India-226001 Department of Biochemistry, Jamia Hamdard University, New Delhi, India
HEMLATA DWIVEDI
Affiliation:
Division of Parasitology, CSIR-CDRI, Lucknow, India-226001
SARIKA SINGH
Affiliation:
Division of Toxicology, CSIR-CDRI, Lucknow, India-226001
WASEEM AHMAD SIDDIQUI
Affiliation:
Department of Biochemistry, Jamia Hamdard University, New Delhi, India
RENU TRIPATHI*
Affiliation:
Division of Parasitology, CSIR-CDRI, Lucknow, India-226001
*
*Corresponding author: Division of Parasitology, P.O.Box No. 173, Central Drug Research Institute (CSIR), Chattar Manzil Palace, Lucknow 226001, India. Tel: +91 522 2612411-18 Extn. 4461. Fax: +91 522 2623405/2623938. E-mail: renu1113@rediffmail.com
Get access Rights & Permissions [Opens in a new window]

Summary

Quinine (QN) and quinidine (QND) have been commonly used as effective and affordable antimalarials for over many years. Quinine primarily is used for severe malaria treatment. However, plasmodia resistance to these drugs and poor patient compliance limits their administration to the patients. The declining sensitivity of the parasite to the drugs can thus be dealt with by combining with a suitable partner drug. In the present study QN/QND was assessed in combination with clarithromycin (CLTR), an antibiotic of the macrolide family. In vitro interactions of these drugs with CLTR against Plasmodium falciparum (P. falciparum) have shown a synergistic response with mean sum fractional inhibitory concentrations (ΣFICs) of ⩽1 (0·85 ± 0·11 for QN + CLTR and 0·64 ± 0·09 for QND + CLTR) for all the tested combination ratios. Analysis of this combination of QN/QND with CLTR in mouse model against Plasmodium yoelii nigeriensis multi-drug resistant (P. yoelii nigeriensis MDR) showed that a dose of 200 mg/kg/day for 4 days of QN or QND produces 100% curative effect with 200 mg/kg/day for 7 days and 150 mg/kg/day for 7 days CLTR respectively, while the same dose of individual drugs could produce only up to a maximum 20% cure. It is postulated that CLTR, a CYP3A4 inhibitor, might have caused reduced CYP3A4 activity leading to increased plasma level of the QN/QND to produce enhanced antimalarial activity. Further, parasite apicoplast disruption by CLTR synergies the antimalarial action of QN and QND.

Keywords

malariadrug resistancequininequinidineclarithromycin
Type
Research Article
Information
Parasitology , Volume 140 , Issue 3 , March 2013 , pp. 406 - 413
Copyright
Copyright © Cambridge University Press 2012

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

REFERENCES

Achan, J., Talisuna, A. O., Erhart, A., Yeka, A., Tibenderana, J. K., Baliraine, F. N., Rosenthal, P. J. and D'Alessandro, U. (2011). Quinine, an old anti-malarial drug in a modern world: role in the treatment of malaria. Malaria Journal 10, 144.CrossRefGoogle Scholar
Awasthi, A., Dutta, G. P., Bhakuni, V. and Tripathi, R. (2004). Resistance reversal action of ketoconazole against mefloquine resistance of Plasmodium yoelii nigeriensis (MDR). Experimental Parasitology 107, 115–119.CrossRefGoogle Scholar
Barat, L. M. and Bloland, P. B. (1997). Drug resistance among malaria and other parasites. Infectious Disease Clinics of North America 11, 969–987.CrossRefGoogle ScholarPubMed
Bhattacharya, A., Mishra, L. C., Sharma, M., Awasthi, S. K. and Bhasin, V. K. (2009). Antimalarial pharmacodynamics of chalcone derivatives in combination with artemisinin against Plasmodium falciparum In vitro. European Journal of Medicinal Chemistry 44, 3388–3393.CrossRefGoogle ScholarPubMed
Calza, P., Medana, C., Padovano, E., Giancotti, V. and Baiocchi, C. (2012). Identification of the unknown transformation products derived from clarithromycin and carbamazepine using liquid chromatography/high-resolution mass spectrometry. Rapid Communications in Mass Spectrometry 26, 1687–1704.CrossRefGoogle ScholarPubMed
Champney, W. S., Tober, C. L. and Burdine, R. (1998). A comparison of the inhibition of translation and 50S ribosomal subunit formation in Staphylococcus aureus cells by nine different macrolide antibiotics. Current Microbiology 37, 412–417.CrossRefGoogle ScholarPubMed
Damkier, P. and Brosen, K. (2000). Quinidine as a probe for CYP3A4 activity: Intrasubject variability and lack of correlation with probe-based assays for CYP1A2, CYP2C9, CYP2C19, and CYP2D6. Clinical Pharmacology & Therapeutics 68, 199–209.CrossRefGoogle ScholarPubMed
Dondorp, A. M., Nosten, F., Yi, P., Das, D., Phyo, A. P., Tarning, J., Lwin, K. M., Ariey, F., Hanpithakpong, W., Lee, S. J., Ringwald, P., Silamut, K., Imwong, M., Chotivanich, K., Lim, P., Herdman, T., An, S. S., Yeung, S., Singhasivanon, P., Day, N. P. J., Lindegardh, N., Socheat, D. and White, N. J. (2009). Reduced in-vivo susceptibility of Plasmodium falciparum to artesunate in Western Cambodia. New England Journal of Medicine 361, 455–467.CrossRefGoogle Scholar
Dorne, J. L. C. M., Walton, K. and Renwick, A. G. (2003). Human variability in CYP3A4 metabolism and CYP3A4-related uncertainty factors for risk assessment. Food and Chemical Toxicology 41, 201–224.CrossRefGoogle ScholarPubMed
Einarson, A., Phillips, E., Mawji, F., D'Alimonte, D., Schick, B., Addis, A., Mastroiacova, P., Mazzone, T., Matsui, D. and Koren, G. (1998). A prospective controlled multicentre study of clarithromycin in pregnancy. American Journal of Perinatology 15, 523–525.CrossRefGoogle ScholarPubMed
Ekland, E. H., Schneider, J. and Fidock, D. A. (2011). Identifying apicoplast-targeting antimalarials using highthroughput compatible approaches. The FASEB Journal 25, 3583–3593.CrossRefGoogle ScholarPubMed
Ho, P., Luo, X., Macauley, J. S., Grigor, M. R. and Wanwimolruk, S. (1998). In vitro hepatic metabolism of cyp3a-mediated drugs quinine and midazolam in the common brush-tailed possum (trichosurus vulpecula). Environmental Toxicology and Chemistry 17, 317–324.Google Scholar
Johnson, J. D., Richard, A. D., Lucia, G., Miriam, L., Norma, E. R. and Norman, C. W. (2007). Assessment and continued validation of the malaria SYBR Green I-based fluorescence assay for use in malaria drug screening. Antimicrobial Agents and Chemotherapy 51, 1926–1933.CrossRefGoogle ScholarPubMed
Kalanon, M. and McFadden, G. I. (2010). Malaria, Plasmodium falciparum and its apicoplast. Biochemical Society Transactions 38, 775–782.CrossRefGoogle ScholarPubMed
Kazim, M., Puri, S. K. and Dutta, G. P. (1991). Comparative evaluation of blood schizontocidal activity of quinine and quinidine against drug resistant rodent malaria. Journal of Communicable Diseases 23, 254–256.Google ScholarPubMed
King, S. M. (1995). Clarithromycin for children. Canadian Journal of Infectious Diseases 6, 69–70.CrossRefGoogle ScholarPubMed
Lell, B. and Kremsner, P. G. (2002). Clindamycin as an antimalarial drug: review of clinical trials. Antimicrobial Agents and Chemotherapy 46, 2315–2320.CrossRefGoogle ScholarPubMed
Mathis, A., Wild, E. C., Boettger, E. C., Kapel, C. M. O. and Deplazes, C. P. (2005). The mitochondrial ribosome as target for macrolide antibiotic clarithromycin in the helminth Echinococcus multiocularis. Antimicrobial Agents and Chemotherapy 49, 3251–3255.CrossRefGoogle Scholar
Mathis, A., Wild, P., Deplazes, P. and Boettger, E. C. (2004). The mitochondrial ribosome of the protozoan Acanthamoeba castellanii is the target for macrolide antibiotics. Molecular and Biochemical and Parasitology 135, 225–229.CrossRefGoogle ScholarPubMed
Mirghani, R. A., Yasar, U., Zheng, T., Cook, J. M., Gustafsson, L. L., Tybring, G. and Ericsson, O. (2002). Enzyme kinetics for the formation of 3-hydroxyquinine and three new metabolites of quinine in vitro: 3-hydroxylation by cyp3a4 is indeed the major metabolic pathway. Drug Metabolism and Disposition 30, 1368–1371.CrossRefGoogle ScholarPubMed
Na-Bangchang, K. and Karbwang, J. (2009). Current status of malaria chemotherapy and the role of pharmacology in antimalarial drug research and development. Fundamental & Clinical Pharmacology 23, 387–409.CrossRefGoogle ScholarPubMed
Nand, N., Aggarwal, H., Sharma, M. and Singh, M. (2001). Systemic Manifestations of Malaria. Journal, Indian Academy of Clinical Medicine 2, 189–194.Google Scholar
Newton, P., Keeratithakul, D., Teja-Isavadharm, P., Pukrittayakamee, S., Kyle, D. and White, N. (1999). Pharmacokinetics of quinine and 3-hydroxyquinine in severe falciparum malaria with acute renal failure. Transactions of Royal Society of Tropical Medicine & Hygiene 93, 69–72.CrossRefGoogle ScholarPubMed
Nielsen, T. L., Rasmussen, B. B., Flinois, J., Beaune, P. and Brosen, K. (1999). In vitro metabolism of quinidine: the (3 s)-3-hydroxylation of quinidine is a specific marker reaction for cytochromep-4503a4 activity in human liver microsomes. The Journal of Pharmacology and Experimental Therapeutics 289, 31–37.Google Scholar
Pai, M. P., Graci, D. M. and Amesden, G. W. (2000). Macrolide-drug interaction: an update. Annals of Pharmacotherapy 34, 495–513.CrossRefGoogle ScholarPubMed
Pinto, A. G., Wanq, Y. H., Chalasani, N., Skaar, T., Kolwankar, D., Gorski, J. C., Lianqpunsaqul, S., Hamman, M. A., Arefayene, M. and Hall, S. D. (2005). Inhibition of human intestinal wall metabolism by macrolide antibiotics: effect of clarithromycin on cytochrome P4503A4/5 activity and expression. Clinical Pharmacological Therapy 77, 178–188.CrossRefGoogle Scholar
Rodrigues, A. D., Roberts, E. M., Mulford, D. J., Yao, Y. and Ouellet, D. (1997). Oxidative metabolism of clarithromycin in the presence of human liver microsomes: major role for the cytochrome p4503a (cyp3a) subfamily. Drug Metabolism and Disposition 25, 623–630.Google ScholarPubMed
Sidhu, A. B. S., Valderramos, S. G. and David, A. (2005). Fidock PfMDR 1 mutations contribute to quinine resistance and enhance mefloquine and artemisinin sensitivity in Plasmodium falciparum. Molecular Microbiology 57, 913–926.CrossRefGoogle Scholar
Singh, S., Srivastava, R. K., Srivastava, M., Puri, S. K. and Srivastava, K. (2011). In-vitro culture of Plasmodium falciparum: utility of modified (RPNI) medium for drug-sensitivity studies using SYBR Green I assay. Experimental Parasitology 127, 318–321.CrossRefGoogle ScholarPubMed
Soyinka, J. O., Onyeji, C. O., Omoruyi, S. I., Owolabi, A. R., Sarma, P. V. and Cook, J. M. (2009). Pharmacokinetic interactions between ritonavir and quinine in healthy volunteers following concurrent administration. British Journal of Clinical Pharmacology 69, 262–270.CrossRefGoogle Scholar
Sullivan, D. J. Jr., Gluzman, I., Russell, D. G. and Goldberg, D. E. (1996). On the molecular mechanism of chloroquine's antimalarial action. Proceedings of the National Academy of Sciences USA 93, 11865–11870.CrossRefGoogle ScholarPubMed
Suzuki, A., Iida, I., Hirota, M., Akimoto, M., Huguchi, S., Suwa, T., Tani, M., Ishizaki, T. and Chiba, K. (2003). CYP isoforms involved in the metabolism of clarithromycin in vitro: Comparison between the identification from the disappearance rate and that from formation rate of metabolites. Drug Metabolism and Pharmacokinetics 18, 104–113.CrossRefGoogle Scholar
Tripathi, R., Pandey, S. K. and Rizvi, A. (2011). Clarithromycin, a cytochrome P450 inhibitor, can reverse mefloquine resistance in Plasmodium yoelii nigeriensis infected Swiss mice. Parasitology 138, 1069–1076.CrossRefGoogle ScholarPubMed
Tripathi, R., Awasthi, A. and Dutta, G. P. (2005). Mefloquine resistance reversal action of ketoconazole-A cytochrome P450 inhibitor, against mefloquine resistant malaria. Parasitology 130, 475–479.CrossRefGoogle Scholar
Uzuegbu, U. E. and Emeka, C. B. (2011). Changes in Liver Function Biomarkers among Malaria Infected Patients in Ikeja Lagos State, Nigeria. Current Research Journal of Biological Sciences 3, 172–174.Google Scholar
Ward, M. B., Sorich, M. J., Evans, A. M. and McKinnon, R. A. (2009). Cytochrome P450 Part 3: Impact of Drug–Drug Interactions. Journal of Pharmacy Practice and Research 39, 55–58.CrossRefGoogle Scholar
White, N. J., Looareesuwan, S., Warrell, D. A., Chongsuphajaisiddhi, T., Bunnag, D. and Harinasuta, T. (1981). Quinidine in falciparum malaria. Lancet 4, 1069–1071.CrossRefGoogle Scholar
Whitty, C. J. M., Chandler., Ansah, E., Leslie, T. and Staedke, S. G. (2008). Deployment of ACT antimalarials for treatment of malaria: challenges and opportunities. Malaria Journal 7, (Suppl 1):S7.CrossRefGoogle ScholarPubMed
Wisedpanichkij, R., Chaijaroenkula, W., Sangsuwanb, P., Tantisawat, J., Boonpraserta, K. and Na-Bangchanga, K. (2009). In vitro antimalarial interactions between mefloquine and cytochrome P450 inhibitors. Acta Tropica 112, 12–15.CrossRefGoogle ScholarPubMed
Wongsrichanalai, C., Pickard, A. L., Wernsdorfer, W. H. and Meshnick, S. R. (2002). Epidemiology of drug-resistant malaria. Lancet Infectious Diseases 2, 209–218.CrossRefGoogle ScholarPubMed
World Health Organization. (2012). Update on Artemisinin Resistance – April. http://www.who.int/malaria/publications/atoz/arupdate042012.pdf.Google Scholar
World Health Organization. (2006). Malaria Treatment Guidelines and Artemisinin Monotherapies. Geneva, Switzerland.Google Scholar
World Malaria Report. (2011). http://www.who.int/malaria/world_malaria_report_2011/WMR2011_noprofiles_lowres.pdf.Google Scholar
Zuckerman, J. M., Qamar, F. and Bono, B. R. (2009). Macrolides, ketolides, and glycylcyclines: azithromycin, clarithromycin, telithromycin, tigecycline. Infectious Disease Clinics of North America 23, 997–1026.CrossRefGoogle ScholarPubMed