Therapy and drug resistance in malaria

Kulkarni, Aniruddha; Kasturi, Leelavathi; Amin, Abdinasir A; Mashankar, V. A.

doi:10.1007/bf02802634

Cited by 6 publications

(3 citation statements)

References 4 publications

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“…CQ is the first-line treatment for P. vivax malaria in India but the exact burden of CQR P. vivax in India is unclear. Since India has already declared its aim to eliminate malaria by 2030 [ 28 ], the detection and monitoring of CQR P. vivax are crucial. In this systematic review, CQ therapeutic efficacy was assessed by in vivo efficacy studies ( n = 1787) and ex-vivo ( n = 141) studies from different malaria-endemic regions in India.…”

Section: Discussionmentioning

confidence: 99%

“…The poor response could have been due to poor CQ absorption in malnourished patients as well. Another study conducted by Kulkarni et al [ 28 ] similarly reported a high prevalence of treatment failures (51.7%) from Mumbai. However, the study’s sample size was very small ( n = 29) and the duration of follow-up was very short (less than 7 days).…”

Section: Discussionmentioning

confidence: 99%

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A systematic review of CQ-resistant Plasmodium vivax malaria infections in India

Nallapati,

Gupta,

Hande

et al. 2023

Pathogens and Global Health

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Introduction Chloroquine (CQ) is the drug of choice for treating uncomplicated Plasmodium vivax (P. vivax) malaria in India. The knowledge about the exact burden of CQ resistance in P. vivax in India is scarce. Therefore, this systematic review aimed to assess the prevalence of CQ resistance in reported P. vivax cases from India. Methods PubMed, EMBASE, and Web of Science, were searched using the search string: ‘Malaria AND vivax AND chloroquine AND (resistance OR resistant) AND India’. We systematically reviewed in-vivo and in-vitro drug efficacy studies that investigated the CQ efficacy of P. vivax malaria between January 1995 and December 2022. Those studies where patients were followed up for at least 28 days after initiation of treatment were included. Results We identified 12 eligible CQ therapeutic efficacy studies involving 2470 patients, Of these 2329 patients were assessed by in-vivo therapeutic efficacy methods and the remaining 141 were assessed by in-vitro methods. CQ resistance was found in 25/1787 (1.39%) patients from in-vivo and in 11/141 (7.8%) patients from in-vitro drug efficacy studies. Conclusion Based on the available studies, the prevalence of CQ resistance in P. vivax was found to be relatively lower in India. However, continued surveillance and monitoring are crucial to identify the emergence of CQ resistance.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A systematic review of CQ-resistant Plasmodium vivax malaria infections in India

Nallapati,

Gupta,

Hande

et al. 2023

Pathogens and Global Health

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“…The development of drug resistance in pathogenic fungi and parasites, such as resistance to azoles, which are inhibitors of the ergasterol sterol biosynthesis enzyme Erg11 in the pathogenic yeast Candida albicans [32][33][34], or resistance to chloroquine and mefloquine in the malarial parasite Plasmodium falciparum, [35][36][37][38] illustrates the enormous public health impact of fungal drug resistance.…”

Section: Effects Of Hsp90 Inhibitors On Drug Resistance In Pathogenmentioning

confidence: 99%

Possible Effects of Early Treatments of Hsp90 Inhibitors on Preventing the Evolution of Drug Resistance to Other Anti-Cancer Drugs

Xiao¹,

Rasouli²,

Ruden³

2007

CMC

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Hsp90 is a chaperone that is critically important for both cancer progression and tumor survival. Hsp90 is an exciting target for anti-cancer drugs because most of the proteins that interact with Hsp90 are known to be in the cell cycle, signaling and chromatin-remodeling pathways. Recent work in fungi has shown that reduction of Hsp90 activity dramatically increases the efficacy of many fungicides. Furthermore, in studies on the evolution of drug resistance in fungi, it has been shown that high levels of Hsp90 increase the rate of the development of fungicide resistance, whereby low levels of Hsp90 decrease the rate of fungicide resistance. Similarly, in humans and mammalian models, Hsp90 inhibitors have been shown to act additively or synergistically with many other cancer therapies for killing both solid tumors and leukemias. Also, several recent studies have shown that Hsp90 inhibitors potentiate the activity of drugs in cancer cells lines that are otherwise resistant to the drug. However, during the evolution of drug resistance in cancer cells, it has not yet been determined whether early exposure to Hsp90 inhibitors slows the rate of developing resistance to other anti-cancer drugs, as would be expected from the fungal studies. In this review, we summarize the effects of the Hsp90 inhibitors geldanamycin and its derivatives with other anti-cancer drugs on killing cancer cells. We also discuss other basic science and clinical studies that need to be done to determine the optimum exposure regimens for Hsp90 inhibitor treatments to maximize its cancer-killing activities, and to minimize the evolution of resistance to other anti-cancer drugs.

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