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American tegumentary leishmaniasis in Brazil: a critical review of the current therapeutic approach with systemic meglumine antimoniate and short‐term possibilities for an alternative treatment
Author(s) -
Carvalho Sílvia H.,
Frézard Frédéric,
Pereira Neila P.,
Moura Alexandre S.,
Ramos Lucinéia M. Q. C.,
Carvalho Gabriel B.,
Rocha Manoel O. C.
Publication year - 2019
Publication title -
tropical medicine and international health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.056
H-Index - 114
eISSN - 1365-3156
pISSN - 1360-2276
DOI - 10.1111/tmi.13210
Subject(s) - meglumine antimoniate , miltefosine , medicine , leishmaniasis , neglected tropical diseases , drug , leishmania , pharmacology , cutaneous leishmaniasis , intensive care medicine , immunology , disease , visceral leishmaniasis , parasite hosting , world wide web , computer science
Objectives Meglumine antimoniate ( MA ; Glucantime®), the 80‐year‐old first‐line systemic treatment for all forms of American tegumentary leishmaniasis ( ATL ) caused by Leishmania (Viannia) braziliensis , Leishmania (Viannia) guyanensis and Leishmania ( Leishmania ) amazonensis , is highly toxic, presents adverse side‐effects and may not attain clinical and parasitological cure. This critical review examines the necessity for intramuscular/intravenous administration of MA , the alternatives to this approach, and the possibilities of developing affordable, accessible and non‐toxic drugs or new delivery methods. Method PubMed searches were performed using the terms ‘cutaneous leishmaniasis’ or ‘American tegumentary leishmaniasis’ in combination with ‘meglumine antimoniate’ or ‘ N –methyl glucamine’ or ‘drug repositioning’ or ‘nanotechnology’. Searches covered a period of 20 years of peer reviewed journals and technical bulletins. We explored the mode of action, pharmacokinetics, toxicity and efficacy of MA , evaluated the progress of ATL therapy in Brazil, and examined the potential of drug repositioning and nanotechnology in accelerating the introduction and/or optimisation of an alternative treatment. Results The evidence suggests that ATL therapy will continue to rely on systemic MA in the foreseeable future even though an intralesional subcutaneous route has evolved over the last 10 years. The chances of developing a novel drug for ATL or a new mode of delivery of MA are low. While MA nanocarriers afford a promising approach, this technology is still in its infancy. A more immediate solution would be the production of a bioequivalent of miltefosine, an efficacious oral agent no longer protected by patent. Conclusion Development of a contemporary treatment requires governmental commitment in bringing together private and public sectors.