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Document Page 365 15 Antitrypanosomiasis Drug Development Based on Structures of Glycolytic Enzymes Christophe L. M. J. Verlinde, Hidong Kim, Bradley E. Bernstein, Shekhar C. Mande, * and Wim G.J. Hol University of Washington, Seattle Washington I. Trypanosomiasis A. Disease and Treatment Human African trypanosomiasis, also called sleeping sickness, is caused by the parasites Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense. These unicellular organisms live freely in the bloodstream of the human host and invade the brain during the later stage of the disease. Without treatment the disease is always fatal [1]. The course of the gambiense form may last from months to years, while T. brucei rhodesiense usually kills within weeks. Sleeping sickness occurs in thirty-six sub- Saharan African countries, putting fifty million people at risk. Each year 25,000 new cases are reported, but the actual number of cases is more likely to be about 250,000 [2]. The current state of antitrypanosomal chemotherapy is dismal; many parasitologists do not want to take the risk of being infected with T. brucei rhodesiense and prefer to study the parasite T. brucei brucei, which is harmless to humans [3]. Not more than four drugs are available to treat the disease: pentamidine, suramin, melarsoprol—all from the first half of this century—and eflornithine, introduced in 1990 (Figure 1). Except for eflornithine, which is an irreversible ornithine decarboxylase inhibitor [4], the mechanisms of the drugs are poorly understood [5]. All four drugs require administration by injection in a hospital setting, which is a major drawback in rural Africa [6]. Pentamidine is useful for treating early stage T. brucei gambiense infection, suramin for both early stage gambiense and rhodesiense infection. The permanent charges on pentamidine * Current affiliation: Institute of Microbial Technology, Chandigarh, India http://legacy.netlibrary.com/nlreader/nlReader.dll?bookid=12640&filename=Page_365.html [4/5/2004 5:31:12 PM]
Document Figure 1 Available drugs for the treatment of human African trypanosomiasis. Page 366 and suramin explain why they show poor oral absorption and do not cross the blood–brain barrier, making them unsuitable for the treatment of late-stage trypanosomiasis. Melarsoprol, an organoarsenical compound, was until 1990 the only drug effective in the late stage of both forms of trypanosomiasis. Unfortunately, it is also highly toxic, causing reactive encephalopathy in up to 10% of the patients, of which about one half die. This deadly complication is well known to villagers of areas where the disease is endemic and, ironically, discourages people from participating in diagnostic surveys. Eflornithine, heralded as the “resurrection drug” upon its introduction [7], cures patients infected with late-stage T. brucei gambiense but is ineffective against the more virulent rhodesiense form. Additionally, it causes bone marrow suppression in half of the patients and occasionally convulsions [6]. A serious concern is that resistance has been reported against each of the four antitrypanosomal drugs [1]. http://legacy.netlibrary.com/nlreader/nlReader.dll?bookid=12640&filename=Page_366.html [4/5/2004 5:31:28 PM]
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Document D ddI, 152 tumour necrosis
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