Opisthorchiasis medical therapy: Difference between revisions

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==Medical Therapy==
==Medical Therapy==
There was unsuccessful use of [[chloroquine]] for opisthorchiasis treatment in 1951-1968.<ref name="WHO 1995"/>
There was unsuccessful use of [[chloroquine]] for opisthorchiasis treatment in 1951-1968.
Thus, currently, the control of opisthorchiasis relies predominantly on [[anthelmintic]] treatment with [[praziquantel]]. The single dose of praziquantel of 40&nbsp;mg/kg is effective against opisthorchiasis and also against [[schistosomiasis]]. A randomised-controlled trial published in 2011 showed that the broad-spectrum anti-helminthic, tribendimidine, appears to be at least as efficacious as praziquantel.


Thus, currently, the control of opisthorchiasis relies predominantly on [[anthelmintic]] treatment with [[praziquantel]].<ref name="Young 2010"/> The single dose of praziquantel of 40&nbsp;mg/kg is effective against opisthorchiasis and also against [[schistosomiasis]].<ref name="WHO 1995"/> A randomised-controlled trial published in 2011 showed that the broad-spectrum anti-helminthic, tribendimidine, appears to be at least as efficacious as praziquantel.<ref>{{cite doi| 10.1016/S1473-3099(10)70250-4}}</ref>
[[Artemisinin]] was also found to have [[anthelmintic]] activity against ''Opisthorchis viverrini''.


[[Artemisinin]] was also found to have [[anthelmintic]] activity against ''Opisthorchis viverrini''.<ref>{{Cite PMID|17975411}}.</ref>
Despite the efficacy of this compound, the lack of an acquired immunity to infection predisposes humans to reinfections in endemic regions. In addition, under experimental conditions, the short-term treatment of ''Opisthorchis viverrini''-infected [[hamster]]s with praziquantel (400&nbsp;mg per kg of live weight) has been shown to induce a dispersion of parasite antigens, resulting in adverse immunopathological changes as a result of oxidative and nitrative stresses following re-infection with ''Opisthorchis viverrini'', a process which has been proposed to initiate and/or promote the development of cholangiocarcinoma in humans.


Despite the efficacy of this compound, the lack of an acquired immunity to infection predisposes humans to reinfections in endemic regions.<ref name="Young 2010"/> In addition, under experimental conditions, the short-term treatment of ''Opisthorchis viverrini''-infected [[hamster]]s with praziquantel (400&nbsp;mg per kg of live weight) has been shown to induce a dispersion of parasite antigens, resulting in adverse immunopathological changes as a result of oxidative and nitrative stresses following re-infection with ''Opisthorchis viverrini'', a process which has been proposed to initiate and/or promote the development of cholangiocarcinoma in humans.<ref name="Young 2010"/>
Given the current reliance on a single trematocidal drug against ''Opisthorchis viverrini'', there is substantial merit in searching for new intervention methods, built on a detailed understanding of the interplay between the parasites and their hosts as well as the biology of the parasites themselves at the molecular level. Furthermore, the characterization of the genes expressed in these parasites should assist in elucidating the molecular mechanisms by which opisthorchiasis initiate and enhance the development of cholangiocarcinoma.
 
Given the current reliance on a single trematocidal drug against ''Opisthorchis viverrini'', there is substantial merit in searching for new intervention methods, built on a detailed understanding of the interplay between the parasites and their hosts as well as the biology of the parasites themselves at the molecular level.<ref name="Young 2010"/> Furthermore, the characterization of the genes expressed in these parasites should assist in elucidating the molecular mechanisms by which opisthorchiasis initiate and enhance the development of cholangiocarcinoma.<ref name="Young 2010"/>
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}

Revision as of 15:58, 30 November 2012

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Medical Therapy

There was unsuccessful use of chloroquine for opisthorchiasis treatment in 1951-1968. Thus, currently, the control of opisthorchiasis relies predominantly on anthelmintic treatment with praziquantel. The single dose of praziquantel of 40 mg/kg is effective against opisthorchiasis and also against schistosomiasis. A randomised-controlled trial published in 2011 showed that the broad-spectrum anti-helminthic, tribendimidine, appears to be at least as efficacious as praziquantel.

Artemisinin was also found to have anthelmintic activity against Opisthorchis viverrini.

Despite the efficacy of this compound, the lack of an acquired immunity to infection predisposes humans to reinfections in endemic regions. In addition, under experimental conditions, the short-term treatment of Opisthorchis viverrini-infected hamsters with praziquantel (400 mg per kg of live weight) has been shown to induce a dispersion of parasite antigens, resulting in adverse immunopathological changes as a result of oxidative and nitrative stresses following re-infection with Opisthorchis viverrini, a process which has been proposed to initiate and/or promote the development of cholangiocarcinoma in humans.

Given the current reliance on a single trematocidal drug against Opisthorchis viverrini, there is substantial merit in searching for new intervention methods, built on a detailed understanding of the interplay between the parasites and their hosts as well as the biology of the parasites themselves at the molecular level. Furthermore, the characterization of the genes expressed in these parasites should assist in elucidating the molecular mechanisms by which opisthorchiasis initiate and enhance the development of cholangiocarcinoma.

References

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