Four hundred forty-eight patients with 929 Echinococcus granulosus hydatid cysts received 3- to 6-month continuous cycles of mebendazole or albendazole treatment and underwent prolonged follow-up by clinical visits and imaging studies (range, 1-14 years) to assess the long-term outcome of treatment. Degenerative changes and relapse were assessed by imaging techniques. At the end of therapy, 74.1% of the hydatid cysts showed degenerative changes. These were more frequent in albendazole-treated than in mebendazole-treated cysts (82.2% vs. 56.1%; P < .001). During long-term follow-up, 104 cysts (22%) had degenerative changes that progressed, whereas 163 cysts (approximately 25%) relapsed. The percentages of relapses in the two drug-treated groups were almost the same. Relapses occurred more frequently in type II cysts of the liver. Cysts recurred most often (78.5%; P < .001) within the first 2 years after treatment ended. Further chemotherapy cycles induced degenerative changes in >90% of relapsed cysts without inducing more frequent or more severe side effects than those observed during the initial cycles.

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The immunological reactivity of Echinococcus granulosus antigen B was evaluated in 30 hydatid patients. Antigen B was purified from sheep hydatid cyst fluid by electroelution from a non-reducing SDS-PAGE gel (AgB). In ELISA and immunoblotting (IB), determining antibody production in sera from patients with hydatid disease and with other parasitic infections, purified AgB showed higher specificity than a partially purified antigen named pH5PPT (100% vs 83% in pH5PPT-ELISA and 58% in pH5PPT-IB). AgB-IB achieved higher sensitivity than AgB-ELISA (80% vs 63%). All AgB-IB positive sera recognized the 12 kDa subunit. Qualitative AgB-IB assessment of IgG isotype responses identified IgG4 as the predominant isotype (87%). The other isotypes showed a lower percentage of positive reactions: IgG1, 33%; IgG2, 21%; and IgG3, 17%. PBMC proliferative assay revealed a cellular response to AgB in 100% of patients' PBMC. These findings confirm antigen B, especially its smallest subunit, as a good diagnostic molecule.