Long-term serological evaluation of patients with cystic echinococcosis treated with benzimidazole carbamates.

Seeking better immunological markers indicating the long-term outcome of cystic echinococcosis (CE) after chemotherapy we studied 23 patients receiving albendazole, clinically followed for 8 years, and grouped ultrasonographically according to therapeutic outcome. Antibody responses against a partially purified fraction of hydatid fluid (HFF) and antigen B (AgB) were evaluated by indirect haemagglutination (IHA), ELISA and immunoblotting (IB). Although IHA titres varied over the course of treatment, differences in mean antibody titres to HFF between groups were significant only at 4 years (P = 0.031). IgG isotype expression remained unchanged during follow-up whereas IgE expression decreased in patients with cured or stable disease. AgB disclosed higher IgG4 expression (P < 10(-4); P = 0.025) and lower IgG1 expression than HFF (P < 10(-4); P = 0.022). IHA antibody titres were higher in patients with progressive than in those with cured or stable disease, even in those with the same cyst type. ELISA isotype profiles differed between groups, particularly for type CE 3, 4 and 5 cysts: higher serum IgG1 and IgG3, lower IgG4 and IgE in patients with cured or stable disease. Although combined serological testing provides scarce information on the long-term outcome of CE after chemotherapy it may be useful for reviewing in a retrospective study the outcome of a cyst and for assessing the host-parasite relationship.

Mixed cryoglobulinemia secondary to visceral Leishmaniasis.

We describe a case of type II mixed cryoglobulinemia, with monoclonal IgMkappa rheumatoid factor, associated with visceral leishmaniasis caused by Leishmania infantum. Involvement of Leishmania antigen(s) in the formation of cryoprecipitable immune complexes was suggested by the fact that cryoglobulinemic vasculitis subsided after antiparasite therapy and that anti-Leishmania antibodies, as well as rheumatoid factor, were enriched in the cryoprecipitate. We observed 2 additional patients with visceral leishmaniasis and cryoglobulinemic vasculitis. All 3 patients had seemingly contracted leishmaniasis in Italy, were hepatitis C virus negative, and were initially diagnosed as having autoimmune disorders. These findings indicate that Leishmania can be an etiologic agent of type II mixed cryoglobulinemia. This parasitosis should be taken into consideration in the differential diagnosis of vasculitides in endemic areas.

Long-term evaluation of patients with hydatidosis treated with benzimidazole carbamates.

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.

Anti-erythrocyte autoimmunization in hydatid disease.

A 73-year-old man with hydatid disease developed autoimmune hemolytic anemia due to IgM cold agglutinin with anti-I specificity. Hemolysis decreased after initiating mebendazole therapy. The cysts notably diminished in size and the red cell autoantibodies disappeared at the end of this treatment. On the basis of these observations, 44 patients with hydatid disease were investigated. One patient showed IgM cold autoantibody with no signs of anemia. In addition, cleavage fragments of C3 were detected on the erythrocyte membranes of 6 patients, following chronic activation of the complement system. We suggest that parasitic antigens may evoke antibodies cross-reacting with the red blood cells of the host.