Family occurrence of schistosomal hepatosplenomegaly and maternal effect

Abstract

In this paper we present a study of members of 265 nuclear families, aged six or more. This study is based of family heredograms, and takes into account the clinical form of schistosomiasis observed before treatment with oxamniquine. The probability of occurrence of two or more cases of hepatosplenomegaly is low, notwithstanding the fact that it was observed in 38 families. Even less frequent is the occurrence of three or more cases observed in 17 families (P = 0.002). The concentration of the hepatosplenic form was higher among siblings than it was among mothers and children, or fathers and children. It was found to be not significant between husband (father) and wife (mother). These observations reinforce the evidence for the presence of a genetic component in susceptibility to the hepatosplenic form of the disease. In cases in which the mother was hepatosplenic there was a higher incidence of hepatosplenic children; the relative risk was a least five times higher than in those in which the father was the affected member (the maternal effect). In cases where both members were affected by the hepatointestinal form, the risk to the filial generation was similar to that of the population in general. Thus, in the process towards severe forms of schistosomiasis mansoni, pre and post natal factors might be involved.

Praziquantel and Upper Gastrointestinal Bleeding in Hepatic Schistosomiasis: A Quasi-Experimental Study

“…Our results also showed individuals with a close family member with HS were more likely to experience more episodes of UGIB. Though a family history of HS has not been directly associated with UGIB, progression of periportal fibrosis before and after PZQ use has been found to cluster in some families [ 9 , 36 – 38 ]. From our study, participants who experienced more UGIB also had a relative leukocytosis.…”

Role of the spleen on the pathogenesis of schistosomal periportal (pipestem) fibrosis of the liver: an experimental approach.

“…These include the role of repeated infections as opposed to a single or few exposures, the age and race of the patients, their blood groups, duration of infection, failure of immunologic modulation, and HLA determinants. [5][6][7][8] The evidence for and against each one of these cofactors is meager and the problem has remained complex and is difficult to solve with materials from human patients. Therefore, the need for an experimental model is crucial.…”