Haptoglobins and rheumatic fever.

Abstract

The haptoglobins are polymorphic ?2-globulins which combine with free haemoglobin (Polonovski and Jayle, 1940). The usual method of haptoglobin typing with starch-gel electro phoresis reveals three phenotypes designated Hp 1-1, 2-1, and 2-2 (Smithies, 1955). A fourth phenotype in which no haptoglobin bands are detected has been classified Hp 0. Special methods reveal 15 possible haptoglobin phenotypes which are produced by the action of five autosomai, allelic, co-dominant genes (HplF, Hpls, Hp2FF, Hp2FS, Hp2SS) at a single locus (Connell et al., 1962 ; Nance and Smithies, 1963). This polymorphism has been studied in many populations. Both racial and regional variations in gene frequencies have been re ported (Parker and Beam, 1961). There is no known reason for such variations, but it is suspected that the //p1 and Hp2 genes are now or have in the past been influenced by one or more selective factors. Evidence for this hypothesis has been presented in a study (Workman et al., 1963) in which the Hp1 gene frequency differences between the West African and American negro populations could not be accounted for on the basis of gene migration alone. Their evidence suggests that the haptoglob'n genes have different adaptive values in the two populations and that the polymorphism may possibly be un stable in the populations studied. The level of haptoglobin in the blood is influenced by a variety of factors. These include inflammation, haemolysis, hormone administration, administration of pyrogens, and probably genetic constitution (Nyman, 1959). Variations re lated to sex (Nyman, 1959), age (Jayle and Moretti, 1962), and haptoglobin phenotype (Smith and Owen, 1961) have also been found. Mean levels of haptoglobin in relation to pheno type in decreasing order are : Hp l-l>Hp 2-l>Hp 2-2. Rheumatic fever is a disease which produces inflammatory changes in connective tissue. During the acute attack serum haptoglobin levels are markedly elevated (Owen et al., 1964). This is probably due to the release of a material from the in flamed tissue which stimulates the hepatic synthesis of hapto globin (Borel et al., 1964). No information concerning the haptoglob'n levels of individuals who have recovered from the acute attack of rheumatic fever is available. The present study was done to compare the distributions of haptoglobin pheno types and haptoglobin levels of a suitable control population with those of a group of adults who had had one or more documented episodes of rheumatic fever or clinically proved rheumatic heart disease some time in the past.