THE ASSOCIATION BETWEEN THE CLINICAL AND LABORATORY MANIFESTATIONS OF LUPUS ERYTHEMATOSUS AND THE GENETICALLY DETERMINED DEFICIENCY OF THE SECOND COMPONENT OF THE COMPLEMENT

Abstract

Lupus Erythematosus is a multifactorial systemic disease, it's genetic component has been suggested by familial aggregation and twin studies (Shai et al, 1999). Deficiencies in proteins of the complement system were among the

first identified genetic risk factors.

The complement deficiency of C2 is the most frequently occurring

Homozygous complement deficiency in humans ( Ratnoff ,1996) .

The molecular abnormality of the most common type ofC2 deficiency the type I deficiency, was identified by ( Johnson et al, 1992). In our study, we have included 52 patients with Systemic Lupus Erythematosus, trying to search for C2 deficient gene whether Heterozygous or Homozygous. Among our series of SLE patients (n=52}, 13 patients proved to be Heterozygous C2 deficient (25%) , while none of our patients showed any evidence of Homozygous C2 deficiency.