<unk>  is a rare X-linked disease in which<unk> , an important complement factor responsible for the stabilization of the alternative C3 convertase, is deficient. There are three forms of<unk> es: Type I, which is identified by the total absence of the<unk>  protein in the plasma, Type II, which is a low but detectable amount of the<unk>  protein in the plasma, and Type III, which is a rare case of normal levels of<unk>  protein, but a dysfunctional variant. One of the first studied cases of<unk>  was in 1980 by Davis and Forrestal. These families had members with only partial deficiencies which resulted in a lowered consumption of the C3 protein.<unk>  was studied again shortly after in 1982 by Sjoholm in which all of the subjects were deceased shortly after the study because of their disease. The largest study of<unk>  was in 1989 by Fijen which included 9 males across 3 generations. Out of the 46 family members in Fijen's study, the 9 who were affected were found to be more susceptible to diseases from the Neisseria genus.
Properdin deficiency
Vitamin K deficiency
Factor I deficiency
Familial isolated vitamin E deficiency
Folate deficiency
Hypodysfibrinogenemia
Factor XIII deficiency
Factor X deficiency