The genetics of XXXX complications.

@entity1 @entity2175 @entity455 @entity6 @entity9199 @entity1723 @entity989 @entity4107
Duration of disease is the major susceptibility factor for @entity455 . @entity455 does not occur without the metabolic abnormality of @entity6 and there is much circumstantial evidence to implicate poor @entity6 control in its pathogenesis. The rate of development and severity of complications, however, are variable even in @entity1 with apparently similar control and about 25% of @entity6 will never develop clinical evidence of @entity455 . Studies of identical twins suggest a genetic component in the pathogenesis of @entity989 in @entity2175 , and less so in @entity1723 , but increased capillary basement membrane thickness does not occur in the non- @entity6 identical co-twins of insulin dependent @entity6 . There may also be genetic heterogeneity not only of @entity6 , but also of its complications, although for a given type of @entity6 the prevalence of @entity455 is often very similar in different racial groups. Associations between several different HLA molecules (particularly @entity4107 ) and @entity455 in @entity1723 have been reported but not consistently confirmed. Recently the finding of an increased frequency of the B3 allotype of the fourth component of complement @entity9199 in subjects with @entity989 has suggested that there is an HLA linked association. Both complement and the immunoglobulins are concerned with humoral immunity and the report of an association between a phenotype of the IgG heavy chain markers on chromosome 14 and @entity989 is of particular interest. These associations appear to be additive but independent. These reports need confirmation but provide the best evidence we have for an immunogenetic component (HLA and non-HLA linked) of the aetiology of @entity455 , at least in @entity1723 . The studies of identical twins, HLA and Gm associations provide good evidence that genetic factors are involved in susceptibility to @entity455 , at least in some @entity6 , although the most relevant genes may not have been identified. Searches for better genetic markers must continue in order to identify those @entity1 at increased risk of developing @entity455 .
