Serum alpha2 macroglobulin and plasma fibrin monomer in diabetic neuropathy and retinopathy

ABSTRACT

Impairment of neural function is one of the most frequent disabling complications of diabetes mellitus. No part of the peripheral nervous system seems spared. Progressive neural impairment may occur in sensory and motor peripheral nerves producing pain, parasthesia or distal muscle weakness [Ward, 1972]. This also occurs in autonomic nervous system producing orthostatic hypotension, sexual impotence and urinary and bowel incontinence [Clarke, et al. 1979]. Although these complications are prominent, the exact cause is still unknown. However, Anderson [1976] suggested that slowing of peripheral nerve activity may be related to metabolic derangements. A relationship between hyperglycemia and peripheral nerve function as measured by nerve conduction velocity has been demonstrated to human subjects. Diabetic retinopathy is considered to be a multifactorial disorder. A relationship between duration of diabetes and development of retinopathy has long been recognised [Caird et al., 1969], mean blood glucose concentration have been reported to be higher, particularly in severe retinopathy. Data related to other factors as cigarette smoking, obesity, blood pressure and. genetic susceptibility are conflicting. William et al., [1983] stated the risk factors in diabetic retinopathy include increasing duration of the disease, presence of other microvascular complications of diabetes and probably hyperglycemia itself. Plasma fibrin-monomer and raised serum gamma 2 macroglobulin have recently been implicated [Wardle et a1., 1973]. The aim of the study is to define and evaluate the various risk factors in diabetic retinopathy and neuropathy in Assiut with particular reference to fibrin monomer and gamma 2 macroglobuin