Why the study?
Are immunological markers altered in diabetics with autonomic neuropathy compared to uncomplicated diabetics and normal controls?
Are immunological markers altered in diabetics with autonomic neuropathy compared to uncomplicated diabetics and normal controls?
Immunological mechanisms, including complement activation and circulating immune complexes, may play a role in the etiology of diabetic autonomic neuropathy.
May implicate immune mechanisms in diabetic autonomic neuropathy; hypothesis-generating and requires prospective validation before any clinical application.
Lymphocytic infiltration of autonomic ganglia found at autopsy and a strong clinical association with iritis suggests that diabetic autonomic neuropathy might have an immunological basis. We measured levels of circulating immune complexes, complement (C3, C4), complement breakdown products (C3d), and insulin antibodies in diabetics with autonomic neuropathy and a history of iritis (n = 17), compared to diabetics of similar age and duration with autonomic neuropathy but no history of iritis (n = 20), and with uncomplicated insulin-dependent diabetics (n = 23), together with normal controls (n = 26). We found higher levels of circulating immune complexes in patients with autonomic neuropathy (irrespective of iritis) compared to normal controls, and differences in C3d levels suggesting complement activation. C4 levels were unexpectedly normal in the diabetics with autonomic neuropathy, in contrast to the uncomplicated insulin-dependent diabetic controls. Insulin antibody levels showed no difference between the three groups of diabetics. These findings suggest that immunological mechanisms may be implicated in the aetiology of diabetic autonomic neuropathy and that further studies are indicated.
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Gilbey et al. (1986) studied this question.
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