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Autonomic Neuropathy in Pregnancy

for IDDM (5-8). In addition, deficient epinephrine and pancreatic polypeptide secretory responses to hypoglycemia in people with IDDM who do not have clinically overt autonomic neuropathy or relevant cardiovascular reflex abnormalities appear to identify individuals who will subsequently develop these abnormalities (9). Thus, the deficient hormonal responses to hypoglycemia may be sensitive markers for early autonomic neuropathy. Because deficient adrenomedullary epinephrine secretion in response to a decrement in plasma glucose is a "demonstrable (neuropathic) disorder. . .that occurs in the setting of diabetes mellitus without other causes for peripheral neuropathy" (1), it should be considered a feature of diabetic neuropathy, although it should not be assumed that its precise cause is the same as that of other features of diabetic neuropathy (6). Thus, it is disappointing that the Report and Recommendations of the San Antonio Conference on Diabetic Neuropathy failed to mention either the adrenal medullae or epinephrine (1). Because deficient adrenomedullary epinephrine secretion contributes to the development of iatrogenic hypoglycemia, which causes substantial morbidity and some mortality in IDDM patients (5,6) and may be a sensitive marker for the development of more traditional forms of diabetic autonomic neuropathy, it seems that this omission should be corrected.