CHLORPROPAMIDE-INDUCED ADH RELEASE, HYPONATREMIA AND CENTRAL PONTINE MYELINOLYSIS IN DIABETES-MELLITUS

Chlorpropamide (CPM) has been reported to produce impaired water excre tion due to the enhancement of renal vasopressin (ADH) action and/or d ue to centrally enhanced ADH release, but it is still unknown whether CPM gives rise to ADH release with a subsequent hyponatremia in diabet es mellitus (DM), which, in turn, causes an impairment of the central nervous system. In 3 patients with DM, who developed hyponatremia duri ng the treatment with CPM, an acute mater load (WL) was carried out in the presence and absence of the drug, and plasma BDH was determined w ith plasma and urine osmolalities. Moreover, in 2 cases, MRI scans of the brain were taken. In all the patients, acute WL tests failed to su ppress completely ADH release in response to changes in plasma osmolal ity in the presence of CPM, which, in turn, resulted in the impaired m ater excretion. In the absence of CPM, an acute WL normally suppressed plasma ADH leading to the diuresis. MRI scans illustrated the presenc e of central pontine myelinolysis. It is likely that CPM might stimula te ADH release in DM with a subsequent hyponatremia and brain damages.