INSULIN EDEMA IN DIABETES-MELLITUS ASSOCIATED WITH THE 3243-MITOCHONDRIAL TRNA(LEU(UUR)) MUTATION - CASE-REPORTS

We encountered a patient with diabetes mellitus due to the 3243 mitoch ondrial tRNA mutation(DM-Mt3243), who developed insulin edema and hepa tic dysfunction after starting insulin. Such a rare phenomenon was unl ikely to be a fortuitous coincidence in mitochondrial diabetes, as non e in 197 non-mutant NIDDM patients had same episode. Moreover, similar leg edema was noticed in another DM-Mt3243 patient, and other two DM- Mt3243 patients had leg edema which responded to coenzyme Q10. These o bservations suggest further a role of mitochondrial function on leg ed ema. The mechanism of his insulin edema may involve vasomotor changes induced by the rapidly glycemic control, because our case of insulin e dema had a prominent increase of strong succinate dehydrogenase reacti ve vessels. Alternatively, myocardial dysfunction might have produced leg edema and hepatic dysfunction, because he had subclinical myocardi al dysfunction, judged by imaging with beta-methyl-p-(I-123)- iodophen yl-pentadecanoic acid. The third explanation is that a rapid improveme nt of glycemic control might have induced hepatic reoxygenation and th e production of reactive oxygen species in the liver that contributed to cell damage. Thus, although we cannot draw definite conclusion, our experiences here suggest that mitochondrial dysfunction is important in the etiology of insulin edema.