Endocrine Abstracts

Introduction: Centropontic myelinolysis (CPM) is a neurological pathology related to axonal demyelination lesions, often localized at the pontine level. For a long time, this condition was attributed to rapid correction of hyponatremia. A few cases of PCM with normal natraemia have been described, in a context of undernutrition, chronic alcoholism, hypokalaemia or hyperglycaemia.

Patient and observation: We report the case of an 18 years old patient, type 1 diabetic for 8 years, admitted for keto-asidosis decompensation. On admission, the patient was conscious, hemodynamically and respiratorily stable, capillary blood glucose was elevated to 6 g/l, with the presence of 3 crosses of acetone and sugar on urine dipstick. The biological workup showed a venous glucose level of 6.16 g/l, a corrected natraemia of 137 mmol/l, a kalemia of 3.7 mmol/l, and low alkaline reserves of 13 meq/l. The emergency was resolved and the patient underwent a thorough clinical examination, which revealed FTT severe staturo-ponderal delay, a micro penis and bilateral paresthesias in all 4 limbs. A hypothalamic-pituitary MRI in search of a central cause of FTT was performed, showing the presence of a pontine lesion suggestive of PCM.

Discussion: PCM was first described in 1959. Microscopically, it is a symmetrical destruction of myelin involving all nerve bundles associated with a loss of oligodendrocytes. Often, it has been attributed to a rapid correction of hyponatremia. In the case of normal natraemia, it can be hypothesized that rapid elevation of blood glucose has the same effect as a rapid infusion of hypertonic saline. MRI remains the imaging technique of choice. An effective but slow correction of the blood sugar level allows a good evolution of the clinical picture.