Hyperglycemia, lumbar plexopathy and hypokalemic rhabdomyolysis complicating Conn's syndrome.

BACKGROUND: Lumbosacral plexopathy is a complication of diabetes mellitus. Conn's syndrome from an aldosterone secreting adenoma may be associated with hypokalemia and rhabdomyolysis but mild hyperglycemia also usually occurs. METHODS: Case description. RESULTS: A 70-year-old male diagnosed as having Conn's syndrome, hypokalemia and mild hyperglycemia developed rhabdomyolysis and lumbar plexopathy as a presenting feature of his hyperaldosteronism. His rhabdomyolysis rapidly cleared following correction of hypokalemia but recovery from the plexopathy occurred slowly over several months. Definite resection of the aldosterone secreting adenomas reversed the hyperglycemia. CONCLUSIONS: Our patient developed lumbar plexopathy resembling that associated with diabetes mellitus despite the presence of only mild and transient hyperglycemia.

Activation of glutamate receptors and glutamate uptake in identified macroglial cells in rat cerebellar cultures.

1. Patch-clamp methods have been used to examine the action of excitatory amino acids on three types of glial cell in cultures of rat cerebellum, namely type-1-like astrocytes, type-2 astrocytes and oligodendrocytes. In addition we have examined glutamate sensitivity of the precursor cell (the O-2A progenitor) that gives rise to type-2 astrocytes and oligodendrocytes. 2. Glutamate (30 microM), quisqualate (3-100 microM), (S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA, 10-30 microM) and kainate (10-500 microM) were applied to cerebellar type-2 astrocytes examined under whole-cell voltage clamp. Each of these agonists induced inward currents in cells held at negative membrane potentials. The currents reversed direction near 0 mV holding potential. N-Methyl-D-aspartate (NMDA, 30-100 microM) or aspartate (30 microM) in the presence of glycine (1 microM) did not evoke any whole-cell current changes in type-2 astrocytes. 3. The distribution of glutamate receptors in type-2 astrocytes was mapped with single- or double-barrelled ionophoretic pipettes containing quisqualate or kainate. Application of these agonists (current pulses 100 ms, 50-100 nA) to cells held at -60 mV evoked inward currents of 20-120 pA in the cell soma and 10-80 pA in the processes. Responses could also be obtained at the extremities of processes (approximately 60 microns from the soma). 4. Quisqualate or kainate (at 30 microM) applied to O-2A progenitor cells from rat cerebellum or optic nerve induced whole-cell currents (quisqualate 20-30 pA; kainate 20-50 pA, holding potential, Vh = -60 mV) that reversed near 0 mV. In common with type-2 astrocytes, the progenitor cells did not respond to NMDA (30 microM). 5. Type-1-like astrocytes produced large inward currents to glutamate (30 microM). These currents remained inward-going at holding potentials as positive as +80 mV and were not accompanied by any apparent noise increase. This result can be explained by the presence of an electrogenic glutamate uptake carrier. In cells kept up to 4 days in vitro, quisqualate, kainate and NMDA each failed to produce any whole-cell current changes, indicating the absence of receptors in type-1-like astrocytes at this stage in culture. Furthermore the glutamate uptake currents in type-1-like astrocytes were inhibited when external Na+ was replaced by Li+, although Li+ was found to pass through the glutamate channel in type-2 astrocytes.(ABSTRACT TRUNCATED AT 400 WORDS)