Citation

Papadimitriou A, Hadjigeorgiou GM, Tsairis P, Papadimitriou E, Ouzounelli C, Ouzounellis T. Eur. Neurol. 1996; 36(3): 142-145.

Affiliation

Neurological Department, Laboratory of Muscle Disease, Red Cross Hospital, Athens, Greece.

Copyright

(Copyright © 1996, Karger Publishers)

DOI

unavailable

PMID

8738943

Abstract

Quail poisoning is known to produce an acute myoglobinuric syndrome. The cause of this syndrome is still unknown. It has been suggested that a toxic effect or a genetic sensitivity plays a major role. Ten patients with a history of quail poisoning were examined to determine their present state and the course of the disease. A muscle biopsy was performed in 2 of these patients who complained of muscle cramps after exercise. The activities of several glycolytic mitochondrial and lipolytic enzymes were estimated. In all 10 patients the physical examination, electromyogram findings and conduction velocities were normal. Serum levels of CK, aldolase and lactic acid were also within normal range. In the 2 patients with cramps, all enzyme activities were normal in muscle tissue. Our findings possibly exclude a preexisting enzyme defect as a cause of myoglobinuria in quail poisoning. Considering that 4 of our patients continued the consumption of quails without further problems, we suggest that the major factor contributing to quail poisoning must be toxic.

Language: en