The Genetic Background to Malignant Hyperpyrexia Revealed by Serum Creatine Phosphokinase Estimations in Asymptomatic Relatives

Serum and urinary myoglobin following an aborted malignant hyperthermia reaction

“…Minimal muscle damage, a s judged by a lack of CK rise. has been reported following M H when anaesthesia w;is terminated promptly [24], when an inadequate dose of daiitrolene had been given prophylactically to ;in MH susceptible individual [25, [29]. The muscle abnormality causing an elevation of pre-operative CK might also be expected to result in an elevated serum myoglobin.…”

Malignant hyperthermia: an investigation of five patients

“…10,17,26,74,81,99,101,108,109,141,143,145,146,150,158,187,188,189 This is not to say that the defects must be confined to skeletal muscle, nor does this necessarily mean that a defect in muscle is the primary lesion. 99,14~…”

Aetiology of Malignant Hyperthermia

“…New findings pinpointed skeletal muscle as the major aetiological factor in acute episodes of MH and demonstrated an association with myopathies. Blood concentrations of creatine phosphokinase correlated at least in part with susceptibility, in non-triggered patients as well as during acute episodes [24,67], Contracture-producing drugs, well known to muscle physiologists, produced lower threshold responses in muscle from susceptible patients [70]. Procaine and lignocaine, perhaps because of effects upon muscle, were noted to be effective in treating clinical episodes [70,71], although lignocaine was later temporarily condemned on theoretical grounds because of its in vitro action in releasing calcium from sarcoplasmic reticulum [8] (see SR: drugs in MH).…”