The high proportion of drug therapeutic failures leading to an admission highlights the need for public education, particularly to prevent non-compliance.

No abstract

The cellular immune response to acetylcholine receptor from Torpedo electric organ was studied in 100 myasthenic patients and 41 healthy subjects. The mean stimulation index (SI) was 2 +/- 0.15 for the patients, and 1.06 +/- 0.08 for the controls. Stimulation was significantly greater when the test medium contained autologous serum rather than a standard universal serum (AB serum). Young patients were generally good responders (SI, 2.39 +/- 0.26), but older patients usually did not respond (mean SI, 1.18 +/- 0.13). Among the younger patients, men had higher responses than women (mean SI, 3.13 +/- 0.63 and 2.05 +/- 0.23, respectively). There was no correlation between degree of lymphocytic reactivity and duration or severity of symptoms.

We studied 11 patients with myasthenia gravis who demonstrated a cellular immune response to acetylcholine receptor (AChR) of the electric organ of Torpedo marmorata. After thymectomy, there was a marked decrease in the patients' lymphocyte reactivity to AChR. The mean reduction of the stimulation index (SI) was 50%, but the response to the nonspecific mitogen phytohemagglutinin (PHA) was not affected. In six cases, the lymphocyte response was measured at intervals up to 22 months after thymectomy; in all six, the immune response to AChR remained decreased. In some cases, the response continued to decrease, even to normal values. The effect of corticosteroid treatment was tested in other patients. The cellular immune response to AChR was significantly lower in treated patients (mean SI, 1.64 +/- 0.25) than in untreated controls (mean SI, 2.41 +/- 0.38), with no significant difference in the response to PHA. These data suggest that a decrease in the cellular immune response to AChR may be one mechanism by which thymectomy and corticosteroids are therapeutic in myasthenia.

Lymphocytes of twenty-seven patients with polymyositis were incubated in vitro with cholinergic receptor rich membranes obtained from the electric organs of Torpedo Marmorata. Lymphocytes of polymyositic patients were slightly stimulated; positive responses were present mainly in patients affected from more than a year. Sensitization against the nicotinic cholinergic receptor may explain the occurrence of the myasthenic syndrome with polymyositis.