Letter: Myasthenic syndrome during treatment with practolol.

Hughes, R.; Zacharias, Farouk

doi:10.1136/bmj.1.6007.460-d

Cited by 20 publications

(6 citation statements)

References 1 publication

(1 reference statement)

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“…Till now, in nonmyasthenic patients, only transitory myasthenic symptoms induced by betablockers have been reported [1][2][3], resolving with the interruption of the drug. The following facts must be emphasized in our case: the patient was fully alert with no motor symptoms before acébutolol was introduced.…”

Section: Discussionmentioning

confidence: 99%

“…Beta-blockers worsen myasthenia gravis (MG) [1][2][3] by a depressant effect on the neuromuscular junction [4,5]. Myasthenic symptoms induced by beta-blockers may occur [1][2][3] in nonmyasthenic patients but are always transient, resolving when the treatment is interrupted.…”

Section: Introductionmentioning

confidence: 99%

“…Myasthenic symptoms induced by beta-blockers may occur [1][2][3] in nonmyasthenic patients but are always transient, resolving when the treatment is interrupted. Here, we report a case of autoimmune MG which began soon after acebutolol therapy was established and which developed at a fulminating course despite drug with drawal.…”

Section: Introductionmentioning

confidence: 99%

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Fulminant Myasthenia Gravis Soon after Initiation of Acebutolol Therapy

Confavreux¹,

Charles²,

Aimard³

1990

Eur Neurol

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We report the case of myasthenia gravis in a 74-year-old woman, 2 weeks after acebutolol had been introduced as the sole treatment for systemic hypertension. The disease developed at a fulminant and fatal course despite drug withdrawal. The possibilities of coincidental association between the two events, triggering of a preexisting latent myasthenia gravis or full induction of the disease by acebutolol, are discussed.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Fulminant Myasthenia Gravis Soon after Initiation of Acebutolol Therapy

Confavreux¹,

Charles²,

Aimard³

1990

Eur Neurol

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“…Key words fi-Adrenoceptor blocker; intrinsic sympathomimetic action, muscle cramps, CPK, CPK-MB, propanolol, carteolol, metoprolol, arotinolol Several forms of myopathy related to treatment with/3-adrenoceptor blockers, including myastenia gravis, toxic myopathy and other forms of myopathy, have previously been reported [1][2][3][4][5]. In those myopathies,/3-adrenoceptor blockers were associated with high serum creatine phosphokinase (CPK) levels and muscle cramps or pain [3,5].…”

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confidence: 96%

Muscle cramps and elevated serum creatine phosphokinase levels induced by ?-adrenoceptor blockers

Imai

Watanabe

Hashimoto

et al. 1995

Eur J Clin Pharmacol

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We have assessed the propensity of beta-adrenoceptor blockers to cause muscle cramps and to raise the serum creatine phosphokinase (CPK) level in 78 patients with essential hypertension. After a control period, a beta-adrenoceptor blocker without intrinsic sympathomimetic activity (ISA; propranolol, metoprolol or arotinolol) was administered for three months. Thereafter, the patients were randomised to receive a beta-adrenoceptor blocker with ISA (pindolol or carteolol) for three months or a beta-adrenoceptor blocker without ISA for a further three months. This pattern was continued until all beta-adrenoceptor blockers had been given. At the end of each period, CPK and CPK-MB levels were measured. Of the 78 subjects, muscle cramps occurred in 27 during treatment with pindolol and 32 during treatment with carteolol. No complaints were made by subjects treated with propranolol and arotinolol, but muscle cramps were reported in 2 treated with metoprolol. While muscle cramps were caused both by pindolol and carteolol in 16 subjects, they were caused by either of these drugs in the remainder of the subjects. Muscle cramp occurred mainly in the calves when the patients were in bed at night. Serum CPK and CPK-MB levels increased significantly during treatment with pindolol (control period vs pindolol, CPK = 96 vs 133 IU.ml-1, CPK-MB = 14 vs 18 IU.ml-1) or carteolol (CPK = 117 IU.ml-1, CPK-MB = 18 IU.ml-1) while the levels during treatment with propranolol, arotinolol and metoprolol did not change from those in the control period.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…the production of anti-acetylcholine receptor (AchR) antibodies (2). Beta-adrenergic blockers also induce myasthenia-like syndrome among patients without MG (1,3). Many other drugs, such as antiarrythmic agents and antibiotics, aggravate or unmask MG and other disorders of the neuromuscular junction (1).…”

Section: Introductionmentioning

confidence: 99%

Myasthenia-Like Syndrome Induced by Overdosage of Cibenzoline.

et al. 1996

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A case of cibenzoline-induced myasthenia-like syndrome is reported. A 67-year-old woman with renal failure and no previous disorder of neuromuscular junction complained of fatigue during climbing up a flight of stairs and experiencing heavy eyelids after administration of100 mg/ day of cibenzoline. Repetitive nerve stimulation tests revealed decrement at 5-10 Hz. After reduction of the dosage, myasthenia-like signs and symptomsdisappeared. The peak cibenzoline concentration was still high even after the dose reduction (666.4 ng/ml). In conclusion, cibenzoline, at a high plasma level, may induce myasthenia-like syndrome without any disorder of the neuromuscular junction. (Internal Medicine 35: 512-514, 1996)

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Letter: Myasthenic syndrome during treatment with practolol.

Cited by 20 publications

References 1 publication

Fulminant Myasthenia Gravis Soon after Initiation of Acebutolol Therapy

Fulminant Myasthenia Gravis Soon after Initiation of Acebutolol Therapy

Muscle cramps and elevated serum creatine phosphokinase levels induced by ?-adrenoceptor blockers

Myasthenia-Like Syndrome Induced by Overdosage of Cibenzoline.

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