Subject(s)
Glycyrrhiza/poisoning , Paralyses, Familial Periodic/chemically induced , Paralyses, Familial Periodic/diagnosis , Adult , Antihypertensive Agents/therapeutic use , Antithyroid Agents/therapeutic use , Diagnosis, Differential , Drug Therapy, Combination , Humans , Male , Methimazole/therapeutic use , Paralyses, Familial Periodic/drug therapy , Potassium Chloride/therapeutic use , Propranolol/therapeutic useABSTRACT
The case of a 42-year-old man is reported, who on four occasions developed a hypokalaemic periodic paralysis after an intramuscular injection of "Ambene". The detailed examination of this patient shows, that it is the primary, autosomal dominant inherited form of hypokalaemic periodic paralysis, and not the secondary form, which is caused by a renal or gastrointestinal loss of potassium. Clinical and electrophysiological, as well as histopathological and electron microscopic findings are presented, showing the typical vacuolar myopathy with submicroscopic tubular structures. In the literature there is evidence for an increased sensitivity of the muscle membrane to insulin with an increased potassium-shift inside the cell in hypokalaemic periodic paralysis. "Ambene" is a combination, which contains amongst other substances dexamethasone and the local anaesthetic drug lidocain. In the present case the paresis was possibly caused by a combined effect of dexamethasone with a consequent hyperglycaemia and lidocain with a change in the excitability of the muscle membrane. The pathophysiological mechanism of hypokalaemic periodic paralysis is discussed in terms of the release by the combination of these two drugs. It has not previously been reported that "Ambene" can provoke a hypokalaemic periodic paralysis. This is a severe side effect because of the resulting cardiac and respiratory problems.
Subject(s)
Aminopyrine/adverse effects , Anti-Inflammatory Agents/adverse effects , Back Pain/drug therapy , Dexamethasone/adverse effects , Hypokalemia/chemically induced , Paralyses, Familial Periodic/chemically induced , Phenylbutazone/adverse effects , Thiamine/adverse effects , Vitamin B 12/adverse effects , Adult , Aminopyrine/therapeutic use , Anti-Inflammatory Agents/therapeutic use , Dexamethasone/therapeutic use , Drug Combinations/adverse effects , Drug Combinations/therapeutic use , Humans , Injections, Intramuscular , Male , Muscles/drug effects , Paralyses, Familial Periodic/diagnosis , Phenylbutazone/therapeutic use , Potassium/blood , Thiamine/therapeutic use , Vitamin B 12/therapeutic useABSTRACT
Although acetazolamide usually prevents paralytic attacks in hypokalemic periodic paralysis, not all patients benefit from this treatment. We studied a father and two sons in whom attack frequency and severity increased on acetazolamide. Administration of triamterene virtually abolished attacks in three separate single-blind trials totaling more than 12 months. Spontaneous and glucose-insulin provoked occurred with only slight hypokalemia. Acetazolamide produced slight hypokalemia and provoked attacks of weakness whereas triamterene increased potassium levels significantly. Certain patients with hypokalemic periodic paralysis are worsened by acetazolamide, perhaps because of its kaliopenic effect. Triamterene may be effective in some of these patients.
Subject(s)
Acetazolamide/adverse effects , Paralyses, Familial Periodic/drug therapy , Acetazolamide/therapeutic use , Adolescent , Adult , Blood Glucose/analysis , Clinical Trials as Topic , Glucose/adverse effects , Humans , Insulin/blood , Male , Middle Aged , Paralyses, Familial Periodic/blood , Paralyses, Familial Periodic/chemically induced , Potassium/blood , Triamterene/therapeutic useSubject(s)
Paralyses, Familial Periodic/etiology , Adolescent , Adrenocorticotropic Hormone , Adult , Aged , Aldosterone/urine , Child , Child, Preschool , Denmark , Diagnosis, Differential , Electrolytes/blood , Epinephrine , Female , Glucose/metabolism , Humans , Hypokalemia/complications , Insulin/metabolism , Male , Middle Aged , Muscles/pathology , Paralyses, Familial Periodic/chemically induced , Paralyses, Familial Periodic/complications , Paralyses, Familial Periodic/drug therapy , Paralyses, Familial Periodic/epidemiology , Pedigree , Physical Exertion , Potassium/analysis , Respiration , Time FactorsABSTRACT
A case report was made of a 24-year-old man suffering from hypogonadotropic eunuchoidism associated with a hypokalemic type of familiar periodic paralysis. The attacks were observed only during the period of continual administration of the oil solution of 115.7 mg of testosterone enanthate and 20.0 mg of testosterone propionate, intramuscularly as a depot. From the findings on this patient, it was concluded that testosterone might possibly play a role in the occurrence of attacks in the case of periodic paralysis.
Subject(s)
Eunuchism/complications , Paralyses, Familial Periodic/chemically induced , Testosterone/adverse effects , Adult , Eunuchism/drug therapy , Humans , Male , Testosterone/administration & dosageABSTRACT
The observation of a 20 years old patient with a periodic paralysis is reported. During a crisis induced by 20 U of insulin and 150 g of glucose, transient hyperaldosteronism was found and the muscular biopsy performed in the left biceps brachii, disclosed vacuoles with a double membrane. The significance of these findings is discussed.