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PubMed1977

Treatment of familial periodic hypokalemia with propranolol (Inderal).

Four patients suffering form familial periodic paralysis with hypokalaemia (FPP) were subjected untreated to standardized induction of paralysis. The induction was repeated after pre-treatment with the beta receptor blocker propranolol (Inderal). In three of the patients propranolol had no or even a negative effect upon the development of paralysis or upon the fall in serum potassium. In one patient a slight prophylactic gain was achieved. It was not possible to demonstrate any difference in the serum level of glucose or insulin during the induction of paralysis according to whether the patients were untreated or treated with propranolol. Short-lasting out-patient treatment of the patient who had apparently had some slight prophylactic benefit from propranolol had to be discontinued after 11 days because of an unusually severe and long-lasting attack. It is concluded that propranolol has no major effect in the treatment of FPP-unlike its favourable effect in thyrotoxic familial periodic paralysis (TFPP).

Acute Disease↗
PubMedDate not supplied

Aetiological, clinical and metabolic profile of hypokalaemic periodic paralysis in adults: a single-centre experience.

BACKGROUND: Hypokalaemic periodic paralysis constitutes a heterogeneous group of disorders that present with acute muscular weakness. In this analysis, we discuss the aetiological factors that appear to be more common in the Indian population. METHODS: From 1995 to 2001, 31 patients presented with periodic paralysis (mean age 34.5 years, range 11-68 years). Of the 31 patients, 19 were men. The clinical and laboratory data of these patients were analysed. Patients were investigated for possible secondary causes of hypokalaemla. RESULTS: There were 13 patients (42%) with renal tubular acidosis, 13 with primary hyperaldosteronism (42%), 2 each with thyrotoxic periodic paralysis and sporadic periodic paralysis, and I with Gitelman syndrome. Of the 13 patients with renal tubular acidosis, 10 had proximal and 3 distal renal tubular acidosis. Three of these patients with renal tubular acidosis had Sjogren syndrome. The patients diagnosed to have renal tubular acidosis had significantly lower serum bicarbonate (18.7 [14.6] v. 29.6 [5.0] mEq/L; p < 0.05) and higher levels of chloride (107.5 [6.0] v. 99.5 [3.4] mEq/L; p < 0.05) compared with those who had primary hyperaldosteronism, although the potassium values were similar (2.4 [0.65] v. 2.26 [0.48] mEq/L; p = 0.43). All patients with primary hyperaldosteronism had hypertension at presentation and were proven to have adrenal adenomas. CONCLUSION: A significant number of patients in this study had secondary and potentially reversible causes of hypokalaemic periodic paralysis. The common causes were renal tubular acidosis and primary hyperaldosteronism. A detailed work-up for secondary causes should be undertaken in Indian patients with hypokalaemic periodic paralysis.

Acidosis, Renal Tubular↗