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Case Reports Indian Pediatrics 2000;37: 1261-1263. |
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Hypokalemic Paralysis During Management of Hypothyroidism |
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Periodic paralysis, associated with transient alteration in serum potassium level, is a well known cause of episodic weakness(1). Hypokalemic periodic paralysis with serum potassium level less than 3.5 mEq/L can sometimes be life threatening. If diagnosed in time and properly treated, the response and recovery is dramatic(2). Primary periodic paralysis is an autosomal dominant disease(3). Secondary periodic paralysis associated with gastroenteritis, diuretic abuse, renal tubular acidosis, villous adenoma of colon, hyperaldosteronism, Bartter syndrome and hyperthyroidism(2,4) is much more common(5). We report a case of periodic paralysis that occurred following management of hypothyroidism.
A 12-year-old girl was noticed to be short-statured and underweight. Two months before admission, she was diagnosed to have hypothyroidism, short stature, pulmonary tuberculosis and severe malnutrition, by a pediatrician. Investigations done showed following blood levels: thyroxine 1.5 mg/dl (normal 4.2 to 13 mg/dl)(6). TSH 42.2 mU/L (normal 2-10 mU/L)(6), and growth hormone 3.6 ng/ml (normal 0.7-6 ng/ml)(6). Sex chro-matin was positive and X-ray chest showed hilar prominence with parenchymal infiltra-tion. Radiograph of the wrist showed six carpal bones (bone age 6 ± 1 yr). The Mantoux test showed 15 mm induration at 48 h. Ultra- sonography of the abdomen and blood levels of transaminases and creatinine were normal. The patient was treated with isoniazid, rifampicin, pyrazinamide and thyroxine (7 mg/kg/day). Forty days later, she developed episodic weakness in both lower limbs and was admitted at SMS Medial College, Jaipur. She recovered spontaneously within a day and was discharged from the hospital. Seven days later, she again developed weakness in both lower limbs and was re- hospitalized. There was no history of fever, diarrhea, vomiting, polyuria and polydipsia. The weakness was not related to excessive exercise, intake of high carbohydrate diet or diuretic abuse. Three male siblings had expired in the neonatal period, the cause was not known. Two female siblings were alive and healthy. There was no history of periodic paralysis in other family members. On examination, the weight was 15 kg (38% of expected), height 113.5 cm (less then 3 standard deviations for age), upper segment to lower segment ratio of 1 : 1 and arm span was 6 cm less than the height. Muscle power was 2/5 in both upper limbs and 3/5 in both lower limbs with hypotonia and deep tendon reflexes were weak. Rest of the neurologic examination and systemic examination were normal. Investigations revealed hypokalemia with serum potassium of 3.4 mEq/L, sodium of 141 mEq/L and chloride of 101.5 mEq/L. The levels of T3 were 80 ng/dl (normal 80-210 ng/dl), T4 5.1 mg/dl and TSH 15.2 mU/L. ECG showed U waves and flattening of T waves in chest leads and lead II. The child received intravenous fluids with 35 mEq/L potassium. The weakness improved within next 24 hours. Other investigations such as blood counts, urine for porphobilinogen, stool examination, abdominal ultrasonography, nerve conduction velocity and electromyographic studies were normal. The child was discharged on oral thyroxine in a dose of 7 mg/kg/day and anti-tubercular drugs. She was advised to take potassium rich foods and to avoid strenuous exercises for 2-3 weeks. On follow up over the next four months, she was euthyroid (T3 180 ng/dl, T4 14 mg/dl, TSH 2.6 mU/L) with normal levels of serum potassium and no recurrence of paralysis. She gained height of 2.5 cm and weight of 2 kg during follow up.
Periodic paralysis may be primary or secondary type. The paralytic attack can last from an hour to several days and the weakness may be generalized or localized(3). Distur-bances of potassium equilibrium may produce a wide range of disorders including myopathy, marked muscle wasting, diminution of muscle tone, power and reflexes(2). The primary hypokalemic periodic paralysis is autosomal dominant and is exacerbated by strenuous exercise, high carbohydrate diet, cold and excitement, which was not found in this case(3). In primary type, episodes of weakness recur frequently while in our case episodes did not recur inspite of normal diet and routine activities. Many cases of secondary hypokalemic periodic paralysis have been reported in association with gastroenteritis, diuretic abuse, renal tubular acidosis, Bartter syndrome, villous adenoma of colon and hyperthyroi-dism(4). There was no history of diarrhea, vomiting or diuretic abuse in the present case. Absence of polyuria, polydipsia, anorexia, vomiting, constipation, profound hypokalemia, hypochloremia and hyponatremia ruled out Bartter syndrome. Similarly, none of clinical features of renal tubular acidosis like polyuria, polydipsia, acidotic breathing, rickets and pathological fractures were present in this case(7,8). Laboratory findings such as normal urinary pH and lack of hyperchloremia during episode of paralysis also excluded the possibilities of renal tubular acidosis. Characteristic features of hyperaldostero- nism like hypertension and polyuria were absent(9). While on therapy with thyroxine and anti-tubercular drugs this patient developed episodic hypokalemic periodic paralysis without any evident precipitating cause. Although isoniazid can cause neuritis, but its association with episodic flaccid weakness has not been reported. Clinical features and investigations did not reveal any evidence of hyperthyroidism that may cause hypokalemic paralysis(3). There was no prior episode of paralysis before initiation of thyroxine therapy and no similar illness in the family. The levels of thyroid hormones and TSH values indicate borderline hypothyroidism. The association of hypokalemic periodic paralysis with hypo-thyroidism has not been reported, to the best of our knowledge. Thyroxine in pharmacological doses, can cause increased potassium excretion and water diuresis in patients with myxedema during initial part of therapy(10). This may result in hypokalemia, especially in a child with severe malnutrition and low stores of total body potassium(2,12). Pediatricians treating child-ren with thyroxine should be aware of this complication. Contributors: SPC conceived and designed the paper and critically revised the manuscript for important intellectual content. She will act as the guarantor for the paper. RKG, KG and HT contributed to case study, literature search and drafting the article.. Funding:
None.
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