Thyrotoxic hypokalemic periodic paralysis as the presenting symptom of silent thyroiditis
A 23-year-old gentleman was admitted with acute onset weakness of both upper and lower limbs after rising from bed. Weakness was more in lower limbs and proximally. The patient had a past history of similar transient weakness in proximal muscle of lower limbs, 3 weeks back -- after a period of rest, from which he had a spontaneous recovery within 6 hours. There was no fatigability, muscle ache, dysphagia, dysphonia, and no history of symptoms suggestive of ocular, sensory, cerebellar, cranial nerve or bladder, and bowel involvement. He had no history of hypertension, kidney, thyroid disease, no history of trauma, fever, recent vaccination or medication like diuretics, exogenous thyroid hormone intake. Heavy exercise, carbohydrate load, vomiting, and diarrhea did not precipitate the weakness. No family member had similar symptoms.\nOn examination his vital signs were normal except a regular heart rate of 102/min; his blood pressure was 122/80 mm of Hg. His neurological examination revealed flaccid weakness of both lower limbs, mainly proximally with a power of MRC grade 2/5, and upper limb power of 3/5. His deep tendon jerks were depressed and plantar reflex was flexor bilaterally. He had no weakness of extraocular muscles, no muscle tenderness. His higher function and sensory and cerebellar functions were within normal limits. His respiratory, cardiovascular, and gastrointestinal examination revealed no obvious abnormalities. There was no goiter or fine tremor. Recurrent episodes of flaccid paralysis followed by quick recovery were suggestive of periodic paralysis.\nHis routine hematological study was normal except a high first-hour ESR of 68 mm/h. Urine routine examination and blood sugar was normal, without any urinary sugar. Biochemical parameters including electrolytes were normal, sodium was 138 mEq/l, and serum calcium was 9.2 mg/dl, except for serum potassium of 1.8 mEq/l (normal -3.5--5). A 24-hour urinary potassium concentration was 10 mEq/day (normal:<20 mEq/ day), urinary potassium-creatinine ratio was 1 mEq/mmol (normal <2), and transtubular potassium gradient (TTKG) calculated as (urine/plasma[potassium])/ (urine/ plasma osmolality) was 1.5 (normal <3), respectively. The findings’ were consistent with hypokalemic periodic paralysis unrelated to any renal potassium loss. There was no history of familial periodic paralysis, chronic diuretic abuse or gastrointestinal disorders causing potassium loss. Fasting urine pH was 4.4 (nl <5) with arterial ph of 7.41 in arterial blood gas, serum bicarbonate of 24 mmol/l was normal ruling out renal tubular acidosis. Ammonium chloride loading test (0.1 g/kg) was normal with urinary pH of 3.6. Electrocardiogram showed sinus tachycardia and ultrasound abdomen was normal without any nephrocalcinosis.\nThe thyroid function test (TFT) showed a depressed TSH: 0.03 mU/ml (normal -0.5--4.7) raised free T4: 2.8 ng/dl (normal -0.6--2.0) and T3-200 ng/dL (normal -70--190) though clinically there were no features of thyrotoxicosis. His TSH receptor antibody was 0.5 U/L (normal <1) and TPO antibody 74 IU/ml (normal <35). TSH receptor antibodies were measured by the receptor assay method with a competitive binding radioreceptor assay manufactured by Immunotech, SA, Marseille, France. A 99mTc pertechnetate thyroid scan revealed decreased uptake of 0.1% (normal 0.4- -1%), consistent with thyroiditis [].\nHis nerve conduction velocity (NCV) was normal but electromyography showed myopathic pattern of weakness with no decrement in muscle action potential on repetitive stimulation and normal creatinine kinase level.\nHe was diagnosed as a case of hypokalemic thyrotoxic periodic paralysis due to silent thyroiditis. He was treated initially with intravenous and later oral potassium (80 meq/day) supplement besides propranolol in the dosage of 120 mg/day. He recovered completely within 4 days and he was discharged on propranolol 80 mg/day. His serum potassium was 4.0 meq/l at discharge. He was followed up regularly and at the end of 2 months TFT was normal. His propranolol was gradually tapered off and he had no fresh attacks even after 2 months of complete propranolol withdrawal.