Hypokalemic periodic paralysis: an unusual cause.

periodic paralysis is a rare disorder characterized by transient attacks of flac-cid paralysis of varying intensity and frequency. Although mostly familial in etiology, several sporadic cases with different causes have been reported, including some resulting from renal tubular acidosis. 1 This article reports the case of a young man with secondary hypokalemic periodic paralysis caused by distal renal tubular acidosis, which was precipitated by glue sniffing. A 27-year-old man with a 13-year history of HIV infection came to the hospital because of a 24-hour history of episodic, gradually increasing weakness of the lower extremities. He reported having had similar episodes twice previously, most recently 6 weeks ago; on those occasions, parenteral administration of fluids improved his condition. Resting after exercise or eating did not precipitate the weakness, and there was no family history of similar illness. He reported no bladder or bowel involvement and had no history of fever, cough, or any recent illness. He had received a diagnosis of dis-tal renal tubular acidosis with hypertension 7 months previously. Despite the strong smell of solvent emanating from him, the patient reported no history of glue sniffing , although family members suggested such a history. Along with his antiretroviral medications (lamivu-dine 150 mg orally daily, efavirenz 600 mg once daily) his treatment regimen included metoprolol succinate 200 mg orally daily and diltiazem extended-release capsules 240 mg orally daily. He also had been prescribed potassium and bicarbonate supplementation. The patient , however, was poorly compliant and was taking no medications at the time of hospital admission and his other episodes of lower extremity weakness. On examination, there was a strong smell of solvent emanating from the patient. He was alert, awake, and oriented. Vital signs were stable, with normal heart rate and rhythm. Lungs were clear to auscultation, and abdominal examination revealed no abnormalities. Cran-ial nerves were all intact. The patient had hypotonic weakness in all four limbs (grade 3/4 strength) and generalized hyporeflexia. Plantar reflexes were negative , and there was no sensory deficit. Laboratory Evaluation Laboratory examination revealed a normal anion gap and hyperchloremic metabolic acidosis with severe hypokalemia. Blood urea nitrogen, serum creatinine, and uric acid levels were within normal limits. Results of a urine drug screen were negative. Urinalysis revealed a pH of 5.5, a specific gravity of 1.006, and no proteinuria or glycosuria. The patient was unaware of his last CD4+ cell count or his viral load. …