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Williams A, Unwin R. 
“Prolonged elevation of serum creatine kinase (CK) without renal failure after ingestion of ecstasy”. 
Nephrol Dial Transplant. 1997 Feb;12(2):361-2.
We would like to report two recent cases of ecstasy intoxication associated with elevated and prolonged circulating creatine kinase, but without acute renal failure. The first case was a 33-year-old previously fit man on holiday from Australia. Three days before presentation, while at a party, he had taken b tablet of ecstasy and danced for several hours, drinking only alcohol. By the following morning, approximately 7 h later, he developed diarrhoea, passing 1-2 loose stool, and generalized muscle aches and pains. The muscular pains were worse the next day and another day later (3 days after taking ecstasy) he noticed that he was passing dark Coca-cola urine, which prompted him to seek medical advice. On examination he looked anxious, but well. He was afebrile, normotensive and had a pulse rate of 100 beats/min. There was no muscle tenderness or firmness. His urine was dark and tested positive for blood and protein, but on microscopy showed only 12 white cells and no red cells per high power field. Bloods tests showed normal serum urea, creatinine and electrolyte concentrations, including potassium, phosphate and calcium, but raised aspartate transaminase (AST; 212 IU/l, normal range 11 55 IU/l ) and creatine kinase (CK; 9200 IU/l, normal range 24 195 IU/l ). An ECG was normal, showing only sinus tachycardia. His CK increased rapidly and peaked at 112 000 IU/l within 24 h of admission. He was treated initially with a forced alkaline diuresis and then maintained on an oral water diuresis, such that he became slightly hyponatraemic. His renal function did not change. However, his CK remained elevated ( 96 800 IU/l by next day), decreasing slowly until he was discharged 5 days later. At that time he felt well and his CK was 6500, but had increased 2 days later to 18 860 IU/l, when he was reviewed in the outpatient clinic, 9 days after ecstasy ingestion (Figure 1). He was seen again, 7 days later, with a CK of 1290 IU/l, and finally after another week, when his CK had declined to near normal, 30 days after his original admission, at 210 IU/l.

The second case was a previously fit 25-year-old woman who presented having collapsed at a party after taking one ecstasy tablet with alcohol. Shortly after her arrival she had a grand mal seizure, which required i.v. diazepam. She was also hyperpyrexial with a temperature of 41.9 C. This was managed with i.v. dantrolene. She was unconscious and transferred to the intensive care unit. She also became hypoglycaemic and required i.v. glucose. An urgent CT scan of her brain was requested because of the uncertain history, but was normal. Within 24 h of admission her platelet count had fallen to < 45000, but there was no evidence of a consumptive coagulopathy, and she was given a platelet transfusion. She was kept well hydrated and her renal function remained normal throughout, although her urine did initially test positive for blood and protein. Her CK peaked at 99 700 IU/l (normal range 24 170 IU/l ) 24 h after admission; 8 days later it was still over 11 000 IU/l, and it was just over 300 IU/l 1 week after discharge, 2 weeks after taking ecstasy.
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