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Drug induced rhabdomyolysis Department of nephrology Overview of rhabdomyolysis • Definition – a syndrome resulting from destruction of skeletal muscle • Classification – Pure exertional rhabdomyolysis – Genetically transmitted defect leading to rhabdomyolysis • Carnitine palmitoyltrasnferase deficiency • McArdle’s disease (myophophorylase deficiency) – Nonhereditary, nonexertional rhabdomyolysis • Precipitating factors leading to nonexertional rhabdomyolysis – – – – – Alcohol Phosphate deficiency Potassium deficiency Bacterial and viral infections Drugs – cocaine, amphetamines, neuroleptics, statins, protein inhibitors, fibrates – Toxins – tetanus, snake, venom, toluene, Tricholoma equestre mushrooms – Direct/ischemic injury • Clinical manifestation – – – – – Muscle weakness, pain, swelling and cramps Compartment syndrome Dark urine Metabolic abnormalities ARF • Direct nephrotoxicity of ferrihemate • Tubular obstruction due to protein, uric acid crystal & myoglobin cast • Renal vasoconstriction • Treatment – – – – – – Fluid replacement Urine alkalization Correction of electrolyte imbalance DIC Dialysis Fasciotomy JASN 2004, 11:1553-1561 Etiology of drug-induced rhabdomyolysis Current Opinion in Pediatrics 2004, 16:206–210 Mechanisms of drug induced rhabdomyolysis • Primary direct toxic effect on the myocyte function • Indirect secondary effect predisposing the myocyte to develop injury • Primary direct toxic effect on the myocyte function – Inhibition of calcium metabolism by the sarcoplasmic reticulum – Impairment of the production of ATP disruption of cell membrane – Alterations in carbohydrate metabolism • Indirect secondary effect predisposing the myocyte to develop injury – Drug-induced coma prolonged immobilization & muscle compression – Seizures – Myoclonus – Trauma, agitation, delirium Licorice • Candy, p-aminosalycylic acid, carbenoxolone sodium, boisson de coco, chewing tobacco and oriental herbal preperation • Glycyrrhizin glycyrrhetinic acid (active form) • Hypokalemia – Impaired glycogen synthesis reduction in energy production during sustained muscle contraction – Reduced muscle cell transmembrane voltage muscle damage – Impairment of normal increase of potassium release during contraction causing vasodilator effect on arterioles ischemia and muscle necrosis F/79 1년에 2회씩 보약을 복용해온 환자로 내원 전 1개월 동안 한약을 복용하였으며, 복용 5일째부터 전심쇠약감 발생, 내원 3일전부터 양하지 무력감으로 누워 지내다 1일전부터 자꾸 자려하는 상태로 내원. M/78 2 년 전부터 감초, 생강 등이 포함된 한약제를 복용하였으며, 이후 고혈압 진단, 투약 중으로 내원 1 주 전부터 양측 하지 근력 약화 발생, 하루 전부터 목을 가눌 수 없을 정도로 심해져 내원. F/55 평소 건강하던 환자로 인후염 증상 지속되어 민간요법으로 감초를 4개월간 복용하였으며, 내원 4 일 전부터 양팔과 다리 근육이 뭉치는 증상 있었으며, 내원 당일 사지마비감을 주소로 내원. CNS drugs • General anesthetic agents and CNS drugs – Narcotics, cyclic antidepressants, benzodiazepines, antihistamines and barbiturates – Prolonged immobilization pressure-induced ischemia • LSD, sympathomimetics and phencyclidine – Derilium or agitation prolonged involuntary muscle contraction Mayo Clinic Proceedings 2004, 79,1031-1034 M/17 생후 3개월 – AAP투여 후 hepatitis with agranulocytosis 10 세 – cefaclor & AAP 투여 중 desquamative dermatitis 14 세 - a febrile eruption after receiving amoxicillin and AAP, intensified after proparacetamol injection Oral challenge with paracetamol febrile exanthema, neutropenia, and a rise of CRP & CPK-MM Allergy 1999, 54:1115