Escitalopram-associated rhabdomyolysis

This case history describes a case of rhabdomyolysis resulting from treatment with escitalopram as monotherapy at the recommended dose. This is a rare and little-known side effect of selective serotonin reuptake inhibitors.

An adolescent in his late teens was referred to the outpatient clinic for child and adolescent psychiatry due to suspicion of an eating disorder. He exercised daily and had lost weight as a result of inadequate energy intake. His condition was interpreted as orthorexia nervosa. During treatment at the outpatient clinic for child and adolescent psychiatry his condition improved, but one year later he showed increasing symptoms of depression, with indication for antidepressant drug treatment. He was taking a calcium supplement with vitamin D due to osteopenia but took no other regular medications during the disease course.

The patient initially benefited from 10 mg escitalopram, but his depressive symptoms increased after six months. The dose was then increased from 10 mg to 15 mg daily. As part of the follow-up at the outpatient clinic for child and adolescent psychiatry, blood tests were taken for screening five days after the dose was increased. These revealed significantly elevated creatine kinase (CK) of > 20 000 U/L (Table 1). He reported no muscle pain but was admitted as an emergency patient to the department of clinical medicine, where he was treated for rhabdomyolysis with intravenous fluid and activity restriction. Serum myoglobin, electrolytes and renal function were normal throughout the disease course.

Serum concentration of escitalopram was within the reference range. Pharmacogenetic testing showed normal activity of the cytochrome P450 enzyme, which is the main metaboliser of escitalopram (CYP2C19), and normal expression of the serotonin transporter SLC6A4. The CK level fell during the six-day hospitalisation period (Table 1). At discharge it was concluded that orthorexia and severe undernutrition was the reason for the development of rhabdomyolysis. No change was made to the medication. The patient expressed clearly that he had normalised his energy intake and refrained from exercise in the days before admission. His current body mass index was 18 kg/m².

Four days after discharge, the patient still had elevated creatine kinase despite cessation of physical activity. Creatine kinase is halved every 1.5 days (1) when the triggering cause is removed. Other causes therefore needed to be considered. Escitalopram as a possible contributory cause of the rhabdomyolysis was suspected, and the drug was therefore gradually discontinued with a reduction of 5 mg every two days. Eleven days after the last intake of escitalopram, the CK level was within the reference range. The elimination half-life of escitalopram is approximately 30 hours, and considerably longer for its principal metabolites (2). The patient's depressive symptoms increased somewhat, and according to the patient's own wishes these were treated with talking therapy at the outpatient clinic for child and adolescent psychiatry.