Psychosomatics 48:348-349, August 2007
doi: 10.1176/appi.psy.48.4.348
© 2007 Academy of Psychosomatic Medicine
Creatine Kinase Elevation Associated With Bipolar Disorder and Ephedrine Abuse
Lonnie A. Borgerding, M.D.,
Timothy W. Lineberry, M.D., and
J. Michael Bostwick, M.D.
Received September 6, 2005; revised June 6, 2006; accepted July 6, 2006. From the Dept. of Psychiatry and Psychology, Mayo Clinic, Rochester, MN. Send correspondence and reprint requests to Lonnie A. Berg, M.D., Dept. of Psychology, Mayo Clinic College of Medicine, Rochester, MN 55905. e-mail: berg.lonnie{at}mayo.edu
© 2007 The Academy of Psychosomatic Medicine
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INTRODUCTION
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Substance abuse is commonly associated with bipolar disorder.1 Implicated substances often include drugs of abuse detected on routine toxicology screens. Creatine kinase (CK) elevations have been associated with medications; injury; disease; and psychotic states, including mania.2,3 We present the case of a bipolar-disorder patient with chronically elevated creatine kinase and a known history of substance abuse.
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Case Report
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Mr. "AT," a 27-year-old man with a history of bipolar disorder and polysubstance dependence, presented to the Emergency Department (ED) complaining of sharp, retrosternal chest pain occurring with physical exertion and emotional stress. Physical exam, vital signs, and ECG were within normal limits. AT was taking valproic acid and olanzapine for bipolar disorder. He admitted to intermittent ephedrine abuse over the past 2 years but denied recent use. He denied any other recent substance abuse. Laboratory evaluation was notable only for an elevated creatine kinase (CK) of 957 IU/liter (normal: 52 IU/liter-336 IU/liter), CK-MB isoenzyme total of 15.8 ng/ml (normal: <6.2 ng/ml), and serum drug screen positive for valproic acid. Mr. AT was hospitalized overnight, ruled out for myocardial injury, and referred for further evaluation by internal medicine and psychiatry. His CK remained elevated for the next 7 weeks. He appeared to be in a persistent hypomanic state, but denied any substance abuse. Because olanzapine was suspected of causing the elevated CK, it was cross-tapered with risperidone. Despite the change to risperidone, he continued to show elevated CK.
Three months after the initial presentation, AT admitted to his psychiatrist that he had been abusing ephedrine during most of the time since his ED visit. He stated that he was now "clean." His persistent hypomania resolved, and he began an outpatient dual-diagnosis treatment program at another facility.
Seven months after his initial ED visit, AT presented in a hypomanic and apparently intoxicated state to his ongoing dual-diagnosis treatment program. He was admitted for acute inpatient psychiatric treatment lasting 2 weeks. Urine drug screening on admission showed an amphetamine-like substance, later determined to be phenylpropanolamine and ephedrine. His CK on admission was elevated, at 1,326 IU/liter.
Within just a few days of inpatient hospitalization, with presumed ephedrine abstinence, his hypomania receded, and his CK normalized to 323 IU/liter. He continued to receive risperidone throughout the hospitalization, ruling out atypical antipsychotic use as the cause of his elevated CK. Before his anticipated discharge, he went out on a brief pass. He returned to the unit in an intoxicated, hypomanic state. The treatment team was highly suspicious that he had used ephedrine. Laboratory testing on his return revealed a CK that was extremely elevated, at 1,538 IU/liter, with normal urine drug screen.
After discharge and 9 days of treatment at a court-ordered chemical-dependency program, he was transferred back to our facility because of ongoing mania and perceived medication management failure. On admission, his CK was again elevated, at 740 IU/liter, with a negative urine drug screen. However, a urine specimen sent to a reference laboratory for quantitative ephedrine detection by gas chromatography showed an ephedrine level of 276 ng/ml. After 3 days of hospitalization, his CK again normalized, to 217 IU/liter.
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Discussion
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There are many known causes for elevated CK. Abnormal CK levels in both schizophrenia and bipolar disorder, in the absence of medications or other obvious causes, has been described.3 Among the many medications known to cause elevated CK are traditional antipsychotics, atypical antipsychotics, other psychotropics, and ephedrine.3,4 In AT’s case, periods of suspected ephedrine use corresponded to elevated CK levels, and abstinence, during inpatient hospitalizations, resulted in normalization of both CK and his manic state. Bipolar disorder is associated with a high frequency of comorbid substance abuse, particularly of stimulants.1 Ephedrine is known to induce mania in patients with and without a previous psychiatric history.5
Ephedrine abuse is very difficult to detect by routine drug screening. It has a very short half-life of 3 hours–6 hours and is rarely a component of routine urine drug screens. Specifically detecting ephedrine use requires suspicion near the time of ingestion and urine gas chromatography, which is both costly and time-consuming, especially if a sample must be sent to a reference laboratory. This case illustrates that CK elevation may be a useful and rapid surrogate marker for ephedrine abuse when it is clinically suspected but routine drug screens are uninformative.
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REFERENCES
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- Winokur G, Turvey C, Akiskal H, et al: Alcoholism and drug abuse in three groups: bipolar I, unipolars, and their acquaintances. J Affect Disord 1998; 50:81–89[CrossRef][Medline]
- Gabow PA, Kaehny WD, Kelleher SP: The spectrum of rhabdomyolysis. Med 1982; 61:141–152
- Meltzer HY: Massive serum creatine kinase increases with atypical antipsychotic drugs: what is the mechanism and the message? Psychopharmacology 2000; 150:349–350[CrossRef][Medline]
- Mansi IA, Huang J: Rhabdomyolysis in response to weight-loss herbal medicine. Am J Med Sci 2004; 327:356–357[CrossRef][Medline]
- Jacobs KM, Hirsch KA: Psychiatric complications of Ma-huang. Psychosomatics 2000; 41:58–62[Free Full Text]
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INTRODUCTION
Case Report
