Rhabdomyolysis is not a well-understood adverse effect of antipsychotic use. Proposed mechanisms suggest involvement of serotoninergic and/or dopaminergic blockade. The purpose of this study was to describe the relationship between antipsychotic use and rhabdomyolysis. Patients admitted with rhabdomyolysis and taking an antipsychotic from January 2009 to October 2011 were included. Background demographics, laboratory data, medical and physical history, concomitant medications, and hospital course data were collected. Of the 673 cases admitted with rhabdomyolysis, 71 (10.5%) were on an antipsychotic. This is significantly greater when compared to the general US population, where only 1.3% of individuals take an antipsychotic drug (P < .0001). Cause of rhabdomyolysis was not documented in 38% of cases, and antipsychotic use was suspected in 10% of cases. No significant correlations were found between antipsychotic type and other patient-specific parameters. Seventeen (25%) of these patients were taking 2 or more antipsychotics. The largest percentage was on quetiapine (Seroquel(®); AstraZeneca, Wilmington, Delaware), the most commonly prescribed antipsychotic in the United States. Antipsychotic use is a risk factor for rhabdomyolysis and seems to be more common in those taking multiple agents. More research needs to be done to determine which antipsychotics have a higher risk and which receptors are involved. Providers should be aware of rhabdomyolysis associated with antipsychotic use.
A 63-year-old male patient with a history of bipolar I disorder presented to the emergency department in an acutely psychotic state. The patient had just returned from vacation in a malarial high-risk area and, as a result, had taken five weekly doses of mefloquine for prophylaxis. The patient's bipolar disorder was being treated with lithium, and he had been stable for about 8 years. All organic causes of psychosis were ruled out. The patient was admitted to the inpatient psychiatric unit and was treated with quetiapine until he was stable enough to return home.
Describe four personality factors with preliminary indications of distinguishing depressed patients from normals, namely those indexed in the O‐A Kit as U. I. 19, U. I. 20, U. I. 25 and U. I. 30. Thirty‐one clinically depressed Ss‐22 inpatients and 9 outpatients‐were administered the O‐A (Objective‐Analytic) battery for these four and the scores compared with those of 30 demographically matched controls. From earlier research and the general psychological theory that concerned these source traits it was hypothesized that depressed Ss would deviate negatively on U. I. 19 and U. I. 25 and positively on U. I. 20 and U. I. 30. A comparison of means that used a one‐tailed t‐test showed significant differences on two of the factors, U. I. 19 and U. I. 20, at p < 0.01 level of significance, and on U. I. 25 and U. I. 30 at p < 0.05 significance level. Thus, the clinical sample showed the hypothesized directions of divergence from the control sample on all four of the factors. Later use of a discriminant function on this pattern of deviations shows a high degree of patient‐control separation (Price, Cattell, & Patrick, Note 1).
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