Effect of cocaine on leakage of creatine kinase from isolated fast and slow muscles of rat

Pagala, Murali; Amaladevi, Bellamakonda; Azad, Deepak; Pagala, Sobhan; Herzlich, Barry C.; Namba, Tatsuji; Grob, David

doi:10.1016/0024-3205(93)90238-x

Cited by 24 publications

(4 citation statements)

References 22 publications

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“…Cocaine overdosage has been reported to be associated with rhabdomyolysis and high SCK activity (e.g., 5,670 IU /L; Pagala et al 1993). Patients 6, 7, and 11 had abused cocaine prior to admission but had normal SCK activities at admission and no evidence of cocaine in urine samples.…”

Section: Discussionmentioning

confidence: 99%

Marked Elevations of Serum Creatine Kinase Activity Associated with Antipsychotic Drug Treatment

Meltzer

1996

Neuropsychopharmacology

139

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Serum creatine kinase (SCK) activity of the skeletal muscle (MM) form is sometimes moderately increased in acutely psychotic patients and may be massively increased as a result of muscle damage. The objective of this study was to characterize the SCK increases in patients treated with novel antipsychotic drugs. SCK activity and myoglobinuria, an index of gross muscle damage, were monitored at varying intervals in schizophrenic or schizoaffective patients treated with antipsychotic drugs. Possible causes of increases in SCK activity, such as trauma, excessive physical activity, exacerbation of psychosis, were assessed. Fifteen instances of massive increases in SCK activity were observed in 11 out of 121 patients (10%) treated with the following antipsychotic drugs: clozapine, loxapine, haloperidol, melperone, risperidone, or olanzapine. These increases in SCK activity were of the MM type and ranged from 1,206 to 177,363 IU/L (median, 9,600 IU/L). Thus, they were much larger than the increases usually found in acutely psychotic patients or patients with neuroleptic malignant syndrome (range, 500-3,000 IU/L). Only the patient with SCK activity of 177,363 IU/L had rhabdomyolysis as evidenced by myoglobinuria. The onset of the increases was from 5 days to 2 years after initiating treatment, and the increases lasted 4 to 28 days (median, 8 days). Flulike symptoms were present in two of the patients, but the others were asymptomatic. The increases were self-limiting in three cases, despite continuing treatment. Two of three cases rechallenged with the same drug again developed large increases in SCK activity within a week. It is unlikely these increases in SCK activity are related to acute psychosis, trauma, or the neuroleptic malignant syndrome. The increase in SCK activity may reflect the ability of the drugs to increase intermittently cell membrane permeability, especially in skeletal muscle, in some vulnerable subjects. A possible role of serotonin in this process is suggested by the pharmacology of most of the offending drugs. However, in some instances, the increases may have been unrelated to drug treatment. There was no evidence that these increases in SCK activity, despite their magnitude, compromised renal function. Routine monitoring of SCK activity of myoglobinuria during treatment with the antipsychotic drugs studied here is probably not necessary.

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Section: Discussionmentioning

confidence: 99%

Marked Elevations of Serum Creatine Kinase Activity Associated with Antipsychotic Drug Treatment

Meltzer

1996

Neuropsychopharmacology

139

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“…9 In studies of isolated, nonperfused rat muscle, cocaine was found to have a direct effect on the tissue, resulting in leakage of CK in a dose-dependent fashion. 16 Serum myoglobin levels were not measured in this study. However, the extent to which direct toxicity can be implicated in cocaine-induced muscle damage is not clear.…”

Section: Discussionmentioning

confidence: 88%

Association of Elevated Umbilical Cord Blood Creatine Kinase and Myoglobin Levels with the Presence of Cocaine Metabolites in Maternal Urine

et al. 1996

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“…However, cocaine-associated rhabdomyolysis also occurs in patients who are neither agitated nor restrained, which may be explained by direct mechanisms of cocaine toxicity [8][9][10]. In vitro studies of murine skeletal muscle incubated with cocaine demonstrated rhabdomyolysis occurred less than one hour after exposure, suggesting a direct toxic effect [16,17]. Authors of an in vivo study highlighted yet another mechanism of cocaine-induced rhabdomyolysis by measuring significantly increased levels of glutathione, a free radical scavenger, and thiobarbituric acid reactive substances, a measurement of lipid peroxidation, in mice treated with a single dose of intravenous cocaine [17].…”

Section: Discussionmentioning

confidence: 99%

The association between cocaine use detected on drug screening and rhabdomyolysis

Richards

Mefford

Patel

et al. 2020

Toxicology Communications

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Rhabdomyolysis is associated with patients presenting to the emergency department who test positive for cocaine on rapid drug screening, including those neither agitated nor restrained. The aim was to determine patient characteristics, frequency, and severity of cocaine-associated rhabdomyolysis. We studied cocaine-positive patients also tested for rhabdomyolysis with creatine kinase (CK) over a six-year period and recorded demographics, vital signs, disposition, diagnoses, and routine labs. We then compared patients with and without rhabdomyolysis. There were 215 patients. The majority were male, black, middle-aged, and smoked tobacco. Psychiatric, neurological, and cardiovascular final diagnostic groups were most common. Other substances detected on drug screening included ethanol (18%) and amphetamines (36%). Rhabdomyolysis (CK ! 1000 U/L) was diagnosed in 54 (25%) patients, with median (IQR) CK of 2052 (1305-4959) and range of 1009-40,647 U/L. There were significant differences in gender, race, disposition, and renal/cardiac laboratory test results between patients with and without rhabdomyolysis. We performed multiple logistic regression analysis to reveal elevated BUN, blunt trauma, male gender, and amphetamines detected on drug screen as associated factors for developing rhabdomyolysis. The frequency of rhabdomyolysis in patients who used cocaine was 25%, with certain associated patient characteristics.

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Effect of cocaine on leakage of creatine kinase from isolated fast and slow muscles of rat

Cited by 24 publications

References 22 publications

Marked Elevations of Serum Creatine Kinase Activity Associated with Antipsychotic Drug Treatment

Marked Elevations of Serum Creatine Kinase Activity Associated with Antipsychotic Drug Treatment

Association of Elevated Umbilical Cord Blood Creatine Kinase and Myoglobin Levels with the Presence of Cocaine Metabolites in Maternal Urine

The association between cocaine use detected on drug screening and rhabdomyolysis

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