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Association between blood carisoprodol:meprobamate concentration ratios and CYP2C19 genotype in carisoprodol-drugged drivers: decreased metabolic capacity in heterozygous CYP2C19*1/CYP2C19*2 subjects?

Carisoprodol is metabolized to meprobamate by the cytochrome P450 enzyme CYP2C19, encoded by the polymorphic CYP2C19 gene. Most studies on carisoprodol metabolism have been carried out on individuals phenotyped for CYP2C19 activity using the probe drug S-mephenytoin. We aimed to investigate whether the ratio of carisoprodol to meprobamate in a 'real life' setting could be predicted by CYP2C19 genotype or, more specifically, if high carisoprodol : meprobamate ratios in drugged drivers could be ascribed to the presence of mutant CYP2C19 alleles. From original material comprising 358 blood samples from apprehended drivers, two polarized groups were selected; a high-ratio group of 11 subjects where the carisoprodol : meprobamate ratio was >1 and a low-ratio control group of 23 subjects where the ratio was <0.31. Genotyping was carried out for the CYP2C19*2, CYP2C19*3 and CYP2C19*4 alleles. DNA samples from 94 healthy blood donors were used as reference material. The number of mutant alleles in the high-ratio and low-ratio groups was significantly higher and lower, respectively, than in the reference material. The increased number of mutant alleles in the high-ratio group was not due to the presence of many poor metabolizers, but to a high number of heterozygous individuals with the genotype CYP2C19*1/*2. This result indicates a gene dosage effect where the carisoprodol : meprobamate ratio reflects the number of active CYP2C19 alleles. The metabolism of carisoprodol to meprobamate is dependent on CYP2C19 genotype. Heterozygous individuals with the CYP2C19*1/*2 genotype have a reduced capacity for metabolizing carisoprodol, and should probably be regarded as intermediate metabolizers of this drug.

Adult↗

Somatic dysfunction during carisoprodol cessation: evidence for a carisoprodol withdrawal syndrome.

Carisoprodol is a commonly used skeletal muscle relaxant with potential for abuse because of its active metabolite, meprobamate, and several reports have suggested that patients abruptly stopping intake of carisoprodol may have a withdrawal syndrome. The authors studied changes in the occurrence of somatic dysfunctions in five patients during an 8-day period following discontinuation from large doses of carisoprodol. Results showed that the number of somatic dysfunctions changed significantly during the withdrawal period. Each patient had an increase in the number of somatic dysfunctions during the first 3 days after cessation of carisoprodol with return to at or near baseline by the eighth day. This was reflected statistically in a significant-within-subjects effect for time. Results of supplemental analyses revealed a significant component of the effect and a trend for the quadratic component to be significant. Increases in the number of somatic dysfunctions during carisoprodol discontinuation support the existence of a carisoprodol withdrawal syndrome.

Adult↗

NTP toxicity studies of carisoprodol (CAS No. 78-44-4) administered by Gavage to F344/N rats and B6C3F1 mice.

[carisoprodol structure: see text] Carisoprodol is a widely used skeletal muscle relaxant and analgesic and is available as a prescription drug. Comparative studies were conducted to determine the toxicity of carisoprodol administered in corn oil and in 0.5% methylcellulose by gavage. Carisoprodol plasma concentrations of rats and mice were measured at the end of the 13-week studies; single-dose plasma carisoprodol analyses were also performed. Genetic toxicity studies were conducted in Salmonella typhimurium, L5178Y mouse lymphoma cells, cultured Chinese hamster ovary cells, and peripheral blood erythrocytes of mice. Groups of 10 male and 10 female F344/N rats received 0, 100, 200, 400, 800, or 1,600 mg carisoprodol per kilogram body weight in corn oil by gavage or 0, 100, 200, 400, or 800 mg/kg carisoprodol in 0.5% methylcellulose by gavage for 13 weeks. Groups of 10 male and 10 female B6C3F1 mice received 0, 75, 150, 300, 600, or 1,200 mg/kg carisoprodol in corn oil by gavage or 0, 600, 1,200, or 1,600 mg/kg carisoprodol in 0.5% methylcellulose by gavage for 13 weeks. Among rats that received carisoprodol in corn oil, survival was similar to that of the vehicle controls. Survival of rats administered carisoprodol in 0.5% methylcellulose was also similar to that of the vehicle controls after adjustment for deaths (two males and one female in the 800 mg/kg group and two females in the 400 mg/kg group). The final mean body weight gain of males administered 1,600 mg/kg carisoprodol in corn oil was significantly less than that of the vehicle controls; the final mean body weights and body weight gains of female rats in the 800 and 1,600 mg/kg groups were significantly greater. In the carisoprodol in 0.5% methylcellulose study, males in the 200 mg/kg group and females in the 100 and 800 mg/kg groups had significantly greater mean body weights and body weight gains than did the vehicle controls. Clinical findings in rats administered carisoprodol in corn oil or in 0.5% methylcellulose included lethargy, ataxia, diarrhea, and prostration; the incidences were dose-related, and females were more sensitive than males to the effects of carisoprodol. In the carisoprodol in corn oil study, differences in hematology and clinical chemistry parameters occurred with no consistent patterns. The effects of carisoprodol in 0.5% methylcellulose on hematology and clinical chemistry parameters were not studied. In the corn oil study, the kidney and liver weights of male and female rats administered 200 mg/kg carisoprodol or greater were generally significantly greater than those of the vehicle controls. In the 0.5% methylcellulose study, liver weights were significantly greater in male rats administered 400 or 800 mg/kg and in female rats administered 800 mg/kg carisoprodol compared to the vehicle controls; however, a consistent effect on the kidney weights was not observed. Nephropathy was observed in male rats administered 400 mg/kg carisoprodol or greater in corn oil; the livers of four males in the 1,600 mg/kg group had centrilobular hypertrophy of hepatocytes. No lesions were observed histopathologically in female rats administered carisoprodol in corn oil. In the carisoprodol in 0.5% methylcellulose study, the severity of nephropathy in males administered 200 mg/kg or greater was enhanced, and the incidence of nephropathy in female rats in the 800 mg/kg group was slightly greater than that in the vehicle controls. Plasma carisoprodol concentrations at the end of 13 weeks generally increased with increasing dose in rats administered carisoprodol in corn oil or in 0.5% methylcellulose. The plasma carisoprodol concentrations in rats administered a single gavage dose of carisoprodol in corn oil also increased with increasing dose. In the carisoprodol in corn oil mouse study, two females each in the vehicle control and 75 mg/kg groups and one female each in the 150 and 600 mg/kg groups were accidentally killed; all males survived to the end of the study. One male and one female administered 1,600 mg/kg carisoprodol in 0.5% methylcellulose died; seven mice were accidentally killed. The mean body weights and body weight gains of mice administered carisoprodol in corn oil were generally similar to those of the vehicle controls. The final mean body weights and body weight gains of all groups of males and females administered carisoprodol in 0.5% methylcellulose were significantly less. Clinical findings in the carisoprodol in corn oil study included lethargy, ataxia, tremors, and prostration in male and female mice. Ataxia, lethargy, convulsions, and prostration were observed in all dosed groups of males and females administered carisoprodol in 0.5% methylcellulose. In the carisoprodol in corn oil study, liver weights were significantly greater in males administered 300 mg/kg or greater and in females administered 150 mg/kg or greater than in the vehicle controls. In the carisoprodol in corn oil study, no gross or microscopic lesions were considered related to carisoprodol administration. Minimal to mild centrilobular hypertrophy was observed in the liver of all dosed groups of males and in females in the 1,200 and 1,600 mg/kg groups in the carisoprodol in 0.5% methylcellulose study. The testis weights of males administered 1,200 mg/kg carisoprodol in corn oil were significantly less than those of the vehicle controls; the sperm motility of males in this group was also significantly less than that of the vehicle controls. There were no significant differences in vaginal cytology parameters between dosed and vehicle control females. At the end of the carisoprodol in corn oil study, the concentration of carisoprodol was above the limit of detection in the plasma of only one male mouse each in the 300 and 1,200 mg/kg groups and in four females in the 1,200 mg/kg group. In mice administered a single gavage dose of carisoprodol in corn oil, plasma concentrations increased with increasing dose; peak plasma concentrations occurred at 20 to 120 minutes in males and 60 to 120 minutes in females. In the carisoprodol in 0.5% methylcellulose study, plasma carisoprodol concentrations of female, but not male, mice increased with increasing dose; peak plasma carisoprodol concentrations occurred at 30 minutes postdosing in all groups of males and females. Results of proportionality and bioavailability studies indicated that single gavage doses of 200 to 800 mg/kg carisoprodol in 0.5% methylcellulose in rats or 300 to 1,200 mg/kg in mice were dose proportional; absolute bioavailability values increased with increasing dose, ranging from 15% to 32% for rats and from 18% to 38% for mice. For rats, the bioavailability of carisoprodol in 0.5% methylcellulose was approximately fivefold that of carisoprodol in corn oil; the Cmax values of the dose in 0.5% methylcellulose were approximately threefold those of the dose in corn oil. For mice, no significant difference was observed in the bioavailability of carisoprodol between the vehicles; however, the Cmax values of the dose in 0.5% methylcellulose were 1.5 to 1.75 times those of the dose in corn oil. Carisoprodol was not mutagenic in any of four strains of Salmonella typhimurium, with or without S9 metabolic activation. It did induce mutations in L5178Y mouse lymphoma cells in the absence of S9; with S9, no mutagenic activity was noted in this assay. Results of the sister chromatid exchange test with carisoprodol in cultured Chinese hamster ovary cells were considered equivocal with and without S9. Chromosomal aberrations in cultured Chinese hamster ovary cells were clearly increased by carisoprodol treatment, particularly in the presence of S9. No significant increases in the frequency of micronucleated erythrocytes were observed in peripheral blood samples from male and female mice administered carisoprodol by gavage for 13 weeks. In conclusion, carisoprodol induced ataxia and prostration in rats and mice, increases in liver weights in rats and mice, and nephropathy in male rats. The bioavailability of carisoprodol in 5% methylcellulose was greater than in corn oil. The no-observed-adverse-effect (NOAEL) level of carisoprodol administered in corn oil or in 0.5% methylcellulose was determined to be 100 mg/kg, compared to the clinical dose of 20 mg/kg per day for adults and 5 to 7.5 mg/kg per day for children.

Animals↗

Impairment due to intake of carisoprodol.

BACKGROUND: Carisoprodol is a centrally acting muscle relaxant commonly used for lower back pain. It is a drug of abuse and has been detected among impaired drivers. Carisoprodol's active metabolite meprobamate is thought to act through the GABA(A) receptor complex and produces a well-known impairing effect. It is unclear whether therapeutic intake of carisoprodol leads to impairment, and the effect of supratherapeutic doses has not been investigated. Possible impairment could further be a product of the parent drug and/or the metabolite meprobamate. The present study aimed to investigate if carisoprodol had an impairing effect by it self. METHODS: From the database at the Norwegian Institute of Public Health, Division for Forensic Toxicology and Drug Abuse 62 cases containing carisoprodol and meprobamate as only drugs were identified. These cases constituted our material. RESULTS: Impaired drivers (73%) had higher blood carisoprodol concentration than not impaired drivers (27%), but no difference in blood meprobamate concentration was found for all the drivers viewed together. Amongst occasional users of carisoprodol, however, there was difference in blood meprobamate concentration between not impaired and impaired drivers. The risk of being judged impaired rose with increasing blood carisoprodol concentration, but not with increasing blood meprobamate concentration. The clinical effects of carisoprodol as measured by the clinical test for impairment (CTI) resembled those of benzodiazepines with some important differences such as tachycardia, involuntary movements, hand tremor and horizontal gaze nystagmus, which may be specific carisoprodol effects. CONCLUSION: Carisoprodol probably has an impairing effect by itself, at least at blood concentration levels above which can be seen after therapeutic intake of the drug.

Analysis of Variance↗

The CYP2C19 genotype and the use of oral contraceptives influence the pharmacokinetics of carisoprodol in healthy human subjects.

AIMS: The aim of the present study was to investigate if subjects with one normal and one non-functional CYP2C19 allele (intermediate metabolizers; IMs) metabolized carisoprodol differently than individuals with two normal CYP2C19 alleles (extensive metabolizers; EMs) We also wanted to investigate whether the use of oral contraceptives influences the metabolism of carisoprodol in EMs and IMs. Impairing effects on psychomotor coordination and feelings of sedation were studied by comparing IMs with EMs following their ingestion of a single dose of 700 mg carisoprodol. METHODS: Thirty-seven healthy Caucasian volunteers participated in the study, of whom 25 were not using any drugs known to interact with CYP2C19, including two poor metabolizers (PMs) (CYP2C19 *2/*2 or CYP2C19 *2 /*4), 11 IMs (CYP2C19 *1/*2 or CYP2C19 *1/*4) and 12 EMs (CYP2C19 *1/*1); the remaining 12 participants were six EMs and six IMs using oral contraceptives. A single oral dose of 700 mg of carisoprodol was given, and blood drug concentrations were followed for 11 h and 45 min. During this time period, different pharmacodynamic measurements were made. RESULTS: IMs had a longer elimination half life (T(1/2)) (127 min; 95% confidence interval (CI) 95, 159) than EMs (96 min; 95% CI 84, 107) and a larger area under the concentration-time curve from 0 to infinity (AUC(0-infinity)) for carisoprodol (16.3 microg h ml(-1) ; 95% CI 11.9, 20.7) than EMs (11.3 microg h ml(-1) ; 95% CI 7.8, 14.8). The use of oral contraceptives was accompanied by larger AUC(0-infinity) for carisoprodol in both EMs (18.5 microg h ml(-1); 95% CI 10.7, 26.3) and IMs (26.0 microg h ml(-1) ; 95% CI 18.8, 33.2). EMs using oral contraceptives also had a longer T(1/2) (117 min; 95% CI 92, 143) and higher maximum carisoprodol concentration than EMs not using oral contraceptives. No significant differences in pharmacodynamic parameters were found between subjects in the different genotype groups or between users and non-users of oral contraceptives. CONCLUSIONS: Subsequent to a single-dose administration of carisoprodol, the carisoprodol AUC was approximately 45% larger in CYP2C19 IMs than in EMs. The use of oral contraceptives increased the AUC by approximately 60% in both EMs and IMs. Despite these pharmacokinetic effects, no significant differences with respect to the CYP2C19 IM and EM genotypes were observed in the acute impairing effects of a single dose of carisoprodol.

Area Under Curve↗

Carisoprodol intoxications: a retrospective study of forensic autopsy material from 1992-2003.

Carisoprodol is commonly prescribed as a centrally acting muscle relaxant, but it is also subject to abuse. The literature describing fatal intoxications with the drug is limited to a relatively small number of cases, and there are inconsistencies with regard to which concentration levels that are toxic. We therefore investigated all forensic autopsies at the Norwegian Institute of Public Health during the period 1992-2003 where carisoprodol was detected. The median concentrations of carisoprodol in intoxication with carisoprodol only or with only minor other analytical findings was 36 mg/l (range 8-65 mg/l; n=5). In the rest of the intoxications, the relevance of carisoprodol relative to the other drugs detected was variable (n=93). When the number of intoxications with carisoprodol each year were divided by the number of defined daily doses (DDD) sold, a fatal toxicity index between 5.6 and 6.9 deaths/1 million DDD was obtained. The total number of cases where carisoprodol was detected increased during the period studied, which correlated to sales figures for the drug. We conclude that carisoprodol can be fatal in concentrations below those indicated in some of the previously published literature. There were, however, only a small number of cases where the cause of death can be attributed to use of carisoprodol alone.

Adolescent↗

Formation of meprobamate from carisoprodol is catalysed by CYP2C19.

Carisoprodol is a muscle relaxant analgesic, which has an active metabolite i.e. meprobamate. We conducted an open three-panel single-dose administration study with 15 healthy volunteers: five poor metabolizers of mephenytoin, five poor metabolizers of debrisoquine and five extensive metabolizers of both substrates. The aim was to investigate if the elimination of carisoprodol and meprobamate is dependent on the two metabolic polymorphisms of mephenytoin and debrisoquine. The subjects were given single oral doses of 700 mg carisoprodol and 400 mg meprobamate on separate occasions. The disposition of carisoprodol was clearly correlated to the mephenytoin hydroxylation phenotype. The mean serum clearance of carisoprodol was four times lower in poor metabolizers of mephenytoin than in extensive metabolizers, which confirms the hypothesis from our previous study that N-dealkylation of carisoprodol cosegregates with the mephenytoin hydroxylation polymorphism. However, mean serum clearance of meprobamate did not differ between the two groups. Also, polymorphic debrisoquine hydroxylation did not influence the elimination of carisoprodol or meprobamate. Poor metabolizers of mephenytoin thus have a lower capacity to metabolize carisoprodol and may therefore have an increased risk of developing concentration dependent side-effects such as drowsiness and hypotension, if treated with ordinary doses of carisoprodol.

Administration, Oral↗

A review of carisoprodol deaths in Jefferson County, Alabama.

BACKGROUND: Carisoprodol is a skeletal muscle relaxant with the potential for abuse. A carisoprodol overdose is rarely considered fatal. Nevertheless, we encountered carisoprodol in several cases, prompting review of our experience. METHODS: We did a retrospective study of cases examined at the Jefferson County Coroner/Medical Examiner Office from January 1, 1986, to October 31, 1997, reviewing investigative reports and autopsy findings. RESULTS: Carisoprodol was present in 24 cases. Seventeen decedents died of acute drug intoxication. Carisoprodol was never the sole drug detected at autopsy, nor was it ever the sole cause of death. Propoxyphene was a co-intoxicant in 8 of the 24 cases. CONCLUSIONS: Carisoprodol causes respiratory depression. Since the mechanism of death was respiratory depression in 82% of the decedents who died of acute intoxication, we consider that carisoprodol was probably responsible, in part, for those deaths. The simultaneous use of propoxyphene and carisoprodol seems to be especially dangerous.

Acute Disease↗

Carisoprodol elimination in humans.

The elimination of the muscle relaxant drug, carisoprodol, was examined in 10 healthy volunteers after an oral dose of 700 mg. In nine subjects, carisoprodol was rapidly eliminated, with a mean half-life of 99 +/- 46 min, and extensively converted to meprobamate. Within 2.5 h after carisoprodol intake, meprobamate serum concentrations exceeded those of carisoprodol. Serum levels of meprobamate recorded (15-25 mumol/L) indicate that meprobamate might contribute to the effect(s) of carisoprodol. One subject eliminated carisoprodol with an overall half-life of 376 min, and only small amounts of meprobamate were recorded. This subject was found to be a poor metabolizer of mephenytoin. In spiked human sera, protein binding of carisoprodol was in the range of 41-67%, whereas meprobamate was bound to a lesser extent, 14-24%.

Adult↗

Carisoprodol as a drug of abuse.

Carisoprodol (available as Soma and in other commercial forms) is a commonly prescribed muscle relaxant. A small group of patients was recently discovered colluding to obtain the drug under false pretenses for the purposes of substance abuse. Animal and human studies have previously shown limited potential for tolerance or abuse, while the evidence for therapeutic efficacy is inadequate. There are two previous case reports of human carisoprodol abuse or dependence, one in which a patient showed signs of a true withdrawal syndrome. A third case involved a fatality linked to carisoprodol abuse. Data from the National Institute on Drug Abuse reveal that overdose and abuse of carisoprodol may be more common than previously suspected. Carisoprodol use should be limited to short-term treatment of acute musculoskeletal conditions involving significant muscle spasm. Suspicions of abuse should be raised by patients requesting the drug by name, "losing" prescriptions, using carisoprodol chronically, or denying the efficacy of less mind-altering alternatives.

Behavior, Addictive↗

Commonly used muscle relaxant therapies for acute low back pain: a review of carisoprodol, cyclobenzaprine hydrochloride, and metaxalone.

BACKGROUND: Low back pain is a leading reason for primary care visits. Many treatment options are available, but some lack scientific support. OBJECTIVE: The aim of this review was to discuss the etiology of low back pain and the relative risks and benefits of muscle relaxants commonly prescribed for the management of back pain. METHODS: We searched Intercontinental Marketing Services data for January 2003 through January 2004 to determine the most commonly prescribed agents for the management of musculoskeletal pain. Carisoprodol, cyclobenzaprine hydrochloride, and metaxalone represented >45% of all such prescriptions. Cochrane Library, MEDLINE, and EMBASE databases were searched (time frame: 1960 through January 2004; search terms: back pain, carisoprodol, cyclobenzaprine, metaxalone, muscle relaxants, and pharmacotherapy) and reference lists of identified articles were hand-searched. RESULTS: Three trials of carisoprodol (N = 197) were located in the Cochrane Library database. Two double-blind, randomized, placebo-controlled trials evaluating the safety and efficacy of cyclobenzaprine hydrochloride (N = 1405) were identified in the literature. Three double-blind, placebo-controlled trials were identified for metaxalone (N = 428) in 2 reports. The types of adverse events seen with these agents involved the central nervous system, including drowsiness/sedation, fatigue, and dizziness. However, the efficacy of cyclobenzaprine hydrochloride was shown to be independent of its sedative effects, which were dose related. The potential for abuse with carisoprodol is of growing concern. CONCLUSIONS: Analgesic pain management for low back pain due to muscle spasm may be combined with a muscle relaxant. Cyclobenzaprine hydrochloride has the most recent and largest clinical trials demonstrating its benefit, but carisoprodol and metaxalone also appear to be effective. However, carisoprodol's usefulness is mitigated by its potential for abuse.

Amitriptyline↗

Simultaneous determination of carisoprodol and acetaminophen in an attempted suicide by liquid chromatography-mass spectrometry with positive electrospray ionization.

An adult female ingested a considerable quantity of carisoprodol/acetaminophen tablets, which are not commercially available in Japan, in an attempt to commit suicide. Generally, because of lack of the appreciable ultraviolet absorbance or fluorescence, carisoprodol and its major metabolite meprobamate are determined by gas chromatography or gas chromatography-mass spectrometry. Complicated derivatization is, however, necessary to that methodology. Thus, we investigated the derivatization-free, highly sensitive, and simultaneous determination of carisoprodol, meprobamate, and acetaminophen by means of liquid chromatography-mass spectrometry (LC-MS) with positive electrospray ionization. A semi-micro ODS column was used. Ammonium acetate solution (10mM) and acetonitrile were used as mobile phase at a flow rate of 150 microL/min using gradient elution. MS parameters were as follows: capillary voltage, 3.5 kV; cone voltage, +30 V; extractor voltage, 5 kV; and ion source temperature, 100 degrees C. Urine samples pretreated by Oasis HLB cartridge, or plasma samples deproteinized by adding ice-cold acetonitrile were analyzed by LC-MS. The limits of quantitation for each compound were as follows: 0.50 ng/mL for carisoprodol; 10 ng/mL for acetaminophen; and 1.0 ng/mL for meprobamate. In the present case, carisoprodol and acetaminophen were the only drugs detected. Meprobamate was also found as the metabolite of carisoprodol in both urine and plasma. The plasma levels of carisoprodol, acetaminophen, and meprobamate on arrival were 29.5, 245, and 46.7 microg/mL, respectively. These levels were extremely high compared with therapeutic plasma concentrations. Despite the high plasma concentrations of these drugs, which correspond to fatal levels, the patient survived.

Acetaminophen↗

Carisoprodol (soma): abuse potential and physician unawareness.

Carisoprodol is a noncontrolled skeletal muscle relaxant whose active metabolite is meprobamate, a Schedule IV controlled substance. Although several case reports have shown that carisoprodol has abuse potential, it continues to be widely prescribed. The usage patterns of 40 patients who had taken carisoprodol for three or more months (20 of whom had no history of substance abuse and 20 of whom carried a diagnosis of substance abuse or dependence) were reviewed and compared and a survey was conducted to assess physician awareness of the abuse potential of the drug. Findings showed that some patients using carisoprodol for over three months may abuse the medication, especially those individuals with a history of substance abuse. A significant percentage of the physician population is unaware of the potential of carisoprodol for abuse and of its metabolism to meprobamate, a controlled substance. Physicians should exercise caution when prescribing carisoprodol, especially if the patient has a history of substance abuse.

Adult↗

Carisoprodol withdrawal syndrome.

A 43-year-old man with chronic back and shoulder pain was treated with hydrocodone. He began taking excessive amounts of the drug, so his physicians stopped prescribing it. The patient then obtained the muscle relaxant carisoprodol on his own from several sources. He was consuming up to 30 or more tablets/day (> or =10,500 mg/day) for several weeks, then abruptly stopped taking the drug. Within 48 hours he developed anxiety, tremors, muscle twitching, insomnia, auditory and visual hallucinations, and bizarre behavior. The symptoms intensified and peaked on the fourth day after carisoprodol cessation. The patient required brief treatment with olanzapine and tapering dosages of lorazepam while the symptoms gradually resolved. To our knowledge, this is the first documented case of a withdrawal syndrome with carisoprodol. The symptoms most likely resulted because of accumulation of meprobamate, the active metabolite of carisoprodol in humans. Clinicians prescribing carisoprodol should be aware of the possibility for abuse or addiction. Further, we recommend that carisoprodol be designated a controlled substance at the federal level.

Adult↗

Carisoprodol intoxications and serotonergic features.

The symptoms and signs of carisoprodol intoxications do not resemble those caused by its metabolite meprobamate. Meprobamate most probably produces its effects through the GABAergic neurotransmitter system. The signs and symptoms of carisoprodol intoxications, however, are not easily explained by interaction with this neurotransmitter system. In the present study, four cases of carisoprodol intoxications are presented with emphasis on the presence of serotonergic signs and symptoms. All four cases fulfilled three different sets of criteria for the diagnosis of serotonin syndrome. These findings could indicate that an increased serotonin level in the central nervous system could explain some of the symptoms and signs of carisoprodol intoxications. This may have implications for the clinical evaluation and treatment of such intoxications. Since few laboratories routinely screen for carisoprodol it is important to keep this drug in mind when encountering intoxications displaying serotonergic symptoms.

Adult↗

Direct and rapid determination of baclofen (Lioresal) and carisoprodol (Soma) in bovine serum by liquid chromatography-mass spectrometry.

Baclofen (Lioresal), a lipophilic analogue of c-aminobutyric acid (GABA), and carisoprodol (Soma), a central nervous system depressant with an unknown mechanism of pharmacologic action, are categorized as muscle relaxants. Baclofen is used clinically in the management of spasticity and its sequelae secondary to severe chronic disorders such as multiple sclerosis and other types of spinal cord lesions. Carisoprodol is used for discomfort associated with acute and painful musculoskeletal conditions. Intoxication from these drugs occurs in both humans and animals necessitating a need for their detection in plasma/serum, tissue, and gastrointestinal contents samples. A sensitive and specific analytical method for detection and quantitation of these compounds using liquid chromatography with positive atmospheric pressure chemical ionization-mass spectrometry was developed. A rapid extraction procedure for both analytes from fortified bovine sera is described. Chromatographic separation was carried out on a C(18) reverse-phase column with a gradient elution of acetonitrile and 0.25% acetic acid. The effluent was directed to the mass spectrometer with fragmentation information for baclofen and carisoprodol obtained in a scan monitoring mode. Linear standard curves for baclofen and carisoprodol were constructed based on at least two corresponding extracted ions over a concentration range of 0.1-50 micro g/mL. The analysis of fortified sera samples demonstrates good accuracy and precision for the method with a limit of detection of 0.5 micro g/mL for carisoprodol (n = 3) and 1 micro g/mL for baclofen (n = 4) and a limit of quantitation of 2 micro g/mL for both compounds. Recoveries at the limit of quantitation were between 75 and 95% for both analytes, with a 4.8-9.3% range in standard deviation.

Animals↗

Transfer of carisoprodol to breast milk.

There is no published information on the transfer of the centrally acting muscle relaxant carisoprodol and its active metabolite meprobamate into breast milk. The objective of this study was to quantify the excretion of carisoprodol and meprobamate in human milk and estimate the dose received by breast-fed infants. The concentrations of carisoprodol and meprobamate were measured in breast milk on 4 consecutive days at steady-state conditions in one woman using carisoprodol 2100 mg/d. The average milk concentrations were 0.9 microg/mL for carisoprodol and 11.6 microg/mL for meprobamate. Based on the milk concentrations measured, the absolute dose ingested by an exclusively breast-fed infant could be estimated at 1.9 mg/kg per day, and the relative dose would be 4.1% of the weight-adjusted maternal dose. No adverse effects were observed in the infant, but the infant was partly fed with formula because of insufficient maternal milk production. Thus, the authors consider that at least during prolonged use, lactation is generally inadvisable until more clinical data are available.

Adult↗

Carisoprodol-induced myoclonic encephalopathy.

CASE REPORT: A 39-year-old man ingested 35 g carisoprodol. He developed agitation, tachycardia, myoclonus, and coma. The blood carisoprodol was 71 micrograms/mL; the meprobamate was 26 micrograms/mL. DISCUSSION: Carisoprodol overdose is thought to induce simple central nervous system depression. This case demonstrates a severe overdose with symptoms more consistent with myoclonic encephalopathy. A review of cases presenting to the San Francisco Division of the California Poison Control System during 1997 suggests that carisoprodol is more commonly associated with agitation and bizarre movement disorders than the current literature suggests. The pharmacology and potential mechanisms of toxicity are discussed. CONCLUSION: Agitation, hypertonia, and a myoclonic encephalopathy may be seen with significant carisoprodol intoxication.

Adult↗