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Included as part of the PRECAUTIONS section.

Sedation

SOMA (carisoprodol) has sedative properties (in the low back pain trials, 13% to 17% of patients who received SOMA (carisoprodol) experienced sedation compared to 6% of patients who received placebo) [see ADVERSE REACTIONS] and may impair the mental and/or physical abilities required for the performance of potentially hazardous tasks such as driving a motor vehicle or operating machinery. There have been post-marketing reports of motor vehicle accidents associated with the use of SOMA (carisoprodol) .

Since the sedative effects of SOMA (carisoprodol) and other CNS depressants (e.g., alcohol, benzodiazepines, opioids, tricyclic antidepressants) may be additive, appropriate caution should be exercised with patients who take more than one of these CNS depressants simultaneously.

Drug Dependence, Withdrawal, and Abuse

In the postmarketing experience with SOMA (carisoprodol) , cases of dependence, withdrawal, and abuse have been reported with prolonged use. Most cases of dependence, withdrawal, and abuse occurred in patients who have had a history of addiction or who used SOMA (carisoprodol) in combination with other drugs with abuse potential. However, there have been post-marketing adverse event reports of SOMA (carisoprodol) -associated abuse when used without other drugs with abuse potential. Withdrawal symptoms have been reported following abrupt cessation after prolonged use. To reduce the chance of SOMA (carisoprodol) dependence, withdrawal, or abuse, SOMA (carisoprodol) should be used with caution in addiction-prone patients and in patients taking other CNS depressants including alcohol, and SOMA (carisoprodol) should not be used more than two to three weeks for the relief of acute musculoskeletal discomfort.

SOMA (carisoprodol) , and one of its metabolites, meprobamate (a controlled substance), may cause dependence [see CLINICAL PHARMACOLOGY].

Seizures

There have been postmarketing reports of seizures in patients who received SOMA (carisoprodol) . Most of these cases have occurred in the setting of multiple drug overdoses (including drugs of abuse, illegal drugs, and alcohol) [see OVERDOSAGE].

Nonclinical Toxicology

Carcinogenesis, Mutagenesis, Impairment of Fertility

Long term studies in animals have not been performed to evaluate the carcinogenic potential of carisoprodol.

SOMA (carisoprodol) was not formally evaluated for genotoxicity. In published studies, carisoprodol was mutagenic in the in vitro mouse lymphoma cell assay in the absence of metabolizing enzymes, but was not mutagenic in the presence of metabolizing enzymes. Carisoprodol was clastogenic in the in vitro chromosoma (carisoprodol) l aberration assay using Chinese hamster ovary cells with or without the presence of metabolizing enzymes. Other types of genotoxic tests resulted in negative findings. Carisoprodol was not mutagenic in the Ames reverse mutation assay using S. typhimurium strains with or without metabolizing enzymes, and was not clastogenic in an in vivo mouse micronucleus assay of circulating blood cells.

SOMA (carisoprodol) was not formally evaluated for effects on fertility. Published reproductive studies of carisoprodol in mice found no alteration in fertility although an alteration in reproductive cycles characterized by a greater time spent in estrus was observed at a carisoprodol dose of 1200 mg/kg/day. In a 13-week toxicology study that did not determine fertility, mouse testes weight and sperm motility were reduced at a dose of 1200 mg/kg/day. In both studies, the no effect level was 750 mg/kg/day, corresponding to approximately 2.6 times the human equivalent dosage of 350 mg four times a day, based on a body surface area comparison. The significance of these findings for human fertility is not known.

Use In Specific Population

Pregnancy: Pregnancy Category C.

There are no data on the use of SOMA (carisoprodol) during human pregnancy. Animal studies indicate that carisoprodol crosses the placenta and results in adverse effects on fetal growth and postnatal survival. The primary metabolite of carisoprodol, meprobamate, is an approved anxiolytic. Retrospective, post-marketing studies do not show a consistent association between maternal use of meprobamate and an increased risk for particular congenital malformations.

Teratogenic effects

Animal studies have not adequately evaluated the teratogenic effects of carisoprodol. There was no increase in the incidence of congenital malformations noted in reproductive studies in rats, rabbits, and mice treated with meprobamate. Retrospective, post-marketing studies of meprobamate during human pregnancy were equivocal for demonstrating an increased risk of congenital malformations following first trimester exposure. Across studies that indicated an increased risk, the types of malformations were inconsistent.

Nonteratogenic effects

In animal studies, carisoprodol reduced fetal weights, postnatal weight gain, and postnatal survival at maternal doses equivalent to 1-1.5 times the human dose (based on a body surface area comparison). Rats exposed to meprobamate in-utero showed behavioral alterations that persisted into adulthood. For children exposed to meprobamate in-utero, one study found no adverse effects on mental or motor development or IQ scores. SOMA (carisoprodol) should be used during pregnancy only if the potential benefit justifies the risk to the fetus.

Labor and Delivery

There is no information about the effects of SOMA (carisoprodol) on the mother and the fetus during labor and delivery.

Nursing Mothers

Very limited data in humans show that SOMA (carisoprodol) is present in breast milk and may reach concentrations two to four times the maternal plasma concentrations. In one case report, a breast fed infant received about 4-6% of the maternal daily dose through breast milk and experienced no adverse effects. However, milk production was inadequate and the baby was supplemented with formula. In lactation studies in mice, female pup survival and pup weight at weaning were decreased. This information suggests that maternal use of SOMA (carisoprodol) may lead to reduced or less effective infant feeding (due to sedation) and/or decreased milk production. Caution should be exercised when SOMA (carisoprodol) is administered to a nursing woman.

Pediatric Use

The efficacy, safety, and pharmacokinetics of SOMA (carisoprodol) in pediatric patients less than 16 years of age have not been established.

Geriatric Use

The efficacy, safety, and pharmacokinetics of SOMA (carisoprodol) in patients over 65 years old have not been established.

Renal Impairment

The safety and pharmacokinetics of SOMA (carisoprodol) in patients with renal impairment have not been evaluated. Since SOMA (carisoprodol) is excreted by the kidney, caution should be exercised if SOMA (carisoprodol) is administered to patients with impaired renal function. Carisoprodol is dialyzable by hemodialysis and peritoneal dialysis.

Hepatic Impairment

The safety and pharmacokinetics of SOMA (carisoprodol) in patients with hepatic impairment have not been evaluated. Since SOMA (carisoprodol) is metabolized in the liver, caution should be exercised if SOMA (carisoprodol) is administered to patients with impaired hepatic function.

Patients with Reduced CYP2C19 Activity

Patients with reduced CYP2C19 activity have higher exposure to carisoprodol. Therefore, caution should be exercised in administration of SOMA to these patients [see CLINICAL PHARMACOLOGY].

Last reviewed on RxList: 12/28/2010
This monograph has been modified to include the generic and brand name in many instances.