J Addict Dis. 1999;18(2):51-6.
Carisoprodol (soma): abuse potential and physician unawareness.

Reeves RR, Carter OS, Pinkofsky HB, Struve FA, Bennett DM.

G.V. (Sonny) Montgomery VA Medical Center, University of Mississippi School of Medicine, Jackson 39216, USA.

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.

Source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10334375&dopt=Abstract soma carisoprodol




Pharmacogenetics. 2003 Jul;13(7):383-8.
Association between blood carisoprodol:meprobamate concentration ratios and CYP2C19 genotype in carisoprodol-drugged drivers: decreased metabolic capacity in heterozygous CYP2C19*1/CYP2C19*2 subjects?

Bramness JG, Skurtveit S, Fauske L, Grung M, Molven A, Morland J, Steen VM.

Norwegian Institute of Public Health, Division of Forensic Toxicology and Drug Abuse, Oslo, Norway. jorgen.bramnesabmed.uio.no

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 CYP




Ann Univ Mariae Curie Sklodowska [Med]. 2002;57(1):143-9.
Blockade of reticular formation activity, due to carisoprodol maternal administration, and its effects on rat skeleton development.

Blicharski T, Burdan F, Malkiewicz J, Piechota G.

Experimental Teratology Unit of Human Anatomy Department, Medical University of Lublin.

The purpose of this experiment was to study the influence of reticular formation blockade, due to carisoprodol maternal administration, on rat skeleton development. The drug was administered three times a day orally by stomach tube at doses: T1--20 mg/kg/24 h, T2--200 mg/kg/24 h, T3--400 mg/kg/24 h. The fetuses obtained on 21st day of gestation were counted and macroscopically examined. Placental and fetal weight, fetal and tail length were checked. After fixation in 95% ethanol the fetuses were stained under single alizarin red S Dawson method and examined under a stereo-dissection microscope. Morphological examination revealed no major malformations. Insignificant number of subcutaneous ecchymose and various skeleton anomalies were observed. The experiment revealed that carisoprodol has no influence on rat skeleton development.

Source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12898916&dopt=Abstract soma carisoprodol