Can you take Levamlodipine with Soma?

The carisoprodol in Soma has a moderate potential interaction with Alcoholism.

Carisoprodol is partially metabolized to meprobamate, a pharmacologically active agent with known addictive potential. According to the manufacturer, abrupt cessation of carisoprodol 100 mg/kg/day (approximately 5 times the recommended daily adult dosage) was associated with mild withdrawal symptoms such as abdominal cramps, insomnia, headache, nausea and chills in some study subjects. In clinical use, psychological dependence and abuse have been rare. Nevertheless, therapy with carisoprodol should be administered cautiously in addiction-prone individuals, such as those with a history of alcohol or substance abuse. It may be prudent to refrain from dispensing large quantities of medication to these patients.

Levamlodipine has a major potential interaction with Aortic Stenosis.

In general, calcium channel blockers (CCBs) should not be used in patients with hypotension (systolic pressure < 90 mm Hg) or cardiogenic shock. Due to potential negative inotropic and peripheral vasodilating effects, the use of CCBs may further depress cardiac output and blood pressure, which can be detrimental in these patients. The use of verapamil and diltiazem is specifically contraindicated under these circumstances.

Levamlodipine has a major potential interaction with Cardiogenic Shock.

In general, calcium channel blockers (CCBs) should not be used in patients with hypotension (systolic pressure < 90 mm Hg) or cardiogenic shock. Due to potential negative inotropic and peripheral vasodilating effects, the use of CCBs may further depress cardiac output and blood pressure, which can be detrimental in these patients. The use of verapamil and diltiazem is specifically contraindicated under these circumstances.

The carisoprodol in Soma has a moderate potential interaction with Drug Dependence.

Carisoprodol is partially metabolized to meprobamate, a pharmacologically active agent with known addictive potential. According to the manufacturer, abrupt cessation of carisoprodol 100 mg/kg/day (approximately 5 times the recommended daily adult dosage) was associated with mild withdrawal symptoms such as abdominal cramps, insomnia, headache, nausea and chills in some study subjects. In clinical use, psychological dependence and abuse have been rare. Nevertheless, therapy with carisoprodol should be administered cautiously in addiction-prone individuals, such as those with a history of alcohol or substance abuse. It may be prudent to refrain from dispensing large quantities of medication to these patients.

Levamlodipine has a major potential interaction with Hypotension.

In general, calcium channel blockers (CCBs) should not be used in patients with hypotension (systolic pressure < 90 mm Hg) or cardiogenic shock. Due to potential negative inotropic and peripheral vasodilating effects, the use of CCBs may further depress cardiac output and blood pressure, which can be detrimental in these patients. The use of verapamil and diltiazem is specifically contraindicated under these circumstances.

Levamlodipine has a major potential interaction with Ischemic Heart Disease.

Increased frequency, duration, and/or severity of angina, as well as acute myocardial infarction, have rarely developed during initiation or dosage increase of calcium channel blockers (CCBs), particularly in patients with severe obstructive coronary artery disease and those treated with immediate-release formulations. The mechanism of this effect is not established. Therapy with CCBs should be administered cautiously in patients with significant coronary artery disease.

Levamlodipine has a major potential interaction with Liver Disease.

Calcium channel blockers (CCBs) are extensively metabolized by the liver. The half-lives of CCBs may be prolonged substantially in patients with severe hepatic impairment, with the potential for significant drug accumulation. In addition, the use of some CCBs has been associated with elevations in serum transaminases, both with and without concomitant elevations in alkaline phosphatase and bilirubin. While these effects may be transient and reversible, some patients have developed cholestasis or hepatocellular injury. Therapy with CCBs should be administered cautiously and often at reduced dosages in patients with significantly impaired hepatic function. Periodic monitoring of liver function is advised.

The carisoprodol in Soma has a moderate potential interaction with Liver Disease.

Carisoprodol is primarily converted in the liver to several metabolites, one of which (meprobamate) is pharmacologically active. The metabolites and a small amount of the parent drug are excreted in the urine. Patients with impaired renal and/or hepatic function may be at greater risk for adverse effects due to drug and metabolite accumulation. Therapy with carisoprodol should be administered cautiously in such patients.

The carisoprodol in Soma has a major potential interaction with Porphyria.

The use of carisoprodol is contraindicated in patients with acute intermittent porphyria. Carisoprodol is partially metabolized to the pharmacologically active meprobamate, which has been reported to precipitate acute attacks of porphyria in susceptible patients.

The carisoprodol in Soma has a moderate potential interaction with Renal Dysfunction.

Carisoprodol is primarily converted in the liver to several metabolites, one of which (meprobamate) is pharmacologically active. The metabolites and a small amount of the parent drug are excreted in the urine. Patients with impaired renal and/or hepatic function may be at greater risk for adverse effects due to drug and metabolite accumulation. Therapy with carisoprodol should be administered cautiously in such patients.