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DRUGS & SUPPLEMENTS
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Carisoprodol:
Flexicamin A (Carisoprodol) Tablets are indicated for the relief of discomfort associated with acute, painful musculoskeletal conditions in adults.
Flexicamin A (Carisoprodol) Tablets should only be used for short periods (up to two or three weeks) because adequate evidence of effectiveness for more prolonged use has not been established and because acute, painful musculoskeletal conditions are generally of short duration [see Dosage and Administration (2) ].
Flexicamin A (Carisoprodol) Tablets are indicated for the relief of discomfort associated with acute, painful musculoskeletal conditions. (1)
Important Limitations:
The recommended dose of Flexicamin A (Carisoprodol) is 250 mg to 350 mg three times a day and at bedtime. The recommended maximum duration of Flexicamin A (Carisoprodol) use is up to two or three weeks.
350 mg Tablets: white, round, unscored tablets debossed "2410 V" on one side and plain on the reverse side.
Tablets: 350 mg (3)
Flexicamin A (Carisoprodol) Tablets are contraindicated in patients with a history of acute intermittent porphyria or a hypersensitivity reaction to a carbamate such as meprobamate.
Carisoprodol has sedative properties (in the low back pain trials, 13% to 17% of patients who received Flexicamin A (Carisoprodol) experienced sedation compared to 6% of patients who received placebo) [see ADVERSE REACTIONS (6.1) ] 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 Flexicamin A (Carisoprodol).
Since the sedative effects of Flexicamin A (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.
In the postmarketing experience with Flexicamin A, 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 Flexicamin A (Carisoprodol) in combination with other drugs with abuse potential. However, there have been post-marketing adverse event reports of 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 Flexicamin A (Carisoprodol) dependence, withdrawal, or abuse, Flexicamin A (Carisoprodol) should be used with caution in addiction-prone patients and in patients taking other CNS depressants including alcohol, and Flexicamin A (Carisoprodol) should not be used more than two to three weeks for the relief of acute musculoskeletal discomfort.
Flexicamin A (Carisoprodol), and one of its metabolites, meprobamate (a controlled substance), may cause dependence [see Clinical Pharmacology (12.3) ].
There have been postmarketing reports of seizures in patients who received Flexicamin A (Carisoprodol). Most of these cases have occurred in the setting of multiple drug overdoses (including drugs of abuse, illegal drugs, and alcohol) [see Overdosage (10) ].
Most common adverse reactions are drowsiness, dizziness, and headache (6.1)
To report SUSPECTED ADVERSE REACTIONS, contact Qualitest Pharmaceuticals at 1‑800‑444-4011 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect rates observed in practice.
The data described below are based on 1387 patients pooled from two double blind, randomized, multicenter, placebo controlled, one-week trials in adult patients with acute, mechanical, lower back pain [see Clinical Studies (14) ]. In these studies, patients were treated with 250 mg of Flexicamin A (Carisoprodol), 350 mg of Flexicamin A (Carisoprodol), or placebo three times a day and at bedtime for seven days. The mean age was about 41 years old with 54% females and 46% males and 74% Caucasian, 16% Black, 9% Asian, and 2% other.
There were no deaths and there were no serious adverse reactions in these two trials. In these two studies, 2.7%, 2%, and 5.4% of patients treated with placebo, 250 mg of Flexicamin A (Carisoprodol), and 350 mg of Flexicamin A (Carisoprodol), respectively, discontinued due to adverse events; 0.5%, 0.5%, and 1.8% of patients treated with placebo, 250 mg of Flexicamin A (Carisoprodol), and 350 mg of Flexicamin A (Carisoprodol), respectively, discontinued due to central nervous system adverse reactions.
Table 1 displays adverse reactions reported with frequencies greater than 2% and more frequently than placebo in patients treated with Flexicamin A (Carisoprodol) in the two trials described above.
Adverse Reaction | Placebo (n=560) n (%) | Flexicamin A (Carisoprodol) 250 mg (n=548) n (%) | Flexicamin A (Carisoprodol) 350 mg (n=279) n (%) |
Drowsiness | 31 (6) | 73 (13) | 47 (17) |
Dizziness | 11 (2) | 43 (8) | 19 (7) |
Headache | 11 (2) | 26 (5) | 9 (3) |
The following events have been reported during postapproval use of Flexicamin A (Carisoprodol). Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
Cardiovascular: Tachycardia, postural hypotension, and facial flushing [see Overdosage (10) ].
Central Nervous System: Drowsiness, dizziness, vertigo, ataxia, tremor, agitation, irritability, headache, depressive reactions, syncope, insomnia, and seizures [see Overdosage (10) ].
Gastrointestinal: Nausea, vomiting, and epigastric discomfort.
Hematologic: Leukopenia, pancytopenia.
The sedative effects of Flexicamin A (Carisoprodol) and other CNS depressants (e.g., alcohol, benzodiazepines, opioids, tricyclic antidepressants) may be additive. Therefore, caution should be exercised with patients who take more than one of these CNS depressants simultaneously. Concomitant use of Flexicamin A (Carisoprodol) and meprobamate, a metabolite of Flexicamin A (Carisoprodol), is not recommended [see Warnings and Precautions (5.1) ].
Flexicamin A (Carisoprodol) is metabolized in the liver by CYP2C19 to form meprobamate [see Clinical Pharmacology (12.3) ]. Co-administration of CYP2C19 inhibitors, such as omeprazole or fluvoxamine, with Flexicamin A (Carisoprodol) could result in increased exposure of Flexicamin A (Carisoprodol) and decreased exposure of meprobamate. Co-administration of CYP2C19 inducers, such as rifampin or St. John's Wort, with Flexicamin A (Carisoprodol) could result in decreased exposure of Flexicamin A (Carisoprodol) and increased exposure of meprobamate. Low dose aspirin also showed an induction effect on CYP2C19. The full pharmacological impact of these potential alterations of exposures in terms of either efficacy or safety of Flexicamin A (Carisoprodol) is unknown.
Pregnancy Category C. There are no data on the use of Flexicamin A during human pregnancy. Animal studies indicate that Flexicamin A (Carisoprodol) crosses the placenta and results in adverse effects on fetal growth and postnatal survival. The primary metabolite of Flexicamin A (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 Flexicamin A (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, Flexicamin A (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. Flexicamin A (Carisoprodol) should be used during pregnancy only if the potential benefit justifies the risk to the fetus.
There is no information about the effects of Flexicamin A (Carisoprodol) on the mother and the fetus during labor and delivery.
Very limited data in humans show that Flexicamin A 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 Flexicamin A (Carisoprodol) may lead to reduced or less effective infant feeding (due to sedation) and/or decreased milk production. Caution should be exercised when Flexicamin A (Carisoprodol) is administered to a nursing woman.
The efficacy, safety, and pharmacokinetics of Flexicamin A (Carisoprodol) in pediatric patients less than 16 years of age have not been established.
The efficacy, safety, and pharmacokinetics of Flexicamin A in patients over 65 years old have not been established.
The safety and pharmacokinetics of Flexicamin A (Carisoprodol) in patients with renal impairment have not been evaluated. Since Flexicamin A (Carisoprodol) is excreted by the kidney, caution should be exercised if Flexicamin A (Carisoprodol) is administered to patients with impaired renal function. Flexicamin A (Carisoprodol) is dialyzable by hemodialysis and peritoneal dialysis.
The safety and pharmacokinetics of Flexicamin A in patients with hepatic impairment have not been evaluated. Since Flexicamin A (Carisoprodol) is metabolized in the liver, caution should be exercised if Flexicamin A (Carisoprodol) is administered to patients with impaired hepatic function.
Patients with reduced CYP2C19 activity have higher exposure to Flexicamin A (Carisoprodol). Therefore, caution should be exercised in administration of Flexicamin A (Carisoprodol) to these patients [see Clinical Pharmacology (12.3) ].
Flexicamin A (Carisoprodol) is not a controlled substance [see Warnings and Precautions (5.2) ]. Discontinuation of Flexicamin A (Carisoprodol) in animals or in humans after chronic administration can produce withdrawal signs, and there are published case reports of human Flexicamin A (Carisoprodol) dependence.
In vitro studies demonstrate that Flexicamin A (Carisoprodol) elicits barbiturate-like effects. Animal behavioral studies indicate that Flexicamin A (Carisoprodol) produces rewarding effects. Monkeys self administer Flexicamin A (Carisoprodol). Drug discrimination studies using rats indicate that Flexicamin A (Carisoprodol) has positive reinforcing and discriminative effects similar to barbital, meprobamate, and chlordiazepoxide.
Overdosage of Flexicamin A (Carisoprodol) commonly produces CNS depression. Death, coma, respiratory depression, hypotension, seizures, delirium, hallucinations, dystonic reactions, nystagmus, blurred vision, mydriasis, euphoria, muscular incoordination, rigidity, and/or headache have been reported with Flexicamin A (Carisoprodol) overdosage. Many of the Flexicamin A (Carisoprodol) overdoses have occurred in the setting of multiple drug overdoses (including drugs of abuse, illegal drugs, and alcohol). The effects of an overdose of Flexicamin A (Carisoprodol) and other CNS depressants (e.g., alcohol, benzodiazepines, opioids, tricyclic antidepressants) can be additive even when one of the drugs has been taken in the recommended dosage. Fatal accidental and non-accidental overdoses of Flexicamin A (Carisoprodol) have been reported alone or in combination with CNS depressants.
Treatment of Overdosage: Basic life support measures should be instituted as dictated by the clinical presentation of the Flexicamin A (Carisoprodol) overdose. Induced emesis is not recommended due to the risk of CNS and respiratory depression, which may increase the risk of aspiration pneumonia. Gastric lavage should be considered soon after ingestion (within one hour). Circulatory support should be administered with volume infusion and vasopressor agents if needed. Seizures should be treated with intravenous benzodiazepines and the reoccurrence of seizures may be treated with phenobarbital. In cases of severe CNS depression, airway protective reflexes may be compromised and tracheal intubation should be considered for airway protection and respiratory support.
The following types of treatment have been used successfully with an overdose of meprobamate, a metabolite of Flexicamin A (Carisoprodol): activated charcoal (oral or via nasogastric tube), forced diuresis, peritoneal dialysis, and hemodialysis (carisoprodol is also dialyzable). Careful monitoring of urinary output is necessary and overhydration should be avoided. Observe for possible relapse due to incomplete gastric emptying and delayed absorption. For more information on the management of an overdose of Flexicamin A (Carisoprodol), contact a Poison Control Center.
Flexicamin A (Carisoprodol) Tablets, USP are available as 350 mg round, white tablets for oral administration. Flexicamin A (Carisoprodol) is a white, crystalline powder, having a mild, characteristic odor and a bitter taste. It is slightly soluble in water; freely soluble in alcohol, in chloroform, and in acetone; and its solubility is practically independent of pH. Flexicamin A (Carisoprodol) is present as a racemic mixture. Chemically, Flexicamin A (Carisoprodol) is N-isopropyl-2-methyl-2-propyl-1,3-propanediol dicarbamate and the molecular formula is C12H24N2O4, with a molecular weight of 260.33. The structural formula is:
Other ingredients in Flexicamin A (Carisoprodol) Tablets, USP include croscarmellose sodium, hydrogenated vegetable oil, hypromellose, magnesium stearate and microcrystalline cellulose.
This in an image of the structural formula of Flexicamin A (Carisoprodol).
The mechanism of action of Flexicamin A in relieving discomfort associated with acute painful musculoskeletal conditions has not been clearly identified.
In animal studies, muscle relaxation induced by Flexicamin A (Carisoprodol) is associated with altered interneuronal activity in the spinal cord and in the descending reticular formation of the brain.
Flexicamin A (Carisoprodol) is a centrally acting skeletal muscle relaxant that does not directly relax skeletal muscles.
A metabolite of Flexicamin A (Carisoprodol), meprobamate, has anxiolytic and sedative properties. The degree to which these properties of meprobamate contribute to the safety and efficacy of Flexicamin A (Carisoprodol) is unknown.
The pharmacokinetics of Flexicamin A (Carisoprodol) and its metabolite meprobamate were studied in a crossover study of 24 healthy subjects (12 male and 12 female) who received single doses of 250 mg and 350 mg Flexicamin A (Carisoprodol). The exposure of Flexicamin A (Carisoprodol) and meprobamate was dose proportional between the 250 mg and 350 mg doses. The Cmax of meprobamate was 2.5 ± 0.5 μg/mL (mean ± SD) after administration of a single 350 mg dose of Flexicamin A (Carisoprodol), which is approximately 30% of the Cmax of meprobamate (approximately 8 μg/mL) after administration of a single 400 mg dose of meprobamate.
250 mg Flexicamin A (Carisoprodol) | 350 mg Flexicamin A (Carisoprodol) | |
Flexicamin A (Carisoprodol) | ||
Cmax (μg/mL) | 1.2 ± 0.5 | 1.8 ± 1.0 |
AUCinf (μg*hr/mL) | 4.5 ± 3.1 | 7.0 ± 5.0 |
Tmax (hr) | 1.5 ± 0.8 | 1.7 ± 0.8 |
T½ (hr) | 1.7 ± 0.5 | 2.0 ± 0.5 |
Meprobamate | ||
Cmax (μg/mL) | 1.8 ± 0.3 | 2.5 ± 0.5 |
AUCinf (μg*hr/mL) | 32 ± 6.2 | 46 ± 9.0 |
Tmax (hr) | 3.6 ± 1.7 | 4.5 ± 1.9 |
T½ (hr) | 9.7 ± 1.7 | 9.6 ± 1.5 |
Absorption: Absolute bioavailability of Flexicamin A (Carisoprodol) has not been determined. The mean time to peak plasma concentrations (Tmax) of Flexicamin A (Carisoprodol) was approximately 1.5 to 2 hours. Co-administration of a high-fat meal with Flexicamin A (Carisoprodol) (350 mg tablet) had no effect on the pharmacokinetics of Flexicamin A (Carisoprodol). Therefore, Flexicamin A (Carisoprodol) may be administered with or without food.
Metabolism: The major pathway of Flexicamin A (Carisoprodol) metabolism is via the liver by cytochrome enzyme CYP2C19 to form meprobamate. This enzyme exhibits genetic polymorphism.
Elimination: Carisoprodol is eliminated by both renal and non-renal routes with a terminal elimination half-life of approximately 2 hours. The half-life of meprobamate is approximately 10 hours.
Gender: Exposure of Flexicamin A (Carisoprodol) is higher in female than in male subjects (approximately 30–50% on a weight adjusted basis). Overall exposure of meprobamate is comparable between female and male subjects.
Patients with Reduced CYP2C19 Activity: Carisoprodol should be used with caution in patients with reduced CYP2C19 activity. Published studies indicate that patients who are poor CYP2C19 metabolizers have a 4-fold increase in exposure to Flexicamin A (Carisoprodol), and concomitant 50% reduced exposure to meprobamate compared to normal CYP2C19 metabolizers. The prevalence of poor metabolizers in Caucasians and African Americans is approximately 3–5% and in Asians is approximately 15–20%.
Long term studies in animals have not been performed to evaluate the carcinogenic potential of Flexicamin A (Carisoprodol).
Flexicamin A (Carisoprodol) was not formally evaluated for genotoxicity. In published studies, Flexicamin A (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. Flexicamin A (Carisoprodol) was clastogenic in the in vitro chromosomal aberration assay using Chinese hamster ovary cells with or without the presence of metabolizing enzymes. Other types of genotoxic tests resulted in negative findings. Flexicamin A (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.
Flexicamin A (Carisoprodol) was not formally evaluated for effects on fertility. Published reproductive studies of Flexicamin A (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 Flexicamin 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.
The safety and efficacy of Flexicamin A (Carisoprodol) for the relief of acute, idiopathic mechanical low back pain was evaluated in two 7-day, double blind, randomized, multicenter, placebo controlled, U.S. trials (Studies 1 and 2). Patients had to be 18 to 65 years old and had to have acute back pain (≤ 3 days of duration) to be included in the trials. Patients with chronic back pain; at increased risk for vertebral fracture (e.g., history of osteoporosis); with a history of spinal pathology (e.g., herniated nucleus pulposis, spondylolisthesis or spinal stenosis); with inflammatory back pain, or with evidence of a neurologic deficit were excluded from participation. Concomitant use of analgesics (e.g., acetaminophen, NSAIDs, tramadol, opioid agonists), other muscle relaxants, botulinum toxin, sedatives (e.g., barbiturates, benzodiazepines, promethazine hydrochloride), and anti-epileptic drugs was prohibited.
In Study 1, patients were randomized to one of three treatment groups (i.e., Flexicamin A (Carisoprodol) 250 mg, Flexicamin A (Carisoprodol) 350 mg, or placebo) and in Study 2 patients were randomized to two treatment groups (i.e., Flexicamin A (Carisoprodol) 250 mg or placebo). In both studies, patients received study medication three times a day and at bedtime for seven days.
The primary endpoints were the relief from starting backache and the global impression of change, as reported by patients, on Study Day 3. Both endpoints were scored on a 5-point rating scale from 0 (worst outcome) to 4 (best outcome) in both studies. The primary statistical comparison was between the Flexicamin A (Carisoprodol) 250 mg and placebo groups in both studies.
The proportion of patients who used concomitant acetaminophen, NSAIDs, tramadol, opioid agonists, other muscle relaxants, and benzodiazepines was similar in the treatment groups.
The results for the primary efficacy evaluations in the acute, low back pain studies are presented in Table 3.
Number of Patients | n=278 | n=269 | ||
Relief from Starting Backache, Mean (SE)b | 1.1 (0.1) | 1.8 (0.1) | ||
2 | Difference between Flexicamin A (Carisoprodol) and Placebo, Mean (SE)b (95% CI) | 0.7 (0.5, 0.9) | ||
Global Impression of Change, Mean (SE)b | 1.7 (0.1) | 2.2 (0.1) | ||
Difference between Flexicamin A (Carisoprodol) and Placebo, Mean (SE)b (95% CI) | 0.5 (0.4, 0.7) | |||
Study | Parameter | Placebo | Flexicamin A (Carisoprodol) 250 mg | Flexicamin A (Carisoprodol) 350 mg |
Number of Patients | n=269 | n=264 | n=273 | |
Relief from Starting Backache, Mean (SE)b | 1.4 (0.1) | 1.8 (0.1) | 1.8 (0.1) | |
1 | Difference between Flexicamin A (Carisoprodol) and Placebo, Mean (SE)b (95% CI) | 0.4 (0.2, 0.5) | 0.4 (0.2, 0.6) | |
Global Impression of Change, Mean (SE)b | 1.9 (0.1) | 2.2 (0.1) | 2.2 (0.1) | |
Difference between Flexicamin A (Carisoprodol) and Placebo, Mean (SE)b (95% CI) | 0.2 (0.1, 0.4) | 0.3 (0.1, 0.4) |
aThe primary efficacy endpoints (Relief from Starting Backache and Global Impression of Change) were assessed by the patients on Study Day 3. These endpoints were scored on a 5-point rating scale from 0 (worst outcome) to 4 (best outcome).
b Mean is the least squared mean and SE is the standard error of the mean. The ANOVA model was used for the primary statistical comparison between the Flexicamin A (Carisoprodol) 250 mg and placebo groups.
Patients treated with Flexicamin A (Carisoprodol) experienced improvement in function as measured by the Roland-Morris Disability Questionnaire (RMDQ) score on Days 3 and 7.
350 mg Tablets: white, round, unscored tablets debossed "2410 V" on one side and plain on the reverse side
49999-064-01
Storage:
Store at 20°-25°C (68°-77°F).
Patients should be advised to contact their physician if they experience any adverse reactions to Flexicamin A tablets.
Patients should be advised that Flexicamin A (Carisoprodol) tablets may cause drowsiness and/or dizziness, and has been associated with motor vehicle accidents. Patients should be advised to avoid taking Flexicamin A (Carisoprodol) before engaging in potentially hazardous activities such as driving a motor vehicle or operating machinery [see Warnings and Precautions (5.1) ].
Patients should be advised to avoid alcoholic beverages while taking Flexicamin A tablets and to check with their doctor before taking other CNS depressants such as benzodiazepines, opioids, tricyclic antidepressants, sedating antihistamines, or other sedatives [see Warnings and Precautions (5.1) ].
Patients should be advised that treatment with Flexicamin A (Carisoprodol) tablets should be limited to acute use (up to two or three weeks) for the relief of acute, musculoskeletal discomfort. In the post-marketing experience with Flexicamin A (Carisoprodol) tablets, cases of dependence, withdrawal, and abuse have been reported with prolonged use. If the musculoskeletal symptoms still persist, patients should contact their healthcare provider for further evaluation.
To report SUSPECTED ADVERSE REACTIONS, contact Qualitest Pharmaceuticals at 1-800-444-4011 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
Manufactured for:
QUALITEST PHARMACEUTICALS
Huntsville, AL 35811
8181281
Revised: 10/2010
R5
image of label
Piroxicam:
Flexicamin A is a NSAID, refers to a group oxicams. This medication has anti-inflammatory, analgesic and antipyretic effect.
The mechanism of action associated with inhibition of the enzyme COX, which leads to inhibition of prostaglandin synthesis from arachidonic acid.
Flexicamin A (Piroxicam) inhibits the aggregation of platelets. For systemic use this medicine reduces the pain syndrome.
When Flexicamin A (Piroxicam) used externally it weakens or suppresses inflammation and joint pain at rest and in motion, reduces morning stiffness and swelling of the joints, increases range of motion.
The analgesic effect occurs within 30 minutes after oral taking. Anti-inflammatory effect manifested by the end of the first week of treatment. After a single dose the effect lasts for 24 hours.
After oral administration Flexicamin A (Piroxicam) is well absorbed from the gastrointestinal tract. Cmax in plasma is reached within 3-5 hours.
The proteins plasma binding is 99%. Flexicamin A (Piroxicam) penetrating the placental barrier, excrets in breast milk.
Metabolized in the liver by hydrolysis and conjugation. Flexicamin A (Piroxicam) is excreted unchanged (5%) and in the form of metabolites, which are displayed in the kidneys and in small amounts in feces. T1/2 is approximately 50 hours.
In patients with liver diseases T1/2 may increases.
For systemic and topical use: articular syndrome (rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, gout), back pain, neuralgia, myalgia, traumatic inflammation of the soft tissue and musculoskeletal system.
For systemic use: dysmenorrhea in patients older than 12 years, acute infectious-inflammatory diseases of upper respiratory tract.
For oral administration the dosage is 10-30 mg 1 time / day. Rectal - 20-40 mg 1-2 times / day. In acute gout, the initial dose is 40 mg 1 time / day in the first 2 days, then 40 mg 1 time per day or 20 mg 2 times / day for 4-6 days. In acute conditions or exacerbation of a chronic process you can enter IM at a dose of 20-40 mg 1 time / day. After the relief of acute process of switching to maintenance therapy with oral forms.
Externally this medicine is applied 3-4 times / day.
Digestive system: common - nausea, anorexia, stomatitis, epigastric pain, diarrhea or constipation, bloating, bleeding gums (due to the inhibition of platelet aggregation); in rare cases - erosive and ulcerative lesions of the gastrointestinal tract, with possible bleeding and perforation, transient elevation of liver enzymes, jaundice and hepatic necrosis with fatal consequences. Typically these side effects develop with chronic administration at doses exceeding 30 mg / day.
Hematopoietic system: anemia (rarely aplastic anemia or hemolytic anemia), thrombocytopenia, leukopenia, eosinophilia.
CNS and peripheral nervous system: possible dizziness, headache, drowsiness, sleep disturbances, depression, anxiety, hallucinations, mood changes, weakness, disturbances of sensitivity, swelling of the eyes, blurred vision, and signs of eye irritation.
Metabolism: rarely - hyperkalemia, hypo- or hyperglycemia, changes in body weight, in some cases - a transient increase of residual nitrogen and creatinine, uremia with hyperkalemia.
Urinary system: acute renal failure (with symptoms of hemorrhagic vasculitis), acute interstitial nephritis.
Allergic reactions: possible itching, redness, rash, pemphigus vulgaris, allergic swelling of face and hands; in some cases - Stevens-Johnson syndrome, Lyell's syndrome; in rare cases - anaphylactic reactions, bronchospasm, urticaria, angioedema, vasculitis, serum sickness.
Dermatological reactions: rarely - photosensitivity, rarely - onycholysis, alopecia.
Other: possible nosebleeds.
Local reaction: possible irritation of the rectum, tenesmus.
For external use: rarely - erythema and itching at the site of application.
Erosive and ulcerative lesions of the gastrointestinal tract in acute phase, indications in a history to bronchial asthma in connection with the use of NSAIDs, violations of porphyrin metabolism, expressed by human liver and kidney failure, pregnancy, lactation, children under the age of 14 years, proctitis (rectal use), increased sensitivity to Flexicamin A (Piroxicam).
Flexicamin A is contraindicated for use in the III trimester of pregnancy. If necessary to use this drug in the I and II trimesters of pregnancy should be related to the expected benefit to the mother and the potential risk to the fetus, due to lack of reliable clinical evidence supporting the safety of Flexicamin A (Piroxicam) in this period.
Flexicamin A (Piroxicam) is excreted in breast milk. If necessary to use this medication during lactation should solve the issue of termination of breastfeeding. Category effects on the fetus by FDA - C.
With caution use Flexicamin A (Piroxicam) if erosive and ulcerative lesions and bleeding from the gastrointestinal tract in history, dyspeptic symptoms of chronic heart failure, hepatic dysfunction and kidney failure, asthma, coagulation disorders, and concomitant administration of oral anticoagulants, allergic reactions to acetylsalicylic acid and other NSAIDs in history.
In the course of treatment is necessary to monitor the functional state of the liver and peripheral blood picture. This medicine should not be used topically in violation of the integrity of the skin.
Must avoid contact with eyes or mucous membranes.
Not recommended for use while Flexicamin A (Piroxicam) and acetylsalicylic acid and other NSAIDs.
This medication Displaces from its association with blood proteins other drugs; reduces the effectiveness of antihypertensive drugs. Compared to other NSAIDs and corticosteroids Flexicamin A (Piroxicam) increases the risk of ulcerogenic action. This drug increases the risk of hyperkalemia when combined with potassium-sparing potassium-based diuretics and other drugs; increases the concentration of phenytoin and lithium in the blood. Anticoagulants increase the risk of bleeding. Aspirin reduces the concentration of Flexicamin A (Piroxicam) in the blood up to 80% of the original.
Symptoms: drowsiness, blurred vision, at very high doses - loss of consciousness, coma.
Treatment: gastric lavage, taking activated charcoal, antacids (to reduce the intake), symptomatic therapy.
Depending on the reaction of the Flexicamin A after taken, if you are feeling dizziness, drowsiness or any weakness as a reaction on your body, Then consider Flexicamin A not safe to drive or operate heavy machine after consumption. Meaning that, do not drive or operate heavy duty machines after taking the capsule if the capsule has a strange reaction on your body like dizziness, drowsiness. As prescribed by a pharmacist, it is dangerous to take alcohol while taking medicines as it exposed patients to drowsiness and health risk. Please take note of such effect most especially when taking Primosa capsule. It's advisable to consult your doctor on time for a proper recommendation and medical consultations.
Is Flexicamin A addictive or habit forming?Medicines are not designed with the mind of creating an addiction or abuse on the health of the users. Addictive Medicine is categorically called Controlled substances by the government. For instance, Schedule H or X in India and schedule II-V in the US are controlled substances.
Please consult the medicine instruction manual on how to use and ensure it is not a controlled substance.In conclusion, self medication is a killer to your health. Consult your doctor for a proper prescription, recommendation, and guidiance.
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The information was verified by Dr. Rachana Salvi, MD Pharmacology