Drug Interactions between sulfasalazine and Xanax

Grapefruit and grapefruit juice may interact with ALPRAZolam and lead to potentially dangerous side effects. Discuss the use of grapefruit products with your doctor. Do not increase or decrease the amount of grapefruit products in your diet without first talking to your doctor. Do not drink alcohol while taking ALPRAZolam. This medication can increase the effects of alcohol. You may feel more drowsy, dizzy, or tired if you take ALPRAZolam with alcohol. Talk to your doctor or pharmacist if you have any questions or concerns.

The use of benzodiazepines with alcohol is not recommended. Patients with acute alcohol intoxication exhibit depressed vital signs. The central nervous system depressant effects of benzodiazepines may be additive with those of alcohol, and severe respiratory depression and death may occur. Therapy with benzodiazepines should be administered cautiously in patients who might be prone to acute alcohol intake.

The use of sulfonamides is associated with large increases in the risk of Stevens-Johnson syndrome, toxic epidermal necrolysis and other serious dermatologic reactions, although these phenomena are rare as a whole. Hepatitis, pneumonitis, and interstitial nephritis have also occurred in association with sulfonamide hypersensitivity. Therapy with sulfonamides should be administered cautiously in patients with severe allergies, bronchial asthma or AIDS, since these patients may be at increased risk for potentially severe hypersensitivity reactions. Patients should be instructed to promptly report signs and symptoms that may precede the onset of cutaneous manifestations of the Stevens-Johnson syndrome, such as high fever, severe headache, stomatitis, conjunctivitis, rhinitis, urethritis, and balanitis. Sulfonamide therapy should be stopped at once if a rash develops.

Benzodiazepines may cause respiratory depression and apnea, usually when given in high dosages and/or by intravenous administration. However, some patients may be susceptible at commonly used dosages, including the elderly, debilitated or severely ill patients, those receiving other CNS depressants, and those with limited ventilatory reserve, chronic pulmonary insufficiency or other respiratory disorders. Therapy with benzodiazepines should be administered cautiously in these patients. Appropriate monitoring and individualization of dosage are particularly important, and equipment for resuscitation should be immediately available if the parenteral route is used. Benzodiazepines, especially injectable formulations, should generally be avoided in patients with sleep apnea, severe respiratory insufficiency, or hypoxia.

The use of sulfonamides is associated with large increases in the risk of Stevens-Johnson syndrome, toxic epidermal necrolysis and other serious dermatologic reactions, although these phenomena are rare as a whole. Hepatitis, pneumonitis, and interstitial nephritis have also occurred in association with sulfonamide hypersensitivity. Therapy with sulfonamides should be administered cautiously in patients with severe allergies, bronchial asthma or AIDS, since these patients may be at increased risk for potentially severe hypersensitivity reactions. Patients should be instructed to promptly report signs and symptoms that may precede the onset of cutaneous manifestations of the Stevens-Johnson syndrome, such as high fever, severe headache, stomatitis, conjunctivitis, rhinitis, urethritis, and balanitis. Sulfonamide therapy should be stopped at once if a rash develops.

The use of sulfonamides has been associated with hematologic toxicity, including methemoglobinemia, sulfhemoglobinemia, leukopenia, granulocytopenia, eosinophilia, hemolytic anemia, aplastic anemia, purpura, clotting disorder, thrombocytopenia, hypofibrinogenemia, and hypoprothrombinemia. Acute dose-related hemolytic anemia may occur during the first week of therapy due to sensitization, while chronic hemolytic anemia may occur with prolonged use. Patients with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency should be observed closely for signs of hemolytic anemia. Therapy with sulfonamides should be administered cautiously in patients with preexisting blood dyscrasias or bone marrow suppression. Complete blood counts should be obtained regularly, especially during prolonged therapy (>2 weeks), and patients should be instructed to immediately report any signs or symptoms suggestive of blood dyscrasia such as fever, sore throat, local infection, bleeding, pallor, dizziness, or jaundice.

Clostridioides difficile-associated diarrhea (CDAD), formerly pseudomembranous colitis, has been reported with almost all antibacterial drugs and may range from mild diarrhea to fatal colitis. The most common culprits include clindamycin and lincomycin. Antibacterial therapy alters the normal flora of the colon, leading to overgrowth of C difficile, whose toxins A and B contribute to CDAD development. Morbidity and mortality are increased with hypertoxin-producing strains of C difficile; these infections can be resistant to antimicrobial therapy and may require colectomy. CDAD must be considered in all patients who present with diarrhea after antibacterial use. Since CDAD has been reported to occur more than 2 months after antibacterial use, careful medical history is necessary. Therapy with broad-spectrum antibacterials and other agents with significant antibacterial activity should be administered cautiously in patients with history of gastrointestinal disease, particularly colitis; pseudomembranous colitis (generally characterized by severe, persistent diarrhea and severe abdominal cramps, and sometimes associated with the passage of blood and mucus), if it occurs, may be more severe in these patients and may be associated with flares in underlying disease activity. Antibacterial drugs not directed against C difficile may need to be stopped if CDAD is suspected or confirmed. Appropriate fluid and electrolyte management, protein supplementation, antibacterial treatment of C difficile, and surgical evaluation should be started as clinically indicated.

Benzodiazepines have the potential to cause dependence and abuse. Tolerance as well as physical and psychological dependence can develop, particularly after prolonged use and/or excessive dosages. However, abrupt cessation following continual use of as few as 6 weeks at therapeutic levels has occasionally precipitated withdrawal symptoms. Addiction- prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance when treated with benzodiazepines. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of benzodiazepine therapy should be undertaken gradually using a dosage- tapering schedule. If withdrawal symptoms occur, temporary reinstitution of benzodiazepines may be necessary.

The manufacturers consider the use of benzodiazepines to be contraindicated in patients with acute angle-closure glaucoma or untreated open-angle glaucoma. These agents do not possess anticholinergic activity but have very rarely been associated with increased intraocular pressure.

The use of sulfonamides is associated with large increases in the risk of Stevens-Johnson syndrome, toxic epidermal necrolysis and other serious dermatologic reactions, although these phenomena are rare as a whole. Hepatitis, pneumonitis, and interstitial nephritis have also occurred in association with sulfonamide hypersensitivity. Therapy with sulfonamides should be administered cautiously in patients with severe allergies, bronchial asthma or AIDS, since these patients may be at increased risk for potentially severe hypersensitivity reactions. Patients should be instructed to promptly report signs and symptoms that may precede the onset of cutaneous manifestations of the Stevens-Johnson syndrome, such as high fever, severe headache, stomatitis, conjunctivitis, rhinitis, urethritis, and balanitis. Sulfonamide therapy should be stopped at once if a rash develops.

The use of sulfasalazine is contraindicated in patients with intestinal obstruction. Approximately one-third of orally administered sulfasalazine is systemically absorbed from the small intestine, while the majority is metabolized by intestinal bacteria to 5-aminosalicylic acid (5-ASA) that remains in the colonic lumen and gets excreted in the feces.

Benzodiazepines are metabolized by the liver, and the metabolites are excreted in the urine. Chlordiazepoxide, clorazepate, diazepam, flurazepam and quazepam undergo oxidative N-dealkylation to active metabolites that are substantially longer-acting than the parent compound. These metabolites then undergo further biotransformation to pharmacologically inactive products before excretion by the kidney. Therapy with benzodiazepines should be administered cautiously at lower initial dosages in patients with impaired renal and/or hepatic function. Agents that are converted to weakly active, short-acting, or inactive metabolites may be preferable in hepatic impairment. Lorazepam, oxazepam and temazepam are conjugated to inactive metabolites, while alprazolam, estazolam and triazolam undergo hydroxylation to weakly active or inactive metabolites.

Hepatotoxicity, including jaundice, diffuse hepatocellular necrosis, hypersensitivity hepatitis and hepatic failure, has rarely been reported in patients receiving sulfonamides. In addition, sulfonamides are partially metabolized by the liver and may accumulate in patients with hepatic impairment. Therapy with sulfonamides should be administered cautiously in patients with liver disease.

The use of sulfonamides is contraindicated in patients with porphyria, since these drugs can precipitate an acute attack.

Benzodiazepines may cause respiratory depression and apnea, usually when given in high dosages and/or by intravenous administration. However, some patients may be susceptible at commonly used dosages, including the elderly, debilitated or severely ill patients, those receiving other CNS depressants, and those with limited ventilatory reserve, chronic pulmonary insufficiency or other respiratory disorders. Therapy with benzodiazepines should be administered cautiously in these patients. Appropriate monitoring and individualization of dosage are particularly important, and equipment for resuscitation should be immediately available if the parenteral route is used. Benzodiazepines, especially injectable formulations, should generally be avoided in patients with sleep apnea, severe respiratory insufficiency, or hypoxia.

Benzodiazepines are metabolized by the liver, and the metabolites are excreted in the urine. Chlordiazepoxide, clorazepate, diazepam, flurazepam and quazepam undergo oxidative N-dealkylation to active metabolites that are substantially longer-acting than the parent compound. These metabolites then undergo further biotransformation to pharmacologically inactive products before excretion by the kidney. Therapy with benzodiazepines should be administered cautiously at lower initial dosages in patients with impaired renal and/or hepatic function. Agents that are converted to weakly active, short-acting, or inactive metabolites may be preferable in hepatic impairment. Lorazepam, oxazepam and temazepam are conjugated to inactive metabolites, while alprazolam, estazolam and triazolam undergo hydroxylation to weakly active or inactive metabolites.

Sulfonamides and their metabolites are eliminated by the kidney. Patients with renal impairment may be at greater risk for adverse effects from sulfonamides due to decreased drug clearance. Dosage adjustments may be necessary and modifications should be based on the degree of renal impairment and severity of infection. Additionally, sulfonamides may cause renal toxicity secondary to crystalluria, including uro- and nephrolithiasis, nephritis, toxic nephrosis, hematuria, proteinuria, and elevated BUN and creatinine. Hydration (8 oz. glass of water with each dose and throughout the day) and adequate urinary output (> 1.5 L/day) should be maintained during sulfonamide administration. Renal function tests and urinalysis should be performed weekly or as often as indicated by the patient's status. Rarely, alkalinization of the urine is necessary.

Benzodiazepines may cause respiratory depression and apnea, usually when given in high dosages and/or by intravenous administration. However, some patients may be susceptible at commonly used dosages, including the elderly, debilitated or severely ill patients, those receiving other CNS depressants, and those with limited ventilatory reserve, chronic pulmonary insufficiency or other respiratory disorders. Therapy with benzodiazepines should be administered cautiously in these patients. Appropriate monitoring and individualization of dosage are particularly important, and equipment for resuscitation should be immediately available if the parenteral route is used. Benzodiazepines, especially injectable formulations, should generally be avoided in patients with sleep apnea, severe respiratory insufficiency, or hypoxia.

The use of benzodiazepines in patients with seizure disorders may increase the incidence or precipitate the onset of generalized tonic-clonic seizures (grand mal). Appropriate anticonvulsant medication might need to be initiated or the dosage increased. Abrupt cessation of benzodiazepine therapy may precipitate seizures and other withdrawal symptoms, particularly after prolonged use and/or excessive dosages. Status epilepticus may occur in patients with a history of seizures withdrawn rapidly from benzodiazepine therapy. Following chronic administration, cessation of benzodiazepine therapy should occur gradually with incrementally reduced dosages. Patients should be advised not to discontinue medication without first consulting with the physician.

The use of sulfasalazine tablets is contraindicated in patients with urinary obstruction.

Sulfasalazine may interfere with the absorption of dietary folic acid. Folate deficiency and megaloblastic anemia have been reported. Therapy with sulfasalazine should be administered cautiously in patients with preexisting folate deficiency or anemia secondary to folate deficiency. Folic acid supplementation (1 mg/day) is recommended in all patients during prolonged therapy.

Crystalluria can occur during sulfonamide therapy due to precipitation of the sulfonamide and/or its N4-acetyl metabolite in the urinary tract. Renal toxicity such as uro- and nephrolithiasis, nephritis, toxic nephrosis, hematuria, proteinuria, and elevated BUN and creatinine has been reported. Hydration (8 oz. glass of water with each dose and throughout the day) and adequate urinary output (> 1.5 L/day) should be maintained during sulfonamide administration. Patients who are dehydrated (e.g., due to severe diarrhea or vomiting) may be at increased risk for the development of crystalluria and lithiasis and should be encouraged to consume additional amounts of liquid or given intravenous fluid. Renal function tests and urinalysis should be performed weekly during prolonged therapy (> 2 weeks). Rarely, alkalinization of the urine is necessary.

Benzodiazepines depress the central nervous system and may cause or exacerbate mental depression and cause suicidal behavior and ideation. Episodes of mania and hypomania have also been reported in depressed patients treated with some of these agents. Therapy with benzodiazepines should be administered cautiously in patients with a history of depression or other psychiatric disorders. Patients should be monitored for any changes in mood or behavior. It may be prudent to refrain from dispensing large quantities of medication to these patients.

Crystalluria can occur during sulfonamide therapy due to precipitation of the sulfonamide and/or its N4-acetyl metabolite in the urinary tract. Renal toxicity such as uro- and nephrolithiasis, nephritis, toxic nephrosis, hematuria, proteinuria, and elevated BUN and creatinine has been reported. Hydration (8 oz. glass of water with each dose and throughout the day) and adequate urinary output (> 1.5 L/day) should be maintained during sulfonamide administration. Patients who are dehydrated (e.g., due to severe diarrhea or vomiting) may be at increased risk for the development of crystalluria and lithiasis and should be encouraged to consume additional amounts of liquid or given intravenous fluid. Renal function tests and urinalysis should be performed weekly during prolonged therapy (> 2 weeks). Rarely, alkalinization of the urine is necessary.

Sulfasalazine may interfere with the absorption of dietary folic acid. Folate deficiency and megaloblastic anemia have been reported. Therapy with sulfasalazine should be administered cautiously in patients with preexisting folate deficiency or anemia secondary to folate deficiency. Folic acid supplementation (1 mg/day) is recommended in all patients during prolonged therapy.

Sulfasalazine may cause hemolytic anemia in patients with glucose-6 phosphate dehydrogenase deficiency. This reaction is frequently dose related. It is recommended to observe these patients closely for signs of hemolytic anemia, and if toxic reactions occur, the drug should be discontinued immediately.

Paradoxical reactions, including excitability, irritability, aggressive behavior, agitation, nervousness, hostility, anxiety, sleep disturbances, nightmares and vivid dreams, have been reported with the use of benzodiazepines in psychiatric patients and pediatric patients with hyperactive aggressive disorders. Such patients should be monitored for signs of paradoxical stimulation during therapy with benzodiazepines. The manufacturers do not recommend the use of benzodiazepines for the treatment of psychosis.

The plasma half-lives of benzodiazepines may be prolonged in obese patients, presumably due to increased distribution into fat. Marked increases in distribution (> 100%) have been reported for diazepam and midazolam, and moderate increases (25% to 100%) for alprazolam, lorazepam, and oxazepam. Therapy with benzodiazepines should be administered cautiously in obese patients, with careful monitoring of CNS status. Longer dosing intervals may be appropriate. When dosing by weight, loading doses should be based on actual body weight, while maintenance dose should be based on ideal body weight to avoid toxicity.

Benzodiazepines depress the central nervous system and may cause or exacerbate mental depression and cause suicidal behavior and ideation. Episodes of mania and hypomania have also been reported in depressed patients treated with some of these agents. Therapy with benzodiazepines should be administered cautiously in patients with a history of depression or other psychiatric disorders. Patients should be monitored for any changes in mood or behavior. It may be prudent to refrain from dispensing large quantities of medication to these patients.

Paradoxical reactions, including excitability, irritability, aggressive behavior, agitation, nervousness, hostility, anxiety, sleep disturbances, nightmares and vivid dreams, have been reported with the use of benzodiazepines in psychiatric patients and pediatric patients with hyperactive aggressive disorders. Such patients should be monitored for signs of paradoxical stimulation during therapy with benzodiazepines. The manufacturers do not recommend the use of benzodiazepines for the treatment of psychosis.

The use of mesalamine and other compounds which contain or are converted to mesalamine has rarely been associated with renal adverse effects, including minimal change nephropathy, acute and chronic interstitial nephritis, and nephrogenic diabetes insipidus. Renal lesions such as renal infarct, papillary necrosis, tubular necrosis and interstitial fibrosis have been reported in high-dose animal studies. Therapy with mesalamine and prodrugs of mesalamine should be administered cautiously in patients with impaired renal function or a history of renal disease. Renal function should be evaluated prior to initiation of therapy and periodically during therapy.

Crystalluria can occur during sulfonamide therapy due to precipitation of the sulfonamide and/or its N4-acetyl metabolite in the urinary tract. Renal toxicity such as uro- and nephrolithiasis, nephritis, toxic nephrosis, hematuria, proteinuria, and elevated BUN and creatinine has been reported. Hydration (8 oz. glass of water with each dose and throughout the day) and adequate urinary output (> 1.5 L/day) should be maintained during sulfonamide administration. Patients who are dehydrated (e.g., due to severe diarrhea or vomiting) may be at increased risk for the development of crystalluria and lithiasis and should be encouraged to consume additional amounts of liquid or given intravenous fluid. Renal function tests and urinalysis should be performed weekly during prolonged therapy (> 2 weeks). Rarely, alkalinization of the urine is necessary.