Can you take Myrac with Sucralfate?

The minocycline in Myrac has a moderate potential interaction with Esophageal Obstruction.

The use of oral tetracycline capsules and tablets has been associated with esophageal irritation and ulceration in patients who ingested the drug without sufficient fluid shortly before bedtime. Therapy with solid formulations of tetracyclines should preferably be avoided in patients with esophageal obstruction, compression or dyskinesia. If the drugs are used, patients should be advised not to take the medication just before retiring and to drink fluids liberally.

The minocycline in Myrac has a moderate potential interaction with Liver Disease.

The use of tetracyclines has rarely been associated with hepatotoxicity. Histologic fatty changes of the liver, elevated liver enzymes, and jaundice have been reported, primarily in patients treated with large doses of intravenous tetracycline hydrochloride (no longer available in the U.S.) but also in patients receiving high oral doses of these drugs. Therapy with tetracyclines should be administered cautiously in patients with preexisting liver disease or biliary obstruction. Reduced dosages may be appropriate, particularly with minocycline and doxycycline, since the former is metabolized by the liver and the latter undergoes enterohepatic recycling. Liver function tests are recommended prior to and during therapy, and the concomitant use of other potentially hepatotoxic drugs should be avoided.

The minocycline in Myrac has a major potential interaction with Noninfectious Colitis.

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.

Sucralfate has a major potential interaction with Phosphate Imbalance.

Sucralfate has phosphate binding properties for which the drug is sometimes used therapeutically. However, hypophosphatemia may occur in some patients, regardless of renal status. Therapy with sucralfate should be administered cautiously in patients with preexisting hypophosphatemia. Monitoring phosphate levels in these patients is recommended.

Sucralfate has a major potential interaction with Renal Dysfunction.

Patients with chronic renal failure or those receiving dialysis have impaired excretion of absorbed aluminum. Additionally, aluminum does not cross dialysis membranes as it is bound to albumin and transferrin plasma proteins. Aluminum accumulation and toxicity (aluminum osteodystrophy, osteomalacia, encephalopathy), have been described in patients with renal impairment. Sucralfate must be used with caution in patients with chronic renal failure.

The minocycline in Myrac has a moderate potential interaction with Renal Dysfunction.

Tetracyclines (except doxycycline) are eliminated by the kidney to various extent. Patients with renal impairment may be at greater risk for tetracycline-associated hepatic and/or renal toxicity (increased BUN with consequent azotemia, hyperphosphatemia, and acidosis) due to decreased drug clearance. Therapy with tetracyclines should be administered cautiously at reduced dosages in patients with renal impairment. Clinical monitoring of renal and liver function is recommended, and serum tetracycline levels may be necessary during prolonged therapy.