Drug Interactions between isoniazid and troleandomycin

Food can decrease the levels of isoniazid in your body. Taking isoniazid on an empty stomach (at least 30 minutes before or 2 hours after a meal) will make it easier for your body to absorb the medication. Avoid drinking alcohol while taking isoniazid because alcohol use may increase the risk of damage to your liver and your risk of experiencing a condition known as peripheral neuropathy (i.E., weakness, numbness, and pain typically in the hands and feet). Your doctor may advise you to take a vitamin B6 (pyridoxine) supplement during your treatment to help prevent peripheral neuropathy. Isoniazid may interact with foods containing histamine or tyramine (e.G., aged cheese, cured meats such as sausages and salami, fava beans, sauerkraut, soy sauce, beer, red wine, skipjack, tuna, mackerel, salmon), which can cause symptoms like headache, sweating, flushing, palpitations, dizziness, lightheadedness, or feeling faint. These foods should generally be avoided. It is important to seek immediate medical care if you experience any severe side effects or symptoms of liver damage such as fever, chills, joint pain or swelling, unusual bleeding or bruising, skin rash, itching, loss of appetite, fatigue, nausea, vomiting, dark colored urine, and/or yellowing of the skin or eyes. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

The use of isoniazid is contraindicated in patients with a history of hepatic injury due to this drug and acute liver disease of any etiology. Caution is advised when using the drug in patients with chronic liver disease or a history of alcoholism. This drug has been associated with severe and sometimes fatal hepatitis, which may occur even after many months of therapy. In a US Public Health Service Surveillance Study of 13,838 persons taking isoniazid, there were 8 deaths among 174 cases of hepatitis. Epidemiologic studies indicate an increased incidence with increasing age, alcohol use, and female gender. As a precautionary measure, routine monitoring of serum transaminases (SGOT, SGPT) and bilirubin may be considered, although a transient and harmless increase in serum transaminase reportedly occurs in 10% to 20% of patients, usually in the first 3 months of therapy. Patients should be advised to promptly discontinue isoniazid therapy and seek medical attention if they experience signs or symptoms suggestive of liver damage such as fever, rash, anorexia, nausea, vomiting, fatigue, right upper quadrant pain, dark urine, and jaundice. Reinstitution of the drug should occur only after symptoms and laboratory abnormalities resolve, with low and gradually increasing dosages.

Isoniazid commonly causes dose-related peripheral neuropathy, which results from the depletion of pyridoxine in the presence of the drug. The neuropathy is usually preceded by paraesthesia's of the feet and hands. Therapy with isoniazid should be administered cautiously in patients with pre-existing peripheral neuropathy or risk factors for developing the condition, such as malnutrition, diabetes and alcoholism. Careful monitoring is recommended on these patients. Pyridoxine (vitamin B6) at a dosage of 10 to 50 mg/day may prevent or attenuate isoniazid-related peripheral neuropathy and is recommended for these patients.

Troleandomycin is primarily excreted by the liver and may accumulate in patients with impaired hepatic function. In addition, the use of troleandomycin has been associated with an allergic type of cholestatic hepatitis, particularly in patients receiving the drug for more than 2 weeks or given repeated courses. Therapy with troleandomycin should be administered cautiously in patients with liver and/or biliary disease. Liver function tests should be monitored during prolonged or repeated courses of therapy, and the drug discontinued if abnormalities develop.

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.

Isoniazid commonly causes dose-related peripheral neuropathy, which results from the depletion of pyridoxine in the presence of the drug. The neuropathy is usually preceded by paraesthesia's of the feet and hands. Therapy with isoniazid should be administered cautiously in patients with pre-existing peripheral neuropathy or risk factors for developing the condition, such as malnutrition, diabetes and alcoholism. Careful monitoring is recommended on these patients. Pyridoxine (vitamin B6) at a dosage of 10 to 50 mg/day may prevent or attenuate isoniazid-related peripheral neuropathy and is recommended for these patients.

The use of isoniazid is contraindicated in patients with a history of hepatic injury due to this drug and acute liver disease of any etiology. Caution is advised when using the drug in patients with chronic liver disease or a history of alcoholism. This drug has been associated with severe and sometimes fatal hepatitis, which may occur even after many months of therapy. In a US Public Health Service Surveillance Study of 13,838 persons taking isoniazid, there were 8 deaths among 174 cases of hepatitis. Epidemiologic studies indicate an increased incidence with increasing age, alcohol use, and female gender. As a precautionary measure, routine monitoring of serum transaminases (SGOT, SGPT) and bilirubin may be considered, although a transient and harmless increase in serum transaminase reportedly occurs in 10% to 20% of patients, usually in the first 3 months of therapy. Patients should be advised to promptly discontinue isoniazid therapy and seek medical attention if they experience signs or symptoms suggestive of liver damage such as fever, rash, anorexia, nausea, vomiting, fatigue, right upper quadrant pain, dark urine, and jaundice. Reinstitution of the drug should occur only after symptoms and laboratory abnormalities resolve, with low and gradually increasing dosages.

Troleandomycin is primarily excreted by the liver and may accumulate in patients with impaired hepatic function. In addition, the use of troleandomycin has been associated with an allergic type of cholestatic hepatitis, particularly in patients receiving the drug for more than 2 weeks or given repeated courses. Therapy with troleandomycin should be administered cautiously in patients with liver and/or biliary disease. Liver function tests should be monitored during prolonged or repeated courses of therapy, and the drug discontinued if abnormalities develop.

Isoniazid commonly causes dose-related peripheral neuropathy, which results from the depletion of pyridoxine in the presence of the drug. The neuropathy is usually preceded by paraesthesia's of the feet and hands. Therapy with isoniazid should be administered cautiously in patients with pre-existing peripheral neuropathy or risk factors for developing the condition, such as malnutrition, diabetes and alcoholism. Careful monitoring is recommended on these patients. Pyridoxine (vitamin B6) at a dosage of 10 to 50 mg/day may prevent or attenuate isoniazid-related peripheral neuropathy and is recommended for these patients.

Isoniazid commonly causes dose-related peripheral neuropathy, which results from the depletion of pyridoxine in the presence of the drug. The neuropathy is usually preceded by paraesthesia's of the feet and hands. Therapy with isoniazid should be administered cautiously in patients with pre-existing peripheral neuropathy or risk factors for developing the condition, such as malnutrition, diabetes and alcoholism. Careful monitoring is recommended on these patients. Pyridoxine (vitamin B6) at a dosage of 10 to 50 mg/day may prevent or attenuate isoniazid-related peripheral neuropathy and is recommended for these patients.

Isoniazid is substantially removed by hemodialysis and should be administered after dialysis.

Caution and close monitoring is advised when using isoniazid in patients with HIV seropositive patients. Patients with pulmonary tuberculosis and HIV infection may have problems with malabsorption. Screening of antimycobacterial drug levels, especially in patients with advanced HIV disease, may be necessary to prevent the emergence of multi-drug resistant tuberculosis.

Isoniazid may cause cerebellar syndrome in patients with chronic kidney disease. Patients with end-stage renal disease have been reported to have an increased risk of developing tuberculosis. Careful monitoring is recommended if this drug is used in patients with severe renal dysfunction. Dosage adjustments in renal impairment are generally not necessary except in slow acetylators with a creatinine clearance below 10 mL/min. Approximately 50% of Blacks and Caucasians are slow acetylators, and most Eskimos and Asians are rapid acetylators.