Drug Interactions between budesonide and chloramphenicol

You should avoid the regular consumption of large amounts of grapefruits and grapefruit juice while taking budesonide. Grapefruit can raise the levels of budesonide in your body and lead to increased side effects. Do not increase or decrease the amount of grapefruit products in your diet without first talking to your doctor.

Chloramphenicol may cause bone marrow depression and other hematologic toxicities, which can be irreversible or reversible. The former type is independent of dose and results in aplastic anemia with a high rate of mortality, generally from hemorrhage or infection. It has been reported following both systemic and topical administration of chloramphenicol and has an estimated incidence of 1 in 25,000 to 1 in 40,000 courses of therapy. Bone marrow aplasia or hypoplasia may occur after a single dose but more often develops weeks or months after the drug has been discontinued. A reversible myelosuppression occurs much more frequently and is characterized by anemia, vacuolation of red blood cells, decreased reticulocyte count, leukopenia, thrombocytopenia, increased serum iron concentrations, and increased serum iron-binding capacity. It is dose-dependent, occurring regularly at chloramphenicol dosages exceeding 4 g/day (in adults) or at plasma drug concentrations >= 25 mcg/mL, and usually responds to withdrawal of the drug. Therapy with chloramphenicol should be administered cautiously, if at all, in patients with preexisting blood dyscrasias and/or bone marrow depression. Complete blood counts and differential reticulocyte counts should be performed in all patients prior to initiating therapy and approximately every 2 days during therapy. Marked depression of blood counts and/or development of other hematologic abnormalities may be indication for withdrawal of chloramphenicol therapy.

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.

Chloramphenicol is primarily inactivated by glucuronyl transferase in the liver and eliminated in the urine as both parent drug and metabolites. In adults with normal renal and hepatic function, only 5% to 15% of a dose of chloramphenicol is excreted unchanged by the kidney, but approximately 30% is excreted when chloramphenicol is administered intravenously as the sodium succinate ester. However, the fraction of drug excreted unchanged may be highly variable, especially in neonates and children. Therapy with chloramphenicol should be administered cautiously in patients with significantly impaired renal and/or hepatic function, since drug accumulation may occur in such patients. The dosage should be reduced based on the degree of impairment as well as plasma drug concentrations.

Chloramphenicol is primarily inactivated by glucuronyl transferase in the liver and eliminated in the urine as both parent drug and metabolites. In adults with normal renal and hepatic function, only 5% to 15% of a dose of chloramphenicol is excreted unchanged by the kidney, but approximately 30% is excreted when chloramphenicol is administered intravenously as the sodium succinate ester. However, the fraction of drug excreted unchanged may be highly variable, especially in neonates and children. Therapy with chloramphenicol should be administered cautiously in patients with significantly impaired renal and/or hepatic function, since drug accumulation may occur in such patients. The dosage should be reduced based on the degree of impairment as well as plasma drug concentrations.

Prolonged use of corticosteroids may cause posterior subcapsular cataracts and elevated intraocular pressure, the latter of which may lead to glaucoma and/or damage to the optic nerves. Therapy with corticosteroids should be administered cautiously nonetheless in patients with a history of cataracts, glaucoma, or increased intraocular pressure. Although adverse effects of corticosteroids may be minimized by local rather than systemic administration, the risks are not entirely abolished. Inhaled and nasally applied drug may be absorbed into the circulation, especially when large doses are used. It is important that the recommended dosages of the individual products not be exceeded and that the lowest effective dosage be used.

Prolonged use of corticosteroids may cause posterior subcapsular cataracts and elevated intraocular pressure, the latter of which may lead to glaucoma and/or damage to the optic nerves. Therapy with corticosteroids should be administered cautiously nonetheless in patients with a history of cataracts, glaucoma, or increased intraocular pressure. Although adverse effects of corticosteroids may be minimized by local rather than systemic administration, the risks are not entirely abolished. Inhaled and nasally applied drug may be absorbed into the circulation, especially when large doses are used. It is important that the recommended dosages of the individual products not be exceeded and that the lowest effective dosage be used.

The use of corticosteroids may rarely precipitate or aggravate conditions of hyperadrenocorticism. Although adverse effects of corticosteroids may be minimized by local rather than systemic administration, the risks are not entirely abolished. Inhaled and nasally applied drug may be absorbed into the circulation, especially when large doses are used. It is important that the recommended dosages of the individual products not be exceeded and that the lowest effective dosage be used. The development of symptoms such as menstrual irregularities, acneiform lesions, cataracts and cushingoid features during inhaled or nasal corticosteroid therapy may indicate excessive use.

The immunosuppressant and anti-inflammatory effects of corticosteroids, particularly in higher dosages, may decrease host resistance to infectious agents, decrease the ability to localize infections, and mask the symptoms of infection. Secondary infections may be more likely to develop. Therapy with corticosteroids should be administered cautiously in patients with an infection, particularly active or quiescent tuberculosis or in hepatitis B carriers. Monitor patients for any new or worsening infection and use with caution in these patients. A serious or even fatal course of chickenpox and measles can occur in susceptible patients. It is important that the recommended dosages of the individual products not be exceeded and that the lowest effective dosage be used.

Some inhaled corticosteroid formulations contain lactose and may cause adverse reactions including cough, wheezing and bronchospasm in patients with severe milk protein allergy or intolerance. Caution is advised.

Corticosteroids are predominantly cleared by hepatic metabolism and impairment of the liver function may lead to their accumulation. Patients with hepatic disease should be closely monitored.

Pharmacologic dosages of corticosteroids may increase the risk of corneal perforation in patients with ocular herpes simplex. Therapy with inhaled and nasal corticosteroids should be administered cautiously in such patients.

Prolonged use of inhaled corticosteroids may be associated with a reduction in bone density. This effect appears to be dose-related and has been reported primarily with high dosages (800 mcg/day or more of beclomethasone or equivalent for 1 year or greater). Reduced levels of total body calcium have also been demonstrated in patients receiving lower dosages. Long-term therapy with inhaled and nasal corticosteroids should be administered cautiously in patients with osteoporosis. It is important that the recommended dosages of the individual products not be exceeded and that the lowest effective dosage be used.

The immunosuppressant and anti-inflammatory effects of corticosteroids, particularly in higher dosages, may decrease host resistance to infectious agents, decrease the ability to localize infections, and mask the symptoms of infection. Secondary infections may be more likely to develop. Therapy with corticosteroids should be administered cautiously in patients with an infection, particularly active or quiescent tuberculosis or in hepatitis B carriers. Monitor patients for any new or worsening infection and use with caution in these patients. A serious or even fatal course of chickenpox and measles can occur in susceptible patients. It is important that the recommended dosages of the individual products not be exceeded and that the lowest effective dosage be used.