Drug Interactions between budesonide and indinavir

Large amounts of food decreases the levels of indinavir in your body. Indinavir should be taken on an empty stomach, at least 1 hour before or 2 hours after a meal. This will make it easier for your body to absorb the medication. Take indinavir with a full glass (8 ounces) of water or skim milk. You may also drink juice, coffee, or tea with this medication. Drink at least 6 glasses of water each day to prevent kidney stones while you are taking indinavir. If you prefer to take the medication with food, eat only a light meal, such as dry toast with jelly, or corn flakes with skim milk and sugar. Avoid eating a high-fat meal.

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.

Crystalluria and nephrolithiasis may occur during treatment with indinavir. The cumulative frequency of nephrolithiasis is substantially higher in pediatric patients (29%) than in adult patients (12.4%; range 4.7% to 34.4% across individual trials) and increases with duration of exposure to indinavir; however, the risk over time remains relatively constant. The incidence is also higher when indinavir is used in combination with ritonavir than when used alone at 800 mg three times a day. In some cases, nephrolithiasis/urolithiasis has been associated with renal insufficiency or acute renal failure and pyelonephritis with or without bacteremia. Therapy with indinavir should be administered cautiously in patients with a current or past history of nephrolithiasis. It is crucial that patients receive adequate hydration. Generally, at least 1.5 L (approximately 48 oz) of fluid per day is recommended for adults during indinavir therapy. Those who are dehydrated may be at increased risk and should be encouraged to consume additional amounts of liquid or given intravenous fluid if necessary. All patients receiving indinavir should be instructed to seek medical attention if they experience potential signs and symptoms of nephrolithiasis/urolithiasis such as flank pain, hematuria, dysuria, anuria, and urinary urgency. A brief interruption (e.g., 1 to 3 days) or discontinuation of therapy may be required.

Crystalluria and nephrolithiasis may occur during treatment with indinavir. The cumulative frequency of nephrolithiasis is substantially higher in pediatric patients (29%) than in adult patients (12.4%; range 4.7% to 34.4% across individual trials) and increases with duration of exposure to indinavir; however, the risk over time remains relatively constant. The incidence is also higher when indinavir is used in combination with ritonavir than when used alone at 800 mg three times a day. In some cases, nephrolithiasis/urolithiasis has been associated with renal insufficiency or acute renal failure and pyelonephritis with or without bacteremia. Therapy with indinavir should be administered cautiously in patients with a current or past history of nephrolithiasis. It is crucial that patients receive adequate hydration. Generally, at least 1.5 L (approximately 48 oz) of fluid per day is recommended for adults during indinavir therapy. Those who are dehydrated may be at increased risk and should be encouraged to consume additional amounts of liquid or given intravenous fluid if necessary. All patients receiving indinavir should be instructed to seek medical attention if they experience potential signs and symptoms of nephrolithiasis/urolithiasis such as flank pain, hematuria, dysuria, anuria, and urinary urgency. A brief interruption (e.g., 1 to 3 days) or discontinuation of therapy may be required.

Crystalluria and nephrolithiasis may occur during treatment with indinavir. The cumulative frequency of nephrolithiasis is substantially higher in pediatric patients (29%) than in adult patients (12.4%; range 4.7% to 34.4% across individual trials) and increases with duration of exposure to indinavir; however, the risk over time remains relatively constant. The incidence is also higher when indinavir is used in combination with ritonavir than when used alone at 800 mg three times a day. In some cases, nephrolithiasis/urolithiasis has been associated with renal insufficiency or acute renal failure and pyelonephritis with or without bacteremia. Therapy with indinavir should be administered cautiously in patients with a current or past history of nephrolithiasis. It is crucial that patients receive adequate hydration. Generally, at least 1.5 L (approximately 48 oz) of fluid per day is recommended for adults during indinavir therapy. Those who are dehydrated may be at increased risk and should be encouraged to consume additional amounts of liquid or given intravenous fluid if necessary. All patients receiving indinavir should be instructed to seek medical attention if they experience potential signs and symptoms of nephrolithiasis/urolithiasis such as flank pain, hematuria, dysuria, anuria, and urinary urgency. A brief interruption (e.g., 1 to 3 days) or discontinuation of therapy may be required.

New onset diabetes mellitus, exacerbation of preexisting diabetes mellitus, hyperglycemia, and some cases of diabetic ketoacidosis have been reported during postmarketing surveillance in HIV-infected patients treated with protease inhibitors. Some patients required either initiation or dosage adjustments of insulin or oral hypoglycemic agents for treatment of these events. In some cases, hyperglycemia persisted despite discontinuation of protease inhibitor therapy. A causal relationship has not been established between protease inhibitor therapy and these events. Monitoring patients for hyperglycemia, new onset diabetes mellitus, or exacerbation of diabetes mellitus should be considered during protease inhibitor therapy.

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.

New onset diabetes mellitus, exacerbation of preexisting diabetes mellitus, hyperglycemia, and some cases of diabetic ketoacidosis have been reported during postmarketing surveillance in HIV-infected patients treated with protease inhibitors. Some patients required either initiation or dosage adjustments of insulin or oral hypoglycemic agents for treatment of these events. In some cases, hyperglycemia persisted despite discontinuation of protease inhibitor therapy. A causal relationship has not been established between protease inhibitor therapy and these events. Monitoring patients for hyperglycemia, new onset diabetes mellitus, or exacerbation of diabetes mellitus should be considered during protease inhibitor therapy.

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.

Indinavir is primarily metabolized by the liver. Patients with liver disease may be at greater risk for adverse effects from indinavir due to decreased drug clearance. Therapy with indinavir should be administered cautiously in patients with liver disease. A dosage reduction to 600 mg three times a day is recommended for patients with mild to moderate hepatic insufficiency due to cirrhosis.

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.