Drug Interactions between lonapegsomatropin and ombitasvir / paritaprevir / ritonavir

Ritonavir should be taken with food to lessen gastrointestinal side effects. It is important that you take this medication exactly as prescribed by your doctor. Do not change your treatment or stop treatment without first talking to your doctor.

Food significantly increases the absorption of paritaprevir. You should take each dose of paritaprevir with a meal. Taking it on an empty stomach may lead to inadequate blood levels and reduced effectiveness of the medication.

Treatment with somatropin and somatrogon is contraindicated in patients with acute critical illness due to any complications following open heart surgery, abdominal surgery, multiple trauma, or acute respiratory failure. Patients with these conditions have an increased risk of mortality.

Somatropin and somatrogon are contraindicated in the presence of any active malignancy. Any preexistent malignancy should be inactive and its treatment should be completed prior to somatropin therapy. This includes the presence of any intracranial tumor. Somatropin and somatrogon should be discontinued if there is any evidence of recurrence.

Somatropin and somatrogon are contraindicated in the presence of any active malignancy. Any preexistent malignancy should be inactive and its treatment should be completed prior to somatropin therapy. This includes the presence of any intracranial tumor. Somatropin and somatrogon should be discontinued if there is any evidence of recurrence.

Somatropin and somatrogon are contraindicated in the presence of any active malignancy. Any preexistent malignancy should be inactive and its treatment should be completed prior to somatropin therapy. This includes the presence of any intracranial tumor. Somatropin and somatrogon should be discontinued if there is any evidence of recurrence.

HBV reactivation has been reported during or after completion of HCV direct-acting antiviral therapy in HCV/HBV-coinfected patients who were not receiving HBV antiviral therapy; some cases resulted in fulminant hepatitis, hepatic failure, and death. Cases have been reported in hepatitis B surface antigen (HBsAg)-positive patients and patients with serologic evidence of resolved HBV infection (i.e., HBsAg negative and hepatitis B core antibody [anti-HBc] positive). HBV reactivation has also been reported in patients using certain immunosuppressant or chemotherapeutic agents; risk of HBV reactivation associated with HCV direct-acting antiviral therapy may be increased in these patients. All patients should be tested for evidence of current or prior HBV infection by measuring HBsAg and anti-HBc before starting HCV direct-acting antiviral therapy. Patients with serologic evidence of current or prior HBV infection should be monitored for clinical and laboratory signs of hepatitis flare or HBV reactivation during HCV therapy and posttherapy follow-up; appropriate patient management for HBV infection should be started as clinically indicated.

HBV reactivation has been reported during or after completion of HCV direct-acting antiviral therapy in HCV/HBV-coinfected patients who were not receiving HBV antiviral therapy; some cases resulted in fulminant hepatitis, hepatic failure, and death. Cases have been reported in hepatitis B surface antigen (HBsAg)-positive patients and patients with serologic evidence of resolved HBV infection (i.e., HBsAg negative and hepatitis B core antibody [anti-HBc] positive). HBV reactivation has also been reported in patients using certain immunosuppressant or chemotherapeutic agents; risk of HBV reactivation associated with HCV direct-acting antiviral therapy may be increased in these patients. All patients should be tested for evidence of current or prior HBV infection by measuring HBsAg and anti-HBc before starting HCV direct-acting antiviral therapy. Patients with serologic evidence of current or prior HBV infection should be monitored for clinical and laboratory signs of hepatitis flare or HBV reactivation during HCV therapy and posttherapy follow-up; appropriate patient management for HBV infection should be started as clinically indicated.

The use of drugs containing paritaprevir in combination with ombitasvir and ritonavir is contraindicated in patients with moderate to severe hepatic impairment (Child-Pugh B and C). No dosage adjustment is required in patients with mild hepatic impairment (Child-Pugh A).

Somatropin and somatrogon are contraindicated in the presence of any active malignancy. Any preexistent malignancy should be inactive and its treatment should be completed prior to somatropin therapy. This includes the presence of any intracranial tumor. Somatropin and somatrogon should be discontinued if there is any evidence of recurrence.

Somatropin and somatrogon is contraindicated in patients with Prader-Willi Syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment. There have been reports of sudden death when somatropin was used in such patients.

Somatropin and somatrogon are contraindicated in the presence of any active malignancy. Any preexistent malignancy should be inactive and its treatment should be completed prior to somatropin therapy. This includes the presence of any intracranial tumor. Somatropin and somatrogon should be discontinued if there is any evidence of recurrence.

Treatment with somatropin and somatrogon is contraindicated in patients with acute critical illness due to any complications following open heart surgery, abdominal surgery, multiple trauma, or acute respiratory failure. Patients with these conditions have an increased risk of mortality.

Somatropin and somatrogon is contraindicated in patients with Prader-Willi Syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment. There have been reports of sudden death when somatropin was used in such patients.

Treatment with somatropin and somatrogon is contraindicated in patients with acute critical illness due to any complications following open heart surgery, abdominal surgery, multiple trauma, or acute respiratory failure. Patients with these conditions have an increased risk of mortality.

Somatropin and somatrogon are contraindicated in the presence of any active malignancy. Any preexistent malignancy should be inactive and its treatment should be completed prior to somatropin therapy. This includes the presence of any intracranial tumor. Somatropin and somatrogon should be discontinued if there is any evidence of recurrence.

Somatropin and somatrogon is contraindicated in patients with Prader-Willi Syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment. There have been reports of sudden death when somatropin was used in such patients.

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.

Patients with or at risk for pituitary hormone deficiency(s) may experience reduced serum cortisol and/or unmasking of central (secondary) hypoadrenalism. Glucocorticoid replacement may require increased maintenance or stress doses. Monitor for reduced serum cortisol and/or the need for glucocorticoid dose increases.

There have been reports of increased bleeding, including spontaneous skin hematomas and hemarthrosis, in patients with hemophilia type A and B treated with protease inhibitors; however, a causal relationship has not been established. In some patients, additional factor VIII was given. In more than half of the reported cases, protease inhibitor therapy was continued or reintroduced. Patients with hemophilia or other coagulation defects should be monitored closely for bleeding during protease inhibitor therapy.

The use of growth hormone has been associated with resistance to insulin. Patients with diabetes mellitus or impaired glucose tolerance should be observed closely during therapy. The dose of antihyperglycemic drugs (insulin or oral/injectable agents) may require adjustment.

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.

Ritonavir may prolong the PR interval in some patients. Postmarketing cases of second or third degree atrioventricular block have been reported. Ritonavir should be administered with caution in patients with underlying structural heart disease, preexisting conduction abnormalities, ischemic heart disease, and cardiomyopathies as these patients might be at increased risk for developing cardiac conduction abnormalities.

Treatment with ritonavir alone or in combination with other protease inhibitors (e.g., lopinavir, saquinavir, tipranavir, fosamprenavir) has resulted in substantial increases in the concentration of total cholesterol and triglycerides. These effects have also been reported with other protease inhibitors but may be the most dramatic with ritonavir. The clinical significance of these elevations is unclear. Marked elevation in triglyceride levels is a risk factor for development of pancreatitis. Triglyceride and cholesterol testing is recommended before starting ritonavir (with or without other protease inhibitors) and periodically during therapy. Lipid disorders should be managed as clinically appropriate.

The use of growth hormone has been associated with the development of hypothyroidism. Patients should be monitored baseline and periodically for adequate thyroid function. Inadequate treatment of hypothyroidism may inhibit the optimal response to growth hormone.

Hepatotoxicity (including jaundice, clinical hepatitis, and hepatic transaminase elevations exceeding 5 times the upper limit of normal) has been reported in patients receiving ritonavir alone or in combination with other antiretroviral drugs. Ritonavir should be administered with caution in patients with preexisting liver diseases, liver enzyme abnormalities, or hepatitis; increased monitoring of AST/ALT should be considered in these patients, especially during the first 3 months of ritonavir therapy. Ritonavir is not recommended for use in patients with severe liver dysfunction.