Drug Interactions between atorvastatin and Rocephin

Grapefruit juice can increase the blood levels of atorvastatin. This can increase the risk of side effects such as liver damage and a rare but serious condition called rhabdomyolysis that involves the breakdown of skeletal muscle tissue. In some cases, rhabdomyolysis can cause kidney damage and even death. You should limit your consumption of grapefruit juice to no more than 1 quart per day during treatment with atorvastatin. Let your doctor know immediately if you have unexplained muscle pain, tenderness, or weakness during treatment, especially if these symptoms are accompanied by fever or dark colored urine. You should also seek immediate medical attention if you develop 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, as these may be signs and symptoms of liver damage. 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 most HMG-CoA reductase inhibitors is contraindicated in patients with active liver disease, decompensated cirrhosis, or unexplained persistent elevations of serum transaminases. HMG-CoA reductase inhibitors are extensively metabolized by the liver. Decreased drug metabolism may lead to accumulation and increased risk of toxicity, including biochemical abnormalities of liver function and, rarely, jaundice, hepatitis, cirrhosis, fatty change in the liver, and fulminant hepatic necrosis. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with a history of liver disease and/or heavy alcohol use. A lower initial dosage may be appropriate, and clinical monitoring of liver transaminase levels according to the individual manufacturer product information is recommended. Patients who develop elevated ALT or AST levels during therapy should be monitored until abnormalities resolve. If an increase above 3 times the upper limit of normal persists, consideration should be given to a reduction in dosage or withdrawal of 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.

Hyperbilirubinemic neonates, especially premature, should not be treated with ceftriaxone for injection. Studies have shown that ceftriaxone can displace bilirubin from its binding to serum albumin, leading to possible risk of bilirubin encephalopathy in these patients.

The use of most HMG-CoA reductase inhibitors is contraindicated in patients with active liver disease, decompensated cirrhosis, or unexplained persistent elevations of serum transaminases. HMG-CoA reductase inhibitors are extensively metabolized by the liver. Decreased drug metabolism may lead to accumulation and increased risk of toxicity, including biochemical abnormalities of liver function and, rarely, jaundice, hepatitis, cirrhosis, fatty change in the liver, and fulminant hepatic necrosis. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with a history of liver disease and/or heavy alcohol use. A lower initial dosage may be appropriate, and clinical monitoring of liver transaminase levels according to the individual manufacturer product information is recommended. Patients who develop elevated ALT or AST levels during therapy should be monitored until abnormalities resolve. If an increase above 3 times the upper limit of normal persists, consideration should be given to a reduction in dosage or withdrawal of therapy.

Ceftriaxone can precipitate in the gallbladder. Sonographic abnormalities and symptoms of gallbladder disease have been reported. Therapy with ceftriaxone should be administered cautiously in patients with preexisting disease of the gallbladder, biliary tract, or liver. Serial abdominal ultrasonography may be appropriate during therapy. The drug should be discontinued in patients who develop signs and symptoms suggestive of gallbladder disease while being treated with ceftriaxone.

Ceftriaxone is eliminated by both renal and hepatobiliary excretion. At usual dosages (i.e. 1 to 2 g/day), adjustments are generally not necessary in either renal or hepatobiliary impairment. However, serum drug concentrations should be monitored periodically, and the dosage decreased accordingly if drug accumulation occurs. In patients with both hepatic and severe renal impairment, ceftriaxone dosage should not exceed 2 grams per day without close monitoring of serum concentrations.

Cases of pancreatitis, possibly secondary to biliary obstruction, have been reported rarely in patients treated with ceftriaxone. Most patients presented with risk factors for biliary stasis and biliary sludge (preceding major therapy, severe illness, total parenteral nutrition). A cofactor role of ceftriaxone-related biliary precipitation cannot be ruled out.

Cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) have been observed in patients receiving statins. The reports are usually not serious, and reversible upon statin discontinuation. Caution is recommended when using these agents in patients with cognitive impairment.

Increases in hemoglobin A1c and fasting serum glucose levels have been reported with the use of certain HMG-CoA reductase inhibitors. Caution should be exercised when using these agents in diabetic patients and close monitoring is recommended.

Ceftriaxone can precipitate in the gallbladder. Sonographic abnormalities and symptoms of gallbladder disease have been reported. Therapy with ceftriaxone should be administered cautiously in patients with preexisting disease of the gallbladder, biliary tract, or liver. Serial abdominal ultrasonography may be appropriate during therapy. The drug should be discontinued in patients who develop signs and symptoms suggestive of gallbladder disease while being treated with ceftriaxone.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

Ceftriaxone is eliminated by both renal and hepatobiliary excretion. At usual dosages (i.e. 1 to 2 g/day), adjustments are generally not necessary in either renal or hepatobiliary impairment. However, serum drug concentrations should be monitored periodically, and the dosage decreased accordingly if drug accumulation occurs. In patients with both hepatic and severe renal impairment, ceftriaxone dosage should not exceed 2 grams per day without close monitoring of serum concentrations.

Alterations in prothrombin times have rarely occurred in patients treated with ceftriaxone. Patients with impaired vitamin K synthesis or low vitamin K stores, such a patients with chronic hepatic disease and malnutrition, require monitoring of prothrombin time during treatment. Vitamin K administration (10 mg per week) might be needed if prothrombin time is prolonged before or during therapy.

Cases of hepatitis have been reported with the use of certain cephalosporins. Transient rise in AST, ALT, and alkaline phosphatase levels have also been observed. Caution and monitoring are recommended when these agents are prescribed to patients with hepatic disorders.

Ceftriaxone can precipitate in the gallbladder. Sonographic abnormalities and symptoms of gallbladder disease have been reported. Therapy with ceftriaxone should be administered cautiously in patients with preexisting disease of the gallbladder, biliary tract, or liver. Serial abdominal ultrasonography may be appropriate during therapy. The drug should be discontinued in patients who develop signs and symptoms suggestive of gallbladder disease while being treated with ceftriaxone.

Alterations in prothrombin times have rarely occurred in patients treated with ceftriaxone. Patients with impaired vitamin K synthesis or low vitamin K stores, such a patients with chronic hepatic disease and malnutrition, require monitoring of prothrombin time during treatment. Vitamin K administration (10 mg per week) might be needed if prothrombin time is prolonged before or during therapy.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

Ceftriaxone is eliminated by both renal and hepatobiliary excretion. At usual dosages (i.e. 1 to 2 g/day), adjustments are generally not necessary in either renal or hepatobiliary impairment. However, serum drug concentrations should be monitored periodically, and the dosage decreased accordingly if drug accumulation occurs. In patients with both hepatic and severe renal impairment, ceftriaxone dosage should not exceed 2 grams per day without close monitoring of serum concentrations.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

Some HMG-CoA reductase inhibitors (e.g., fluvastatin) have not been studied in patients with severe renal dysfunction or end-stage renal disease. Some others (e.g., pitavastatin, simvastatin) require a dose reduction when used in this group of patients. Caution and close monitoring are advised when using these drugs in patients with renal dysfunction.

Cephalosporins have been implicated in triggering seizures. Nonconvulsive status epilepticus, encephalopathy, coma, asterixis, neuromuscular excitability, and myoclonia have been reported with cephalosporins, particularly in patients with a history of epilepsy and/or when recommended dosages of cephalosporins were exceeded due to renal dysfunction. Dosage should be adjusted based on the degree of renal function. Anticonvulsant therapy should be continued in patients with known seizure disorders. If CNS adverse reactions including seizures occur, patients should undergo a neurological evaluation to determine whether treatment should be discontinued.

Alterations in prothrombin times have rarely occurred in patients treated with ceftriaxone. Patients with impaired vitamin K synthesis or low vitamin K stores, such a patients with chronic hepatic disease and malnutrition, require monitoring of prothrombin time during treatment. Vitamin K administration (10 mg per week) might be needed if prothrombin time is prolonged before or during therapy.