Ezetimibe/atorvastatin (trade names Liptruzet, Atozet) is a cholesterol lowering combination drug. In the United States, it was approved in May 2013, by the Food and Drug Administration for the treatment of elevated low-density lipoprotein (LDL) in patients with primary or mixed hyperlipidemia as adjunctive therapy to diet. It has also been approved to reduce elevated total cholesterol and elevated LDL in patients diagnosed with homozygous familial hypercholesterolemia as an adjunctive treatment to other hyperlipidemia treatments.Some cardiologists opposed the approval, because the combination reduced LDL cholesterol in a clinical trial, but it did not reduce heart disease. A clinical trial studying the endpoints of heart attacks, strokes and heart-related deaths is scheduled to conclude in 2014.Liptruzet was withdrawn from sale by its manufacturer in June 2015, but not for reasons of safety or effectiveness. Mechanism of action
This combination drug works to reduce cholesterol levels through two different pathways. The ezetimibe component of the medication works by inhibiting cholesterol absorption from food while the atorvastatin component inhibits intrinsic cholesterol production in the liver. Safety
The drug is not safe to use in patients with active liver disease or unexplained persistent elevations in hepatic transaminase. Women that are pregnant or may become pregnant should not use the drug. It is a teratogenic agent that may disrupt the growth and development of a fetus. Immediate discontinuation is recommended in patients that become pregnant while taking this drug. Adverse effects
Commonly reported adverse effects include:
Musculoskeletal pain
Elevated liver enzymes (AST and ALT)
Gastrointestinal problems such as abdominal pain and nausea

See also
Ezetimibe
Ezetimibe/simvastatin


== References ==
Mutations that inactivate the nonessential glycerophosphate transporter render bacteria resistant to fosfomycin.Prescribing fosfomycin together with at least another active drug reduces the risk of developing bacterial resistance. Fosfomycin acts synergistically with many other antibiotics, including aminoglycosides, carbapenems, cephalosporins, daptomycin and oritavancin. Enzymes conferring resistance to fosfomycin have also been identified and are encoded both chromosomally and on plasmids.Three related fosfomycin resistance enzymes (named FosA, FosB, and FosX) are members of the glyoxalase superfamily. These enzymes function by nucleophilic attack on carbon 1 of fosfomycin, which opens the epoxide ring and renders the drug ineffective. The enzymes differ by the identity of the nucleophile used in the reaction: glutathione for FosA, bacillithiol for FosB, and water for FosX.In general, FosA and FosX enzymes are produced by Gram-negative bacteria, whereas FosB is produced by Gram-positive bacteria.FosC uses ATP and adds a phosphate group to fosfomycin, thus altering its properties and making the drug ineffective. Side effects
The drug is well tolerated and has a low incidence of harmful side effects. Mechanism of action
Despite its name (ending in -omycin) Fosfomycin is not a macrolide, but a member of a novel class of phosphonic antibiotics. Fosfomycin is bactericidal and inhibits bacterial cell wall biogenesis by inactivating the enzyme UDP-N-acetylglucosamine-3-enolpyruvyltransferase, also known as MurA. This enzyme catalyzes the committed step in peptidoglycan biosynthesis, namely the ligation of phosphoenolpyruvate (PEP) to the 3-hydroxyl group of UDP-N-acetylglucosamine. This pyruvate moiety provides the linker that bridges the glycan and peptide portion of peptidoglycan.