Interactions and contraindications
Elvitegravir is metabolised via the liver enzyme CYP3A. Substances that induce this enzyme can reduce elvitegravir concentrations in the body, potentially triggering the development of resistant virus strains. Consequently, co-administration of strong CYP3A inducers is contraindicated; examples are rifampicin, the anticonvulsants carbamazepine, phenobarbital and phenytoin, as well as St Johns wort.Glucuronidation of elvitegravir is facilitated by the enzymes UGT1A1 and 3, resulting in increased blood plasma levels when taken together with strong UGT1A inhibitors such as ritonavir and other HIV protease inhibitors. (But ritonavir also increases elvitegravir levels by inhibiting CYP3A.) Furthermore, elvitegravir is a weak to medium inducer of CYP1A2, CYP2C19, CYP2C9, CYP3A, and a number of UGTs; the clinical relevance of these findings is however unclear. Pharmacology
Mechanism of action
Elvitegravir inhibits the enzyme integrase of HIV-1, and of HIV-2 to a lesser extent. The virus needs this enzyme to integrate its genetic code into the hosts DNA. Pharmacokinetics
The drug is taken by mouth. When taken together with ritonavir and a meal, it reaches highest blood plasma concentrations after four hours. Bioavailability is better with fatty meals. In the bloodstream, 98–99% of the substance are bound to plasma proteins. It is metabolized mainly by CYP3A oxidation, and secondly by UGT1A1 and 3 glucuronidation. Nearly 95% are excreted via the feces, and the rest via urine. Plasma half-life when combined with ritonavir is 8.7 to 13.7 hours. References
External links
"Elvitegravir". Drug Information Portal. U.S. National Library of Medicine.
Ventricular aneurysms are one of the many complications that may occur after a heart attack. The word aneurysm refers to a bulge or pocketing of the wall or lining of a vessel commonly occurring in the blood vessels at the base of the septum, or within the aorta. In the heart, they usually arise from a patch of weakened tissue in a ventricular wall, which swells into a bubble filled with blood. This, in turn, may block the passageways leading out of the heart, leading to severely constricted blood flow to the body. Ventricular aneurysms can be fatal. They are usually non-rupturing because they are lined by scar tissue. A left ventricular aneurysm can be associated with ST elevation. Signs and symptoms
Ventricular aneurysms usually grow at a very slow pace, but can still pose problems. Usually, this type of aneurysm grows in the left ventricle. This bubble has the potential to block blood flow to the rest of the body, and thus limit the patients stamina. In other cases, a similarly developed pseudoaneurysm ("false aneurysm") may burst, sometimes resulting in the death of the patient. Also, blood clots may form on the inside of ventricular aneurysms, and form embolisms. If such a clot escapes from the aneurysm, it will be moved in the circulation throughout the body. If it gets stuck inside a blood vessel, it may cause ischemia in a limb, a painful condition that can lead to reduced movement and tissue death in the limb.