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Atripla (Tenofovir)

Atripla DF was approved in 2001 as an antiretroviral drug (ARV) for people with HIV infection. In US treatment guidelines, Atripla is listed as a preferred drug for people just starting ART. Atripla nephrotoxicity is characterized by proximal tubular cell dysfunction that may be associated with acute kidney injury or chronic kidney disease. Withdrawal of the drug leads to improvement of analytical parameters that may be partial. Understanding the risk factors for nephrotoxicity and regular monitoring of proximal tubular dysfunction and serum creatinine in high-risk patients is required to minimize nephrotoxicity.

Other names for this medication:
Tenofovir, Atripla, Tenvir, Trioday, Truvada, Viraday, Viread,

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Atripla is used in combination with other medicines for the treatment of the infection caused by the human immunodeficiency virus (HIV). HIV is the virus that causes acquired immunodeficiency syndrome (AIDS).

Atripla will not cure or prevent HIV infection or AIDS. It helps keep HIV from reproducing and appears to slow down the destruction of the immune system. This may help delay problems that are usually related to AIDS or HIV disease from occurring. Atripla will not keep you from spreading HIV to other people. People who receive this medicine may continue to have some of the problems usually related to AIDS or HIV disease.

Atripla is also used to treat chronic (long-term) hepatitis B virus (HBV) infection.

This medicine is available only with your doctor's prescription.

This product is available in the following dosage forms:

  • Tablet
  • Powder

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Health promotion data for state health departments: telephone versus in-person survey estimates of smoking and alcohol use. Dental trauma occur in childhood and adolescence with consequences in time and costs for both patient and family. Effects of glucose concentration on respiration and glycolysis of ascites tumor cells.

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Intravaginal application to hypoestrogenic women gave similar results, but of much lower magnitude (highest value, 20 times baseline). Interaction of acetylcholine esterase with fluorescent analogs of acetylcholine. Cognitive phenotyping of amyloid precursor protein transgenic J20 mice. The stiffening of titin partly compensates for the muscle weakness in these patients by augmenting submaximal active tension generation.

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