Atazanavir

  

This newsletter has been edited by:
Mrs. Colleen Whitelaw
Dr. Leon Regensberg

Contributors:
Prof. Gary Maartens
Prof. Mark Cotton
Dr. Graeme Meintjes
Dr. Steve Andrews


Please contact the AfA clinical staff on 0800 22 77 00 to make changes to your patient�s authorized medicines.

Please include current contact information for patients on the AfA application form. This is essential in order to allow us to make contact with patients, particularly those requiring post-exposure or mother to child transmission prophylaxis.

It would also be appreciated if we could be provided with information about any patient deaths that may occur. This information is important for monitoring the outcomes of the programme.

Please remember to include the correct ICD10 codes on your claims to avoid delays in payment.

 


Atazanavir (Reyataz�) is a protease inhibitor (PI) that has recently been registered in South Africa. It has several advantages over currently available PIs, but also has a few disadvantages. Resistance is discussed in the next article.
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Resistance mutations and atazanavir

  
 
Among treatment-naive patients failing atazanavir-containing regimens, a proportion (29% in one study) will select for its signature mutation the I50L. This mutation alone causes an 8-fold reduction in susceptibility to atazanavir resulting in high level resistance to the drug. However, unlike most other protease inhibitor (PI) mutations, rather than causing PI cross resistance this mutation increases susceptibility to other PIs.
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Early antiretroviral therapy (ART) in infants  
 
Until recently, there have been no definitive guidelines on when to initiate ART in infants. Even in the USA, where most favour early initiation of treatment, there is some ambivalence. Symptomatic infants below 12 months of age with any immune suppression (CD4 percentage <25% or CD4 count < 1500 X106/L) and any level of plasma HIV RNA are offered therapy.
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Hepatotoxicity when using adjusted dose Kaletra� with rifampicin

  
 
Rifampicin induces the metabolism of protease inhibitors (PIs), resulting in dramatic reductions in the concentrations of all PIs except full dose ritonavir (which is poorly tolerated). The induction by rifampicin can be overcome by either doubling the dose of Kaletra� or adding additional ritonavir to give an equal ratio of lopinavir: ritonavir (in Kaletra� lopinavir: ritonavir is 4:1, so in adults add 300 mg ritonavir 12 hourly to Kaletra� so that patient will get 400 mg lopinavir and 400 mg ritonavir 12 hourly).
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Clinical, virological and immunological responses to HAART

  
 
With the first-line antiretroviral regimen most patients will demonstrate clinical, immunological and virological improvement to therapy. Response to second line therapy and beyond is dependant on the duration of antiretroviral failure, accumulation of resistance mutations, availability of clean drug(s) and complexity of future regimens. In all situations high levels of adherence are associated with the best responses.
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NNRTI vs boosted PI regimens

  
 
The respective efficacies of non-nucleoside reverse transcriptase inhibitor (NNRTI) vs boosted protease inhibitor (PI) regimens have been extensively studied in the past five years.
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