BHIVA audits adherence to UK treatment guidelines

This article is more than 22 years old.

UK treatment guidelines are being broadly followed, according to an audit of UK treatment centres carried out by the British HIV Association and presented at the group's annual conference on April 20.

The audit shows broad application of the BHIVA guidelines among UK treatment centres, said Dr Margaret Johnson, but highlighted problems with access to viral load testing able to quantify all HIV sub-types accurately. Late diagnosis also continues to present a problem in terms of ensuring that treatment can begin before CD4 cell counts fall below the 200 cells/mm3 level at which the risk of opportunistic infections grows.

146 centres submitted patient data to the audit, and a further two were able to answer questions about the availability of drugs and diagnostic tests. Approximately half of respondents to the audit were centres looking after less than 100 patients.

Glossary

nucleoside

A precursor to a building block of DNA or RNA. Nucleosides must be chemically changed into nucleotides before they can be used to make DNA or RNA. 

resistance testing

Laboratory testing to determine if an individual’s HIV strain is resistant to anti-HIV drugs. 

boosting agent

Booster drugs are used to ‘boost’ the effects of protease inhibitors and some other antiretrovirals. Adding a small dose of a booster drug to an antiretroviral makes the liver break down the primary drug more slowly, which means that it stays in the body for longer times or at higher levels. Without the boosting agent, the prescribed dose of the primary drug would be ineffective.

reverse transcriptase

A retroviral enzyme which converts genetic material from RNA into DNA, an essential step in the lifecycle of HIV. Several classes of anti-HIV drugs interfere with this stage of HIV’s life cycle: nucleoside reverse transcriptase inhibitors and nucleotide reverse transcriptase inhibitors (NRTIs) and non-nucleoside reverse transcriptase inhibitors (NNRTIs). 

protease inhibitor (PI)

Family of antiretrovirals which target the protease enzyme. Includes amprenavir, indinavir, lopinavir, ritonavir, saquinavir, nelfinavir, and atazanavir.

Six per cent of centres were either unaware of, or had not read, the 2000 British HIV Association treatment guidelines at the time the audit took place (autumn 2001). 74% said that the guidelines had influenced care at their centre (suggesting that many centres were already applying the approaches set out in the guidelines before the 2000 guidelines were published).

Access problems

Although guidelines on treatment were being applied with a high degree of consistency, some problems with access to diagnostic tests were apparent:

  • 82.3% of centres had access to resistance testing and were able to use it when clinically desirable, while 9.5% did use resistance testing, but not as often as they wished.
  • 8.4% of centres still did not have access to ultrasensitive resistance testing.
  • 15% of centres did not have access to viral load testing that was able to quantify all sub-types effectively.
  • The only problems regarding drug access were reported in relation to Kaletra and boosted protease inhibitors, where two centres had experienced problems in gaining approval to prescribe these drugs, while three centres reported problems with approval for Trizivir on the grounds of price.

Individual patient data

Data from 2044 patients were submitted (centres were asked to provide data on 50 consecutive patients seen during the audit period).

The sample broadly reflected data on patients receiving care previously gathered by the Communicable Disease Surveillance Centre (the SOPHID project), although patients exposed through sex between men and women were somewhat over-represented (43.8% vs 32.4% in SOPHID).

Four per cent of patients had CD4 cell counts below 50 and 18% had CD4 counts between 50 and 200 cells/mm3, with a further 27% between 201 and 350. Just under 75% of patients audited were receiving antiretroviral therapy, 72.4% receiving three or more drugs and 1.8% receiving two drugs.

The majority of individuals receiving treatment (55%) were receiving two nucleoside analogues and a non-nucleoside reverse transcriptase inhibitor (NNRTI), while 25% were receiving two nucleoside analogues and a protease inhibitor (or boosted PI). Eight per cent were receiving triple NRTI therapy and 12% were receiving a regimen of three drug classes, dual therapy or a hydroxyurea-containing regimen.

Amongst patients receiving three or more drugs, 59% had viral load below 50 copies/ml and a further 18% had viral load below 500 copies/ml, with 10% between 500 and 10,000 copies/ml. Ten per cent could be described as having serious virological rebound, with viral load above 10,000 copies/ml. Just over 80% of those who started treatment during 2000 had viral load below 500 copies/ml by the time of the audit, and over 80% of those who started treatment between 1996 and 1999 also had viral load below 500 copies/ml. Even in patients who started treatment before 1996, approximately two-thirds had viral load below 500 copies, suggesting that in nucleoside analogue-experienced patients HAART has proved more successful than expected.

In patients starting treatment in 2000, more than half had CD4 cell counts below 200 when they started HAART, and by 2001 the proportion had grown to just under 60%. The tendency to start treatment late appeared to be driven substantially by late diagnosis of HIV infection. When patients were stratified according to CD4 count at diagnosis of HIV, it was apparent that few patients diagnosed with CD4 counts above 200 were waiting until their CD4 cell counts fell below 200 to start treatment (9% waited until this point). 272 of 330 patients who started treatment with CD4 counts below 200 were undiagnosed until their CD4 cell counts fell below this level.