AIDS TREATMENT UPDATE, August 1995
Edward King

The protease inhibitor AG1343 has significant anti-HIV effects, according to the preliminary results of a trial at London's Kobler Centre.

The trial recruited HIV-positive men with CD4 counts above 200 who had never taken anti-HIV drugs before. Full results were reported for ten participants who received AG1343 at a dose of 300 mg three times daily for 4 weeks. Levels of HIV in their blood decreased by a maximum average of 80% and their CD4 count increased by a maximum average of 200.

A further ten people received a higher dose - 600 mg twice daily. They experienced maximum average decreases in viral load of 91%, and maximum CD4 increases averaging 138.

These figures were calculated by taking the peak measurement for each person i.e. the highest CD4 count they reached, or the lowest viral load, then averaging them out across all of the participants receiving that dose. In fact, there were wide variations, with some people having very small responses to treatment while others had much larger responses.

There was also no clear link between changes in viral load and changes in CD4 count. Some participants had minimal changes in viral load but substantial CD4 increases, while others who had large decreases in viral load had only small rises in their CD4 counts.

The only reported side-effects were fatigue, nausea, headache and poor concentration in some participants. Diarrhoea was also a problem, although this seems to have been caused by the capsules in which the drug was enclosed, and not by the drug itself.

A new trial has recently begun in the USA, using higher doses of AG1343 in a new tablet formulation.

* Septrin changes

The Department of Health has announced changes to the list of infections for which the antibiotic Septrin is recommended. However, the drug remains the best option for treating or preventing PCP.

Septrin is the tradename for the drug co-trimoxazole, made by Glaxo-Wellcome. Until now it has been a licensed treatment for a range of infections, including urinary tract infections and bronchitis. However, following a review by the Medicines Control Agency, Glaxo-Wellcome has agreed to limit the list of infections for which it is recommended.

Septrin is actually two drugs, not one; each tablet contains a mixture of the antibiotics trimethoprim and sulphamethoxazole. For many infections trimethoprim on its own is just as effective as the Septrin combination. Prescribing advice such as that in the British National Formulary has advised doctors to use trimethoprim instead of Septrin for these infections for some time.

However, Septrin remains a recommended drug for treating or preventing PCP because animal tests show that trimethoprim alone is not effective against the PCP organisms. Studies have shown that for people who can tolerate it, Septrin offers better protection against PCP than any other drug, and also prevents toxoplasmosis.

* Diagnosis & survival

An article in the British Medical Journal has suggested that early knowledge of one's HIV status may delay the onset of AIDS but does not result in better survival after the diagnosis of AIDS.

Doctors at St Mary's Hospital in London compared two groups of people - those who had a positive HIV test before they developed AIDS (Group A), and those who only found out that they were HIV-positive when they developed their first AIDS-defining illness (Group B). 49% of people in Group A started taking AZT and 62% started taking PCP prophylaxis before they developed AIDS. In Group B no-one used either AZT or prophylaxis.

People in Group A had lower CD4 counts at the time they developed AIDS than those in Group B, and were more likely to develop the AIDS illnesses associated with more severe immune damage. This implies that in Group A, treatment helped to delay the onset of AIDS, preventing milder infections such as PCP and keeping them symptom-free until they had developed a greater degree of immune damage.

Once they had been diagnosed with AIDS, people in Group A lived for significantly shorter than people in Group B. This is logical, because people in Group A developed AIDS at a more advanced stage of immune damage than people in Group B, and developed more serious AIDS-defining events than people in Group B.

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