AZT Life-Saving or Death-Dealing?
by author David Crowe
A South African court case might answer the question of whether AZT, the currently advertised AIDS drug, is life-saving or death-dealing. The lawsuit only claims damages for one man believed to be killed by AZT, but if it’s successful the precedent could send shock waves around the world. The lawsuit was brought against GlaxoSmithKline, the manufacturers of the drug, by the wife of James Hayman, who died less than a year after starting a course of treatment.
In July 1997 Hayman was prescribed one month’s supply of AZT along with the similar drug 3TC. Although there were no visible signs of his illness at that time, he immediately became very sick, experiencing continual diarrhea, vomiting, headaches, tiredness, anemia, muscle weakness, cramps, pain and weight loss. Because of this, he stretched his prescriptions over two months and then refused to renew them. However, even after stopping drug therapy, his diarrhea, vomiting, tiredness, muscle weakness and weight loss continued. He died in June 1998, having lost about one-third of his total body weight.
The lawsuit is unique and of such great importance because it does not claim that an unexpected side-effect of AZT caused the death, but that activation of the drug in the human body is impossible and that its only effect is toxicity. The implication is that the billions of dollars worth of AZT already sold has only hastened the deaths of AIDS victims, exposing GlaxoSmithKline to a potentially fatal onslaught of lawsuits.
AZT has been the foundation stone of the AIDS drug construction for several reasons. It was first approved in 1987 and it is still one of the biggest sellers, although it’s usually used in two or three drug "cocktails" rather than alone. It is also the main drug used to prevent HIV transmission from mothers to their babies and the one most often used instead of a placebo in clinical trials of new AIDS drugs. This lawsuit could be the trumpet call that brings the walls of AZT tumbling down.
AZT has a well-documented dark side due to numerous debilitating or fatal side-effects. One of the most common advertisements in AIDS journals is for a substance that is designed to combat anemia caused by AZT–an anemia so severe that without blood transfusions patients will die. Much of the damage to blood, bone marrow, nerves and muscle is believed to arise from effects on mitochondria, the essential energy-regulating organelles inside every cell.
Drug Dilemma
AZT is supposed to work by interfering with the most basic mechanism of life--cell division. DNA is a chain of molecular beads known as nucleotides. One of these is thymidine, of which AZT is a defective analog, a bead that can be threaded on to the chain but stops further growth by preventing the addition of natural nucleotides. This mechanism is believed to stop HIV from inserting itself into human DNA and has the potential to stop normal cell division as well as replication of mitochondria.
AZT can only be incorporated into DNA after it has three phosphate molecules added to it (as is true for normal nucleotides as well), a process known as triphosphorylation. This is because it is prescribed as a nucleoside (without any phosphates) rather than a nucleotide. The phosphates must be added by natural mechanisms within the cell, a process that the drug label specifically claims does occur.
The problem is that most of the available scientific evidence shows that only a tiny fraction of AZT is ever triphosphorylated. Sixteen studies are quoted in the lawsuit. Each shows that only a tiny fraction (0.01 or 0.001 per cent) is triphosphorylated. A scientific review paper published in 1999 provided a great deal of ammunition for this argument. Not surprisingly, this research has been widely ignored by an AIDS research community that is dependent on funding from pharmaceutical companies and staffed by researchers determined to get rich by inventing the next new "AZT."
A Legal Threat
David Crowe is president of the Alberta Reappraising AIDS Society at 403-220-0129 or aras.ba.ca.
Source: alive #230, December 2001

