Send response to journal:
Nicholas Bennet wrote:
"PACTG 076 clearly showed the usefulness of AZT (the current standard of care)."
"However, since vitamin A is a teratogen, excess supplementation could be far more deleterious to the fetus than the relative risk of HIV infection."
Why is Dr. Bennett concerned about vitamin A harming infants, yet AZT is perfectly acceptable when there is a wealth of data showing it is a teratogen, mutagen and carcinogen, which in turn leads to neurological problems, mitochondrial dysfunction and death? Does Dr. Bennett have proof that AZT is less toxic than vitamin A? Is vitamin A more carginogenic, more strongly oxidising than, and more destructive to mitochondria than AZT (among other body tissues)? This is a critical question when one considers the unequivocal data showing 'the current standard of care' to be potently toxic and harmful to infants.
A few examples can best illustrate this:
1. In the study, 'Rapid disease progression in HIV-1 perinatally infected
children born to mothers receiving zidovudine monotherapy during
pregnancy', reported in May 1999 in AIDS, (13:927-33) de Martino et al.
2. In June 2000, De Souza et al. published their findings in Journal of
Acquired Immune Deficiency Syndromes (1;24(2):154-61) concerning the
Effect of prenatal zidovudine on disease progression in perinatally HIV1-
infected infants. Their objective was to:
3. In July 2000, in the Journal of Infectious Diseases (182(1):104-11), Kuhn et
al. reported in their study of 325 HIV-positive children born between 1986
and 1997 until death or diagnosis with AIDS, under the title, 'Disease
progression and early viral dynamics in human immunodeficiency virus
infected children exposed to zidovudine during prenatal and perinatal
periods.' Their findings were summarised in a report by Reuters Health:
In 1991 Hayakawa et al., warned in their paper, 'Massive Conversion Of Guanosine To 8-Hydroxy-Guanosine In Mouse Liver Mitochondrial DNA By Administration Of Azidothymidine', published in Biochemical and Biophysical Research Communications (176, 87-93), ‘it is urgently necessary to develop a remedy substituting this toxic substance, AZT’.
Lamperth et al., in 'Abnormal skeletal and cardiac muscle mitochondria induced by zidovudine (AZT) in human muscle in vitro and in an animal model,' published in Laboratory Investigations, 1991 Dec;65(6):742 -51), described AZT as a ‘mitochondrial toxin’.
The French Paediatric HIV Infection Study Group, which followed up a ‘large..cohort’ of ‘2644 of 4392 children..exposed to antiretrovirals’ confirmed that, as opposed to the unexposed, ‘Children exposed to nucleoside analogues during the perinatal period are at risk of a neurological syndrome associated with persistent mitochondrial dysfunction... a risk about 30 times higher than that in the general population.’
Hart et al. propose a mechanism by which AZT mitochondrial toxicity causes neurological damage in their paper, 'Acetyl-l-carnitine: a pathogenesis based treatment for HIV-associated antiretroviral toxic neuropathy', AIDS 2004, 18:1549–1560: ‘Nucleoside analogue reverse transcriptase inhibitors (NRTI) disrupt neuronal mitochondrial DNA synthesis, impairing energy metabolism and resulting in a distal symmetrical polyneuropathy (DSP), an antiretroviral toxic neuropathy (ATN) that causes significant morbidity..’
Divi RL et al. reported 'Mitochondrial damage and DNA depletion in cord
blood and umbilical cord from infants exposed in utero to Combivir.'
AIDS. 2004 Apr 30;18(7):1013-1021.
It's ok though, these are JUST mitochondria. It could be said that a positive antibody test in a pregnant mother, while not being proof of 'HIV' infection, predicts mitochondrial dysfunction in their unborn infants (that is, AZT usage).
In new research, 'Low efficacy of nevirapine (HIVNET012) in preventing perinatal HIV-1 transmission in a real-life situation', by Quaghebeur et al published in AIDS 2004 Sep 3;18:1854-1856, the researchers found that when ‘in a real-life situation in Kenya’ they tried the HIVNET 012 regimen (a hit of nevirapine each for mother and child), it was an unmitigated flop: ‘The perinatal HIV-1 transmission rate at 14 weeks was 18.1%, similar to the 21.7% before the intervention. These data call for further evaluation of the simple nevirapine regimen in field conditions, and underline the need for alternative strategies.’
A paper about fatal and other serious 'Maternal Toxicity With Continuous Nevirapine in Pregnancy: Results From PACTG 1022,' by Hitti et al. had sobering news to report on 1 July 2004 in the Journal of Acquired Immune Deficiency Syndromes (36(3):772776). Their objective: To compare the safety of nelfinavir and nevirapine-based antiretroviral treatment in HIV -1-infected pregnant women’, giving seventeen of thirty-eight pregnant women ‘nevirapine with zidovudine plus lamivudine’, and the rest the latter two drugs with nelfinavir in place of nevirapine. Within two to twenty-six weeks of treatment, drug toxicity caused five women in the AZT+3TC+nevirapine group – twenty-nine per cent of them – to abandon the drugs. But it was too late for an ailing African-American woman (who had been admitted perfectly healthy into the study) after her baby was delivered by caesarian section from her: ‘1 subject developed fulminant hepatic failure and died, and another developed Stevens-Johnson syndrome.’
In this case, it appears caesarian section was about as 'effective as AZT'.
I've repeatedly asked this question of Christopher Noble, who has avoided answering it. So I'll ask Dr. Bennett.
Why is AZT being used when:
1) De Souza et al., Journal of Acquired Immune Deficiency Syndromes (1;
24(2):154-61), Effect of prenatal zidovudine on disease progression in
perinatally HIV1-infected infants.
Competing interests: None declared