Læknaneminn - 01.04.1997, Blaðsíða 129

The drug-AIDS hypothesis'
its kind, the Concorde trial, found no prophylactic
value, but instead revealed a 25% higher mortality in
AZT recipients than in untreated controls 343. In view
of these awkward results Seligmann et al. reached the
patronizing conclusion: “The results of Concorde do
not encourage the early use of zidovudine [AZT] in
symptom-free HlV-infected adults” 160.
8) A study that treated HlV-positive, intravenous
drug users from New York with AZT observed: “The
rate of CD4 lymphocyte depletion did not appear to
slow after the initiation of zidovudine therapy...”.
This Ied to the conclusion: “Our data failed to provide
evidence for an effect of zidovudine on the depletion of
CD4+ lymphocytes, but the direction of the modeling
results suggested that zidovudine users in this sample
may have experienced more rapid CD4+ cell deple-
tion” 87.
9) As of 1994 the American NIAID and the CDC
promoted the prevention of maternal HIV transmis-
sion with AZT 45, l84,185,344. But the costs of the hypo-
thetical triumph of reduced HIV transmission in terms
of birth defects and abortions were omitted from the
reports of the original trial ls4’185,344-M7. However a study
from outside the US reported 8 spontaneous abortions,
8 therapeutic abortions and 8 serious birth defects,
including holes in the chest, abnormal indentations at
the base of the spine, misplaced ears, triangular faces,
heart defects, extra digits and albinism among the
babies born to 104 AZT-treated women. But these
bewildering results were interpreted as just “not prov-
ing safety, thus lending tenuous support to the use of
this drug” 20°.
Indeed, “spontaneous” or therapeutic abortion as a
result of AZT was not an unforseeable accident. A
review in The Lancet on “non-surgical abortion” docu-
rnents that chemotherapeutic drugs, like methotrexate,
have been used to abort normal and ectopic pregnan-
cies since 1952 188. The article concedes early “con-
cerns over teratogenicity”, but concludes: “used cor-
rectly, the method could bring great benefits” 18S.
10) In 1996, the American National Institute of
Child Health and Human Development reported the
consequences of AIDS prophylaxis with AZT for HIV-
positive babies: “In contrast with anecdotal clinical
observations and other studies indicating that zidovu-
dine favorably influences weight-growth rates, our
analysis suggests the opposite. Because our analysis of
zidovudine effect on standardized growth outcomes
was based on limited numbers of patients (no more
than 10 at any one visit with prior zidovudine use) and
because we could not control for stage of HIV disease
in the study design, the result indicating no effect or a
negative effect of zidovudine on growth should be
interpreted with caution. Presumably, zidovudine use
is confounded by progression of HIV disease. The
observation that standardized LAZs [Iength for age
scores] were lower after the start of zidovudine therapy
than before may suggest merely that sicker infants
received zidovudine. However, our fmdings suggest
that the widely held view that antiretroviral treatment
improves growth in children with HIV disease needs
further study” 205. Thus AZT toxicity was shifted to HIV.
But if the lower health standards of AZT-treated
babies were due to prior “HIV disease”, it would have
been necessary to conclude that AZT failed to reverse
or even maintain the “HIV disease” of these babies.
But that possibility was not mentioned nor apparently
even considered by the AZT-doctors. Moreover, the
likelihood that AZT was the cause of the babies’ dis-
eases was obscured by averaging the diseases of AZT-
treated with those of untreated HlV-positive babies (see
7.7.).
11) The disquieting observation that AZT increases
the annual lymphoma risk of HlV-positives 50-fold,
from 0.3 to 14.5%, per year was resolved by the NCI
director, Samuel Broder and his collaborators, by
claiming a victory for AZT: “Therefore, patients with
profound immunodeficiency are living longer [on
AZT], theoretically allowing more time for the devel-
opment of non-Hodgkin lymphoma or other malig-
nancies” 19S.
Conclusions. The extent of the evasions, obfusca-
tions, and outright censorship of the abundant drug-
AIDS connections suggests that AIDS researchers must
at least suspect that recreational drugs and AZT cause
AIDS. Considering that most AIDS researchers have
graduated from university with at least some apprecia-
tion of the central importance of DNA synthesis,
somewhere in the Richard Feyman-recesses of their
minds they must be aware of the high toxicity of DNA
chain-terminators. Even if they did not understand
that life depends on continued DNA synthesis, the
complete failure of drugs like AZT to cure or prevent
AIDS should have inspired concern.
LÆKIMANEMINN
127 1. tbl. 1997, 50. árg.