| 
Past Issues
Volume 15, number 2/3
February/March 2001
Contents
Trust Me, I'm a Doctor
The real story behind the new federal treatment guidelines
My HAART Will Go On
The current state of "salvage" for the highly experienced
Nose Job
Sinusitis and HIV
Leapin' Lipids!
Managing a changing metabolism
Twenty Years with AIDS
Recalling Michael Callen's watershed 1993 speech
Hit Hard, Later...?
By Mark Harrington
1. November 1996: Déjà Vu All Over Again?
Notes from a panel discussion at the NIH in Washington, D.C.: "Principles
of HIV Therapy":
Today we heard the depressing news about cross-resistance developing
between protease inhibitors. It made for a toxic cocktail.
As I left the auditorium I bumped into [Merck virologist] Emilio
Emini.
Harrington: So what do you do if you fail Crixivan?
Emini: [sighs] We don't know what to do.
Harrington: Take two new nucleosides and nevirapine?
Emini: Yeah. And pray.
No one had yet assessed the healing effects of prayer on viral
load. This was what we'd come to.
In the lobby of the Interior Department I ran into a colleague
who was wild with fear and disappointment.
Colleague: I'm going to die.
Harrington: This is everything we were hoping wouldn't happen.
Colleague: I don't have anything to switch to. I'm going to
stop everything.
Dawn Averitt tried to calm our colleague down.
Averitt: Why don't you wait for your next viral load?
Colleague: I'm already back at baseline!
Averitt: But your CD4 count is 250, and it was down to 60 in
January.
Colleague: True, but my viral load is back to half a million.
Averitt: Why don't you wait until you get your latest numbers
and see what your resistance profile is?
Colleague: I'm going to go outside and have a nervous breakdown.
We went outside. It was frigid, and fragile snowflakes swirled
around in the wind. Sometimes the gap between how the researchers
felt and how we felt becomes an abyss. They were excited about the
endless possibilities opened up by the research advances of 1996;
we were terrified about the limited treatment options facing people
who had exhausted most of the current arsenal of antiretroviral
therapy. What to do with those whose viral load refused to go undetectable?
What to do with those who added a protease inhibitor to a failing
two-drug regimen and now appeared doomed to develop resistance,
or worse — especially with ritonavir and indinavir — cross-resistance
to all other protease inhibitors? What to do with those who jumped
aboard last year's [1995's] bandwagon, AZT+3TC, and now appeared
likely to have developed 3TC resistance and, with it, cross-resistance
to ddI, ddC and possibly 1592 [abacavir]? The Chinese menu approach
to antiretroviral treatment suddenly looked much less appetizing,
and much less nourishing.
...Many of the researchers present did not share the activist sense
that we were facing a crisis that, if handled improperly, might
make things worse than before. This was not the prevailing view
propounded by gun-happy virologists, drug-happy pharmaceutical companies,
media captivated by a surprising good-news story and many people
with HIV still struggling to absorb the complex developments of
1996. Just that week, back-to-back articles in The Wall Street Journal
and The New York Times Magazine, both written by HIV-infected journalists,
declared that the epidemic was virtually over. We were staring into
the precipice while others were still climbing the hill.
Toxic cocktail. TAGline 4:2, February 1997
2. 2001: A Conspiracy of Silence?
A newly revised set of US government guidelines on when to start
(WTS) antiretroviral therapy, despite repudiating the "hit early,
hit hard"strategy which has predominated in the USA since the Vancouver
AIDS conference in 1996, merited only a peripheral presence at the
8th Annual Retrovirus Conference held in Chicago from 3 to 8 February
2001.
Neither the chairs of the Health and Human Services guidelines
panel nor the organizers of the Conference appeared especially eager
to highlight the significant modifications that appeared in the
February 2001 update of the Guidelines for the Use of Antiretroviral
Agents in HIV-Infected Adults and Adolescents. (hivatis.org/guidelines/AAFEB05S.PDF)
Prior to the Conference I heard a rumor that the Conference organizers
had turned down a request by guidelines panel co-chairs Anthony
S. Fauci of NIAID and John Bartlett of Johns Hopkins University
for a press conference to announce the new guidelines. So, at the
opening press session I questioned Retrovirus chair Connie Benson
of the University of Colorado whether they had indeed turned down
a request by Drs. Fauci and Bartlett. "Not at all," said Dr. Benson,
who is also a co-chair of the government's top HIV clinical research
program. It turns out the only request she heard had come from a
NIAID press person. "Do you think I would actually turn down Dr.
Fauci?" she asked. And in fact, as the Conference opened, the only
document NIAID had shown the Conference organizers was an anemic
two-page press release; the Retrovirus press person had to download
a copy of the new Guidelines from the Internet.
Why the low-key reception? Well, just as enthusiasm for the early
use of AZT was deflated by the release of the Concorde study results
in 1993, so do the 2001 treatment guidelines finally depose the
ailing "hit early, hit hard"strategy. But for some, old strategies
die hard.
Rather than trumpeting the changes by holding a press conference
before the world's leading AIDS reporters in Chicago and admitting
"Whoops! We were wrong! We screwed up! Maybe treating everyone with
a viral load over 5,000 to 10,000 HIV RNA copies/mL wasn't such
a great idea after all," the Guidelines panel co-chairs and the
Retrovirus organizers all felt it was more opportune — or more
expedient — to skate over the matter as casually as possible,
as though the new Guidelines represented a simple and relatively
uncontroversial recalibration of the standard of care.
3. An Honest Mistake?
Of course, we have been covering this controversy for a long time,
as these titles show:
- Hitting it early, hard: the aftermath — The fickle (and
unforgiving) fashion of antiretroviral therapies: early treatment
choices and their unintended consequences, TAGline 3:7,
October 1996;
- START stopped: Nearly everyone agrees on the need for "strategy"
type clinical studies — and that's where consensus ends,
TAGline 4:3, March 1997;
- The twilight of eradication: Infectious HIV persists after up
to two-and-a-half years of tripledrug therapy, due to a non-decaying
third compartment: "It's the immune system after all," TAGline
4:11, December 1997;
- Data drought: As treatment euphoria ebbs, stubborn uncertainties
resurface but are unlikely to be resolved: "Unacceptable collective
evasion," TAGline 6:4, June 1999;
When Mark Schoofs from The Wall Street Journal called me,
he said, "This is a good thing. People don't have to go on therapy
as early."
"Well, yes," I said, "but it would have been much better to have
a clear answer from a randomized, controlled trial [RCT] by now."
"Well, Tony Fauci says that's unfeasible."
"Well, if he says so, it must be true," I replied, "but if they'd
started one in 1996, we might know the answer by now."
"You sound angry."
"I am angry. Thousands of people were put on therapy too early,
and some of them developed life-threatening side effects, or resistance,
and they would have been fine if they had just waited."
Was failing to seek evidence for such a sweeping policy just an
honest mistake? A gush of euphoria that the long, dark night of
AIDS was over? Well, of course those promulgating the original standard
of care were sincere — but they defaulted from their obligation
as scientists to prove that their expert opinions were actually
correct — and, considering the emergence of long-term side
effects and widespread cross-resistance, it doesn't seem that they
were.
4. The New When to Start Guidelines in a Nutshell
- Previous guidelines recommended that treatment be offered to
everyone with a CD4 count below 500/mm3.
- The current guidelines recommend that treatment be offered to
everyone with a CD4 count below 350/mm3.
- Previous guidelines recommended that treatment be offered to
everyone with a viral load over 10,000 (bDNA) or 20,000 (RT-PCR).
- The current guidelines recommend that treatment be offered to
everyone with a viral load over 30,000 (bDNA) or 55,000 (RT-PCR).
- As before, therapy is recommended for all those with clinically
defined AIDS, a CD4 count below 200/mm3, or with HIV-related
symptoms.
[Other significant changes in the new Guidelines include the addition
of indinavir/ritonavir and lopinavir/ritonavir (Kaletra) to the
"preferred" initial regimens, extensive new sections on adherence
and drug-related adverse effects, and a section on women and viral
load.]
5. Why the Change Now?
The death of the eradication hypothesis?
The NIH press release distributed at the Conference quoted Dr.
Fauci as saying, "we know that we cannot eradicate HIV infection
with currently available medications" (NIH 2001). However, we have
known that HAART cannot eradicate HIV ever since the discovery at
the laboratories of Bob Siliciano, Doug Richman, and Tony Fauci
in 1997 of latent HIV reservoirs in resting provirally-integrated
CD4 cells. The original HHS Guidelines came out that same year,
so the "hit early" approach could not have been based solely or
even mainly on the feasibility of eradication.
Treat HIV like any other infectious disease?
In the minds of some, the "hit early" approach was based on the
idea that, in Bruce Walker's words, we should "treat HIV-1 like
any other infection — treat it." Well, yes. The question is,
when? HIV-1 is not much like other infections. Some, such as bacterial
infections, can be cured with antibiotics. Obviously, if HIV could
be cured, we would try to cure people. Persistent viral infections,
such as herpes, cannot be cured, and we do not treat them chronically,
but only when outbreaks occur. HIV is not like bacterial infections
or like herpes. It cannot be cured, it is chronic and persistent,
it never goes into full latency (unlike herpes), and treatment requires
complex, expensive, sometimes toxic, combination therapy. Full adherence
is difficult if not impossible, and the development of drug resistance
is a constant threat.
Solid results from evidence-based medicine?
In the NIH press release, Fauci went on to say that the revised
Guidelines present "evidence-based recommendations for initiating
antiretroviral therapy that take into account both the benefits
and potential risks..." However, the Guidelines themselves admit
that "The optimal time to initiate antiretroviral therapy is not
known."
The "evidence" to which Dr. Fauci referred is a random grab bag
of observational studies which are contradictory and hardly definitive.
One can conclude whatever one wants to from these observational
studies — if you favor early treatment, you can find studies
that do too, and if you favor later therapy, other studies will
back you up.
Weaker evidence from observational studies?
Observational studies, despite their limitations, are practically
the only "evidence" we have right now about the clinical benefits
of various starting thresholds. Several large cohort studies presented
at the Retrovirus conference in February 2001 — most of them
in poster form because they did not fit the preferred world-view
of the Conference organizers — suggest that, while starting
when the CD4 count is below 200 is clearly less effective than starting
when it's above, there is no difference among groups starting with
higher CD4 cut-offs; even very high viral load may make little difference.
Some examples:
The British Columbia Cohort
No apparent difference in clinical outcome whether one starts when
CD4 >200 or CD4 >350.
In British Columbia, AIDS care is free and antiretrovirals are
centrally distributed to all eligible HIV-positive individuals.
Over 5,400 participants have enrolled; currently over 2,600 are
on antiretrovirals. Robert Hogg and colleagues looked at all HIV-positive
men and women over 18 years old and totally antiretroviral naive
who were first prescribed triple therapy (containing either a PI
or an NNRTI plus two NRTIs) between August 1996 and September 1999.
Analysis was by (slightly censored) intent to treat. They assessed
rates of mortality by different CD4 and HIV RNA thresholds.
One thousand, two hundred and nineteen HIV-positive adults fit
the study criteria. Nine hundred and nine of these (74.6%) received
a PI-based regimen, while 310 (25.4%) received an NNRTI. Median
follow-up was 20 months. 1,034 participants (85%) were men, and
185 (15%) were women. At baseline the median age was 37, the median
CD4 count 280 cells/mm3, and the median plasma HIV RNA
was 120,000 copies/mL.
By the end of January 2000, 86 deaths had occurred (7%). "Fourteen
were not attributed to AIDS and were censored as non-events at the
time of death; the remaining 72 deaths gave a crude mortality rate
of 5.9%." Cumulative 12-month mortality was 3.2%.
The investigators stratified the results by various CD4 and RNA
break points. For example, in early 2000, they used the "new" threshold
of 350 cells and a viral load over 30,000. No difference was found
in mortality between those who started with a CD4 count over 350
and those with CD4 between 200 to 350. By contrast, mortality was
higher in the group that started with a CD4 below 200. Baseline
viral load appeared to make little difference when cutoffs of <5,000,
5,000 to 30,000, and >30,000 were used.
Therefore, they used their own data to identify "natural" break
points (see chart, this page).
After adjustment by multivariate analysis, no baseline viral load
level was associated with greater or lesser survival. A baseline
CD4 count below 200 predicted worse survival. There was little difference
between those starting withCD4 counts between 200 to 350 and those
starting with >350.
Having a baseline CD4 count below 50 cells/mm3 at baseline
increased the risk of mortality by seven-fold compared with those
starting with over 200 (p<0.001), while starting with a CD4 count
between 50 to 199 had a three-fold greater risk (p<0.001). Having
a baseline viral load over 200,000 copies/mL appeared to increase
the risk by about 1.75-fold, but the result was not statistically
significant.
The BC investigators concluded that "the effectiveness of antiretroviral
therapy on survival is independent of plasma HIV-1 RNA levels, AIDS,
and protease inhibitor use at baseline, but dependent on CD4 levels....
The effectiveness of therapy on survival becomes compromised in
patients [who] start with CD4 counts below 200/mm3 "
(Hogg 2001).
Three caveats should be recognized about extrapolating from the
BC cohort study to, for example, the USA:
- The sample size was small. Even though data were available on
1,219 individuals, only the 72 who died of HIV-related causes
(5.9%) provided mortality data. Therefore the sample size is actually
relatively small (hence the large confidence intervals in the
multivariate analysis).
- The length of follow-up was short — a median of 20 months,
with an inter-quartile range between 11 and 30 months. Longer
follow-up might show different results (for example, an increasing
benefit with starting at an intermediate CD4 count or a higher
viral load).
- Access to care is far more equitable in British Columbia than
it is in the USA.
European Cohorts — No apparent difference in virologic
outcome whether one starts when CD4>200 or CD4>350.
Although not presented at Retrovirus, a reassuringly complementary
study — this time assessing virologic rather than clinical
outcomes — was presented at the 5th International Congress
on Drug Therapy in HIV Infection at Glasgow in October 2000. This
was a meta-analysis by Andrew Phillips and others of virologic outcomes
from three European HIV cohorts — the Swiss HIV Cohort Study,
the Frankfurt HIV Cohort, and the EuroSIDA study. They looked at
virologic outcomes by baseline CD4 count and HIV RNA in 2,742 individuals
who were HAART-naive.
In summary, neither baseline CD4 nor RNA appeared to significantly
affect risk of rebound in these three observational cohorts.
Phillips and colleagues concluded that, "So long as the CD4 count
remains above 200/mm3 and the viral load remains below
100,000 copies/mL, there is no evidence that lower CD4 counts and
higher viral loads are associated with poorer responses to antiretroviral
therapy" (Phillips 2000).
Poor Swiss study design fails to deter Retrovirus organizers
from highlighting it in a dubious late-breaker
A bizarre Swiss analysis highlighted as a Retrovirus late-breaker
— even though it involved a smaller sample than either the
BC or another cohort from The University of Alabama, Birmingham,
both of which were relegated to a poster session — involved
a case-control study from the Swiss cohort. "Treatment-naive individuals
with CD4 >350/mm3 when starting HAART between January
1996 and December 1999 were matched with untreated controls by baseline
time, HIV RNA, CD4 count, IV drug use, age, and gender.... 363 cases
were matched with 363 controls." Twenty-eight percent were female
and 25% had a history of IV drug use. Median baseline CD4 counts
were 487 and 498, and RNA levels were 4.2 and 4.1 logs.
Median follow-up times were lopsided, with 2.1 years among cases
and only 1.3 years among controls. The event rate was low. Four
cases (1.1%) and 16 controls (4.4%) developed an AIDS-defining condition,
while four cases (1.1%) and 12 controls (3.3%) died.
Among the bizarre features of this study was the fact that the
investigators didn't even appear to look at lower CD4 thresholds,
such as 200. Of course, starting above 350 is likely to be better
than not starting at all. Moreover, the overall event rate (20 cases
of AIDS, 16 deaths) was quite low — 2.75% for AIDS and 2.2%
for death. Finally, the case-control methodology is riddled with
potential for bias. These deficiencies failed to deter the Retrovirus
conference organizers from highlighting this paper as a late-breaker,
and hailing it in their helpful notes to the press as a study that
"supports [sic] the increasing [sic] body of evidence that earlier
treatment is immunologically and clinically beneficial..." [Highlighted
Abstracts from the 8th Annual Retrovirus Conference, p. 20].
Toxicity, Adherence, Resistance, and Cost?
The real reasons for the change in guidelines include:
- The unexpected plethora of serious drug-related adverse events,
such as elevations in liver and metabolic enzymes, facial lipoatrophy,
fat redistribution, kidney stones, lipodystrophy, metabolic complications,
neuropathy, osteonecrosis, etc., and less common but sometimes
fatal complications such as hypersensitivity reactions, lactic
acidosis, pancreatitis, hepatic steatosis, Stevens-Johnson syndrome,
and end-organ liver and kidney disease.
- The extreme difficulty in achieving perfect adherence, and the
high probability of treatment failure in the face of less than
perfect adherence;
- The increasing prevalence of drug resistance and cross-resistance,
limiting future treatment options and creating a large pool of
individuals who are multi-drug resistant and often resort to complicated,
toxic, highly expensive mega-HAART regimens;
- The cost of therapy; and
- The unexpected resilience and restorative capacity of the immune
system, which no one expected when HAART was first introduced,
and which enables most people, once their CD4 count goes durably
over 200 cells/mm3, to become able to stop taking primary
or secondary prophylaxis for PCP, MAC, CMV, cryptococcosis, toxoplasmosis,
and other opportunistic infections.
6. What next?
It would be nice if we could really have treatment guidelines based
on evidence from well-controlled studies. But perhaps we missed
the chance to initiate such studies because so many were captivated
by the euphoria that accompanied the adoption of HAART after 1996.
Sometime in 1997, when David Barr and I were in Anthony Fauci's
corner office at NIAID, we asked him to support a major clinical
trial of when to start. "It's the most important question in HIV
therapy," he agreed. But nothing happened. During the 1998 adult
AIDS clinical trials recompetition, NIAID once again missed the
opportunity to encourage or force the research community to address
the question.
In early 2000, after considerable activist pressure, the NIAID
Division of AIDS appeared to recommend $42 million in funding for
a when-to-start trial, and held several workshops to discuss methodology
and feasibility issues. These initiatives were smothered in the
cradle by AACTG leadership and community representatives in their
thrall who dismissed the feasibility of long-term research. They
were finally buried at the NIAID Council meeting in January 2001.
As the press started to get hold of the new treatment guidelines,
it was natural to ask Dr. Fauci why there were no clinical trials
to answer what appeared to be such an important question. Even though
the NIAID-sponsored feasibility studies had yet to be completed,
Fauci told ABC News, in a story aired on January 31, 2001, that
such a study would be "logistically impossible to do.... No one
has yet been able to come up with a protocol" (Eisner 2001).
Some have suggested doing a WTS study in a developing country.
But in places that can barely afford HAART or the necessary infrastructure,
treating people with CD4 counts over 350, or even over 200 cells/mm3,
may be a luxury they can't afford, even if some so-far undetected
benefit actually accrues to such a strategy.
At the Retrovirus conference, one of the leading figures in the
Adult ACTG told me that, having dismissed the idea of a randomized
WTS study with clinical endpoints, the AACTG is now exploring the
feasibility of (1) smaller randomized WTS studies looking at viral
load, CD4 counts, and other laboratory parameters, and (2) establishing
a larger observational cohort which, supposedly, could shed light
on the question.
There are several problems with this approach. The smaller randomized
study withsurrogate markers simply wouldn't answer the question
of whether people who start treatment earlier live longer or not.
Obviously CD4 counts would be higher, and RNA levels lower, in the
group that was treated earlier. But, this might not affect longer-term
outcomes. The prospective observational study would be as expensive
as a 'real'trial, wouldn't answer the question any sooner than a
randomized controlled trial, and would suffer from all the limitations
of the observational studies described above.
It appears unlikely that any of the NIH-funded trials networks
will do a controlled clinical endpoint study looking at WTS. It
appears even less likely that such a study could be carried out
in resource-poor developing country settings. Perhaps the Europeans,
in conjunction with other developed countries such as Canada or
Australia, may do such a study but clinicians in those countries
already tend to start treatment later.
More likely, we'll have to continue to rely on observational studies
with accumulating inferences, hints and clues from smaller randomized
studies, as well as new and emerging insights about the predictors
and correlates of various drug-related adverse events, to guide
the standard of care for the next few years.
As someone who's spent the last 12 years of my life trying to encourage
more and better AIDS research, and has worked with community groups
to help push Congress and three presidents to provide more resources
for that research, it's profoundly disappointing that the leaders
of the research effort — both at NIH and in the lavishly funded
AACTG and the smaller, but still substantial CPCRA — have signally
failed to do anything more to address the question of when to start
than to reluctantly replace one set of guidelines based on expert
opinion with another.
References
DHHS/Henry J. Kaiser Family Foundation Panel on Clinical Practices
for the Treatment of HIV Infection. Guidelines for the use of antiretroviral
agents in HIV-infected adults and adolescents. February 2001.
Eisner R. "Hit later, hit hard" with AIDS drugs: Federal government
to announce new AIDS treatment policy. ABC News, 31 January 2001.
Hogg RS, Yip B, Wood E, et al. Diminished effectiveness of antiretroviral
therapy among patients initiating therapy with CD4+ cell counts
below 200/mm3. Abstract 342, 8th CROI, Chicago, IL, February
2001.
NIH News Release. HIV treatment guidelines updated for adults and
adolescents. 5 February 2001.
Opravil M, Ledergerber B, Furrer H, et al. Clinical benefit of
early initiation of HAART in patients with asymptomatic HIV infection
and CD4 counts >350/mm3. Abstract LB6, 8th CROI, 2001.
Phillips AN, Staszewski S, Weber R, et al. Viral load change in
response to antiretroviral therapy according to the baseline CD4+
lymphocyte count and viral load. Abstract PL3.4, 5th International
Conference on Drug Therapy in HIV Infection, Glasgow, UK, 2000.
AIDS 2000;14(suppl 4):S3.
All TAGline articles are available at www.treatmentactiongroup.org
| European Cohorts
— Baseline Characteristics |
|
| |
Baseline CD4
Level |
| |
N |
<200 |
200 to 349 |
<350 |
| Swiss HIV Cohort Study |
1,492 |
50% |
25% |
25% |
| Frankfurt HIV Cohort |
701 |
45% |
29% |
26% |
| EuroSIDA |
549 |
44% |
32% |
25% |
|
| Total |
2,742 |
47% |
27% |
25% |
|
| Gender (% female) |
|
25% |
26% |
25% |
| MSM |
|
42% |
45% |
45% |
| IDU |
|
25% |
23% |
21% |
| Heterosexual |
|
39% |
31% |
30% |
| Age at starting |
|
37 |
35% |
34% |
| When started |
|
9.97 |
9.97 |
10.97 |
| Previous AIDS |
|
34% |
7% |
4% |
| Viral load |
|
52 log 10 |
4.8 log |
4.6 log |
| CD4 count |
|
79 |
274 |
465 |
| Phillips and colleagues assessed virologic outcomes
by two measures — the relative hazard of achieving an "undetectable"
viral load (RNA <500 copies/mL) by 32 weeks, and, among those
who achieved an undetectable viral load, those whose viral load
went back above 500. (They did not appear to distinguish between
cases where the RNA rise was a blip or when it was a breakthrough.) |
| European Cohorts
— Virologic Response by Baseline CD4 and RNA |
|
| Relative Hazard (RH) of RNA
<500 copies/mL by 32 weeks |
| By baseline CD4 |
| CD4 >350 |
1.00 |
| CD4 200 - 349 |
1.07 (0.96 - 1.20, p=0.23) |
| CD4 <200 |
0.88 (0.79 - 0.99, p=0.03) |
| By baseline RNA |
| RNA <10,000 |
1.00 |
| RNA 10,000 - 99,999 |
1.03 (0.90 - 1.18, p=0.82) |
| RNA >100,000 |
0.70 (0.61 - 0.80, p<0.0001) |
| Only a baseline CD4 below 200 or an RNA above
100,000 was significantly predictive of a lower likelihood of
becoming undetectable at 32 weeks. |
Raise the Titanic!
By Bob Huff
Salvage therapy sounds pretty desperate: "What can we possibly
do to rescue this foundering carcass from the Deep Six?" This isn't
to say that a person with two T-cells, serious treatment toxicity
problems and a virus that's resistant to every drug in the book
doesn't need help. People with HIV are still dying. The deaths may
come from liver failure or lymphoma these days, but people with
very few T-cells can still waste away and die from a classic AIDS
illness if not managed properly.
Even very immune-suppressed people, if they are treatment naive
and have a drug-susceptible virus can, with time and diligence,
hope to recover immune competency to a point where prophylactic
medication may safely be stopped. And many people in the US still
discover their diagnosis at that late stage. But for an increasing
number of individuals who have been on therapy long enough to have
run the gamut of available drugs, constructing a treatment regimen
when there are no good options increasingly starts to feel like
a salvage operation.
Failure
Viral load breakthroughs can take many forms, from one time "blips"
to overgrowth with multi-drug resistant (MDR) virus. Inadequate
drug levels are almost always the reason for unsuppressed virus,
with missed or late doses being the most common cause of inadequate
drug levels. But other conditions can also lower drug levels in
the blood. Certain medications can speed up the removal of a drug
from the liver, and some cells can actually "learn" to expel foreign
drug molecules from within. Viral load levels can soar if treatment
is stopped for more than a week — whether due to intolerable
toxicity, weariness with the regimen, or the need for a "holiday."
Any occasion for a burst of viral replication while on antiretroviral
therapy can lead to another, more worrisome, source of virological
failure. Loss of susceptibility to antiretroviral therapy, also
known as drug resistance, can occur whenever a viral mutation arises
capable of replicating despite the presence of drugs. Since resistance
allows replication and replication breeds resistance, there is a
critical need to find new ways to fight viral strains that have
become resistant to multiple HIV drugs. When an individual experiences
immunological failure subsequent to loss of viral suppression, the
need for a "salvage" strategy can become urgent lest clinical failure
follow.
The current state of the art for rescuing an individual from virological
(and the much more serious immunological) failure is to switch or
add new drugs, with choices guided by genotype and phenotypic susceptibility
testing. These tests allow a physician to construct an "optimized"
regimen containing drugs suited to an individual's viral sensitivities.
Optimized therapy may also include a drug to boost blood levels
of one of the other agents, or, if available, may include an experimental
drug with a unique resistance profile.
A more aggressive strategy, sometimes called "Mega-HAART," advocates
piling on five, six, or more drugs, both approved and experimental,
to beat the virus into submission. Usually, these intense regimens
will include an agent to boost the blood levels of one of the other
drugs.
Unfortunately, second and third regimens rarely work as well as
the first one, and the toxicity of such intense drug regimens can
become intolerable. Although "salvage patients" are often the most
willing to attempt demanding regimens, they are also those least
able to tolerate them.
A few novel strategies for addressing this problem are being tested.
One approach proposes removing drug pressure with a structured treatment
interruption in order to allow a switch in the dominant viral population
from drug resistant to drug susceptible. This, in fact, can occur.
But, unless a new drug from an untried class is added when treatment
is restarted, attempts to suppress the shifted virus in a durable
and sustained fashion using formerly used drugs have been disappointing.
Another concept already practiced by some clinicians, but not yet
tested in a clinical trial, is to place patients with multi-drug
resistant virus on a simple HAART regimen that suppresses wild-type
virus at the expense of allowing a moderately unsuppressed MDR strain
to survive. The theory here is that the MDR virus is less able to
replicate and infect new cells than its ancestral "wild-type" strain.
If this is true, then an individual would be better off with an
unsuppressed amount of "crippled" virus. Studies have shown that
"failing" drug regimens may continue to have significant antiviral
activity that contributes to keeping MDR virus in check. This approach
is also supported by observational reports that individuals who
remain on "failing" regimens and receive careful medical management
can have relatively few clinical problems.
Since none of the above are excellent options, there is an urgency
for new drugs with unique resistance profiles to move through the
development pipeline.
Experimental Agents
Individuals who have experienced disease progression despite treatment
are often first in line to try the latest drugs as they become available,
whether on the market, through expanded access programs, or in clinical
trials.
Since a single new drug added to failing background therapy will
be the only active agent against the dominant viral strain, this
situation is virtually the same as being treated with only one drug.
Single drug therapy, or monotherapy, has long been recognized to
give only temporary benefits. Although a single drug may provide
a short-term reduction of viral load, viral replication can continue
under monotherapy and viral mutations often arise that soon render
the new drug useless. Adding one drug at a time has led many patients
down a path of serial monotherapy, eking out a small benefit from
each new agent before giving in to resistance. Patients who have
been on multiple drug regimens over the years may have developed
resistance to virtually every drug in every class. Many of these
individuals find themselves chronically looking to the next new
drug in the pipeline for hope.
One Is Not Enough
To increase the chances for durable viral suppression, some clinicians
feel at least two new drugs with unique resistance profiles should
be added to a background therapy that has been optimized with guidance
from resistance test results. The problem is finding two new drugs;
often only one or two experimental drugs become available each year.
One way to proceed would be to hold off switching regimens until
two novel agents are available, then start them both at the same
time. But because the drug development process is so sluggish, at
any time there might be one new drug available through an expanded
access program with another expected to come to market "any day."
So constructing an optimum regimen when all else is failing requires
patience and a steady flow of new drugs.
Another possibility for some is to get access to new drugs through
a clinical trial. But what kind of trial design can provide an optimized
regimen to every participant? The risks of serial monotherapy have
also been recognized in the research setting. If a clinical trial
is comparing one new drug to placebo — each on top of an optimized
background regimen — then individuals on the treatment arm
may experience temporarily lowered virus levels, but at the price
of becoming resistant to the new drug. Those on the placebo arm
may have unchanged viral levels yet retain susceptibility to the
new drug for future use. Who's better off?
The problems of designing trials for "salvage therapy" reflect
the problems of constructing regimens for multiple treatment experienced
individuals. One solution is to offer more than one experimental
drug to everyone in the trial.
In January 2001, the Federal Food and Drug Administration (FDA)
convened a meeting of researchers, drug sponsors and community members
to discuss the problems of developing drug trials for "salvage"
populations. In sponsoring the meeting, the FDA was signaling their
acknowledgment that data from trials leading to the approval of
new drugs conducted in exclusively drug-naive populations are no
longer as compelling as they once were and that trials with treatment-experienced
individuals are not only acceptable for registration but are welcome.
Information from controlled trials about the use of drugs for heavily
treatment-experienced patients would be extremely valuable to have.
But for the pharmaceutical manufacturers, these studies pose difficult
problems and hold significant risks. The rate of adverse events
in "salvage" trials are likely to be relatively high since the participants
have advanced disease and may be clinically less stable — and
a high rate of adverse events can make a drug look bad. For the
same reason, drugs in these trials are also unlikely to show comparable
efficacy to that seen in a treatment-naive population. Yet with
sixteen antiretroviral drugs on the market, individuals with MDR
virus are those most in need of new options.
In 1999, the FDA removed one obstacle to these trials by declaring
that multiple investigational agents in a trial may be acceptable.
In the past it had been presumed that more than one experimental
drug would "muddy the waters" to such an extent that the FDA would
reject any data from such a trial. The change was a big step forward,
yet old beliefs lingered and some in the industry were slow to accept
the shift in policy.
But allowing two experimental drugs in a study doesn't eliminate
all problems. Imagine a situation where all participants in a trial
receive optimized background therapy that includes one previously
untried or experimental drug. Add to this either the study drug
or a placebo. Those on the treatment arm may benefit from substantial
viral suppression because they are getting two new drugs, but those
on the placebo arm risk developing resistance to the single new
drug in the background regimen.
One way past the "virtual monotherapy" problem is to offer every
participant two experimental drugs in the background regimen, then
randomize the third between placebo and the experimental drug the
manufacturer is trying to have approved. This means that every participant
will receive at least two new drugs with novel resistance profiles
— the minimum thought necessary to sustain suppression of MDR
virus for more than a few months — and some will receive three.
The complications are daunting. Interactions between HIV drugs
are common and one drug may unexpectedly affect the blood levels
of another. The source of common adverse events may be difficult
to attribute to a particular experimental drug. Worse, an unforeseen
serious toxicity might emerge that permanently taints every drug
in the complicated combination.
Even with a green light from the FDA, the problem of gaining cooperation
between multiple manufacturers remains. An experimental drug can
only be provided by its manufacturer; it can't simply be purchased.
This means that the sponsors of each experimental, but non-study
drug, must agree to participate in the trial and supply their agents
for free. So far it hasn't happened. Given the incentives for pharmaceutical
developers to keep a tight rein on how their drug candidates are
used, and the risks inherent in developing drugs in the MDR population,
the barriers to launching optimal "salvage" trial designs are steep.
Free Falling
Other trial designs have been proposed, but they are less satisfactory
from the community's point of view. One scheme is to randomize participants
to receive either the experimental drug or placebo for an initial
two-week period of monotherapy. All participants would then start
optimized therapy plus the new drug and continue to be monitored
for several months. The idea is to show that the drug can produce
a short-term reduction in viral load compared to placebo during
the first few weeks, then to show that the drug is safe and tolerable
when part of a treatment regimen for a longer period of time.
This is an expedient plan for rapidly bringing drugs to market
and a plan favored by drug company representatives at the FDA meeting.
Yet the risk of developing resistance during the short period of
monotherapy worries community critics like Carlton Hogan of the
Coalition for Salvage Therapy (CST). The CST has pressed for minimizing
reliance on these studies, asking that periods of monotherapy be
kept as short as possible.
One point was affirmed by all sides at the FDA meeting: Those in
need of "deep salvage," — those with absolutely no other options
— should not have to depend on clinical trials to get drugs.
Compassionate use programs and expanded access should be widened
to ensure that no one is left without hope of rescue.
Sinusitis: All Stuffed
Up and Nowhere To Go
By Glen Hillson
Reprinted from Living + Magazine, Jan/Feb 2001.
A publication of the BC Persons With AIDS Society, www.bcpwa.org
It's that time of year when many of us with HIV become stricken
with sinusitis and other upper respiratory illnesses that often
seem to drag on for weeks, sometimes months. Sinusitis is one of
the most common afflictions of PWAs in the late winter and early
spring, although it can occur anytime throughout the year. Increased
concentrations of airborne environmental toxins, particularly in
urban areas, are a major factor leading to higher rates of respiratory
illness in the general population. HIV infection further increases
vulnerability because of depleted immune capacity. Although sinusitis
is relatively common among people with HIV, it can be very debilitating
and painful. Sinus infections become chronic (last more than 30
days) in about half of all cases.
What are sinuses?
Sinuses are hollow cavities in the bones in the front of the skull.
Their function is to protect the lungs by warming and humidifying
the air that we breathe. Sinuses are lined with membranes where
mucous is produced to filter and flush bacteria and other pathogens
from the air. When sinuses are healthy, the mucous drains easily
through small passages into the nostrils or throat. Sinusitis is
inflammation of the sinus membranes.
Four individual sinuses collectively compose the network of paranasal
sinuses. They are named after the skull bones where they are situated.
The largest are the maxillary sinuses, which are in the cheek areas
on both sides of the face extending from the bottom of the eye socket
to the upper jaw bone. The sphenoidal sinuses are behind and below
the eye orbits (the bony cavity where the eye is located) toward
the base of the skull. Ethmoidal sinuses are immediately in front
of and below the sphenoidal sinuses on either side of the top of
the nose. The frontal sinuses are located above the eyebrows.
Each sinus is lined with tissue called ciliated upper-respiratory
epithelium. The epithelium lies on top of a mucous membrane. The
mucous membrane is well supplied with blood and mucous-secreting
goblet cells that keep the membrane moist. This enables the membrane
to warm and hydrate the air we breathe. Small inhaled particles
are captured in the mucous and are then moved toward the back of
the throat to be swallowed or coughed.
Symptoms and Diagnosis
Acute sinusitis is usually preceded by a viral infection such as
cold or flu. Symptoms include nasal congestion, colored discharge,
pain, headache, and, frequently, fever. Movement, especially bending
forward, usually amplifies pain. The location of the pain can be
an indicator of which sinuses are inflamed. Pain can occur in the
cheeks, lower forehead, behind the eyes, and on the sides of the
nose. Teary eyes and sensitivity to light can also occur.
The symptoms of chronic sinusitis are usually similar but less
severe and seldom include fever. They can also include postnasal
drip (drainage from the sinus passages into the back of the throat).
This postnasal drip frequently causes throat irritation and persistent
cough.
Diagnosis of sinusitis is usually based on symptoms and individual
medical history rather than on laboratory tests, although x-rays,
CT scans, MRIs, cultures, and endoscopies may help in further evaluation.
Causes
Bacterial pathogens and, to a lesser extent, viruses are the most
common causes of sinus-itis. In persons with severe immuno-suppression,
aspergillosis, a fungal infection, can also be a cause.
Infection is not the only cause of sinus problems. Both food and
airborne allergens can aggravate the sinuses. Underlying dental
infections, smoking, snorting cocaine, overuse of nasal sprays,
rapid changes in air pressure (airplane travel, deep-sea diving)
may also be contributing factors.
Prevention and Treatment
Allergy
Successful treatment of sinusitis is largely dependent on identifying
the cause. And in the case of allergy-induced sinusitis, treatment
starts with prevention. Reducing exposure to dust and pollens can
effectively reduce allergens. Plants, cut flowers, animals, and
house dust can all be factors. Removing rugs and stuffed toys, vacuuming
frequently, damp mopping, changing air filters in heating systems
regularly, and installing free-standing air filters can all help
to control house dust which may contain a variety of allergens.
Eliminating milk products from the diet may be helpful since they
thicken mucous and can impair normal drainage.
Naturopathic physicians recommend supplementing the diet with Vitamins
A, C, and E, as well as zinc, selenium, bioflavinoids, and essential
fatty acids (evening primrose oil, blackcurrant oil, or flaxseed
oil), for regulation of sinus function.
Antihistamines may also be considered, although they can also cause
mucous to thicken and may, therefore, impede proper drainage.
Acute sinusitis
Optimal treatment for acute sinusitis requires accurate diagnosis
of the cause. Fever and colored mucous may indicate a need for antibiotics.
The main aim of treatment is to promote proper drainage of the sinus
cavities. Decongestants are usually recommended as adjuncts to antibiotics.
They may be topical nasal sprays or systemic oral decongestants
such as pseudoephedrine. Providing adequate hydration with steam
(with thyme or eucalyptus oil added) or a cool mist humidifier and
using hot and cold compresses may help to promote drainage and reduce
inflammation. Sniffing warm salted water through the nose and then
expelling it is another way to remove infectious material. Be warned—this
method can be extremely unpleasant and painful.
Chronic sinusitis
If persistent bacterial infection is thought to be the cause of
chronic sinusitis, then more aggressive antibiotic therapy may be
indicated. Intranasal steroids in the form of a spray are also prescribed
to reduce inflammation.
Occasionally, surgery is required as a last resort to widen the
nasal passages.
A variety of suggested alternative therapies are included in the
table below. Herbs and homeopathic remedies should only be used
under the guidance of a qualified practitioner. Always inform your
medical doctor when using any of these remedies.
Sources:
Beta—Leslie Hanna—March 1996
POZ Magazine—Lark Lands, PhD—9/97
Body Positive Information Room—Tony Davies
Positively Aware—Scott McCallister, MD—Jan/Feb 1995
Step Perspective—Laury McKean, RN
Antibiotics for Sinusitis
amoxicillin
TMP-SMX
clarithromycin
cephalosporin
cefuroxime axetil
cefpodoximine
iprofloxacin
clindamycin |
| Alternative
Therapies |
|
| Homepathy |
Hydrotherapy |
Herbal Medicines |
Traditional Chinese Medicine |
Chiropractic |
· arsenicum album
· kalium bichromium
· nux vomica
· mercurius iodatus
·
silicea |
· nasal flush with either salt water or one tsp. powdered
goldenseal mixed with a cup of water |
· purple coneflower
· ephedra
·
goldenseal
· Oregon grape
· horseradish
· yarrow
· garlic
· wild indigo
· elderflower
· stinging nettle
·
fenugreek |
· acupuncture
· acupressure
·
Pe Min Kan Wan (a mixture of concentrated rare herbs) |
|
Lipids and Lifestyle
By Tamil Kendall
Reprinted from Living + Magazine, Sep/Oct 2000.
A publication of the BC Persons With AIDS Society, www.bcpwa.org
Metabolic changes among HIV-positive individuals are increasingly
common. PWAs are seeking answers and alternatives to medications
to treat such changes in blood lipid levels as hypercholesteremia
(high blood cholesterol levels), hypertriglyceridemia (high blood
levels of triglycerides, a type of fat), and both conditions together,
called hyperlipidemia (high fat levels in the blood). Hardening
of arteries caused by fat deposits or fat plaques (atherosclerosis)
is a related concern. All of these conditions are risk factors for
cardiovascular disease, heart attacks, and development of diabetes.
What causes these metabolic changes is still open to debate. Protease
inhibitors have been fingered since they are known to alter levels
of blood lipids and change glucose and insulin metabolism, and also
because these conditions began to be widely discussed during the
HAART (highly active antiretroviral therapy) era. However, it is
likely that HIV itself plays a role in these metabolic changes.
Early in HIV infection, metabolism begins to alter. Lipid abnormalities
in HIV-positive individuals were evident before protease inhibitors
were used. A 1989 study of wasting revealed that people living with
HIV/AIDS had higher triglycerides than HIV-negative individuals.
Before HAART, many PWAs also showed decreased HDL (good) cholesterol
and were thought to be at increased risk of atherosclerosis. Thus,
some say that HIV is a partial cause of high blood lipid levels
and lipodystrophy.
Nevertheless, there is considerable evidence to suggest that antiretroviral
medications are contributing to metabolic changes.
Mitochondria are the "power plants" of human cells—they help
produce energy and process fat. Nucleoside analogue reverse transcriptase
inhibitors (NRTIs) may cause damage to mitochondria by interfering
with an enzyme called mitochondrial DNA polymerase gamma. Mitochondria
need this enzyme to reproduce and its inhibition can result in damaged
and fewer mitochondria available to do the work. Associated with
this condition are a host of problems, including "fatty liver" (hepatic
steatosis), which is a build-up of fat in liver cells that can affect
the way the liver functions.
Protease inhibitors, too, could possibly be interfering with two
proteins involved in fat metabolism that are structurally similar
to the HIV protease enzyme. Malfunctioning of these proteins could
lead to hyperlipidemia and insulin resistance.
There are probably numerous interrelated causes of changes in blood
lipid levels, and it will likely be a long time before the causes
are determined and definitive treatment guidelines are established.
What we do know is that lifestyle choices that have proven effective
for treating heart disease and diabetes can help prevent and manage
these metabolic changes. Diet and exercise are effective and should
be the first priority. Ask your doctor about cholesterol-lowering
drugs called statins.
If you are looking for something extra, the herbs and supplements
described below are used in a variety of complementary treatment
systems and may be helpful. However, no clinical trials proving
their effectiveness have been completed. Nor are there specific
tests for HIV-positive individuals whose metabolic changes may be
caused by antiretroviral medications.
Nutrition
While you want to avoid fat, PWAs' greater need for protein means
that instead of going on an extremely restricted diet, you should
consider switching from hamburger to a tuna sandwich (hold the mayo).
The following diet suggestions were developed especially with PWAs
in mind by Diana Peabody, RD, nutritionist at the Oak Tree Clinic
in Vancouver:
- Get more omega–3 fatty acids from fish or flaxseed. If
fresh fish is too expensive, get canned tuna or salmon in water.
If you take fish oil, make sure it is from the body of the fish,
as opposed to cod liver or halibut liver oil.
- Substitute animal protein with soy protein such as tofu.
- Choose monosaturated fats, such as olive oil, canola oil, and
flax oil.
- Increase your fiber intake with brown rice, quinoa, barley,
whole grain bread, and cereal.
- Eat lots of vegetables and more legumes like dried beans, peas,
and lentils.
- Limit simple carbohydrates like sugar, candy, sweet foods, pop,
Boost/Ensure, and, perhaps surprisingly, fruit juice!
- Avoid greasy and fried foods, such as chips and fast food restaurant
items.
- Use less saturated fat (hard fat like butter, lard, dairy fat,
and meat fat).
- Avoid "hydrogenated" oil.
Exercise
Exercising for only fifteen minutes once or twice a day helps!
Aerobic exercises such as walking, swimming, and biking, are particularly
good. If these are too strenuous, try yoga, tai chi, or qigong.
Always try to do some physical activity after a large meal.
Relax!
A controlled study (Stroke, March 2000;31), suggested transcendental
meditation, independent of diet and exercise, reduced atherosclerosis.
In this study, the thickness of the artery walls was reduced among
meditators compared to those in the control group. The researchers
estimated that the amount of reduction would make the meditators
11% less likely to have a heart attack and 7–15% less likely
to have a stroke. Other studies have demonstrated that meditation
lowers average walking (ambulatory) blood pressure among men with
normal blood pressure and increases exercise tolerance among men
with heart disease.
Cut Down on Alcohol and Cigarettes
Alcohol raises the triglyceride levels in your blood and weakens
the immune system. Smoking is a major risk factor for heart disease.
Smoking also increases oxidative stress, which may increase viral
replication and further weaken the immune system. Oxidative stress
is also a risk factor for atherosclerosis. Recently, Ohio researchers
found that HIV-positive smokers were nearly eight times more likely
to develop lung damage than smokers without HIV.
While quitting smoking is a desirable health choice, it is a difficult
one. Your doctor should provide suggestions and support to help
you quit.
- The Patch or nicotine gum can help ease withdrawal.
- In clinical trials, acupressure and acupuncture have helped
patients successfully quit smoking.
- Hypnosis, behavioral interventions, and special vitamin regimes
can also help.
- Cut down on caffeine, as it increases symptoms of tobacco withdrawal
in the first few days.
- Drink lots of water.
Vitamins and Supplements
- Studies show that Vitamin C may reduce blood lipid levels. Vitamin
E may help prevent the oxidizing or hardening of fat in the arteries.
- Lycopene, found in tomatoes, is an antioxidant. Researchers
at the University of Toronto have suggested two glasses of tomato
juice a day. The darker the fresh tomato, the more lycopene.
- Carnitine assists in transporting fat into the mitochondria.
- Niacin (Vitamin B3) reduces cholesterol. The major
side effects are burning, flushing, and itching.
Herbs and Foods
For high blood fat levels, cayenne, seaweeds, garlic, onions, mushrooms
(shitaake, maitake, and reishi), psyllium, guggilipid, fenugreek,
oats, green tea, safflower, crataegus fruit, lecithin, and ginger
may be helpful.
Guggilipid is a standardized extract from the myrrh tree that is
used in India to lower high cholesterol and high triglycerides.
It is said to work by increasing liver metabolism of LDL cholesterol
and stopping blood platelets from sticking to each other, thereby
lowering the risk for coronary artery disease. Taking guggul (the
unpurified form) has caused diarrhea, mild nausea, and restlessness.
People with inflammatory bowel syndrome, diarrhea, or liver problems
should avoid guggilipid.
In Addition:
- Traditional Chinese medicine suggests drinking tea with meals
helps disperse fat and aids digestion.
- Safflower is believed to promote circulation, reduce blood lipids,
and break up blood clots.
- Crataegus fruits (shanza or Chinese hawthorn) are thought to
eliminate accumulations, promote energy flow, and disperse coagulations.
Crataegus is said to activate the blood, bring down blood pressure,
aid digestion, treat "fatty liver," and reduce lipid levels in
the blood. Do not take it with digoxin.
- Lecithin granules may help protect liver cells and move fat
from the liver and decrease cholesterol. Take one teaspoon three
times a day.
- Ginger may be good for getting rid of bad fat as well as for
treating nausea. A recent experiment with mice showed that dietary
consumption of ginger resulted in reductions in plasma triglycerides
and LDL (bad cholesterol).
Remarks of Michael
Callen to the New York Congressional Delegation, 1983
By Michael Callen (1955–1993)
Twenty years ago this summer, the first published reports appeared
about a strange, new disease affecting homosexuals living in America's
largest cities. Later in 1981, Michael Callen, a young gay man living
in New York, was diagnosed with the immune disorder that would eventually
be known as AIDS. Despite intense fear and stigma swirling around
the disease, Callen began speaking out about his experience as a
person with AIDS. He was a founder of the PWA empowerment movement
and a co-author of "How to Have Sex in an Epidemic," the first public
health pamphlet to distinguish between safe and unsafe sex practices
based on risk of infection.
In May of 1983, Callen spoke to a breakfast meeting of New York
congressmen and women. While some of the irrationality of the time
has passed — William F. Buckley no longer suggests tattooing
AIDS carriers — many of the issues Callen spoke of discussing
with his friends sound familiar:
"We talk about how we're going to buy food and pay rent when
our savings run out."
"We talk about the pain we feel when our lovers leave us out
of fear of AIDS."
"We compare doctors and treatments and hospitals."
Conditions for most people with HIV in the US have improved
considerably over 20 years. That said, there is still no cure and
no vaccine, even as young people continue to become infected at
an alarming rate. Meanwhile, in other parts of the world, fear,
stigma, and lack of treatments threaten to make the worst days of
the epidemic at home seem almost benign.
In 2001, one discussion among people with AIDS continues everywhere:
"What we talk about is survival."
I am a gay man with AIDS and I have been asked to speak to you
this morning to personalize the tragedy of AIDS. I will attempt
to do this, but since what brings us together is the fact that you
are politicians, I will also try to explain how the political context
surrounding AIDS inevitably becomes part of the experience of each
AIDS patient.
Each person's experience with AIDS is different. I can only tell
you my story.
I was diagnosed with AIDS in December, 1981, although I believe
I was immune depressed for over a year before.
I have been hospitalized twice since then and continue to have
my health monitored by my physician and by a number of privately
funded research projects.
Although I believe I will beat this disease, I am continually confronted
by media reports telling me that no one has recovered from this
syndrome, and that my chances of living past 1984 are poor. Figures
provided by the Centers for Disease Control indicate that 80 percent
of those diagnosed when I was are now dead.
My life has become totally controlled by AIDS and my fight to recover.
I begin each day by checking my body for Kaposi's sarcoma lesions
and other signs of serious health complications. I am subject to
fevers and night sweats and an almost unendurable fatigue. I live
with the fear that every cold or sore throat or skin rash may be
a sign of something more serious.
At age 28, I wake up every morning to face the very real possibility
of my own death.
I am a member of a support group for AIDS patients which meets
once a week in the cramped offices of the National Gay Task Force.
In addition, in August of 1982, I formed a support group of gay
men who have been diagnosed with AIDS. Because we have no community
service center or other space in which to meet, the support group
I formed meets in my living room.
Whatever I am asked by members of the media or by curious healthy
people what we talk about in our groups, I am struck by the intractable
gulf that exists between the sick and the well. What we talk about
is survival.
We talk about how we're going to buy food and pay rent when our
savings run out.
We talk about how we are going to earn enough money to live when
some of us are too sick to work.
We talk about how it feels to get fired from our jobs because of
unjustified fears of raging and lethal contagion — fears based
on ignorance and unfounded speculation — fears which are being
fanned by the Centers for Disease Control's endorsement of the view
that we may be carrying and spreading a lethal, cancer-causing virus
— fears that AIDS may be spread by casual, non-sexual contact
which are being spread by men like Dr. Anthony Fauci of the National
Institutes of Health.
We talk about the pain we feel when our lovers leave us out of
fear of AIDS.
We talk about the friends who have stopped calling.
We talk about what it feels like when our families refuse to visit
us in the hospital because they are afraid of catching that "gay
cancer."
We talk about what it feels like to be kept away from our nieces
and nephews and the children of our friends because our own brothers
and sisters and friends are afraid we'll infect their children with
some mysterious, new, killer virus.
We compare doctors and treatments and hospitals.
We share our sense of isolation: how it feels to watch doctors
and nurses come and go wearing gowns, gloves and masks.
We share our anger that there are doctors and health care workers
who refuse to treat AIDS patients.
We share our tremendous sense of frustration and desperation at
being denied treatments such as plasmapheresis because many hospitals
fear that our blood may "contaminate" the machines.
We share our fears about quarantine — the rumors that separate
wards are being created to isolate us from other patients —
rumors that certain hospital workers' unions have threatened to
strike if forced to treat AIDS patients or wash their laundry —
rumors that closed hospitals are being readied for the quarantine
of AIDS patients and maybe even healthy members of at-risk groups.
We talk about our fears that the personal data we have volunteered
to the CDC to help solve the mystery of AIDS may be used against
us in the future. We are asked if we have had sex with animals.
We are asked to detail sexual practices which are illegal in a number
of states. We are asked to admit to the use of illegal drugs. The
answers to these questions are stored in government computers. We
are asked for trust that the confidentiality of this information
is being safeguarded — only to find out that the CDC has already
made available its list of AIDS patients to The New York Blood Center.
We wonder who else has seen this information.
Mostly we talk about what it feels like to be treated like lepers
— treated as if we are morally, if not literally, contagious.
We try to share what hope there is and to help each other live
our lives one day at a time.
What we talk about is survival.
AIDS patients suffer in two basic ways. We suffer from a life-threatening
illness, and we suffer the stigma attached to being diagnosed with
AIDS.
The end to both aspects of this suffering depends on finding the
cause(s) and cure(s) for AIDS. And that can only happen if research
money is released in amounts proportional to the seriousness of
this health emergency. In order to confront and challenge the ignorance
and insensitivity which we, as AIDS patients, must face on a daily
basis, we need answers to the pressing questions of cause, cure
and contagion.
The political context in which AIDS is occurring cannot be ignored.
AIDS is affecting groups that remain disenfranchised segments of
American society: homosexual men, heroin abusers, Haitian immigrants
and hemophiliacs. This so-called 4-H club has been joined by prisoners
(most of whom are either Hispanic, IV drug abusers or both); female
prostitutes; and the children of high risk groups who are also victims
of poverty.
Despite the fact that in the four years since AIDS was first recognized,
AIDS has killed more people than swine flu, toxic shock syndrome,
Legionnaires disease and the Tylenol incident combined, the response
of the federal government to AIDS — the worst epidemic since
polio — has been to ignore it and hope it just goes away. If
such a deadly disease were affecting more privileged members of
American society, there can be no doubt that the government's response
would have been immediate.
As a gay man, I could never decide whether I should be pleased
with how far the gay rights movement has come since 1969 or whether
I should be disgusted and angered at how far we have to go.
The government's non-response to the AIDS crisis has answered this
question for me.
I was raised as a small-town boy from Ohio: white, male and middle
class. As a gay man, the pain I suffered from prejudice was largely
emotional—not for the most part economic. So my political response
was modified by patience. On the whole, I believed in democracy.
I believed in America.
I felt it would only be a matter of time before education and the
destigmatization of gayness would bring me my rights.
But now I am fighting for my life. I am facing a life and death
crisis that only the resources of the federal government can end,
and I am shocked to find how naive I've been.
Not only is my government unwilling to grant my right to love whom
I choose — my right to be free from job discrimination —
my right to the housing and public accommodation of my choosing.
This same government—my government—does not appear to
care whether I live or die.
Prejudice and oppression are words often bandied about too freely.
But the tragedy of AIDS has made many gay men take a new look at
the situation of America's other disenfranchised groups. We are
beginning to see that homophobia and racism are not, as some of
us thought, totally unrelated. We are beginning to see that America's
fear and ignorance of homosexuals and its hate and bigotry toward
black and brown people are not just co-incidental. We are beginning
to see that a Haitian infant dying in poverty in the South Bronx
and the death of a white, middle class gay man in Manhattan are
sadly, but undeniably, interconnected.
These are the politics of AIDS. When the history of this country's
response to this health crisis is written, it will stand as yet
another appalling example of America's apathy, indifference and
inaction.
History teaches that such prejudice and bigotry ultimately poison
the whole society—not just those at whom it is directed. If
the personal suffering of human beings is not enough to motivate
you to fight for increased AIDS funding, let me offer you another
way to justify to your constituents the release of federal research
funds.
Newsweek recently called AIDS "the medical mystery of the century"
Solving this mystery will surely benefit all Americans — indeed
all humankind. Finding the cause of AIDS may well hold the key to
cancer — maybe to all disease.
Do not allow the shortsightedness of prejudice to delay us any
longer from discovering how the immune system defends us from disease.
Whatever you and your colleagues do or don't do, whatever sums
are or are not allocated, whatever the future holds in store for
me and the hundreds of other men, women and children whose lives
will be irrevocably changed — perhaps tragically ended —
by this epidemic, the fact that the Congress of the United States
did so little for so long will remain a sad and telling commentary
on this country and this time.
I do not envy you your role in this matter any more than you must
envy mine. 1983 is a very bad year to be an elected official, just
as it is a very bad year to be a gay man, a Haitian entrant or a
child living in poverty. And surely when you first dreamed of holding
public office you did not, in the furthest reaches of your imagination,
foresee that your duties would include having breakfast on a Monday
morning with a homosexual facing a life-threatening illness. You
can be sure that ten years–five years–or even one year
ago, I could not have imagined the possibility that I, too, would
be up here begging my elected representatives to help me save my
life. But there you are. Here I am. And that is exactly what I am
doing.
Thank you.
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