gilbert@tce.COM (Gilbert Cornilliet) (02/27/91)
==============================================================================
HISTORY IN THE MAKING: MACS AT YEAR SEVEN
by Michael S. Gottlieb, M.D. and Sheila Hutman
In 1983, shortly before the human immunodeficiency virus had been identified
as the cause of AIDS, Richard Kaslow, M.D. of the National Institute of
Allergy and Infectious Diseases (NIAID) encouraged the Institute to initiate
a study of the natural history of AIDS in homosexual men at four universities
in Baltimore, Pittsburgh, Los Angeles, and Chicago. The National Cancer
Institute (NCI) provided additional support for the Multi-Center AIDS Cohort
Study (MACS) in an effort to further the study of AIDS-related malignancies
among homosexual men. In the process of designing the study, researchers at
the four sites, working closely with project officers at the NIAID and NCI,
agreed that collaborating would enable them to collect both more and better
quality information about the new disease.
The principal investigators at the four centers, John Phair, M.D. of the
Northwestern School of Medicine in Chicago and the Howard Brown Clinic, B.
Frank Polk, M.D. of the Johns Hopkins School of Hygiene and Public Health in
Baltimore, Charles Rinaldo, M.D. of the University of Pittsburgh School of
Public Health, and Roger Detels, M.D. of the UCLA School of Public Health
became partners in the Multicenter AIDS Cohort Study (MACS), the largest
project of its kind in the world. Subsequently, Alvaro Munoz, Ph.D. of the
Johns Hopkins School of Hygiene and Public Health joined them as head of the
Data Coordinating Center for the study. Tragically, Dr. Polk died at age 45
of a brain tumor in 1988. His colleague, Alfred Saah, M.D. has taken over as
the Principal Investigator for the Johns Hopkins center. Dr. Kaslow continues
to be actively involved in the study.
Between April 1984 and March 1985, 4,954 sexually active homosexual and
bisexual men between the ages of 18 and 68 who did not have AIDS were
enrolled in the study. The prospective follow-up which this cohort receives
consists of semiannual visits to the medical centers for interviews, physical
exams, and laboratory evaluations. More frequent telephone or mail contact
has been maintained with the men in the cohort who have developed AIDS. Of
the 661 who have progressed to full-blown AIDS, close to 70% have died.
Eighty-seven percent of the original participants 4,293 men do not have
AIDS. Of these, about 1,524 are currently seropositive and 2,769 are
seronegative. Approximately 77% of those who are well were seen in 1990 for
their 11th and 12th follow-up visits. Compliance with the demands of the
project has remained excellent.
The time and energy that this incredible group of volunteers has committed to
the study for no remuneration is truly remarkable and has rarely, if ever,
been witnessed before. Dr. Rinaldo pointed out that these men have been
subjected to extensive physical examinations and detailed interrogations
about their personal lives, and required to donate multiple tubes of blood
twice a year since 1984. "Although some are HIV negative or HIV positive and
asymptomatic, others are infected and getting sicker along the way. Still,
they remain dedicated to helping us better define the natural history of HIV,
the mechanisms underlying the disease process, and the variations in
progression in different individuals. They know that the more we learn, the
sooner we will be able to develop therapeutic and vaccine protocols and to
apply them appropriately," Dr. Rinaldo said.
MAJOR CONTRIBUTIONS
The Multi-Center AIDS Cohort Study has produced some of the most important
information we have about HIV infection. Dr. Detels believes that the cohort
feature of the project has been invaluable. "It has enabled us to follow the
natural history of HIV infection as the disease evolves. Moreover, since some
of the participants became infected after they entered the study, we are able
to document the course of their disease from beginning to end," Dr. Detels
said.
One important reason for the creation of the study was NIAID interest in
establishing a National AIDS Biological Specimens Repository, according to
Lewis Schrager, M.D., NIAID Project Officer for the MACS. Originally, the
MACS stored blood, semen, and urine samples for eventual use in identifying
the infectious agent for which basic scientists were looking. Following the
announcement of the discovery of HIV in 1984, these samples became important
in finding the answers to questions such as: At what stage of disease is the
virus most prevalent in the blood? Do certain markers of immune system
activation correlate with the progression of HIV-induced disease?
The establishment of this repository has allowed the investigators to look
for new information in the first samples taken. "After the HIV antibody test
became available, we had to go back to see who was infected," Dr. Detels
said. The tests showed that 1,809 (36.5%) of the men had been seropositive
for HIV-1 at the time of their enrollment, and 3,145 were seronegative at
entry. As of October 1990, 376 (12%) had seroconverted.
When it became clear that HIV disease was caused by an infectious agent, the
MACS investigators set out to learn how that agent was transmitted. Seeking
to identify risk factors responsible for the occurrence and clinical
expression of HIV infection, an early MACS study looked at the demographics,
lifestyles, sexual practices, recreational drug habits, and medical histories
of the participants. Investigators found that the factor most strongly
associated with prevalent HIV infection was receptive anal intercourse.
Rectal trauma also was found to play a role. This included reports of
receptive fisting, enemas, or blood around the rectum, and the observation of
scarring, fissures, or fistulas on rectal examination.
"As soon as we knew the major route of transmission among homosexual men, we
could provide practical information to the gay community on how to stop the
spread of HIV," Dr. Detels said. A MACS study confirmed that the highest rate
of seroconversion occurred among men who reported practicing both receptive
and insertive anal-genital intercourse. Two hundred thirty-two men (8%)
became HIV+ during the course of this study. When each of these groups was
compared with individuals who did not practice anal intercourse, the risk of
infection was 76 times higher among participants who reported practicing both
receptive and insertive intercourse, 36 times higher among those practicing
receptive intercourse only, and 10 times higher among those practicing
insertive intercourse only. This study, published in 1989, also demonstrated
clearly that (1) condoms provided significant but not complete protection
against infection; (2) among homosexual men, infection may rarely occur
through sexual activities other than anal-genital intercourse; and (3) the
number of men in the study engaging in high-risk behavior is declining.
During its first four years, the MACS documented the natural history of HIV
infection prior to therapeutic interventions. Today, most participants who
are symptomatic or have a CD4 count below 500 are receiving medications to
counter HIV or its infectious sequelae. Thus, it is no longer possible to
study the "natural" evolution of HIV.
Now the MACS is looking at disease in men on various treatment schedules. "It
is more difficult to know if we are seeing disease mechanisms or drug
results," Dr. Detels observed. "But we have the advantage of being able to
study a broader spectrum of individuals than investigators engaged in
clinical trials do. We know the biologic history of HIV in our subjects and
how quickly or slowly they are developing disease. Aware of the factors that
lead to the stage of disease in which they are, we know how long they have
been infected and how their immune systems have changed over time. Clinical
trial investigators recruit patients who are further along in the course of
disease; therefore, they don't know the complete natural history of disease
in their participants."
High on the MACS agenda is another crucial issue related to the development
of HIV disease: What portion of HIV+ people will become symptomatic? We know
that the shortest incubation period for HIV is one year; the average is 10
years, and some infected individuals remain asymptomatic for as long as 10-15
years. This wide range suggests that other factors may determine when and if
an individual will develop disease. Much effort is now being devoted to
attempts to discover what is going on during the disease-free time and to
identify factors that may enhance or inhibit progression of infection. Other
viruses as well as genetic susceptibility have been proposed as possible
co-factors.
The MACS also is searching for easier ways to predict the likelihood of
disease. Assays of CD4+ T cell levels, the most reliable parameter of immune
deficiency, are expensive and difficult to administer. "We're looking at
other biochemical factors that may help physicians monitor the course of
disease," Dr. Detels said. Tracking viral progression is important because
treating a patient before he or she becomes symptomatic may delay the onset
of active disease. Other factors that provide predictive information as
markers of immune activity may also indicate the course of pathological
changes. "In one of our recent studies, we conclude that serum levels of
neopterin, beta2-microglobulin, or IGA also can be used to provide predictive
information. Because they are cheaper and easier to use than the measurement
of CD4+ cells, they may be useful for physicians who want to follow the
course of infection in their patients," Dr. Detels said.
A major emphasis of the Pittsburgh group is research on the
immunopathogenesis of HIV infection. They are seeking to find out how the
virus may mutate over time and alter its genetic characteristics, thereby
preventing the immune response from keeping it in check. As the virus
overwhelms the immune system, the infected individual develops AIDS. "The
answers to these questions could have profound implications on the natural
history of the virus and on developing treatment and vaccine protocols," Dr.
Rinaldo said. A significant contribution from the Chicago MACS resulted from
a collaborative effort with investigators from the University of Michigan
headed by Jill Joseph, M.D. The study looked at the coping strategies used by
gay men in dealing with the epidemic. It culminated in a productive
evaluation of psychological stresses and their impact upon behavioral changes
within the Chicago cohort.
THE MULTI-FACETED NATURE OF THE MACS
Dr. Rinaldo expressed it eloquently when he said, "The texture, the fabric of
each center is different from that of the others." Variation occurs not only
in the research interests of the investigators, but also in the
characteristics of the cohort population at each site. In Chicago, for
example, participants were recruited primarily from the Howard Brown Memorial
Clinic which was established by the gay community to meet the health needs of
gay men in the mid '70s. "We owe the tremendous cooperation of the Chicago
cohort to the clinic," said Dr. Phair.
Pittsburgh was the only MACS site where AIDS had not reached epidemic
proportions by 1984. All four centers have worked closely with their
respective gay communities, but the Pittsburgh investigators had to begin by
building a cohesive community. They helped expand the existing gay
organizations, develop a local AIDS task force, and strengthen the health
care delivery system, reported Dr. Rinaldo. "We didn't want to be seen as
unsympathetic academicians, divorced from the people, using them for our own
scientific purposes. We succeeded in winning their trust by making it clear
that we really wanted to help them."
In Los Angeles, the gay community was very supportive and gays were eager to
participate in the study. In Pittsburgh, few gays perceived themselves as at
risk for HIV infection. MACS researchers there had to develop "unorthodox"
recruitment techniques. The most successful of these were "road shows" that
involved recruiting participants at health clubs or at gay bars in the wee
hours of the morning.
Even after enrollment was complete, Pittsburgh investigators had to stay on
their toes to maintain participation in the study.
For the next round of follow-ups, they plan to offer cholesterol testing to
their cohort because (1) there seems to be increased incidence of heart
disease in people who are HIV+, and (2) the subjects are reaching ages which
place them at risk for chronic diseases.
The diverse backgrounds of the investigators contribute to the
multi-disciplinary nature and the varied approaches of some of the studies.
Not surprisingly, disagreement is common among this group, but the
researchers emerge from each battle over protocol and data interpretation the
richer for it. "We learn from each other," Dr. Detels said. "New hypotheses,
new studies, and a sharper focus come from our encounters. I stand in awe,
watching ideas bombard us from every direction and finally coalesce into a
real study. Each of us wants the research to be the best you can get."
Perhaps it is this common goal that keeps the leaders together and friends.
Working along with the P.I.'s are an exceptional group of researchers with
specialities in immunology, virology, and molecular biology. In addition to
these traditional areas of biomedical research, the MACS has begun to address
issues concerning health services utilization by HIV-infected individuals.
Dr. Schrager is pleased that this is one of many new directions the MACS is
taking. "It offers one more way of taking advantage of what the study offers
us. By asking a few more questions, we can acquire a tremendous new set of
data that may be very important for health policy formulation," he said.
Detels laughed as he thought back to a 1982 study in which he invited UCLA
students to have their immune status tested and to report their prior sexual
activities. The entire project cost less than $1000. The MACS which grew out
of that and similar pilot projects is now a $70 million program, funded at
least until September 1991. The P.I.s are now applying for a 4-year
extension.
"We couldn't do this without good people," Roger Detels admitted. He is
convinced that the success of the MACS is due in particular to the
extraordinary men who are meeting the demands of the project in an effort to
help others; to the dedicated staff who are implementing the research; and to
the investigators who are stretching their capabilities to incredible heights
in creating and directing the studies.
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PRACTICAL APPLICATIONS OF NUTRITION
by Brian Smith, D. C.
This is an actual case history of a patient who is currently under my care. I
use this case to illustrate the use of nutrition in the management of HIV
infections. This case is specific for the individual involved, and this
article should not be construed as a recommendation of treatment for anyone
other than the individual involved.
A 28 year old female presented herself to this office requesting nutritional
guidance. She had been referred by a colleague. The patient is in her first
trimester of pregnancy. She relates that she has been HIV positive since
November 1987. She has taken no specific course of action since that time.
She has decided to have this child and is seeking nutritional counseling. She
further stated her desire to refrain from any prescription drug use.
Her health history is remarkable for cervical dysplasia in 1987 and 1988,
pneumonia, and a history of "cold sores." Her family health history
demonstrates a tendency to cancer on the maternal side.
Physical examination revealed a well-nourished female, 55.5 inches in height,
weighing 119.5 lbs. Her reclining blood pressure was 106/76. Review of
previous medical records demonstrated a low red blood count (3.96, normal is
4.8+/-0.6), high sedimentation rate and low lymphocyte count. Urinary PH was
low at 3.5. A hair analysis showed extremely high levels of copper in her
hair. No T-cell subsets had been performed.
New lab work demonstrated a mildly elevated serum copper, depressed red blood
counts, hemoglobin and hematocrit. Her platelet count was low at 142,000. Her
T-cell subsets demonstrated a T-4 count of 305 and a T-8 of 729 and a low
ratio of 0.4. Her P-24 antigen was negative and the Beta-2-M was within the
normal range at 2.1 mg/1.
She was advised on a nutritional approach incorporating a high protein, low
fat moderate carbohydrate diet and a regimen of nutritional therapeutic
substances to counteract the anemia, the adrenal insufficiency (as evidenced
by the fall in blood pressure when assuming an erect posture plus subjective
complaints) and to bolster the immune system. This included a good multiple
vitamin/mineral complex, vitamin C, DMG, certain B vitamins, chromium and a
product used to bolster her immunity to a number of pathogens. It was
recommended she maintain visits to her chiropractic doctor who utilized a
variety of techniques, adjustive and reflex, to assist her. She was also
under the care of an ob/gyn who is knowledgeable in homeopathics.
After one month, the patient complained of severe headaches. She was referred
to a neurologist for evaluation. This doctor was not sympathetic to the
patient and quickly alienated her by his pronouncements that she was inept
and she should seek medical consultation and refrain from what she was doing.
The patient was angered by this attitude. A report from the neurologist was
no help in that the appropriate laboratory tests were not ordered. I ordered
tests for toxoplasmosis and cryptococcus which came back negative for recent
infections. We decided to continue with conservative care and her headaches
soon abated.
Follow up laboratory work showed a worsening in the platelet count, first to
63,000 (normal 150,000 to 450,000), then to 39,000 within 2 weeks. Other lab
work showed continued anemia and slightly elevated liver enzymes. A
nutritional protocol for low platelets was immediately started. This
consisted of beta-carotene, germanium, liver, supportive complexes, sesame
seed oil and the amino acid methionine. She was referred to a hematologist
for a complete work up. Within two weeks her platelet count had risen to
60,000. The hematologist recommended a continued course of conservative care
and voiced his hesitancy of the use of AZT. A bone marrow biopsy revealed the
low platelet count is due to a peripheral destruction problem. A trial of
gamma-globulin was done to assure us that the patient will not have an
adverse reaction if this is again needed as her delivery date approaches. Her
platelet count rose to 139,000 and we will monitor it continuously.
Her T-cell subsets have remained at approximately the same levels and she has
experienced no health concerns other than the ones listed above. She reports
feeling great and is anxious to have her child. She has gained over 20 lbs.,
her blood pressures have normalized in their response to assuming an erect
position and the baby is quite active. We will continue to monitor her other
laboratory abnormalities and focus on them now that the low platelet count
has been successfully handled.
This case presents many questions that require extensive thought. Will the
child be HIV+? Statistics show that there is 30 to 50% chance a child will
be. The study groups however are slanted in that these mothers are, for the
majority, IV drug users, they have poor nutrition and usually are in an
environment not generally supportive. Intrauterine infection does not appear
likely as research shows that the umbilical cords are usually negative for
infection markers. This question has been on the mind of this patient
constantly. It has been decided by her and her husband to have this child.
She wants to breast feed the child. Are there problems with this? All the
evidence isn't yet in on this question. Breast feeding does pose a problem in
that the virus has been found in mothers' milk. We are currently looking into
options such as pasteurization or freezing of her milk to inactivate the
virus.
This case demonstrates the use of nutritional therapeutics in an especially
difficult case. Fetal and maternal nutrition are serious concerns. Add to
this an HIV infection and we have a very complicated picture. This case also
points out the necessity to use health care professionals that are
knowledgeable in HIV infections and that are not closed-minded. Make sure
that all the people you consult with are accustomed to treating persons with
HIV infections.
(Dr. Brian A. Smith is a chiropractor who has been involved with the care of
HIV+ individuals since beginning practice here in 1987. He can be reached at
213.559.6584 for consultation.)
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CLARITHROMYCIN: A BATTLE FOR TIME
by Jim Corti
Like Pentamidine's offering major resolution to PCP, Clarithromycin seems to
be of significant help in resolving MAI. Doctors ranging from those having
the aggressive qualities of Robbie Jenkins to those with the solid
conservatism of physicians at USC and UCLA are using the American developed
but European distributed antibiotic for successful treatment of Mycobacterium
avium.
Studies in Paris have demonstrated efficacy with clarithromycin (trade name
Klacid) where the traditional drugs are, for the most part, a failure against
MAI. There is strong evidence of overwhelming success by physicians using the
drug after importation for compassionate use by individual patients in this
country.
My purpose in writing is not to advocate or promote Klacid; its performance
speaks for itself. Rather, it is to stress the need for rapid, emergency
measures to be taken for this drug to be provided by third party players,
i.e. insurance companies, institutions, governmental systems. The drug is
expensive, but not nearly expensive as the traditional regimen. The use of
clarithromycin would result in tremendous savings for third party providers.
And that is usually the bottom line in determining who gets what and where
they can get it.
Trials are just now scheduled to begin with the NIH. This could mean forever
on this drug if it gets lost in some black hole in Bethesda. There is some
potential for the drug to be approved for pediatric inner ear infections,
resulting in possible early access via that route, but it's still a long
shot. There is certainly a growing group of people who are very vocal on
their success with the drug. I believe that it is incumbent on the membership
and leadership of organizations like Being Alive and Project Inform to hammer
on this particular issue.
We seem to have a winner. This is not some obscure high tech semi-promise.
This issue needs to be resolved as quickly as possible and the drug put into
the hands of the sick people whose lives could be given better quality and
the one thing we all ask for, time! This cannot be kept as a rich person's
medicine imported for the few who can afford the price. Political action has
to be taken, Gulf War be damned. Push and call for action, now!
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EARLY CARE FOR HIV DISEASE
Early Care for HIV Disease is a guide to help individuals at early stages of
HIV infection maintain or improve their physical and psychological health.
There are chapters on treatment for HIV infection, diet and nutrition, paying
for medical care, clinical trials and psychological coping. The book also
features an extensive resource section for further contacts and more
specialized reading, as well as a glossary of medical terms. Dr. Mathilde
Krim of AmFAR has written an eloquent forward to the book that addresses the
many people who do not yet know if they are infected with HIV.
To find out more about the book and how to obtain a copy, call the San
Francisco AIDS Foundation Hotline at 415.863.AIDS.
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EPO APPROVED!
The FDA approved a license for Procrit, a synthetic form of erythropoietin
(EPO), which significantly reduces anemia in people treated with AZT. A
protein formed in the kidneys, EPO stimulates the production of red blood
cells. EPO had already been licensed for patients with kidney failure and is
marketed by Amgen, a pharmaceutical company, as a product called Epogen.
Another company, Ortho Biotech, conducted trials of their version of EPO in
people with AIDS. While these trials progressed, Ortho provided free EPO
though a treatment-IND program. Now Ortho's drug, with the market name
Procrit, has been licensed for anemia in HIV-infected patients.
Procrit is an extremely expensive drug; one dose (7000 units) will cost about
$70. Patients typically need three doses a week and Ortho speculates that the
annual cost will be from $6000-8500. Ortho says that no one will pay more
than $8500 a year, no matter how much drug they need. The company will
provide the drug free of charge to people without insurance if their annual
income is under $25,000. When a company spokesperson was informed that the
AIDS Drug Assistance Program provides certain drugs free to people whose
income is below $44,000, she replied, "I'll check into that." Let's hope so.
For more information about Procrit, call 1.800.523.7739. For more information
about indigent patient programs, call 1.800.553.3851.
reprinted from GMHC Treatment Issues, January 10, 1991.
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HOW PROTEASE INHIBITORS WORK
by Michael S. Gottlieb, MD
We expect that a new class of drugs will become available in 1991. These are
called protease inhibitors. How do they work? When a virus reproduces, it has
to make new proteins. Proteins start out like strings of beads and, in this
case, the beads are substances called amino acids. It turns out that HIV is
not very efficient with respect to making proteins. It makes the strings of
beads too long and then later cuts the string to the right length, using a
scissors. In this case, the scissors is an enzyme called protease. If these
strings of beads are left too long, the virus simply cannot use them.
Several companies have developed drugs which are inhibitors of the scissors,
inhibitors of the protease enzyme. These drugs clearly work in the test tube.
At least two companies, Hoffman LaRoche and Merck, have developed these drugs
and have begun Phase I toxicity testing in Europe. We should expect results
of these studies in the early part of 1991 and this will probably be a hot
topic at the VII International Conference on AIDS set for June in Florence,
Italy. In the meantime, keep your ears open for the latest developments on
these compounds.
Other drugs of interest are the TIBO drugs developed in Belgium. These drugs
also work against the virus in the test tube by a mechanism completely
different from AZT and its cousins, and completely different from the
protease inhibitors. Phase I trials of these drugs are also in progress in
Europe.
A good question is why these new drugs are being studied in Europe, rather
than in the United States. It is anybody's guess, but mine is that drug
companies are worried about possible interference in their drug development
programs by AIDS activists. The AIDS response movement is far less developed
in Europe and the companies can study drugs, at least initially, in a
relative political vacuum. This is unfortunate and perhaps is a situation
which can be corrected with some dialogue between the activists and the
pharmaceutical industry.
(Michael S. Gottlieb, MD, specializes in HIV patient care in his private
practice and is the Medical Director of the Immune Suppressed Unit at Sherman
Oaks Community Hospital. He can be reached at 818.501.2600.)
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COMMON SKIN DISEASES IN HIV INFECTION
by Alan Cantwell, Jr., MD
Troublesome skin conditions often accompany HIV infection. In fact, skin
disease may be one of the earliest signs of possible HIV infection. As
progressive immune system damage occurs, skin diseases become more frequent
and persistent, and more resistant to treatment.
In this article, I will discuss the most common HIV-associated skin diseases.
However, it is important to note that all of these conditions can appear in
people who are not HIV-positive. HIV infection is determined by blood
testing, never by skin analysis.
Skin opportunistic infections due to viruses, bacteria, yeast and fungi, may
appear during the course of HIV-infection. Viral-caused warts, especially
perianal warts can be annoying. Fortunately, most anal warts respond to
painless treatment with podophyllin applications. Anal wart sufferers should
use plenty of baby powder to keep the area dry. Anal sex aggravates the
condition, and increases the risk of contagion to sex partners.
Viral-caused Molluscum Contagiosum are persistent and asymptomatic
pimple-like papules usually found on the face, chest, and groin. A physician
can treat the lesions by pricking them open and removing the core of virus
material.
Viral herpes simplex infections (better known as "cold sore blisters") are
most often found on the lips, the genitals, and the perianal area. Treatment
with acyclovir (Zovirax) ointment is specific. Severe, recurrent Herpes
simplex infection can be treated with oral acyclovir.
Herpes Zoster ("shingles") is another viral blistering condition which occurs
suddenly in a localized body area, such as a cheek, one arm, or one side of
the trunk. The herpes zoster virus actually attacks the physical nerves, as
well as the skin. Shingles can be painful and treatment by a physician is
essential. The condition lasts 4-6 weeks, and many patients require
disability and bed rest.
Fungus-caused "Athletes foot" and "Jock itch" are very common. The toe and
fingernails may also become infected. In severe cases the fungus can be
treated with an oral antifungal antibiotic, such as griseofulvin. Yeast skin
infections are less common, but may appear in moist areas, such as the groin
and perianal area, the armpits and the mouth. There are various prescription
creams that are curative.
Dry, itchy skin can be a problem for persons with ARC and AIDS. I advise less
frequent bathing, less soap, warm showers rather than hot, plenty of sleep
and stress reduction. Skin lotions and creams such as Lubriderm, Vaseline
Intensive Care, Eucerin, or similar products, should be applied as needed.
A "Dandruff" rash known as Seborrheic Dermatitis affects the scalp, behind
the ears, the forehead and eyebrow area, the perianal area, and sometimes the
chest and groin. Treatment consists of mild cortisone creams. Stress and poor
sleep habits are often at the root of stubborn cases.
Occasionally an AIDS patient will complain of a chronic, intensely itchy rash
that affects the whole body. This type of rash may be caused or aggravated by
the drugs prescribed for HIV infection. There is also the possibility that
the rash may be directly due to the toxic effects of HIV. At any rate, this
frustrating and difficult to treat condition (usually diagnosed as
"non-specific dermatitis") often requires management by a dermatologist.
No discussion of HIV-associated skin disease would be complete without
mention of Kaposi's sarcoma (KS). KS is the most dreaded skin disease
because, by definition, a KS diagnosis means AIDS. To the untrained eye,
there are various red and purple lesions which can resemble KS. Thus, a skin
biopsy should be done to confirm a suspected KS diagnosis.
KS sometimes appears as the earliest sign of AIDS. Not infrequently the
patient feels perfectly healthy. A KS diagnosis in such a patient can be
devastating psychologically, as well as physiologically.
How should KS be treated? The treatment of KS is controversial, especially
when the person is healthy and when the lesions are few in number. In
considering KS treatment options, there are some points worth discussing.
First of all, there is no cure for KS at this time. Secondly, some physicians
are now eager to start treatment early in the disease, when only a few
lesions are present. Other physicians may recommend no treatment at all when
lesions are few in number.
Patients with few, small skin KS lesions can have them "burned off." Larger
lesions can be radiated. Other treatment options are interferon injections
and chemotherapy, especially when the lesions are rapidly increasing in
number. As mentioned, neither interferon nor chemotherapy are curative. Some
people cannot tolerate treatment with interferon due to the side effects.
Chemotherapy for KS can be dangerous because it can result in further damage
to the immune system, resulting in serious and life-threatening opportunistic
infections. If internal lesions of KS develop, chemotherapy may be the only
treatment choice.
It should be noted that AZT does not necessarily prevent the development of
KS. Interestingly, my longest surviving AIDS patient is a Black man with
extensive KS lesions of the legs for over 5 1/2 years. He has never had AZT,
interferon, or chemotherapy, although he has received some local radiation to
some lesions. He claims that stress definitely aggravates his KS lesions, and
he works hard to minimize it in his life.
The cause of KS is not known. My own published research indicates that
cell-wall bacteria are the infectious agent causing this disease. Because
there is no current antibiotic to eradicate these microbes, the only body
defense against KS is the immune system. Thus, KS patients should be wary of
any therapy that further damages their immune system. Most AIDS patients do
not die from KS, but rather from opportunistic infections of more serious
nature.
Most HIV-positive individuals will not experience difficult skin problems.
With the exception of KS, there is beneficial treatment available for most of
the common HIV-associated skin diseases.
(Dr. Cantwell is an HMO-based dermatologist who has practiced in Hollywood
for over 25 years. He is the author of AIDS: the Mystery and the Solution,
AIDS and the Doctors of Death, and The Cancer Microbe. Inquiries concerning
his AIDS and cancer research and writings can be directed to: Aries Rising
Press, P.O. Box 29532, Los Angeles, CA 90029.)
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End of Being Alive Newsletter (February 1991 part 2/2)turner@lance.tis.llnl.gov (Michael Turner) (03/02/91)
In article <1991Mar1.103442.26897@cs.ucla.edu> gilbert@tce.COM (Gilbert Cornilliet) writes: > >COMMON SKIN DISEASES IN HIV INFECTION >by Alan Cantwell, Jr., MD > >[extensive deletion] >No discussion of HIV-associated skin disease would be complete without >mention of Kaposi's sarcoma (KS). KS is the most dreaded skin disease >because, by definition, a KS diagnosis means AIDS. To the untrained eye, >there are various red and purple lesions which can resemble KS. Thus, a skin >biopsy should be done to confirm a suspected KS diagnosis. >[more deleted] >It should be noted that AZT does not necessarily prevent the development of >KS. Interestingly, my longest surviving AIDS patient is a Black man with >extensive KS lesions of the legs for over 5 1/2 years. He has never had AZT, >interferon, or chemotherapy, although he has received some local radiation to >some lesions. He claims that stress definitely aggravates his KS lesions, and >he works hard to minimize it in his life. > >The cause of KS is not known....Most AIDS patients do >not die from KS, but rather from opportunistic infections of more serious >nature. >[more deleted] I read recently that the links between KS and HIV infection are increasingly weak--that KS shows up in many HIV- gay and bisexual men who are not in the usual "risk group" (Italian men) for this otherwise-rare disease. I don't have the report on hand. I recall that it was printed in the S.F. Chronicle, and was based on data released by CDC with Robert Gallo's imprimatur (but with no comment from him.) This is interesting in that AIDS was first known informally as "gay cancer" on the basis of widespread KS diagnoses in the early 80s. Dr. Gallo, who had nearly his whole career as a virologist invested in the theory of viral causes for cancer, now has his career invested in the theory of viral causes for AIDS. For him to now release data suggesting that the original trail- marker for the HIV/AIDS connection was not a valid one is *very* interesting. That AZT is "not necessarily" (maybe not at all? what does he mean?) effective in preventing KS seems to further weaken the connection. Obviously, this should be confirmed by someone with more credentials in AIDS epidemiology, but it would seem that the "definition" (in part, that "KS means AIDS") should be reviewed. Is KS really an HIV-related disease? Or is it due to other immunosuppressive cofactors that just happen to correlate closely with risk for HIV infection? Another disturbing thing: since KS was one of the first diseases linked to HIV, epidemiological data about KS is among the oldest data we have. For this break in the HIV causal link to KS to be so long in coming is suspicious. Gallo's bias (viral causes for cancer) is obvious. Could this bias have delayed the announcement? By years, perhaps? The virtual CDC monopoly on AIDS epidemiology data makes it that much harder to say. Perhaps this data should be put in the public domain. --- Michael Turner turner@tis.llnl.gov