gilbert@tce.COM (Gilbert Cornilliet) (03/14/91)
Hi there!
This is a selection of articles (mostly medical) from
the March 1991 Being Alive Newsletter.
I am one of the editors of this Newsletter.
Comments, suggestions, critics, submission of articles, etc
are welcome. My E-mail address is gilbert@tce.com.
Please share this information with your friends.
Take care.
Gilbert.
======== TABLE OF CONTENTS ========
HOPE FOR GENE THERAPY IS REAL, IF NOT YET IMMEDIATE
MEDICAL UPDATE: JANUARY 28, 1991
A REPORT TO THE COMMUNITY ON COMPOUND Q
ADDENDUM TO A PROPHYLAXIS PROTOCOL
FOSCARNET EXPANDED ACCESS PROGRAM
L.A. PHYSICIANS AIDS FORUM: NEW TREATMENT FOR PCP
NIH BEGINS PHASE I STUDY OF ADVANCED REVERSE TRANSCRIPTASE INHIBITORS
NEWS AND VIEWS
HIV SYSTEM OF CARE
PEOPLE WITH HIV/AIDS AND SEX
REMINDER: DOCTORS ARE NOT PERFECT
================================================================
HOPE FOR GENE THERAPY IS REAL, IF NOT YET IMMEDIATE
by Walt Senterfitt
According to UCLA's Dr. Steven Miles, writing in the AIDS Medical Update
Newsletter, "these are exciting times. It will not be long in the future when
HIV-infected individuals can look forward to a genetic therapy for their
disease."
Dr. Miles cautions that there is no gene therapy on the immediate horizon of
clinical trial and use. Several major hurdles remain to be overcome.
Nevertheless, the excitement of this normally cautious and judiciously
pessimistic academic physician is palpable. We present a summary of his
reviews of recent developments after some background gleaned from recent
articles in the journals Nature, Science, and the New England Journal of
Medicine.
BACKGROUND
Creation of practical therapies based on genetic or molecular manipulation of
living cellular material has been one of the most exciting biomedical
developments of the past decade. Recombinant DNA technology, for instance,
has already created several agents of already proven or potential clinical
value.
Nobel Prize-winning discoveries in the 1980's by Drs. Thomas Cech and Sidney
Altman that a form of RNA (known as ribozymes) can act as an enzyme,
functioning as a sort of "molecular scissors," opened the way for RNA-based
genetic engineering as well. These ribozymes are also being developed as
direct therapeutic weapons against RNA viruses (including HIV). One
application being tested in the laboratory is use of a special RNA form known
as a "hammerhead ribozyme" to disarm any HIV particles not yet integrated
into host cells in the body, essentially by cutting up the viral RNA into
ineffective pieces which are then destroyed by other enzymes.) Paralleling
this progress has been a rapid leap in the ability to decode the location and
function of specific genes. The HIV-1 genome, for instance, though still far
from fully understood, has been much better characterized already than any
other virus. In addition to the three essential genes found in most
retroviruses, HIV-1 has at least six additional genes which perform distinct
but coordinated roles. This remarkable complexity probably underlies the
profound and diverse pathogenicity of HIV-1, but may also be the virus's
Achilles heel in presenting a number of specific targets for disruption.
"Gene transfer" technology is under rapid development at the cutting edge of
this research. The name refers to the process by which a gene manufactured or
manipulated outside the body is then transferred into affected or other
target cells in the body. The aims of this transfer are diverse, and
theoretically limitless: to replace defective genes with healthy ones, to
confer immunity against infection, to induce specific therapeutic action,
perhaps to help rebuild a damaged immune system.
To effect such a transfer requires a "vector," a way of getting replacement
or therapeutic genes into host cell nuclei. The most promising current
approach, for all diseases under study, is to use retroviruses which have
been rendered defective. In other words, one wants a virus which will do its
work of transferring the desired gene and then self destruct, or at least be
incapable of reproducing itself. For HIV disease, that has meant using
mutated or "denatured" variants of the HIV-1 itself.
Though gene transfer is in its infancy, the rate of progress in the last two
or three years has been astounding to most observers. NIH last year approved
a gene transfer protocol to allow and regulate experimental applications in
human subjects. Experiments are being planned to attempt to correct genetic
defects underlying such diseases as cystic fibrosis and muscular dystrophy as
well as to implant healthy blood-cell producing "stem cells" into the bone
marrows of leukemia patients.
RECENT DEVELOPMENTS IN HIV RESEARCH
Dr. Miles' guarded optimism is based in part on several papers published
within the past six months. Though all still at the "bench science" level,
they extend our knowledge and understanding of the possible mechanisms by
which genetic therapy may be accomplished for persons with HIV infection.
One study presented a novel solution to one problem in establishing what's
known as "intracellular immunity." The latter process involves genetically
altering primary stem cells to make them immune to subsequent infection or
incapable of "expressing" or carrying out specific gene-directed functions.
For instance, a T helper lymphocyte might be made immune to HIV infection, or
an already-infected one made incapable of manufacturing new virus.
Another study demonstrated with greater specificity than ever before the
"packaging site" in the genetic material of retroviruses, a key component of
the mechanism necessary to "repackage" replicated viral material into new
virus particles capable of infecting new cells.
A third study used the results from the second to produce HIV with the
packaging site snipped out. The authors showed that this defective virus
particle could infect but not replicate in new cells. In a second step they
also revised the gene responsible for forming new virus envelope (analogous
to cell walls in bacteria) so that even if new virus was packaged by a
failure of step one, it would still be defective and incapable of infecting
new cells. And thirdly, they bound a neomycin-resistant gene to the defective
HIV. Then they showed that in cell culture the genetically-engineered HIV
could in fact "transfect" CD4 cells, transferring its deliberately dfefective
genetic material into the host cell's DNA just like "wild" HIV does. They
demonstrated that this process did confer resistance to further infection by
pathogenic HIV as well as rendering the intracellular HIV incapable of
reproduction. This study was exciting in itself, and also evokes the concrete
possibility of introducing any number of other functional capacities into
target cells.
A final study showed the possibility of using other, nonretroviral vectors,
as well as engineered defective HIV, to introduce particular RNA species
("antisense messenger RNA" in this case) into the target cell's DNA. Those
cells with the highest levels of antisense RNA incorporated into their
genomes had high levels of resistance to HIV infection, although the
protection was not complete after 29 days.
SIGNIFICANCE AND REMAINING HURDLES
The capacity to produce HIV virions (infectious virus particles) which
package specific RNA species is an important discovery. These HIV virions can
be forced to incorporate high levels of RNA which may contain antisense,
ribozyme, or promoter- specific sequences which can act individually and in
concert to decrease HIV replication after transfer to target cells. By using
the HIV virions, all CD4-bearing cells can be effectively "immunized" against
subsequent infection with HIV.
Despite the excitement generated by these papers and the successes of their
different approaches to the problem of genetic therapy, several major hurdles
remain before this can be attempted in clinical practice.
The first problem is that the specificity of the packaging- control sequence
is only relatively good, not yet watertight against "leaks" in the system.
More fine-tuning research is needed to impart a greater degree of safety to
this procedure.
A second problem involves the selection of which cells to target for
"intracellular immunization." Current approaches use modified HIV to bind to
all CD4-bearing cells (including T helper cells and macrophages). This could
potentially impart high levels of resistance to CD4 cells, providing it takes
place prior to infection of these cells with "wild" HIV. However, for persons
already infected with HIV, this could mean relatively few CD4 cells are
uninfected and thus able to be immunized. Ideally, other targets can be found
for intracellular immunization. One approach finding some preliminary success
is to use another receptor target such as CD34 which is on the stem cells
that are precursors to all the T-lymphocytes. Perhaps the HIV virion could be
genetically altered to bind to CD34 rather than CD4 as a point of entry, and
then transfer to these stem cell precursors an immunity to HIV which would
then be inherited by all their T cell offspring. Thus, HIV infected persons
would gradually create a new set of immune lymphocytes alongside their
infected ones. Clearly more research is needed, but preliminary results from
other related studies have demonstrated that this process is possible.
The final problem is the maintenance of consistently high enough levels of
these genetically-engineered RNA species in the target cells. In other words,
these genes have to not only reach the target cells but stay around long
enough and in great enough numbers to effectively immunize the host cells. So
far, the process sometimes "takes" and sometimes doesn't last. Several
approaches are being employed in the attempt to overcome this inconsistency.
CONCLUSION
To quote again from Dr. Miles, "In the past, we have told patients that once
infected, `you're infected for life.' With the advent of these genetic
therapies, we can now provide hope for these patients. We may, in fact, be
able to immunize patients against further effects of HIV infection.
Theoretically, with the use of ribozymes and other specific RNA or DNA
sequences, patients could even be rendered free of infectious HIV viral RNA
indefinitely. This latter event is a long shot. However, given the rapid pace
and success demonstrated to date in this field, this may not be an impossible
feat."
================================================================
MEDICAL UPDATE: JANUARY 28, 1991
Presented by Mark Katz, M.D. and reported by Jim Stoecker
LANCET LOOKS AT LO
For some time now, we have been reading, mainly in the New York Native, about
the research of Dr. Lo of Washington's Armed Forces Institute. Lo discovered
a virus-like organism in the cells of KS patients. This micro organism was
neither a virus nor a bacterium and Lo termed his discovery Mycoplasma
incognitus.
From this research, Lo postulated that HIV may not be the cause of AIDS, but
rather a cofactor. The real culprit might be the mycoplasma that he was
seeing. Last summer, Dr. Luc Montagnier, the co-discoverer of HIV, joined Lo
in suggesting that HIV was not the sole cause of AIDS.
Now Lo's mycoplasma is receiving serious attention from the British Medical
Research Council. A recent article in the respected British medical journal
Lancet, entitled "Mycoplasma and AIDS - What Connection?", called for the
further collection of data on the existence of these organisms in AIDS
patients. The authors also called for the development of suitable animal
models. The Lancet article concludes, "Skepticism there may be, but the
findings of Lo and colleagues are hard to dismiss."
HIV-INFECTED CHILDREN
When an HIV-infected woman gives birth, we know that the child will be born
with HIV antibodies. Only about a third of these children, however, are
actually infected with HIV. It is still an open question why some are
infected and others are not. Some postulate that genetics may be a strong
factor.
Among the children who are HIV-infected, there are differing courses of
disease progression. A recent article in the American Journal of the Diseases
of Childhood reports that there appears to be a bimodal course. About 20% of
children infected in the womb become ill soon after birth and live less than
one year. The other 80% appear to develop AIDS at the rate of other infected
populations. For these children, the median age for diagnosis is about 6
years, while about a quarter remain healthy at age 10. More research is
needed to understand the determinants of this apparent bimodal distribution.
TRANSFUSIONS AND HIV INFECTION
Blood transfusions would seem to be the most direct way to transmit HIV. The
Annals of Internal Medicine recently included a study of 124 persons who
received HIV-infected blood transfusions in 1984 (Note: since the development
of the HIV antibody test in 1985, all blood donations are routinely screened
for HIV.) 89.5% of these recipients are HIV+. The interesting fact, however,
is that 10.5% are HIV-.
This brings up many questions about why not everyone exposed to HIV becomes
infected. Perhaps genetics and/or environmental factors provide protection
from HIV infection. The authors of the above study speculated that the
quantity of the virus being transmitted is crucial. There may be a certain
volume required for HIV infection to occur.
PSYCHOLOGICAL IMPACT OF HIV INFECTION
More and more, we are seeing studies on the psychological impact of HIV
infection. A report in the Journal of Applied Social Psychology looked at the
psychological adjustment of three groups of gay men. Researchers found that
asymptomatic HIV+ men showed poorer adjustment overall than those who were
symptomatic or uninfected. The asymptomatic HIV+ group reported more death
anxiety, less optimism, and a greater severity of psychological distress than
either the symptomatic HIV+ or HIV- groups.
The authors suggest that the uncertainty of the future is the major reason
for these results. Perhaps it is the mixed messages that asymptomatics
receive. On the one hand are the hopes for future therapies and, on the
other, the ever-present possibility of decline into disease before those
hopes are realized.
CD4 ABSOLUTE NUMBERS: HELP OR TYRANNY?
No single value elicits as much anxiety in HIV-infected people as the
absolute CD4 count. Those who are HIV+ know the fear and trembling that these
numbers can bring on. Today, the CD4 count remains the most widely used
surrogate marker. More and more, however, we are seeing a preference for
using the percentage of all lymphocytes which are CD4 helper cells.
This percentage fluctuates much less widely than the absolute CD4 count. The
count can vary in the same person from day to day. This variability is a
source of much of the anxiety surrounding these numbers. The percentage
offers a more stable picture of what is really going on.
As a general rule, the percentage of CD4 can be interpreted as follows:
40% Normal
30% Mild Immune Suppression
20% Moderate Immune Suppression
10% Marked Immune Suppression.
AMPLIGEN RETURNS
Ampligen has been around for some time. The early medical data was quite
encouraging. Ampligen appeared to have both antiviral and immune-enhancing
effects.
In 1987, widespread testing began in the US. The Ampligen used in this
testing was packed in plastic, frozen, and then thawed by heating. Soon after
the trials began, patients began to experience rashes and flushing. Once
researchers switched to thawing at room temperature, the rashes disappeared.
Not too long into the study, however, some people in the study group began to
report the onset of opportunistic infections and the study was soon halted.
Researchers determined that Ampligen is chemically altered when packed in
plastic. The drug is now being manufactured and then stored in glass. New
trials are now starting up across the US. We may yet have good news to report
about Ampligen.
DONORS NEEDED FOR PASSIVE IMMUNOTHERAPY STUDY
All 225 recipients have been selected for a local study of passive
immunotherapy. Donors, however, are still needed. Donors must be HIV+ and
preferably asymptomatic. The blood of potential donors is screened for
adequate levels of anti-p24 antibodies. If you are interested in donating
blood for this study, call Hemacare at 213.654.0565. Donors are paid and can
donate several times a month.
ASPIRIN AS IMMUNE BOOSTER
The lowly aspirin is now being looked at for possible immune enhancing
effects. The theory is that aspirin may increase the production of
interferons and interleukins in the body and thus boost the T cell count.
There have been anecdotal reports that one 325 mg tablet every other day has
caused both CD4 counts and percentages to go up. Aspirin, however, does not
have any antiviral properties.
Search Alliance is set to begin a study here in Los Angeles of the
immune-enhancing effects of aspirin in people with CD4 counts above 250. We
await further reports.
AZITHROMYCIN UPDATE
Azithromycin has been shown to be reasonably effective against toxoplasmosis.
Pfizer, the manufacturer of the drug, is now making azithromycin available
via a compassionate use protocol. This protocol requires that the patient has
failed on the standard anti-toxoplasmosis medications. For more information
about the Pfizer program, call Dr. Michael DeBruin at 203.441.5701.
DAAN HERBAL THERAPY
Oriental medicine certainly has a part to play in the fight against HIV. One
oriental medical approach is DAAN herbal therapy, recently studied in Los
Angeles by oriental doctors Chung and Kim, in association with USC's Dr. Mark
Rarick.
The herbal formula used in the study consisted of eleven herbs formulated by
Dr, Chung of Korea. Eighty-three people began the study. Most were
asymptomatic, while some were symptomatic. The herbal formula was taken once
a month for twelve months. Results show an overall fall in beta-2
microglobulin. CD4 counts for symptomatics stabilized over the twelve months,
while the counts of asymptomatics showed some rise after six months and then
a leveling off.
It should be noted that study partcipants were not taking AZT. The Korean
doctors believe that the way that AZT works is not compatible with the way
that the herbs work. AZT might lessen or even hinder the effects of the
herbal formula.
It should also be noted that about half of those who began the study did not
complete it. Some wanted to go back on AZT. Others found the side effects
intolerable.
Most participants experienced some side effects such as fever, rash and
diarrhea. The Korean doctors see this as a natural purging of the infection
and a sign of the herbs' potency and efficacy. Such side effects seemed to
diminish over time.
Doctors Chung and Kim have now opened a store front at 8060 Melrose Ave., Los
Angeles, to dispense DAAN herbal therapy. The phone number is 213.653.5300.
Be aware that DAAN is not inexpensive, with the current cost a few hundred
dollars a month.
NOTE:
Next month, Dr Mark Rarick will discuss DAAN herbal therapy at the Being
Alive Medical Update. See page 1 for
details.
================================================================
A REPORT TO THE COMMUNITY ON COMPOUND Q
by Robert S. Jenkins, MD, Gary P. Jacobs, MD,
Dotsie M Anfenson, RN, and Jane Barnett, LVN
For a little over a year we have been involved in the administration and
supervision of tricosanthin (Compound Q) in our medical practice. We use the
Chinese product as we do not yet have access to the American product. We do
not promote or encourage anyone to take this drug. We have made it available
in our practice in order to study its effectiveness and to provide a
relatively safe, medically supervised place to receive this drug which can
cause anaphylactic reactions (severe allergic reactions associated with falls
in blood pressure and difficulty in breathing).
Our year's experience with Q has taught us how to safely administer it, what
premedications to give and which patients should not be given the drug. Many
of the answers to these questions can be found in the text of this article.
Generally, patients with fewer than one hundred T4-cells should probably not
be infused with Q because of the risk of neurological complications
(lethargy, stupor, seizures, coma and brain death); also anyone, even with
more than 100 T4-cells, experiencing neurological problems (HIV Dementia, HIV
Encephalitis) should not do Compound Q. The dose of Q we used last year will
be increased this next year and our premedications will change. Finally, our
data collection and dosing schedules need to be more tightly controlled to
obtain more useful data.
We have approximately 75 patients who started or tried Compound Q this past
year. Of the 75 patients, there are 23 on whom we have useful data. There are
several reasons why there is not useful data on the other 50 patients. Those
reasons include:
1 Some patients experienced severe flu-like symptoms and chose to quit.
2 Patients would become frustrated after their first set of depressed
T4-cells and quit the study.
3 Some attrition from people moving out of the area.
4 Some of the patients did not comply with our requests for T4-cells on a
regular basis and from the same laboratory.
5 We still have 38 patients taking the drug but some of them started too
recently to have useful information available.
The graph summarizes the useful data we have available on our patients over
an average eight month period with the solid black bars representing T4-cells
of patients who did not take Q and the hatched bars representing Q patients.
They have been categorized into five different groups depending on their
starting T4-cells (0-99, 100-199, 200-299, 300-399 and 400-499). Total number
of patients is 23. The non-Q patients were blindly picked from our own
patient charts by an observer who did not know the patients T4-cell results.
This is the only way we knew to "control" the study; we felt it unethical to
perform a placebo controlled study with this drug.
Looking at the results, the only group to show an overall rise in T4-cells
was the 0-99 T4-cell group. This is also the group that we had the most
trouble with in terms of neurological problems. Also, none of the patients in
this group had reversal of their overall immune status. A 60% increase in
this group may only represent an increase from 30 to 48 T4-cells, not
statistically significant.
The other groups all had overall declines in their T4-cells, and except for
the 400-499 group, the declines in the Q group were less than the non-Q
group. One problem with the 400-499 group is that the non-Q patients picked
as controls showed slight increases as opposed to the Q receiving group. We
decided to just report the data as we pulled it, as opposed to going back and
pulling more non-Q patients in the 400-499 group to "alter our control
group." Thus, it appears that the patients who did Q in the 400-499 group did
worse than those people who did not take Q.
This bar graph shows averages of the whole group. Individually a few patients
did very well with remarkable rises in T4-cells; unfortunately, these
remarkable rises in some patients were offset by some remarkable declines in
T4-cells in a few other patients. It does seem that some of the patients
stabilized their T4-cells. It also seems that the patients who continued with
Compound Q had less opportunistic infections than they might have otherwise
had, but this is mostly speculation and it is difficult to extrapolate this
information from a small sample size such as this. Patients also reported a
sense of well-being and increased energy after the infusions. Some patients,
despite falls in T4-cells, continued to take the drug because of this sense
of well-being. I think people need to keep in mind that the results we have
reported with Q are as good, if not better than, as those reported with AZT
prior to AZT's approval. On the downside, Q is more toxic and dangerous than
AZT and should be administered carefully and under medical supervision.
Another problem we experienced was that approximately 20% of the patients
experienced severe anaphylactic reactions and dramatic falls in blood
pressure, difficulty in breathing, nausea, vomiting and hives. These
reactions require immediate treatment with epinephrine and/or Benadryl, but
none of our patients suffered any permanent effects. This is the main reason
for doing Q in the presence of someone who knows how to treat anaphylactic
reactions.
A more serious problem, but occurring much less frequently, is the neurologic
sequelae: lethargy, stupor, coma, seizures and brain death. One of our
patients died, and one other had seizures and coma from which he has
essentially recovered. The patient who died had 140 T4-cells a month prior to
his death and had three previous infusions of Q prior to his last infusion.
We strongly feel that Q should be administered only by physicians who are
willing and able to hospitalize any patient who has a serious complication
from Q, and for medical-legal reasons, we must only take care of our own
complications.
Our year long experience with Q raises as many questions as it answers.
Primarily, Q did not pan out to be the panacea we had all hoped for. Our
experience differs from San Francisco's, and the reasons for this are not
entirely clear. We did have a smaller group, and overall the Los Angeles
group was probably sicker than the San Francisco group.
In good conscience, we can neither advocate nor promote the use of this drug.
We are encouraged enough to start and, we hope, complete the next phase of
our Q experience with 45 patients over the next eight to nine months.
(Remember this is the Chinese Q; not Genelabs Q). If any remarkable benefits
are seen we will certainly make them public before the end of the study. We
wish to acknowledge the brave patients who devoted their time, finances, and
emotional energy to the project to date.
================================================================
ADDENDUM TO A PROPHYLAXIS PROTOCOL
by Robert S. Jenkins, MD and Gary P. Jacobs, MD
Since our original prophylaxis protocol was written in November 1990, there
are four topics on which we wish to elaborate. Those four are pneumocystis
pneumonia, toxoplasmosis, cryptosporidium and mycobacterium avium.
PNEUMOCYSTIS PNEUMONIA (PCP) PROPHYLAXIS
In November of 1990, Kaiser Los Angeles made public their data on Bactrim as
pneumocystis pneumonia prophylaxis. Of 116 people in their study, there was a
zero incidence of pneumocystis pneumonia with patients on one Bactrim DS pill
three days a week. Pentamadine by comparison has at least a 10-15%
breakthrough rate for PCP per year. The downside of Bactrim is that
approximately 30% of the patients demonstrate some sort of allergic reaction;
for this reason one might want to consider using Dapsone 100 mgs three days a
week as PCP prophylaxis, as Dapsone overall seems to have less incidence of
allergic reactions.
Dapsone's one drawback is that it can cause hemolytic anemia in patients who
have a Glucose-6-Phosphate-dehydrogenase deficiency. This occurs in less than
5% of the population, and there is a screening test one can perform to test
for deficiency of G6PD. We are not running this test routinely as yet, but if
anemia on Dapsone becomes a problem in our practice, we may consider running
this test more routinely.
Our current recommendation for PCP prophylaxis is Dapsone 100 mg three times
a week (M-W-F). If one is allergic to either Bactrim or Dapsone, one may want
to try the other as there is not 100% crossover of allergy from one drug to
the other. Bactrim is a sulfa compound and Dapsone is a sulfone, akin to
cousins as opposed to brothers/sisters. We are now taking people off
Pentamadine if they can tolerate either Dapsone or Bactrim, although some
patients want to be "complete" in their prophylaxis and are doing both
aerosolized Pentam and either Dapsone or Bactrim.
TOXOPLASMOSIS PROPHYLAXIS
There is controversy as to whether Bactrim or Dapsone will prophylax against
Toxoplasmosis. Whether either one is adequate prophylaxis against
Toxoplasmosis is not known. Using pyrimethamine as prophylaxis against
Toxoplasmosis seems rather severe as pyrimethamine (a folate inhibitor) can
cause decreases in one's white blood cell count and may require the use of
leucovorin to "rescue" the white cells. Recently a trial of pyrimethamine as
prophylaxis for Toxoplasmosis has been proposed by AMFAR. This seems to be
rather drastic prophylaxis but might be indicated in patients with positive
IgG or IgM antibodies to Toxoplasmosis. A formal study evaluating the
efficacy of Bactrim or Dapsone as Toxoplasmosis prophylaxis would be welcome
and possibly more valuable than the proposed AMFAR study of pyrimethamine.
CRYPTOSPORIDIUM PROPHYLAXIS
Since our original publication, we have treated approximately 12 patients
with active crypotosporidium infection. In our experience, early on treatment
with Humatin seems to be more effective against active infection whereas
Diclazuril was much less effective. Combination of both drugs was not
beneficial. We feel that prophylaxis should remain with Humatin 250
milligrams, two capsules a day. We now feel that Diclazuril is not proving
effective and that patients should use Humatin as prophylaxis against
cryptosporidium, not Diclazuril or Clinicox. As added interest, the new
macrolide antibiotic, Azithromycin, is being considered for treatment of
cryptosporidium although this is purely speculation at present.
MYCOBACTERIUM AVIUM INTRACELLULARE (MAI) PROPHYLAXIS
In our recent experience we had started a number of patients on
Clarithromycin. Many patients started the drug as emperic therapy for "fevers
of unknown origin" (FUO), i.e., patients without specific diagnoses for their
daily fevers. A significant number of these people (more than 95%) have had
dramatic improvement in well being and elimination of fevers by taking 1.5
gms a day for 1 to 2 weeks, followed by 250 mg to 500 mg a day as long term
maintenance. We are now recommending the use of Clarithromycin as MAI
treatment and/or prophylaxis and not using Clofazamine as an alternative
given that Clarithromycin is working so well. This is different from our
previous recommendation of using either Clarithromycin or Clofazamine as MAI
prophylaxis.
For prophylaxis in asymptomatic people, one tablet (250 milligrams) a day is
the recommenced dosage. The cost continues to be a problem, $3-4 per tablet,
but the money is well spent considering the rapidly progressive and virile
nature of MAI once the infection takes control.
==============================================================================
End of Being Alive Newsletter (March 1991 - part 1/2)