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ALERT – Vitamin A is probably simple antidote to bird flu, mainstream literature shows

You read it here first – hold those billions, Vitamin A blocks bird flu lung devastation

All the panic over H5N1 seems a little overblown when you consider that the virus has been around for eight years at least without morphing into a deadly human version that can sweep the globe from human to human. The very same H5N1 was the cause of the “Avian flu” outbreak in Hong Kong in 1997.

But just to reduce the hysteria a few more notches, we have decided to relent on our decision (at the end of the previous post) to be kind to the drug companies, officious officials, army of doomsayers and worryworts, posturing politicians, and all the other people whose interests mesh smoothly with maximum flu alarm, and announce with a trumpet fanfare the final solution to bird flu.

We at New AIDS Review thus proudly note today (Sun Nov 20), apparently for the first time in any form of media outside the medical literature, the references that tell what the ultimate solution to bird flu surely is: a modest dose of Vitamin A to anyone who contracts it.

You read right. The $7.2 billion question is this: why spend billions upon billions on massive and uncertain preventive measures such as

a) executing the few chickens owned by poor Asian families who may depend on them for survival

b) the unlikely effort to prevent H5N1 spreading among domestic fowl by vaccinating 5.1 billion birds in China and billions elsewhere in Asia (the Chinese eat 14 billion chickens a year, so even if a gigantic army of vaccinators is successfully recruited and swings into action, they will have to keep at it forever, as if they were repainting a hundred Golden Gate bridges annually),

c) stockpiling enough vaccine for humans which if it can be done will take months and may be evaded anyway by the evolving virus, and

d) distributing enough antivirals like Tamiflu to sink a ship when there is some question as to whether they will be effective against this virus (according to the British Medical Journal current issue 2005;331;1266 ‘How the Media Caught Tamiflu’)

when, according to the mainstream medical literature lying under the noses of the pontificating pundits and overly political scientists such as Anthony Fauci and the CDC brass who are on every TV channel this morning chinking their medals and repeating what the media have been hearing for months, the simple solution to H5N1 is this: give anyone who contracts deadly bird flu a dose of Vitamin A.

This will do the trick because Vitamin A reliably blocks the pathway of creation of deadly Tumor Necrosis factor in the lungs, which is the aspect of bird flu which is so deadly.

That is what the referenced papers say which we list below, which are readily available to any of these heroes of health for their bedtime reading.

Government without time to read

Why this grand army of well paid advisors, experts, commentators, WHO statisticians, field workers, corporate chieftains, Presidential advisors, think tank wonks, fast-talking current affairs hosts, and other luminaries have somehow overlooked them in their rush to judgement we hesitate to imagine.

Could it be that, in this age of information deluge, opinion making of every kind in the hottest issues of the day has now become completely divorced from factual information if that data is buried in any form of publication other than newspaper headlines and book reviews?

If so, it bodes ill for the future. Certainly there are already two huge signs that this is now true: Katrina and Iraq. In both cases, extensive written advisories were completely ignored.

As we all know, there were plenty of warnings in the form of levee engineering reports that a strong hurricane would flood New Orleans out of existence, written years before Katrina struck. So many, in fact, that even the leisurely PBS had time to send a documentary crew down there to make the same point some years ago.

In the case of Iraq, a report of thousands of pages of what to do with the country once the war was won was prepared by the State Department, in consultation with all kinds of experts and exiled Iraqis, for the Bush administration in advance of the invasion.

According to the New Yorker, it was filed in the White House waste basket.

The Avian flu-TNF-Vitamin A paper trail

Here are the references on Vitamin A and what they say, courtesy of library research by Robert Houston, long time medical investigator and nutrition researcher in New York City, who has lectured at the New School and frequently advises reporters on health and medical topics. He now writes to us:

Can Vitamin A Tame Bird Flu?

NewAIDSreview.com scoops the world’s media by being the first to reveal that recent scientific studies point to vitamin A as a potential remedy for bird flu.

It should be noted however that the normal requirement of vitamin A is only 5000 units per day (1.5 mg), and that the therapeutic levels range from 25,000 to 100,000 units (about 7 – 28 mg).

Unlike vitamin C, it cannot be taken in gram amounts; in fact, severe toxicity has occurred at 300 mg (1 million units). Other nutrients, such as the omega-3 fatty acids of fish oil, can also help to reduce TNF overproduction.

(see Grimble, R. et al. The ability of fish oil to suppress tumor necrosis factor-a production… Am J Clin Nutr 76:454-9, 2002.)

At these tiny amounts it should be possible to defend every person on earth from avian flu for a fraction of the cost of Tamiflu. There is already a system in place for distributing Vitamin A to children in seventy countries.

Here is the paper trail that Houston followed that shows fairly conclusively that a little Vitamin A will tame Avian Flu:

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How we know that Vitamin A tames Avian Flu:

1. A report in 1996 stated that vitamin A counteracts TNF in the joints in the case of arthritis caused by Lyme disease, a finding which has been ignored by the Lyme disease establishment.

(Cantorna, M. and Hayes, E. Vitamin A deficiency exacerbates murine Lyme arthritis. J Infec Dis 174:747-51, 1996.)

2. Then it was shown in 2000 that vitamin A deficiency can result in injury to the lungs.

(Baybutt, R. et al. Vitamin A defiency injures lung and liver parenchyma and impairs function of rat type II pneumocytes. J Nutr 130(5):1159-65, 2000.)

3. Then two studies found that vitamin A protects the lungs from damaging effects of TNF.

(Besnard, V. et al. Protective role of retinoic acid from antiproliferative action of TNF-a on lung epithelial cells. Am J Physiol Lung Cell Mol Physiol 2822: L863-L871, 2002. First pub Dec 7 2001)

(Am J Physiol Lung Cel Mol Physiol 282: L863-71, 2002; Torii, A. et al. Vitamin A reduces lung granulomatous inflammation… Eur J Pharmacol 497 335-342, 2004.)

4. The fact that H5N1 flu targets the lungs and that TNF collects there was established in July also. The paper showed that avian flu occurs primarily in the lungs.

Bangkok investigators wrote that “We investigated a patient with fatal H5N1 influenza. Viral RNA was detected by PCR (reverse transcription-polymerase chain reaction) in lung, intestine, and spleen tiossue, but positive stranded viral RNA indicating viral replication was confined to the lung and intestine. Tumor necrosis factor was seen in lung tissue…In contrast to disseminated infection documented in other mammals and birds, H5N1 viral replication in humans may be restriucted to the lung and intestine, an the major site of H5N1 viral replication in the lung is the pneumoctye.

(Influenza A replication sites in human sites in humans. Uiprasertkul M, etc al. Mahidol University, Bangkok, Thailand. Emerg Infect Dis 2005 Jul 11 (7):1036-41.)

5. A study from the National Health Research Institute in Taipei at the same time reported that vitamin A (retinoic acid) suppresses TNF production and does so by blocking the same signalling pathway (p38 kinase) which bird flu activates.

(Ho, L. et al. Retinoic acid blocks pro-inflammatory cytokine-induced matrix metalloproteinase production… Biochemical Pharmacology 70:200-208, July 15, 2005.)

6. The key breakthrough was published two months ago in August, confirming why the avian flu virus H5N1 is more deadly than other flu viruses. Scientists at the University of Hong Kong studied the H5N1 flu which broke out in Hoing King in 1997 and found that it hyperinduces tumor necrosis factor (TNF) in the body’s immune cells, causing severe autoimmune damage in the lungs where the virus localizes.

They say they hope that “these results may provide insights into the pathogensis of H5N1 disease and rationales for the development of novel therapeutic strategies.”

(Lee, D.C. et al. Hyperinduction of tumor necrosis factor alpha expression in response to avian influenza virus H5N1. J Virol 79(16):10147-54, Aug. 2005. The University of Hong Kong, Queen Mary Hospital,Pokfulam, Hong Kong Special Administratiuve Region, People’s Republic of China.)

As the last paper suggests, this knowledge about the modus operandi of Avian Flu can be used for the “development of novel therapeutic strategies”.

Our “novel strategy” is to ramp up Vitamin A production to straospheric levels and make sure there is enough for every man, woman and child on the planet. Since that would cost less than a few cents each, we reckon, it would save all of $10 billion right there in WHO salaries, Tamiflu patent royalties, Anthony Fauci television appearances, and all the other costs that modern health defenses are now saddled with.

But why haven’t Anthony Fauci and his cohorts at the NIH and CDC, not to mention the WHO, come up with this themselves? Why do they need an obscure onlooker to point it out to them?

It’s their job, after all, to protect us from this gigantic threat which they are saying may ruin the world. The ever authoritative Dr Fauci was saying on TV last night that, even if the virus never appears in lethal form, a vast effort to defend against it will be well worth the billions we can shovel at it. Shouldn’t Dr Fauci read the medical literature in between his many sessions under the TV lights repeating the same smug alarms?

One possibility as to why the medical authorities don’t know all this from reading their own literature, at bedtime if necessary, emerges from this sequence. It does help to be a nutrition expert who has researched Lyme disease, which is a relatively neglected and somewhat disputed area.

But then, so is nutrition a relatively neglected area, medically speaking, it seems to us. As a cause and cure of ailments, it is surely much more relevant than is suspected by many doctors in our commercial, drug-oriented system.

But of course, the unpatentable Vitamin A is no path to profits for the maker of Tamiflu, Swiss pharmaceutical giant Roche, a leader in an industry where profits are not as easy to come by these days.

Having the right drug in hand for a superbug can rescue the situation very rapidly for a drug company in hard times, as the case of Viropharma shows. Crucial Antibiotic Rescues Biotech Maker’s Finances

On the other hand, as the case of Viropharma also shows, meddling with Mother Nature by dosing her with an ever increasing array of drugs can lead to unintended side effects which make it ever more important to consider the more natural alternative of nutrient supplements. Apparently in this case it is drugs that beget the need for yet another drug:

C. difficile disease occurs when antibiotics used to treat a different infection wipe out the beneficial bacteria that normally reside in the colon. That leaves an opening for C. difficile, which is resistant to most antibiotics. The bacteria form spores that can persist for months on surfaces like toilets and can be transferred to patients from the hands of health care workers or visitors.

Is it too much to ask that Dr Fauci and his battalions of scientists and health workers take up our suggestion and research the saner route of a safe nutritional alternative in dealing with what they present as the global health threat of all time?

And while they are at it, perhaps they might apply the same revisionist thinking to AIDS, which according to the mainstream scientific literature they are also ignoring is the highest mountain of theoretical scientific and medical garbage that has ever accumulated.

(show)

The New York Times

November 9, 2005

Crucial Antibiotic Rescues Biotech Maker’s Finances

By ANDREW POLLACK

Roche, whose drug Tamiflu is in great demand as a preparation for a possible influenza pandemic, is not the only company reaping a financial windfall from a treatment for a contagious disease. And in this case, the health threat is not merely a potential one.

ViroPharma, a formerly struggling biotechnology company, sells Vancocin, the only drug approved to treat Clostridium difficile, a bacterium that already kills thousands of people a year in this country and is apparently becoming more common and more deadly.

The life-saving drug has turned out to be a financial lifesaver for ViroPharma which, almost by serendipity, acquired the American rights to Vancocin last November. Since then, in response to rising demand, the company has increased the price of the drug – its only product – three times by a total of 80 percent, to about $800 for a course of treatment.

With Vancocin sales expected to more than double this year to $120 million, ViroPharma, based in Exton, Pa., is profitable for the first time in its 11-year history. Its stock price is up 14-fold since reaching a 52-week low in April. On Monday, it rose nearly 15 percent, after the company announced higher-than-expected third-quarter profit and raised its estimate for sales of Vancocin this year, then it declined 91 cents yesterday, to $23.19.

But some doctors say the price increases are exploiting growing fears of the bacterium, while placing a burden on patients and those who take care of them. “It’s absolutely outrageous,” Dr. Daniel M. Musher, an infectious-disease specialist at the Veterans Affairs Medical Center in Houston, said of the price increases.

ViroPharma executives, as well as some other doctors and Wall Street analysts, defend the price as still relatively low compared with some other antibiotics like Azactam from Elan and Zyvox from Pfizer that are used to treat other infections. Those drugs can cost $1,000 to $2,000 for a course of treatment. They note, too, that ViroPharma has started a program to provide the drug free to those who cannot afford it.

And the company says that after losing money for years, it needs its profits from Vancocin to expand production of the drug and continue developing other potentially promising treatments for other diseases.

Vancocin’s target bacterium, known in scientists’ shorthand as C. difficile, causes severe diarrhea and a type of colitis, mainly in elderly hospitalized patients. According to one estimate, there are about 400,000 cases and about 5,000 deaths a year in the United States.

But comprehensive statistics are not available, and there is now some evidence that the incidence of infections has doubled since 2000 and that some cases are occurring outside hospitals.

Moreover, several hospitals have had outbreaks of a supervirulent strain that produces about 20 times as much colon-damaging toxin as typical strains. The toxic strain has been found so far in 14 states, as well as in Canada, Britain, the Netherlands and Belgium.

“This is another superbug,” said Dr. L. Clifford McDonald, an epidemiologist at the Centers for Disease Control and Prevention. At the annual conference in April of the Society for Healthcare Epidemiology of America, a session on C. difficile was entitled Apocalypse Next.

An outbreak of the virulent strain in Quebec province has killed hundreds of people since 2003, with one expert estimating the toll as high as 2,000. An outbreak in 2000 led to 44 colectomies, the removal of part of the colon, at the University of Pittsburgh Medical Center, and 20 deaths.

At Somerset Medical Center in New Jersey, nearly 10 percent of deaths last year were in patients infected with C. difficile, double the rate of the previous two years, according to a poster presented at a meeting of the Infectious Diseases Society of America last month in San Francisco.

C. difficile disease occurs when antibiotics used to treat a different infection wipe out the beneficial bacteria that normally reside in the colon. That leaves an opening for C. difficile, which is resistant to most antibiotics. The bacteria form spores that can persist for months on surfaces like toilets and can be transferred to patients from the hands of health care workers or visitors.

Vancocin is an oral form of a powerful antibiotic, vancomycin, which is usually given intravenously. Low-cost generic versions of the intravenous drug are available, but reaching C. difficile in the colon is best done through oral medication.

While Vancocin is the only drug formally approved for C. difficile, most doctors first try off-label use of a generic antibiotic, metronidazole, which costs $10 to $80 for a course of treatment. Two studies published this year suggest that metronidazole is effective 70 to 80 percent of the time. While there is no head-to-head study showing Vancocin to be better, many doctors are starting to use it first, especially in severe cases.

That trend has helped ViroPharma, which is sponsoring seminars for physicians about C. difficile. “Vancocin is the treatment for your mother,” Dr. Colin Broom, ViroPharma’s chief scientific officer, said in an interview. “Metronidazole is the treatment for your mother-in- law.”

Dr. Broom was echoing a long-running joke in the field. But in a recent medical journal commentary asking, “Is it O.K. for Mom?” Dr. Dale N. Gerding, of the Hines Veterans Affairs Hospital and Loyola University medical school in Chicago, wrote that in most cases metronidazole still is effective – although patients should be monitored closely for signs that the drug is not working.

At its founding in 1994, ViroPharma set out to find a cure for the common cold, or at least a drug that would directly fight the cold virus rather than merely treat symptoms. But in 2002, the Food and Drug Administration rejected its drug, pleconaril, over safety questions. In the next two years, ViroPharma shrank to 35 employees from 435 .

With cash running low last year, the company began to look for a drug it could acquire to generate revenue. The investment bank Piper Jaffray had just had a deal fall through with a small biotechnology company to buy Vancocin from the drug’s developer, Eli Lilly, which has been de-emphasizing antibiotics. So Piper approached ViroPharma.

“We had never heard of the product,” said Michel de Rosen, ViroPharma’s chief executive. “We had never heard of C. diff.”

But ViroPharma noticed that prescriptions were growing and learned of the new superstrain of the bug. So last November, ViroPharma paid $116 million – double the company’s market value at the time – for the United States rights to Vancocin, borrowing about half the money needed. (Lilly still sells the drug outside the United States.)

ViroPharma executives say the drug’s success has surprised them. “We did not expect the change in medical need would be so rapid,” Mr. de Rosen said.

United States sales of Vancocin rose from $28 million in 2002 to $40 million in 2003 and $54 million last year, according to executives. The company said on Monday that it expected sales this year to surpass $120 million. ViroPharma’s stock market value is now about $1.3 billion.

The company raised prices for the drug by about 17 percent in December, an additional 26 percent in March and 22 percent more in August. Mr. de Rosen defended those moves, saying Lilly had not increased the price for 17 years. And even at the new price, he said, Vancocin saves money for the health care system by shortening hospital stays.

Dr. Neil O. Fishman, director of health care epidemiology and infection control at the University of Pennsylvania Health System and a consultant for the company, said that because Vancocin was a life-saving drug, “the price becomes nominal” – especially, he said, compared with cancer drugs that cost tens of thousands of dollars and might prolong lives by only a few months.

Wall Street analysts have reacted positively to the price increases. Thomas Wei of Piper Jaffray wrote in a note to investors in September that because Vancocin still cost less than comparable drugs for other life-threatening infections, prices could rise as much as 65 percent further. He predicted that the price would reach $1,000 by 2007.

“Given the lack of alternatives for the treatment of severe or complicated C. difficile associated diarrhea,” his note said, “there is the potential that there could be further upside to our new assumptions.”

In a survey of 44 doctors conducted in September by Lazard, more than two-thirds said the price increases would not cause them to reduce the use of Vancocin and nearly half said they expected to increase their use in the next 12 months.

But some doctors say their hospitals avoid paying for Vancocin by having patients swallow a generic intravenous form of vancomycin. While its unpleasant taste can cause nausea, some doctors say the two forms of the drug are essentially the same.

Dr. August J. Valenti, director of epidemiology and infection prevention at the Maine Medical Center, said this method saves $600 a treatment. His hospital took infection control measures after the number of cases of C. difficile began rising in 2002. “We were beginning to see far more relapses, and relapses after relapses,” Dr. Valenti said.

New drugs aimed at C. difficile, as well as a vaccine, are now in development by various companies, and some experts say they are needed. Genzyme is in the final phase of clinical trials of tolevamer, which works by binding and immobilizing the toxins produced by the bacteria. Because tolevamer is not an antibiotic, Genzyme hopes it will reduce relapses. Others developing drugs include ActivBiotics, Oscient Pharmaceuticals, Romark Laboratories, the team of Optimer Pharmaceuticals and Par Pharmaceutical, and the team of Medarex and the nonprofit Massachusetts Biologic Laboratories. Acambis is working on a vaccine.

Henri A. Termeer, Genyzme’s chief executive, said Vancocin’s price had risen because ViroPharma “looked at it as a single opportunity and they are utilizing it in that sense.” But he predicted that once competition arrived, the “tremendous pricing flexibility” that ViroPharma has had “may not be sustainable over time.”

* Copyright 2005 The New York Times Company

4 Responses to “ALERT – Vitamin A is probably simple antidote to bird flu, mainstream literature shows”

  1. Robert Houston Says:

    New AIDS Review is to be commended for its splendid review of the recent research indicating that vitamin A may be a useful treatment for avian flu. A number of collateral sociological issues have been brilliantly framed by Truthseeker, who may one day take off his black cape and mask and be revealed as one of the world’s foremost science writers.

    Some may object that even if vitamin A counteracts TNF, the dosage required may be higher than the safe physiological range. It is thus pertinent to quote from the recent study by J. Ho et al. (Biochem Pharm 70:200, 2005 – item 5 in the “paper trail”), which involved human cells:

    Pro-inflammatory cytokines like interleukin-1 and tumor necrosis factor alpha play pivotal roles in immunopathogenesis… In this study we examined the possible effects and mechanisms of vitamin A… The results indicated that physiological concentrations of vitamin A appeared to be enough to provide certain protection from the immunopathogenesis… (emphasis added)

  2. Robert Houston Says:

    The above findings by L.J. Ho et al. of the National Health Research Institute in Taiwan indicate that moderate therapeutic levels of vitamin A can curb TNF wherever it may occur in the body. Earlier this month a world authority on vitamin A, Alfred Sommer, M.D., former Dean of the Johns Hopkins School of Public Health, told the Washington Post:

    In all the studies that have been done, and there are many, the net benefit of taking a large dose of vitamin A supplement two or three times a year has been overwhelmingly positive. One can get an overdose of vitamin A, but that would only occur if one took very large doses for very long periods of time… We knew that children were vitamin A deficient in many parts of the world… even very mild vitamin A deficiency, before children even develop night blindness, increased their risk of severe and deadly infectious diseases. (Washingtonpost.com, Nov. 4, 2005)

    The world owes a debt of gratitude to Truthseeker for bringing the important new findings on vitamin A and bird flu to public attention. The point is not that vitamin A is a cure but rather that it may be a lifesaver, which can neutralize the lethal aspect of bird flu. This is not my “original research” but rather the careful work of world-class scientists in China and elsewhere, which I merely collected in a literature search through Medline – something Fauci et al. should try sometime.

  3. Robert Houston Says:

    Corroborative Studies

    A recent review of vitamin A from the Harvard School of Public Health (1) provides additional studies concerning its effect on tumor necrosis factor (TNF). Because the Hong Kong researchers specified the hyperinduction of TNF in macrophage cells of the immune system as the main pernicious effect of avian flu virus (D.C. Lee et al., J Virol, Aug. 2005 – item 6 in “paper trail”), it’s pertinent that several studies have found that vitamin A blocks TNF in macrophages (2-4). As early as 1994 it was found that vitamin A (retinoic acid) “almost completely inhibited the production of TNF by macrophages,” according to scientists at M.D. Anderson Cancer Center in Houston, Texas (4).

    The Harvard review also referenced a small clinical trial. Conducted at the University of Oslo in 2000, it found that “Vitamin A supplementation in patients with low vitamin A levels resulted in…decreased tumor necrosis factor-a levels” (5). The dosage was only 6500 IU per day, just slightly above the daily requirement and about 1/15th the therapeutic dosage, yet the TNF levels of the patients fell in half.

    An article on “Vitamin A and Avian Flu” is due to appear next month in the Townsend Letter for Doctors (Feb/March 2006), based on the research revealed in New AIDS Review.

    1. Villamor, E. and Fawzi, W. Effects of vitamin A supplementation on immune responses… Clin Microbiology Revs 18:446-464, July 2005.
    2. Mathew, J. and Sharma, R. Effect of all-trans-retinoic acid on cytokine production in a murine macrophage cell line. Int J Immunopharmacology 22:693-706, 2000.
    3. Motomura, K. et al. Destabilization of TNF-a mRNA by retinoic acid in hepatic macrophages. Am J Physiol Endocrinol Metab 281:E420-E429, 2001.
    4. Mehta, K. et al. Inhibition by all-trans-retinoic acid of tumor necrosis factor and nitric oxide production by peritoneal macrophages. J Leukocyte Biol 55:336-342, 1994.
    5. Aukrust, P. et al. Decreased vitamin A levels in common variable immunodeficiency: vitamin A supplementation in vivo enhances immunoglobulin production and downregulates inflammatory responses. Eur J Clin Invest 30:252-259, 2000.

  4. james Says:

    Nac NIH/NCI 2001 study reverses established KS in vivo model and doubles the life span. KS occurs in the absence of “aquired immune defiency” it is not caused by either hhv-8 or immune suppression low cd4.

    Whats really crazy about all in this article this is that sadly the article does not get the “hiv” protease inhibitors have their anti KS effects regardless of “viral” presence or non presence. Even with “viral” rebound “drug resistance” as already shown PI’s have the anti apoptosis effects independent of “viral” presence or non presence. And of course independent of “CD4” levels LOL.

    I hope you dont mind but I would like to repost the previouse two references about “hiv” specific LOL protease inhibitors treating non “hiv” kaposi Sarcoma in vitro and invivo and now trialed in humans. I would like to post them in the KS not aids post on here becusause they belong there as well, these two posts are interlinked because others and I hypothesise the “hiv” P.I.’s act like antioxidants sometimes interefering with apoptosis/cell death INDEPENDENT of “viral” presence or not particulary so with activated t cells.

    PPPPPPSSSSSSSSSSSSTTTTTTTTT
    REMEMBER NAC INHIBITS?REVERSES KS IN VIVO< WELL P.I’S RAISE GSH AS WELL AS REDUCING OXIDATIVE STMULI JUST LIKE NAC DOES.

    xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
    http://www.thebody.com/catie/switch_ks.html

    Canadian AIDS Treatment Information Exchange
    French Doctors Suggest That Therapy Switch May Cause KS Relapse

    By Sean R. Hosein

    July 8, 2003

    Kaposi’s sarcoma (KS) is a tumour that usually appears on the skin and most commonly affects gay and bisexual men with HIV/AIDS. KS was more common in North America and Western Europe at the beginning of the AIDS epidemic than it is now. Although KS most commonly affects the skin, over time, as immunity weakens, KS tumours can develop inside the body, particularly near lymph nodes and the digestive tract and in mucous membranes such as the mouth. As the tumours grow they can block lymph vessels, causing fluid to build up, which results in discomfort, further complications and even death. Treatments available for KS include radiation and chemotherapy, but these have seldom resulted in a cure for KS in people with HIV/AIDS (PHAs).
    In the mid-to-late 1990s, protease inhibitors (PIs) became widely available in high-income countries. When used as part of combination therapy, PIs helped put KS into remission. Researchers suspected that this occurred because PI combination therapy raised CD4+ cell counts and reduced levels of HIV in the blood. The changes in cell counts and viral load allowed the immune system a chance to begin repairing itself and perhaps to better fight KS tumours.

    However, this theory may now have to be reexamined, based on new findings from Paris, France. There, doctors reported that five PHAs who switched from a PI-based regimen to a regimen based on non-nukes (NNRTIs), such as efavirenz (Sustiva, Stocrin) or nevirapine (Viramune), had relapses in their KS.

    PI Therapy
    At the time the PHAs were originally diagnosed with KS, all five had “widespread” skin tumours. They received chemotherapy and/or radiation therapy. Eventually they took PI-based combination therapy for about 2½ years, and their KS went into remission and cleared up. However, three of the PHAs’ therapy was eventually unable to suppress HIV levels; the remaining two wanted simpler regimens. So doctors changed their combinations to ones based on non-nukes instead of PIs.

    After the Switch
    On average, the KS relapsed one year after the PHAs switched from PIs to a non-nuke. At the time the relapse occurred, in four of the five PHAs, CD4+ cell counts were relatively high — ranging between 350 and 1,300 cells. Also, in four of the five PHAs, viral loads were low — fewer than 20 copies.

    PIs and KS
    The doctors note that the recurrence of KS in their patients cannot be explained by low CD4+ counts or high viral loads. In seeking other explanations, the doctors report certain results of test-tube and animal experiments done by researchers. In these experiments, PIs seem to prevent the growth and development of KS tumours. The drugs appear to do this by blocking the production of growth factors (chemical messengers) needed by KS cells. Moreover, exposure to PIs caused KS cells to die.

    The report by the French doctors about KS relapse is interesting. However, much more study and analysis is needed to confirm these findings in other PHAs as well as to reconcile them with results from other clinical trials where combination therapy with either PIs or NNRTIs resulted in the regression of KS.

    In the meantime, the French doctors warn that other doctors should use caution when switching their patients who previously had KS from a PI to an NNRTI.

    References
    Sgadari C, Barillari G, Toschi E, et al. HIV protease inhibitors are potent anti-angiogenic molecules and promote regression of Kaposi sarcoma. Nature Medicine 2002; 8(3):225-232.
    Gaedicke S, Firat-Geier E, Constantiniu O, et al. Anti-tumor effect of the human immunodeficiency virus protease inhibitor ritonavir: induction of tumor-cell apoptosis associated with perturbation of proteasomal proteolysis. Cancer Research 2002; 62(23):6901-6908.
    Bani-Sadr F, Fournier S and Molina JM. Relapse of Kaposi’s sarcoma in HIV-infected patients switching from a protease inhibitor to a non-nucleoside reverse transcriptase inhibitor-based highly active antiretroviral therapy regimen. AIDS 2003;17(10):1580-1581.
    Gill J, Bourboulia D, Wilkinson J, et al. Prospective study of the effects of antiretroviral therapy on Kaposi’s sarcoma-associated herpes virus infection in patients with and without Kaposi’s sarcoma. Journal of Acquired Immune Deficiency Syndromes 2002;31(4):384-390.

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