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#18408 From: "jim98122x" <jim98122x@...>
Date: Fri Sep 1, 2006 7:14 am
Subject: Re: why bother with Radiesse?
jim98122x
Offline Offline
Send Email Send Email
 
Why would anyone waste their money on this?
By their own admission, the stuff does not last (their own words):

Radiesse provides a correction that has been proven to last one year without surgery.

Radiesse is not permanent and therefore avoids the risks associated with permanent materials.
(you mean the risk of not having to fork out a couple of thousand dollars all over again?  Risk to whom, the plastic surgeon?)

and if that's not bad enough (again, their own words...)

Its unclear where this  material should be injected (dermally or sub dermally) to achieve correction of
facial defects.

and

It tends to be unforgiving if not applied properly.

Um, yeah, sounds great....step right up!....who wants to be first to get it for facial wasting?  Guinea Pigs,  anyone....?   ( but you got cash, right?)

Am I missing something here?  This stuff doesn't even last as long as Sculptra, which is already too short-lived.
I 'm pretty  sure if this is the stuff he was talking about (but they all sound the same),  that Dr. Peter Englehard was talking about when he told me "don't waste your time on that stuff, it's really expensive and it doesn't even last 6 months".  He said the same thing about Restylane.

Where's the US approval for Bio Alcamid and PMMA?  This looks like another obvious "off label" play where they get approval on the backs of HIV+ patients but are really aiming at the rich-old-lady market.

JimS.
Seattle

--- In PozHealth@yahoogroups.com, PoWeRTX@... wrote:
>
>
> I had a call with Bioform, the makers of Radiesse yesterday. I am
> organizing a group of treatment activists to meet with them to discuss their patient
> assistance program design soon. We still do not know what the cost for HIV
> related work will be or what the patient assistance program will look like. I am
> hoping that they will be as easy to work with as Dermik (Sculptra) was.
>
> From FACIALWASTING.ORG:
>
> Radiesse (also called Radiense) is (calcium hydroxylapatite, (CaHA)
> microspheres suspended in an aqueous polysaccharide gel. Radiance, the newest
> product in the market, is not approved in the US as a facial filler yet but
> doctors are using it under an IDE study. It is manufactured by Bioform of
> Franksville, Wisconsin. In general, calcium hydroxylapatite has safely been used in
> the body for many applications including dental applications where bone
> build-up is needed for reconstruction and also in block form for cosmetic
> applications such as cheek, jaw, cranial and chin implants (hard bony areas).
> Calcium hydroxylapatite creates a lattice where the surrounding cells can be
> incorporated from ossification in bony areas to a stable scaffold in which soft
> tissue can grow. The calcium hydroxylapatite microspheres are suspended in a
> polysaccharide carrier which holds the microspheres in place until it is
> resorbed and the collagenation takes place. When injected in soft tissue, away from
> bone, fibroblasts work by building reportedly a non-scar tissue collagen
> type, thus creating volume in the treatment area. Its unclear where this
> material should be injected (dermally or sub dermally) to achieve correction of
> facial defects. It is being used in small quatities for wrinkle treatment and lip
> augmentation. It tends to be unforgiving if not applied properly. An allergy
> test is supposedly not needed. The especulated longevity is 2 to 5 years .
>
> More about a study here: _http://der
> matology.cdlib.org/102/therapy/HIV/comite.html_ (http://dermatology.cdlib.org/102/therapy/HIV/comite.html)
>
>
> INFORMATION FROM THE COMPANY:
> *************************************************
>
> RADIESSE® FACT SHEET
> WHAT IS RADIESSE
> Radiesse is a next-generation, long-lasting product used for soft tissue
> augmentation.
> · Radiesse consists of calcium-based microsphere technology that
> naturally promotes the growth of a patient’s own collagen.
> · Radiesse provides a correction that has been proven to last one
> year without surgery.
> · Radiesse is not permanent and therefore avoids the risks associated
> with permanent materials.
> HOW IT WORKS
> Radiesse is an injectable product consisting of tiny calcium-based particles
> that replace volume loss and also stimulate new collagen growth for
> long-lasting clinical results.
> · Radiesse is gently injected into the skin in very small amounts
> with a very fine needle. Its exclusive calcium-based microsphere technology
> contains tiny particles of calcium-based powder that form a scaffold around which
> the body produces new collagen to naturally restore the fullness and
> contours of the face. The tiny microspheres gradually break down into calcium and
> phosphate ions that are naturally absorbed by the body over time.
> · Radiesse’s biocompatible composition is harmonious with the body
> and poses virtually no risk of an allergic reaction.
> WHAT IT TREATS
> Radiesse is a long-lasting soft tissue augmentation material used to correct
> facial wrinkles and folds, such as nasolabial folds. It also used to correct
> facial lipoatrophy (facial wasting) associated with HIV therapy.
> WHAT SETS RADIESSE APART
> Radiesse is different because it is a next-generation product that is
> long-lasting.
> THE PROOF:
> Years of rigorous clinical testing and use by physicians in more than
> 200,000 patients worldwide demonstrate that Radiesse is safe and effective.
> Further, clinical studies show that the average Radiesse treatment lasts one year.
> WHO STANDS BY RADIESSE:
> BioForm Medical is a privately-held medical device company that develops and
> commercializes injectable implants for soft tissue augmentation.
> ML00179-00
>
> ********************************************
>
>
> Radiesse® 12-Month HIV Facial Lipoatrophy
> CLINICAL study BACKGROUNDER
>
> Trial Background:
> o A multi-site, clinical study examining the safety and efficacy of
> Radiesse injections for restorative treatment of HIV-associated facial
> lipoatrophy.
> o Conducted by BioForm Medical, Inc., a privately-held medical
> device company specializing in injectable products for soft tissue augmentation.
> o Trial conducted under an Investigational Device Exemption (IDE)
> granted by the FDA.
> Trial Design:
> o Conducted at three medical centers in the United States, including
> two centers in New York City and one in San Francisco.
> o 100 patients with HIV-associated facial lipoatrophy were enrolled
> in the trial.
> o All study patients received an injection of Radiesse during initial
> visit and were seen one month later for touch up injections as necessary.
> o Additional follow up conducted at three and six months.
> Key Findings:
> o Patients were scored by their physician for improved appearance on
> the Global Aesthetic Improvement Scale (GAIS). Finding 12 months after
> treatment with Radiesse showed:
> · 32 percent of patients’ appearance were Very Much Improved
> · 52 percent of patients’ appearance were Much Improved
> · 16 percent of patients’ appearance were Improved
> · 0 percent of patients’ appearance was Unchanged
> · 0 percent of patients’ appearance was Worse
> o During the study, patients were asked how treatment with Radiesse
> had affected their quality of life. At 12-months follow up:
> · 100 percent of patients said that treatment with Radiesse had been
> beneficial
> · 99 percent of patients said they were more confident about their
> appearance after treatment with Radiesse
> · 99 percent of patients said they would recommend treatment with
> Radiesse
> · 98 percent of patients said that they felt more attractive after
> treatment with Radiesse
> · 97percent of patients said that they felt their emotional state
> had improved after treatment with Radiesse
> o Radiesse was safe and well tolerated, with no serious
> device-related adverse events reported. In all 100 patients, Radiesse was proven safe for
> injection.
> Data Publication/ Presentation:
> Study results were presented at the recent meetings of the American Society
> of Plastic Surgery (ASPS) and American Academy of Facial Plastic and
> Reconstructive Surgery (AAFPRS).
> Findings were published in a special supplement of the September 2005 issue
> of Plastic Surgery Journal.
> Current Indications:
> Radiesse is currently approved in the U.S. for treatment of the following
> conditions:
> * Oral/Maxillofacial Defects
> * Vocal Fold Insufficiency
> * Radiographic Tissue Marking
>
> ML00180-00
>
> Regards,
>
> Nelson Vergel
> powerusa dot org
>

#18407 From: PoWeRTX@...
Date: Fri Sep 1, 2006 12:11 am
Subject: 10,000 steps to lose weight
nelsonvergel
Offline Offline
Send Email Send Email
 
To lose belly fat, get a pedometer and take 10,000 steps a day
 
 
 
Regards,

Nelson Vergel
powerusa dot org

#18406 From: PoWeRTX@...
Date: Thu Aug 31, 2006 3:03 pm
Subject: Fwd: Silicone treatments for HIV lipoatrophy in SF
nelsonvergel
Offline Offline
Send Email Send Email
 
In a message dated 8/31/2006 2:00:59 P.M. Central Standard Time, ZSkinCenter writes:
Dear Mr. Vergel,

A patient brought to my attention your excellent page about lipoatrophy reconstructive procedures on facial wasting.org.  I wanted to send you a note just to let you know that there IS someone here in San Francisco providing microdroplet silicone treatments for HIV patients with lipoatrophy.  I have had my practice at CPMC Medical Center for eight years now and have been doing lipoatrophy correction procedures since 1996.  Patients have been coming to me since 2002 for silicone treatments, and we have not had one single side effect or complication with the microdroplet procedure, and with consistently excellent results.  I generally treat one to three patients per day.  We also provide Sculptra treatments, but I just wanted to let you know that the silicone option (and it is an excellent one) is available to patients here in San Francisco.

Sincerely,

Gaetano Zanelli, M.D.
45 Castro St. Suite 215
San Francisco, CA   94114
(415) 487-1846
 
Regards,

Nelson Vergel
powerusa dot org
Dear Mr. Vergel,

A patient brought to my attention your excellent page about lipoatrophy reconstructive procedures on facial wasting.org.  I wanted to send you a note just to let you know that there IS someone here in San Francisco providing microdroplet silicone treatments for HIV patients with lipoatrophy.  I have had my practice at CPMC Medical Center for eight years now and have been doing lipoatrophy correction procedures since 1996.  Patients have been coming to me since 2002 for silicone treatments, and we have not had one single side effect or complication with the microdroplet procedure, and with consistently excellent results.  I generally treat one to three patients per day.  We also provide Sculptra treatments, but I just wanted to let you know that the silicone option (and it is an excellent one) is available to patients here in San Francisco.

Sincerely,

Gaetano Zanelli, M.D.
45 Castro St. Suite 215
San Francisco, CA   94114
(415) 487-1846

#18405 From: hoppefaith@...
Date: Fri Sep 1, 2006 12:31 am
Subject: Re: Hep A re-vax for hiv +.. A question to the group
bjncarlsbad
Offline Offline
Send Email Send Email
 
A few days ago  I had a re-vaccination of Hep A vaccine because my levels showed borderline.. The  last time I was vaccinated was  primary on Oct 2001 and secondary on June 2002 (6 MONTHS  later) . My question?? After my vax from a few  days ago., do I get another vax in 6 months to serve as my secondary vax in this series , as is normal protocol,or just stick with the one addl booster that I just had ?? Or check lab values in 6 months to see if  levels are borderline again??? thanks.. Luke.

#18404 From: PoWeRTX@...
Date: Fri Sep 1, 2006 12:34 am
Subject: A new option for HIV facial wasting to be approved in the US soon
nelsonvergel
Offline Offline
Send Email Send Email
 

I had a call with Bioform, the makers of Radiesse yesterday.  I am organizing a group of treatment activists to meet with them to discuss their patient assistance program design soon. We still do not know what the cost for HIV related work will be or what the patient assistance program will look like. I am hoping that they will be as easy to work with as Dermik (Sculptra) was.

 

From FACIALWASTING.ORG:

 

Radiesse (also called Radiense) is  (calcium hydroxylapatite, (CaHA) microspheres suspended in an aqueous polysaccharide gel.  Radiance, the newest product in the market, is not approved in the US as a facial filler yet but doctors are using it under an IDE study.  It is manufactured by Bioform of Franksville, Wisconsin.  In general, calcium hydroxylapatite has safely been used in the body for many applications including dental applications where bone build-up is needed for reconstruction and also in block form for cosmetic applications such as cheek, jaw, cranial and chin implants (hard bony areas). Calcium hydroxylapatite creates a lattice where the surrounding cells can be incorporated from ossification in bony areas to a stable scaffold in which soft tissue can grow. The calcium hydroxylapatite microspheres are suspended in a polysaccharide carrier which holds the microspheres in place until it is resorbed and the collagenation takes place.  When injected in soft tissue, away from bone, fibroblasts work by building reportedly a non-scar tissue collagen type, thus creating volume in the treatment area. Its unclear where this material should be injected (dermally or sub dermally) to achieve correction of facial defects. It is being used in small quatities for wrinkle treatment and lip augmentation. It tends to be unforgiving if not applied properly. An allergy test is supposedly not needed. The especulated longevity is 2 to 5 years .

 

More about a study here: http://dermatology.cdlib.org/102/therapy/HIV/comite.html

 

 

INFORMATION FROM THE COMPANY:

*************************************************

 

RADIESSE® FACT SHEET

 

WHAT IS RADIESSE 

 

Radiesse is a next-generation, long-lasting product used for soft tissue augmentation.

 

·        Radiesse consists of calcium-based microsphere technology that naturally promotes the growth of a patient’s own collagen.  

 

·        Radiesse provides a correction that has been proven to last one year without surgery.

 

·        Radiesse is not permanent and therefore avoids the risks associated with permanent materials.

 

HOW IT WORKS

 

Radiesse is an injectable product consisting of tiny calcium-based particles that replace volume loss and also stimulate new collagen growth for long-lasting clinical results.

 

·        Radiesse is gently injected into the skin in very small amounts with a very fine needle. Its exclusive calcium-based microsphere technology contains tiny particles of calcium-based powder that form a scaffold around which the body produces new collagen to naturally restore the fullness and contours of the face. The tiny microspheres gradually break down into calcium and phosphate ions that are naturally absorbed by the body over time.

 

·        Radiesse’s biocompatible composition is harmonious with the body and poses virtually no risk of an allergic reaction.

 

WHAT IT TREATS

 

Radiesse is a long-lasting soft tissue augmentation material used to correct facial wrinkles and folds, such as nasolabial folds.  It also used to correct facial lipoatrophy (facial wasting) associated with HIV therapy.

 

WHAT SETS RADIESSE APART

 

Radiesse is different because it is a next-generation product that is long-lasting.

 

THE PROOF:

 

Years of rigorous clinical testing and use by physicians in more than 200,000 patients worldwide demonstrate that Radiesse is safe and effective. Further, clinical studies show that the average Radiesse treatment lasts one year.

 

WHO STANDS BY RADIESSE:

 

BioForm Medical is a privately-held medical device company that develops and commercializes injectable implants for soft tissue augmentation.

 

ML00179-00

 
********************************************
 

Radiesse® 12-Month HIV Facial Lipoatrophy

CLINICAL study BACKGROUNDER

 

Trial Background:

o       A multi-site, clinical study examining the safety and efficacy of Radiesse injections for restorative treatment of HIV-associated facial lipoatrophy. 

o       Conducted by BioForm Medical, Inc., a privately-held medical device company specializing in injectable products for soft tissue augmentation.

o       Trial conducted under an Investigational Device Exemption (IDE) granted by the FDA.

Trial Design:

o       Conducted at three medical centers in the United States, including two centers in New York City and one in San Francisco.

o       100 patients with HIV-associated facial lipoatrophy were enrolled in the trial.

o       All study patients received an injection of Radiesse during initial visit and were seen one month later for touch up injections as necessary.

o       Additional follow up conducted at three and six months.


Key Findings:

 

o       Patients were scored by their physician for improved appearance on the Global Aesthetic Improvement Scale (GAIS).  Finding 12 months after treatment with Radiesse showed:

·        32 percent of patients’ appearance were Very Much Improved

·        52 percent of patients’ appearance were Much Improved

·        16 percent of patients’ appearance were Improved

·        0 percent of patients’ appearance was Unchanged

·        0 percent  of patients’ appearance was Worse

 

o       During the study, patients were asked how treatment with Radiesse had affected their quality of life.  At 12-months follow up:

·        100 percent of patients said that treatment with Radiesse had been beneficial

·        99 percent of patients said they were more confident about their appearance after treatment with Radiesse

·        99 percent of patients said they would recommend treatment with Radiesse

·        98 percent of patients said that they felt more attractive after treatment with Radiesse

·        97percent of patients said that they felt their emotional state had improved after treatment with Radiesse

 

o       Radiesse was safe and well tolerated, with no serious device-related adverse events reported.  In all 100 patients, Radiesse was proven safe for injection.

Data Publication/ Presentation:

Study results were presented at the recent meetings of the American Society of Plastic Surgery (ASPS) and American Academy of Facial Plastic and Reconstructive Surgery (AAFPRS).

 

Findings were published in a special supplement of the September 2005 issue of Plastic Surgery Journal. 

Current Indications:

Radiesse is currently approved in the U.S. for treatment of the following conditions:

  • Oral/Maxillofacial Defects
  • Vocal Fold Insufficiency
  • Radiographic Tissue Marking

 

 

ML00180-00

 

Regards,

Nelson Vergel
powerusa dot org

#18403 From: vaeagle2@...
Date: Thu Aug 31, 2006 8:51 pm
Subject: The Antidote for a High-Fat Meal
eesdc_2001
Offline Offline
Send Email Send Email
 
Exercise: The Antidote for a High-Fat Meal

By Kathleen Doheny
HealthDay Reporter 45 minutes ago

THURSDAY, Aug. 31 (HealthDay News) -- So, you've just polished off a meal high
in fat, and now you're feeling guilty? Wait an hour or two, then get a little
exercise, and you can reverse the potential damage to your arteries, a new study
suggests.

And you don't even have to head to the gym for that exercise. "We're talking
about a walk, we're not talking about changing your clothes and sweating," said
Janet P. Wallace, a professor of kinesiology at Indiana University, and lead
investigator for the study.

The study, coincidentally, follows another study published earlier this month in
the Journal of the American College of Cardiology in which researchers found
that eating just one piece of carrot cake high in saturated fat and drinking a
milkshake can reduce the body's ability to protect itself against heart disease.

The fat in the cake and shake, it seems, reduces the ability of the body's
"good" cholesterol -- the high-density lipoprotein, or HDL -- to do its job
--protecting the inner lining of the arteries from inflammatory substances that
promote vessel-clogging plaque.

According to Wallace, after a fatty meal, arteries lose their ability to expand
in response to an increase in blood flow. The effect peaks four to six hours
after eating -- usually just in time for your next meal. So, four hours after a
fatty meal, your arteries look like those of a person with heart disease, she
said.

"That post-meal period is a hot topic among all the researchers in heart
disease, diabetes and obesity," Wallace said. "That period sets up the
environment for the artery to be unhealthy. And when the artery is unhealthy,
that is when it leads to heart disease, insulin resistance and other problems."

To see if exercise could make a difference, Wallace and her colleagues studied
eight healthy 25-year-olds, looking at three scenarios. Each of the participants
-- five men and three women -- completed all three scenarios. They ate a low-fat
breakfast. They ate a high-fat breakfast. And they ate a high-fat breakfast
followed two hours later by a 45-minute walk on a treadmill at a moderate pace.
The high-fat meal contained about 48 grams of fat and the low-fat one actually
had no fat; each consisted of about 940 calories.

The researchers used a blood pressure cuff to measure blood flow in the brachial
artery, located in the arm, before and after each scenario. "The brachial artery
represents what is going on in the arteries of the heart," Wallace said.

After the high-fat meal alone, the brachial artery dilation dropped from 6
percent to 4 percent, Wallace said. "The ideal range is about 6 to 10," she
said. "A range of 3 to 5 is not good."

After the low-fat meal, dilation went from 6 percent to 6.5 percent, a slight
improvement.

But, "after the high-fat meal and exercise, it went from 6 percent (before the
meal) to 8 and a half percent," she said.

"Exercise does great things, and this obviously shows exercise is very effective
in counteracting that high-fat meal," Wallace added.

The study results were published in the September issue of the European Journal
of Applied Physiology.

Next, Wallace hopes to study the effect of exercise before a high-fat meal. "I
think we will find it works as well." She emphasized that her research isn't
meant to encourage people to indulge in high-fat fare. But she's realistic:
"There are people who are going to eat high-fat meals," she said.

If you're a fatty-food fan, Wallace suggests some exercise -- after getting your
doctor's OK.

But Jeannie Moloo, a Sacramento, Calif., registered dietitian and a spokeswoman
for the American Dietetic Association, offered a caveat about the study: "We
need to keep in mind the results apply only to the population investigated and
that was young, healthy and physically active adults. The small number of
subjects, only eight, makes it difficult to tell if there are differences in
responses between men and women."

And Moloo, like Wallace, cautioned that the research isn't an excuse to indulge
in fatty foods.

More information

To learn more about a healthy diet, visit the American Dietetic Association.

http://news.yahoo.com/s/hsn/20060831/hl_hsn/exercisetheantidoteforahighfatmeal

#18402 From: "lvrofnatur" <LvrOfNatur@...>
Date: Thu Aug 31, 2006 7:50 pm
Subject: re: drugs
rachelsmename
Offline Offline
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Personally, I would be upset if azt was removed from the market because I've been on it since 1996 and I have had an  undetectable viral load ever since. So it does provide great help in viral control for some. 
 
>>>I think AZT (Retrovir) along with d4T (Zerit) should be removed from the
market as they provide minimal viral control while over the long term
causing long term damage to the energy producing structures in human
cells known as the Mitochondria.

#18401 From: "Norm Stuart" <nspop2@...>
Date: Thu Aug 31, 2006 8:24 pm
Subject: Re: Reyataz does not affect lipid metabolism, even with Norvir boost
norm_w_stuart
Offline Offline
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Are you referring to the unfolded protein response (UPR) studies in mouse macrophages? Its interesting if they can show an increase in SREBP's in human macrophages. What's more important is the mechanism behind increased levels of SREBP's if this actually occurs.

C-Reactive Protein creates foam cells when it accumulates in macrophage-rich regions of developing atherosclerotic lesions and mediates uptake of native low-density lipoprotein (LDL) by macrophages, thereby potentially contributing to foam cell formation. So normalizing C-Reactive Protein is important regardless of the cause.

Many have observed an increase in blood pressure, with long-term use of protease inhibitors, and an associated rise in C-Reactive Protein. Others suggest that this is a normal aging effect unrelated to protease inhibitor use. This is why studies like Don Kotler's comparing lipodystrophy in normally aging HIV negative people with lipodytrophy in aging people with HIV. Unless you have the comparison, you can't be sure what you're really observing.

--- In PozHealth@yahoogroups.com, Butch Kara <longjohnmaniac@...> wrote:
>
> Norm, I was unaware that any protease inhibitors had been implicated in increasing C-reactive protein, which, as many of us know, is a marker for inflammation. My CRP tests always came back very low while I was on ritonovir, sequinavir, and lopinavir. Chronic HIV does cause elevated CRP as it's an inflammatory disease, which fact was mentioned in the first article I cited. However, the second mechanism of atherogenesis (forming arterial plaque) referred to in both articles has nothing to do with inflammation or elevated C reactive protein - they are talking about up-regulation of particular genetic expressions by the PI class of drugs, including atazanvir, which may increase arterial plaque by turning macrophages into foam cells (as well as by other routes at the cellular level). If so, despite either a good lipid and/or good inflammation profile, PI's may still pose a unique risk for developing heart disease.
> Tom in MO
>
> Original message:
> Re: Reyataz does not affect lipid metabolism, even with Norvir boost
> Posted by: "Norm Stuart" nspop2@... norm_w_stuart
> Date: Wed Aug 30, 2006 6:41 am (PDT)
>
> The episodic or chronic increase in C-Reactive Protein, associated with
> protease inhibitors, appears to be directly mediated by an increase in
> blood pressure, which in turn many believe is caused by increased body
> mass.
> There is no reliable evidence to associate this with Reyataz. Others
> have noted this same rise in blood pressure and C-Reactive Protein in
> people with HIV who have not been treated with protease inhibitors, and
> relate this to normal aging.
> Regardless of the cause, C-Reactive Protein can be normalized with
> either of two Angiotensin-2 Receptor Blockers, Micardis (telmisartan)
> and Benicar (olmesartan).
> Both of these ARBs virtually eliminate inflammation in the
> cardiovascular system, and also greatly reduce any existing
> inflammation
> in the liver and kidneys regardless of the cause. I agree with those
> who
> believe that arterial plaquing is a response to cardiovascular
> inflammation. Eliminate the inflammation and you have probably
> eliminated the arterial plaquing.
> Micardis provides the additional benefit that it can reduce elevated
> blood sugar. Micardis is structurally similar to the diabetic drug
> Actos
> (pioglitazone) being tested in people with HIV for lipodystrophy.
> Having taken both, I can say they both normalize blood pressure and
> C-Reactive Protein equally well, and Micardis does reduce HBA1C,
> essentially a hemoglobin measure of peak blood sugar levels.
> Micardis is slightly less convenient in that each tablet comes in a
> foil
> bubble pack in a box, whereas Benicar tablets are dispensed in a small
> bottle. The equivalent dose (not yet published) is 40 mg of Benicar
> equals 80 mg of Micardis.
>
>
> . Re: Reyataz does not affect lipid metabolism, even with Norvir
> boost
> Posted by: "Butch Kara" longjohnmaniac@... longjohnmaniac
> Date: Tue Aug 29, 2006 10:42 pm (PDT)
> Although it's good that even boosted atazanavir doesn't mess with
> your lipid levels, there may be more to PI's and atherosclerosis than
> lipid levels - it's been suspected for several years that PI's promote
> atherosclerosis through another mechanism. Apparently (see second citation
> below) this also includes atazanavir (Reyataz).
> Tom in MO
>
> J. Clin. Invest. 111:317-318 (2003). doi:10.1172/JCI200317746.
> Copyright ©2003 by the American Society for Clinical Investigation
> Commentary
> HIV protease inhibitors and atherosclerosis
> David Y. Hui
> Department of Pathology, University of Cincinnati College of
> Medicine, Cincinnati, Ohio, USA
> Address correspondence to: David Y. Hui, Department of Pathology,
> University of Cincinnati College of Medicine, 231 Albert Sabin Way,
> Cincinnati, Ohio 45267-0529, USA. Phone: (513) 558-9152; Fax: (513) 558-2141;
> E-mail: huidy@...
> The advent of highly active antiretroviral therapy (HAART), including
> the use of HIV protease inhibitors (PIs) has significantly reduced the
> morbidity and mortality of AIDS in HIV infected patients.
> Unfortunately, the adverse effects of PIs, including dyslipidemia, lipodystrophy,
> insulin resistance, and premature atherosclerosis, are cause for concern
> for their use in chronic management of HIV infection (1, 2). At
> present, the relationship between HAART and premature atherosclerosis in
> HIV-infected patients is unclear. Lipid abnormalities and insulin resistance
> induced by PIs can certainly increase the risk of premature
> atherosclerosis. Chronic inflammation associated with HIV infection, particularly
> the increased level of C reactive protein (3), may also contribute to
> accelerated atherosclerosis in these patients. Whether the treatment
> regimen alone directly contributes to accelerated atherosclerosis,
> however, has not been scrutinized vigorously.
> In this issue of the JCI, Dressman et al. showed that HIV PIs
> directly promote atherosclerosis in mice (4). Importantly, the authors
> demonstrated that PIs at a dosage that did not induce hyperlipidemia are
> potent promoters of atherosclerosis, thus providing the first evidence for a
> direct effect of PIs in atherosclerosis. Although the in vivo studies
> were performed in genetically-engineered mouse models of
> atherosclerosis, their in vitro results that PIs also induced foam cell formation in a
> human macrophage cell line are of significance.
> The study by Dressman et al. (4) also suggested that PIs directly
> promote atherosclerosis by inducing CD36 gene expression in macrophages.
> This observation is consistent with the documented role of macrophage
> CD36 in atherosclerosis (5). However, the results were in direct contrast
> to another study, which reported that PIs decreased monocyte CD36
> levels in healthy volunteers and HIV-infected individuals (6). The
> discrepancy between the two studies may be due to differences in experimental
> design. Whereas Dressman et al. examined CD36 mRNA and protein expression
> in mouse macrophages and differentiated human THP-1 cells, Serghides
> and colleagues focused on CD36 expression in human monocytes and
> undifferentiated THP-1 cells. Thus, it is possible that PIs have opposite
> effects on CD36 expression in monocytes and macrophages. If this turns out
> to be the case, PI-induced down regulation of CD36 expression in
> monocytes and other cell types may be responsible for impaired glucose
> tolerance, insulin resistance, and hyperlipidemia (6), whereas their
> up-regulation of macrophage CD36 may promote foam cell formation and
> atherosclerosis (4). CD36 is a major fatty acid transporter in tissues
> with high metabolic capacity (5). Its down-regulation in tissues such as
> the heart, adipose, and skeletal muscle would impair fatty acid
> utilization and decrease insulin responsiveness in these tissues, thus
> resulting in glucose intolerance, insulin resistance, and hyperlipidemia. These
> two effects may act synergistically in promoting premature
> atherosclerosis.
> Dressman et al. (4) also found that PI-induced macrophage CD36
> expression is related to the activation of PPAR in a protein kinase C
> dependent manner. How compounds designed to inhibit protease activity
> influence protein kinase C activity and activate PPAR gene transcription
> remains unclear. However, it is now established that PIs, particularly
> ritonavir, are also inhibitors of proteasome-mediated protein degradation
> pathways (7, 8). These include their inhibition of activated SREBP
> degradation, resulting in constitutive activation of SREBP-1 and SREBP-2
> responsive genes (8). Since activated SREBPs are also promoters of PPAR
> expression (9), the PI-induced PPAR and CD36 expression may be mediated via
> PI-induced activated SREBP accumulation in the macrophage nucleus. This
> hypothesis would predict that PIs promote atherosclerosis through two
> mechanisms, both involving increased SREBP activity (Figure 1). One
> mechanism is through PI-induced metabolic complications that
> increased the risk of atherosclerosis; the other mechanism is a direct
> effect of PIs on macro-phage foam cell formation. If this hypothesis is
> proven correct, then novel compounds that inactivate SREBP activity may
> be designed and used to alleviate both metabolic and cellular
> complications that pro-mote cardiovascular events associated with HAART.
>
> ***************
> Molecular Pharmacology Fast Forward
> First published on June 23, 2005; DOI: 10.1124/mol.105.012898
>
> HIV Protease Inhibitors Activate the Unfolded Protein Response in
> Macrophages: Implication for Atherosclerosis and Cardiovascular Disease
> Huiping Zhou, William M. Pandak, Jr., Vijay Lyall, Ramesh Natarajan,
> and Phillip B. Hylemon
> Department of Microbiology & Immunology (H.Z., P.B.H.), Division of
> Gastroenterology, Department of Internal Medicine and McGuire Veterans
> Affairs Medical Center (W.M.P.), Department of Physiology (V.L.), and
> Division of Pulmonary and Critical Care Medicine, Department of Internal
> Medicine (R.N.), Virginia Commonwealth University, Richmond, Virginia
>
> Human immunodeficiency virus (HIV) protease inhibitors have been
> successfully used in highly active antiretroviral therapy for HIV-1
> infection. Treatment of patients infected with HIV with HIV protease
> inhibitors is unfortunately associated with a number of clinically significant
> metabolic abnormalities and an increased risk of premature
> atherosclerosis and myocardial infarction. However, the cellular/molecular
> mechanisms of the HIV protease inhibitor-induced lipid dysregulation and
> atherosclerosis remain elusive. Macrophages are the most prominent cell type
> present in athe rosclerotic lesions and play essential roles in both
> early lesion development and late lesion complications. In this study, we
> demonstrate that three different HIV protease inhibitors (ritonavir,
> indinavir, and atazanavir) induce endoplasmic reticulum stress and
> activate the unfolded protein response in mouse macrophages. Furthermore, at
> therapeutic concentrations (5-15 µM), these HIV protease
> inhibitors were found to increase the levels of transcriptionally
> active sterol regulatory element binding proteins, decrease endogenous
> cholesterol esterification, cause the accumulation of free cholesterol in
> intracellular membranes, deplete endoplasmic reticulum calcium stores,
> activate caspase-12, and increase apoptosis in macrophages. These
> findings provide possible cellular mechanisms by which HIV protease
> inhibitors promote atherosclerosis and cardiovascular disease in HIV-1 infected
> patients treated with HIV protease inhibitors.
> Received March 16, 2005; accepted June 23, 2005
> Address correspondence to: Dr. Phillip B. Hylemon, Department of
> Microbiology and Immunology, Virginia Commonwealth University, P.O. Box
> 980678, Richmond, VA 23298-0678. E-mail: hylemon@...
>
>
> Original message:
> Reyataz does not affect lipid metabolism - even with Norvir boost
> Posted by: "Norm Stuart" nspop2@... norm_w_stuart
> Date: Tue Aug 29, 2006 6:36 am (PDT)
>
> Impact of Boosted vs Unboosted Atazanavir-based Regimens on the Lipid
> Profiles of HIV Positive Patients
> Conclusion
> The authors concluded, "There does not appear to be a difference
> between
> atazanavir and atazanavir/ritonavir [in their effect] on total
> cholesterol and triglycerides over the first 3 months
>
>
> ---------------------------------
> Do you Yahoo!?
> Everyone is raving about the all-new Yahoo! Mail.
>


#18400 From: "Norm Stuart" <nspop2@...>
Date: Thu Aug 31, 2006 7:23 pm
Subject: Re: new member / Zerit vs new meds & Sculptra
norm_w_stuart
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The other more effective drug for ITP was probably Rituxan, a monoclonal antibody to CD20. This attaches to "B cells" and marks them for destruction. Removing the current population of B cells often stops ITP. Rituxan is also a super treatment for B cell lymphoma. Apart from the occassional allergic reaction, Rituxan is remarkably side-effect free.

As for Carnitine. Once d4T has killed off 85% of your mitochondria, you will probably experience metabolic problems from this for the rest of your life, even though you stopped taking d4T thirty years ago. If there is re-popualtion of mitochondria, it appears to be very slow.

Carnitine is like a train of boxcars, available to bring raw materials to the mitochindria. If 85% of your Mitochondria are gone, then adding boxcars to keep the remaining mitochondrial factories well supplied will help the remaining mitochondria operate at full capacity. So taking Carnitor / Carnitine will help.

But boxcars won't protect the mitochondrial factories from bombing raids by d4T or AZT. If the factory machinery is damaged, more raw material won't help. There will already lots of raw material waiting on the shipping dock to be processed, which can't be processed because the machinery is damaged.

People taking protease inhibitors have eleated lipids due to a problem with the PPAR-alpha nuclear structures being inhibited. Since this doesn't have anything to do with Mitochondria, Carnitine won't help solve this problem - but Tricor can. 

 

--- In PozHealth@yahoogroups.com, "Bill Gaul" <wgaul1@...> wrote:
>
> Norm -
>
> The thrombocytopenia was determined to be ITP - an immune reaction to the Crixivan. It was sudden in onset (only caught it because I was in the second week of a Phase 1 study) and repeated on re-challenge. It's rare, but is established as a side effect now. There was an article published in the journal "Blood" on my case. The hematologist I saw after the second onset (the first was treated with Immune-globulin) said I was producing very healthy platelets, even though reduced in number, so I had no symptoms. Apparently thrombocytopenia causes lower counts - and - less healthy platelets usually. They did say they were surprised I didn't even bruise from blood draws. That 11,000 is very low and dangerous. The ER physician that did my intake looked under my watch band and said "hmm..." after he got the test results. He was expecting purple markings. I cleared the second bout with prednisone. The more effective treatment wasn't approved by Merk, and also supposedly isn't as effective with repeated use.
>
> What doesn't make sense about your statement about Carnitor is: What about new and undamaged fat cells? Wouldn't improved function help to prevent the kind of changes mitochondrial damage causes, and maybe even further DNA damage? It's certainly worth a try - and cheaper than liposuction. I don't think Zerit is the only problem med in this area. I haven't taken it for four years now, and still have a lot of metabolic repercussions. I wouldn't disagree on the facial wasting issue re: Zerit, since it usually doesn't reverse and I've had it for about five years, or more.
>
> BG
> ----- Original Message -----
> From: Norm Stuart
> To: PozHealth@yahoogroups.com
> Sent: Tuesday, August 29, 2006 4:33 PM
> Subject: [PozHealth] Re: new member / Zerit vs new meds & Sculptra
>
>
> Taking L-Carnitine can help improve the production of remaining mitochondria in people who have depleted mitochondria populations.
>
> While I have no idea what drugs you were being given for low platelet counts, I am not aware of any treatments which make the remaining platelets more effective. All treatments for thrombocytopenia I know of are designed to reduce the destruction of platelets or increase production of platelets.
>
> With a platelet count of 11,000 (compared with a more normal range of 140,000 to 250,000) it would be safe to say that these tretaments were not working well, regardless of what they were.
>
> Your lack of symptoms, such as bruising, is not unusual. Often, low platelet levels do not lead to clinical problems; rather, they are picked up on a routine full blood count. Occasionally, there may be bruising, nosebleeds and/or bleeding gums - but this is not typical in thrombocytopenia. But if you received an injury, only a blood transfusion would have saved your life.
>


#18399 From: PoWeRTX@...
Date: Thu Aug 31, 2006 3:02 pm
Subject: I am looking for help
nelsonvergel
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Gang
 
I am looking to hire someone for 10 hours or so to look at archives in pozhealth and pull out good emails that may help people who are just joining (frequently asked questions, etc). I am planning to make a free e-book available with "best of pozhealth"
 
I am looking for someone who:
1- understands medical terms
2-is stable and self directed
3- knows how to format in MS Word
4- keeps his/her word
5- has the time
 
 
Please email me directly
 
Regards,

Nelson Vergel
powerusa dot org

#18398 From: PoWeRTX@...
Date: Thu Aug 31, 2006 2:51 pm
Subject: No more emails on the Kaiser study
nelsonvergel
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Per the moderator
 
Good points were raised from both sides of the argument.
 
Thanks
 
Regards,

Nelson Vergel
powerusa dot org

#18397 From: PoWeRTX@...
Date: Thu Aug 31, 2006 2:34 pm
Subject: U.S. ADAP Waiting Lists Shrink, but Not for Long, Report Warns
nelsonvergel
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U.S. ADAP Waiting Lists Shrink, but Not for Long, Report Warns
The number of Americans on AIDS Drug Assistance Program (ADAP) waiting lists has dropped sharply in the last few months, but the respite may be only temporary, according to the latest "ADAP Watch" released by the National Alliance of State and Territorial AIDS Directors. The report said that 310 people in five U.S. states were currently on a waiting list to receive HIV meds, down from 791 people in nine states in February. However, some of the states that were able to eliminate their waiting lists this year are on the verge of starting new ones, and several other states have recently introduced new restrictions or expect to do so soon, the report says. Click Here
 
Regards,

Nelson Vergel
powerusa dot org

#18396 From: WEBcfm@...
Date: Thu Aug 31, 2006 2:15 pm
Subject: Fwd: a question for you
WEBcfm@...
Send Email Send Email
 
In a message dated 8/30/2006 1:02:07 AM Eastern Daylight Time, WEBcfm writes:
Hi Nelson,
I noticed a posting of yours, and I thought I had saved it, but I can't find it.  It was about some kind of hair gel with 2.5 minoxidil and something about Nizoril shampoo.
I've always had a full and healthy head of hair, but lately it looks like there's a gerbil in the drain after showering.  I looked in the hair care isle at the store today and all I saw was Rogaine, and it was 5.0, and it was like a lotion.  I think it was between $30 and $50, depending on the size.  I didn't see any GEL, or anything with a lesser strength.
Also, I have prescription strength Nizoril shampoo..is that the shampoo you were referring to? 
Can you give me a brand name of the other product, and tell me where I might find it.  Maybe there's a bar code with an order number, and the company name.
My viral load was undetectable for quite awhile, and six mo's ago it went up to 12,000..then the next visit to the doctor it went up to 49,000.  I'm wondering if this could have something to do with my hair falling out.  I'm 53 yrs old and still have alot of hair! 
I also had a urinary tract infection that lasted six months.  It was from getting a cystoscopy. They pushed bacteria inside me with the instrument, and it took several rounds of different antibiotics to clear it up.  I don't know if that has anything to do with the hair loss.
By the way, I met you at the Mid Fairfield Dinner in Norwalk Ct, where you were the speaker.  I was the guy with the beard and glasses..and hair..lol. 
BTW I did get six Sculptra treatments...looks pretty good now!
If you could send me the info on these hair products, I'd appreciate it.
Thanks very much!  I learn alot on this mailing list..thank u for creating it.
:) Charlie
Hi Nelson,
I noticed a posting of yours, and I thought I had saved it, but I can't find it.  It was about some kind of hair gel with 2.5 minoxidil and something about Nizoril shampoo.
I've always had a full and healthy head of hair, but lately it looks like there's a gerbil in the drain after showering.  I looked in the hair care isle at the store today and all I saw was Rogaine, and it was 5.0, and it was like a lotion.  I think it was between $30 and $50, depending on the size.  I didn't see any GEL, or anything with a lesser strength.
Also, I have prescription strength Nizoril shampoo..is that the shampoo you were referring to? 
Can you give me a brand name of the other product, and tell me where I might find it.  Maybe there's a bar code with an order number, and the company name.
My viral load was undetectable for quite awhile, and six mo's ago it went up to 12,000..then the next visit to the doctor it went up to 49,000.  I'm wondering if this could have something to do with my hair falling out.  I'm 53 yrs old and still have alot of hair! 
I also had a urinary tract infection that lasted six months.  It was from getting a cystoscopy. They pushed bacteria inside me with the instrument, and it took several rounds of different antibiotics to clear it up.  I don't know if that has anything to do with the hair loss.
By the way, I met you at the Mid Fairfield Dinner in Norwalk Ct, where you were the speaker.  I was the guy with the beard and glasses..and hair..lol. 
BTW I did get six Sculptra treatments...looks pretty good now!
If you could send me the info on these hair products, I'd appreciate it.
Thanks very much!  I learn alot on this mailing list..thank u for creating it.
:) Charlie

#18395 From: PoWeRTX@...
Date: Thu Aug 31, 2006 2:35 pm
Subject: Body Fat Changes in People With HIV: A Talk With Todd Brown, M.D.
nelsonvergel
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Body Fat Changes in People With HIV: A Talk With Todd Brown, M.D.
Todd Brown, M.D., is an HIV researcher with the Johns Hopkins School of Medicine; his research focuses on metabolic and skeletal problems in HIV-infected people. In this interview with The Body PRO's David Wohl, M.D., Dr. Brown discusses the research he presented at AIDS 2006 regarding lipodystrophy in HIV-infected patients. Click Here
 
Regards,

Nelson Vergel
powerusa dot org

#18394 From: John Barrow <pozbod@...>
Date: Thu Aug 31, 2006 6:29 pm
Subject: Kaiser, redux
johnftl59
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One last comment, before blood spatters from the dead horse contaminate the list, further.

I just find this discussion terribly ironic. Here we have a small scale study, let's assume honest in intent, that detects a single positive parameter with a very small N. Every other parameter fails to show benefit, including what must be presumed to be the key endpoint, improvements in neuropathy.

Is anyone really impressed by a 25% increase in T cells in the treatment group, when that treatment group started, somehow, with about 25% fewer t cells than the control groups? It seems logical that in an impoverished patient demographic, nutrition is a good thing, but I don't feel the ground shifting under anything. The treatment group caught up to the control group, it did not surpass it.

Is the question of D4T/DDI consequences worth looking at today? And George, I was on that combo in 1995! And got off ASAP, when PIs became available. It is dangerous to use that combo, for risks of pancreatitis, neuropathy, etc. It's hard to believe there were large numbers of people using it in 2003, as the risks were well known by then.

And how come, all of a sudden, questioning the motives of a guy who sells highly marked up vitamins is unfair, when every legitimate drug study is rejected because of possible financial links to drug companies by the vitamin lobby here?

Topic dead, discuss among yourselves............


John Barrow




#18393 From: PoWeRTX@...
Date: Thu Aug 31, 2006 2:34 pm
Subject: Selenium Improves HIV Treatment Response in Nigerian Randomized Study
nelsonvergel
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Selenium Improves HIV Treatment Response in Nigerian Randomized Study
Dramatic results from a large study in Nigeria suggest that patients with advanced HIV disease who take selenium supplements along with their antiretrovirals could experience a CD4+ cell count boost twice as quickly as patients who take antiretrovirals alone. All of the 340 Nigerians who took part in the 72-week study had extremely low CD4+ cell counts when they started treatment, suggesting the impact of selenium may be much greater for patients who are diagnosed late in the course of their infection. Patients who took a daily dose of 200 micrograms of selenium with their antiretrovirals also experienced more weight gain, fewer opportunistic infections and higher hemoglobin levels. Click Here
 
Regards,

Nelson Vergel
powerusa dot org

#18392 From: PoWeRTX@...
Date: Thu Aug 31, 2006 10:10 am
Subject: Topical Version of Protease Inhibitor May Treat HPV
nelsonvergel
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Topical Version of Protease Inhibitor May Treat HPV

by Tim Horn

August 29, 2006 (AIDSmeds)—British researchers at the University of Manchester have discovered a new use for an already approved HIV treatment. The HIV protease inhibitor lopinavir, one of the two drugs in Kaletra®, appears to be active against human papillomavirus (HPV), one of the most common sexually transmitted infections and responsible for precancerous and cancerous lesions of the anus and cervix.

Throughout the world, many HIV-positive men and women undergo surgery and other invasive procedures to remove to remove precancerous and cancerous lesions caused by HPV infection every year. But if the University of Manchester research pans out, it may be possible to treat these lesions topically, using a cream, gel, or ointment version of lopinavir. The discovery may be even more significant in developing countries which lack surgical facilities and where HPV-related cervical cancer is one of the most common forms of cancer in women.

Ian Hampson, MD, of the School of Medicine's Division of Human Development and Reproduction and his colleagues report that lopinavir – and to a lesser extent indinavir (Crixivan®) – selectively killed HPV-infected cervical cancer cells in test tube studies. Because Kaletra is already available as a liquid formulation, Dr. Hampson suggests, it may work by direct application to HPV lesions.

The research is to be published in the September issue of the journal Antiviral Therapy and is also being presented at the 23rd International Papillomavirus Conference & Clinical Workshop in Prague on September 5th.

As explained by Dr. Hampson, "It is very exciting to find such a significant new use for this HIV drug which is already licensed and FDA-approved for oral administration. We are currently exploring the means of delivering this drug directly to the affected tissue. We would then move to a clinical trial. If this proves successful we could see the treatment available fairly rapidly."

He added: "Anti-HPV vaccines are currently in the process of being licensed but, not all lesions will be prevented and not all women will be vaccinated. A non-surgical therapy will have significant advantages – better preservation of obstetric function, the potential for use in resource-poor settings such as underdeveloped countries and it may appeal more to women than surgery.”

While the immediate plan is to study topical lopinavir in HIV-negative women with cervical HPV disease, it is likely that men and women with anal lesions caused by HPV – along with HIV-positive people with cervical and anal HPV involvement – will be included in clinical trials as well. 

 
Regards,

Nelson Vergel
powerusa dot org

#18391 From: John Barrow <pozbod@...>
Date: Thu Aug 31, 2006 3:01 am
Subject: Re: drugs
johnftl59
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"I just got better info of what my friend is going to start on.
Zidovudine, Retrovir, and Trevada. Does this sound like a good
combination? He was on Viread, Kalatra, And Epivir. The Epivir failed
and they gave him something else that put him in ICU with a VERY high
fever and Very low blood pressure. Any info would greatly be accepted."

I think there's some information missing here.

Zidovudine is the chemical name and Retrovir the brand name for AZT. It would be strange to mix AZT with Tenofavir and FTC, the medications in Truvada.

I have no idea which drug gave him problems, though if I had to guess, it would be Abacavir.



John Barrow




#18390 From: Butch Kara <longjohnmaniac@...>
Date: Thu Aug 31, 2006 4:02 am
Subject: Re: Reyataz does not affect lipid metabolism, even with Norvir boost
longjohnmaniac
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Norm, I was unaware that any protease inhibitors had been implicated in increasing C-reactive protein, which, as many of us know, is a marker for inflammation.  My CRP tests always came back very low while I was on ritonovir, sequinavir, and lopinavir. Chronic HIV does cause elevated CRP as it's an inflammatory disease, which fact was mentioned in the first article I cited.   However, the second mechanism of atherogenesis (forming arterial plaque) referred to in both articles has nothing to do with inflammation or elevated C reactive protein - they are talking about up-regulation of particular genetic expressions by the PI class of drugs, including atazanvir, which may increase arterial plaque by turning macrophages into foam cells (as well as by other routes at the cellular level).   If so, despite either a good lipid and/or good inflammation profile, PI's may still pose a unique risk for developing heart disease.
Tom in MO
 
Original message:
Re: Reyataz does not affect lipid metabolism, even with Norvir boost
Posted by: "Norm Stuart" nspop2@... norm_w_stuart
Date: Wed Aug 30, 2006 6:41 am (PDT)
 
The episodic or chronic increase in C-Reactive Protein, associated with
protease inhibitors, appears to be directly mediated by an increase in
blood pressure, which in turn many believe is caused by increased body
mass.
There is no reliable evidence to associate this with Reyataz. Others
have noted this same rise in blood pressure and C-Reactive Protein in
people with HIV who have not been treated with protease inhibitors, and
relate this to normal aging.
Regardless of the cause, C-Reactive Protein can be normalized with
either of two Angiotensin-2 Receptor Blockers, Micardis (telmisartan)
and Benicar (olmesartan).
Both of these ARBs virtually eliminate inflammation in the
cardiovascular system, and also greatly reduce any existing
inflammation
in the liver and kidneys regardless of the cause. I agree with those
who
believe that arterial plaquing is a response to cardiovascular
inflammation. Eliminate the inflammation and you have probably
eliminated the arterial plaquing.
Micardis provides the additional benefit that it can reduce elevated
blood sugar. Micardis is structurally similar to the diabetic drug
Actos
(pioglitazone) being tested in people with HIV for lipodystrophy.
Having taken both, I can say they both normalize blood pressure and
C-Reactive Protein equally well, and Micardis does reduce HBA1C,
essentially a hemoglobin measure of peak blood sugar levels.
Micardis is slightly less convenient in that each tablet comes in a
foil
bubble pack in a box, whereas Benicar tablets are dispensed in a small
bottle. The equivalent dose (not yet published) is 40 mg of Benicar
equals 80 mg of Micardis.
 
 
. Re: Reyataz does not affect lipid metabolism, even with Norvir
boost
Posted by: "Butch Kara" longjohnmaniac@... longjohnmaniac
Date: Tue Aug 29, 2006 10:42 pm (PDT)
Although it's good that even boosted atazanavir doesn't mess with
your lipid levels, there may be more to PI's and atherosclerosis than
lipid levels - it's been suspected for several years that PI's promote
atherosclerosis through another mechanism. Apparently (see second citation
below) this also includes atazanavir (Reyataz).
Tom in MO
J. Clin. Invest. 111:317-318 (2003). doi:10.1172/JCI200317746.
Copyright ©2003 by the American Society for Clinical Investigation
Commentary
HIV protease inhibitors and atherosclerosis
David Y. Hui
Department of Pathology, University of Cincinnati College of
Medicine, Cincinnati, Ohio, USA
Address correspondence to: David Y. Hui, Department of Pathology,
University of Cincinnati College of Medicine, 231 Albert Sabin Way,
Cincinnati, Ohio 45267-0529, USA. Phone: (513) 558-9152; Fax: (513) 558-2141;
E-mail: huidy@....
The advent of highly active antiretroviral therapy (HAART), including
the use of HIV protease inhibitors (PIs) has significantly reduced the
morbidity and mortality of AIDS in HIV infected patients.
Unfortunately, the adverse effects of PIs, including dyslipidemia, lipodystrophy,
insulin resistance, and premature atherosclerosis, are cause for concern
for their use in chronic management of HIV infection (1, 2). At
present, the relationship between HAART and premature atherosclerosis in
HIV-infected patients is unclear. Lipid abnormalities and insulin resistance
induced by PIs can certainly increase the risk of premature
atherosclerosis. Chronic inflammation associated with HIV infection, particularly
the increased level of C reactive protein (3), may also contribute to
accelerated atherosclerosis in these patients. Whether the treatment
regimen alone directly contributes to accelerated atherosclerosis,
however, has not been scrutinized vigorously.
In this issue of the JCI, Dressman et al. showed that HIV PIs
directly promote atherosclerosis in mice (4). Importantly, the authors
demonstrated that PIs at a dosage that did not induce hyperlipidemia are
potent promoters of atherosclerosis, thus providing the first evidence for a
direct effect of PIs in atherosclerosis. Although the in vivo studies
were performed in genetically-engineered mouse models of
atherosclerosis, their in vitro results that PIs also induced foam cell formation in a
human macrophage cell line are of significance.
The study by Dressman et al. (4) also suggested that PIs directly
promote atherosclerosis by inducing CD36 gene expression in macrophages.
This observation is consistent with the documented role of macrophage
CD36 in atherosclerosis (5). However, the results were in direct contrast
to another study, which reported that PIs decreased monocyte CD36
levels in healthy volunteers and HIV-infected individuals (6). The
discrepancy between the two studies may be due to differences in experimental
design. Whereas Dressman et al. examined CD36 mRNA and protein expression
in mouse macrophages and differentiated human THP-1 cells, Serghides
and colleagues focused on CD36 expression in human monocytes and
undifferentiated THP-1 cells. Thus, it is possible that PIs have opposite
effects on CD36 expression in monocytes and macrophages. If this turns out
to be the case, PI-induced down regulation of CD36 expression in
monocytes and other cell types may be responsible for impaired glucose
tolerance, insulin resistance, and hyperlipidemia (6), whereas their
up-regulation of macrophage CD36 may promote foam cell formation and
atherosclerosis (4). CD36 is a major fatty acid transporter in tissues
with high metabolic capacity (5). Its down-regulation in tissues such as
the heart, adipose, and skeletal muscle would impair fatty acid
utilization and decrease insulin responsiveness in these tissues, thus
resulting in glucose intolerance, insulin resistance, and hyperlipidemia. These
two effects may act synergistically in promoting premature
atherosclerosis.
Dressman et al. (4) also found that PI-induced macrophage CD36
expression is related to the activation of PPAR in a protein kinase C
dependent manner. How compounds designed to inhibit protease activity
influence protein kinase C activity and activate PPAR gene transcription
remains unclear. However, it is now established that PIs, particularly
ritonavir, are also inhibitors of proteasome-mediated protein degradation
pathways (7, 8). These include their inhibition of activated SREBP
degradation, resulting in constitutive activation of SREBP-1 and SREBP-2
responsive genes (8). Since activated SREBPs are also promoters of PPAR
expression (9), the PI-induced PPAR and CD36 expression may be mediated via
PI-induced activated SREBP accumulation in the macrophage nucleus. This
hypothesis would predict that PIs promote atherosclerosis through two
mechanisms, both involving increased SREBP activity (Figure 1). One
mechanism is through PI-induced metabolic complications that
increased the risk of atherosclerosis; the other mechanism is a direct
effect of PIs on macro-phage foam cell formation. If this hypothesis is
proven correct, then novel compounds that inactivate SREBP activity may
be designed and used to alleviate both metabolic and cellular
complications that pro-mote cardiovascular events associated with HAART.
***************
Molecular Pharmacology Fast Forward
First published on June 23, 2005; DOI: 10.1124/mol.105.012898
HIV Protease Inhibitors Activate the Unfolded Protein Response in
Macrophages: Implication for Atherosclerosis and Cardiovascular Disease
Huiping Zhou, William M. Pandak, Jr., Vijay Lyall, Ramesh Natarajan,
and Phillip B. Hylemon
Department of Microbiology & Immunology (H.Z., P.B.H.), Division of
Gastroenterology, Department of Internal Medicine and McGuire Veterans
Affairs Medical Center (W.M.P.), Department of Physiology (V.L.), and
Division of Pulmonary and Critical Care Medicine, Department of Internal
Medicine (R.N.), Virginia Commonwealth University, Richmond, Virginia
Human immunodeficiency virus (HIV) protease inhibitors have been
successfully used in highly active antiretroviral therapy for HIV-1
infection. Treatment of patients infected with HIV with HIV protease
inhibitors is unfortunately associated with a number of clinically significant
metabolic abnormalities and an increased risk of premature
atherosclerosis and myocardial infarction. However, the cellular/molecular
mechanisms of the HIV protease inhibitor-induced lipid dysregulation and
atherosclerosis remain elusive. Macrophages are the most prominent cell type
present in atherosclerotic lesions and play essential roles in both
early lesion development and late lesion complications. In this study, we
demonstrate that three different HIV protease inhibitors (ritonavir,
indinavir, and atazanavir) induce endoplasmic reticulum stress and
activate the unfolded protein response in mouse macrophages. Furthermore, at
therapeutic concentrations (5-15 µM), these HIV protease
inhibitors were found to increase the levels of transcriptionally
active sterol regulatory element binding proteins, decrease endogenous
cholesterol esterification, cause the accumulation of free cholesterol in
intracellular membranes, deplete endoplasmic reticulum calcium stores,
activate caspase-12, and increase apoptosis in macrophages. These
findings provide possible cellular mechanisms by which HIV protease
inhibitors promote atherosclerosis and cardiovascular disease in HIV-1 infected
patients treated with HIV protease inhibitors.
Received March 16, 2005; accepted June 23, 2005
Address correspondence to: Dr. Phillip B. Hylemon, Department of
Microbiology and Immunology, Virginia Commonwealth University, P.O. Box
980678, Richmond, VA 23298-0678. E-mail: hylemon@...
Original message:
Reyataz does not affect lipid metabolism - even with Norvir boost
Posted by: "Norm Stuart" nspop2@... norm_w_stuart
Date: Tue Aug 29, 2006 6:36 am (PDT)
Impact of Boosted vs Unboosted Atazanavir-based Regimens on the Lipid
Profiles of HIV Positive Patients
Conclusion
The authors concluded, "There does not appear to be a difference
between
atazanavir and atazanavir/ritonavir [in their effect] on total
cholesterol and triglycerides over the first 3 months


Do you Yahoo!?
Everyone is raving about the all-new Yahoo! Mail.

#18389 From: PoWeRTX@...
Date: Thu Aug 31, 2006 12:48 am
Subject: a patient reports having the "novel patterm of fat accumulation"
nelsonvergel
Offline Offline
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Just about two weeks ago, I showed my ID doctor at the VA here in
Atlanta, the fat accumulation under my arms (as the picture in the
attached message shows).  I have worked out most of my adult life and
I have very defined pecs.  The muscle definition extends toward and
under my arms, and then there are two huge fat accumulation deposits
under my arms.  From the back, it looks like I have very defined
delts. 

About 5 years ago I had a buffalo hump that was removed by the VA
hospital, due to the fact that I could not turn my head and was
unable to sleep.

I was on Zeret at the time, but have since been taken off this med.

I would be most interested in getting into a STUDY or obtain more
information regarding the fat accumulation under my arms if anyone
knows of this.  I would be happy to send pictures of this if needed.

I have been HIV+ since 1989 and my current T cells are 618 with a VL
of undetectable.

Thank you
George in Atlanta
 
Regards,

Nelson Vergel
powerusa dot org

#18388 From: "swhoutx025" <atoyota@...>
Date: Thu Aug 31, 2006 1:42 pm
Subject: Re: Looking for Legal expertise. Ref: Patient who clearer HIV but refuses to help
swhoutx025
Offline Offline
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As much as I would wish the fellow would participate,,, he is not a
lab rat and has free will.  We are not a fascist country (despite a
lot of what is going on lately) and coercing someone legally "for
the greater good" seems dispicable and morally wrong...

Just becuase he is mentally ill, unemployed, and on disability does
not dimish his rights!

--- In PozHealth@yahoogroups.com, PoWeRTX@... wrote:
>
> Dr Susan Diamond from Dallas is looking for an attorney who  may
want to do
> some research on legal ways to convince someone to cooperate with
researchers
> for the greater good. I would appreciate if anyone can refer me
to  any legal
> groups that could help on this case.
>
>
> ******************************
> I am a physician in private practice in Dallas, Texas and have
been taking
> care of AIDS patients for almost 20 years.
>
> Last year I came  across a patient in my practice who had
detectable HIV in
> his system and was  treated with 3 drugs including Crixivan for a
number of
> years.  He then  stopped his medications when he lost his job and
yet remained
> undetectable for  over 2 years.
>
> In collaboration with Dr. Roger Bedimo, head of Infectious
Disease at the
> VAH in Dallas his blood was sent to Dr. Richard Koup's group at
the NIH.  Dr.
> Joe Casazza, a senior investigator at the NIH analyzed the
samples and found
> that the patient had developed an immune tolerance.   Although Dr.
Casazza had
> seem this before he had never seen a patient with such  a strong
and robust
> response that was so easy to study.
>
> Unfortunately,  the patient decided that he did not want to
participate any
> further.  He  has a long history of severe mental illness and is
unemployed and
> on  disability.
>
> It is a shame he can choose not to participate further and  that
he unique
> response to HIV cannot be studied further to help elucidate the
immune system's
> reaction to control  HIV.
>
> *********************************************
>
>
>
>
> Regards,
>
> Nelson Vergel
> powerusa dot  org
>

#18387 From: John Barrow <pozbod@...>
Date: Thu Aug 31, 2006 3:09 am
Subject: Re: Jon Kaiser is a true champion
johnftl59
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"ttacking someone through his work is notorious enough, but to attack one of
our own fighters, someone who is going against the mainstream to validate
options that he has seen work in his patients the same way Joan Priestley
saw them work before Kaiser did is so twisted, I wonder whether it's worth
it to exchange in this group at all."

Michael, darling. Is this you speaking? Mr "you're all prostitutes and liars?"

The only thing is that this study is getting hyped like a cure for cancer. He looked at many parameters, and found zip.

The treatment group managed to catch up to the control group in CD4 counts. Why were they so different to begin with? That seems weird, if they really were a control group.

On patient could have had an infection, and severely biased the results when you're talking about a 15 member group.

It's really pretty underwhelming.



John Barrow




#18386 From: "Bill Gaul" <wgaul1@...>
Date: Thu Aug 31, 2006 3:57 am
Subject: Re: Re: new member / Zerit vs new meds & Sculptra
upstatedv8
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Norm -
 
The thrombocytopenia was determined to be ITP - an immune reaction to the Crixivan. It was sudden in onset (only caught it because I was in the second week of a Phase 1 study) and repeated on re-challenge. It's rare, but is established as a side effect now. There was an article published in the journal "Blood" on my case. The hematologist I saw after the second onset (the first was treated with Immune-globulin) said I was producing very healthy platelets, even though reduced in number, so I had no symptoms. Apparently thrombocytopenia causes lower counts - and - less healthy platelets usually. They did say they were surprised I didn't even bruise from blood draws. That 11,000 is very low and dangerous. The ER physician that did my intake looked under my watch band and said "hmm..." after he got the test results. He was expecting purple markings. I cleared the second bout with prednisone. The more effective treatment wasn't approved by Merk, and also supposedly isn't as effective with repeated use.
 
What doesn't make sense about your statement about Carnitor is: What about new and undamaged fat cells? Wouldn't improved function help to prevent the kind of changes mitochondrial damage causes, and maybe even further DNA damage? It's certainly worth a try - and cheaper than liposuction. I don't think Zerit is the only problem med in this area. I haven't taken it for four years now, and still have a lot of metabolic repercussions. I wouldn't disagree on the facial wasting issue re: Zerit, since it usually doesn't reverse and I've had it for about five years, or more.
 
BG
----- Original Message -----
Sent: Tuesday, August 29, 2006 4:33 PM
Subject: [PozHealth] Re: new member / Zerit vs new meds & Sculptra

 

Taking L-Carnitine can help improve the production of remaining mitochondria in people who have depleted mitochondria populations.

While I have no idea what drugs you were being given for low platelet counts, I am not aware of any treatments which make the remaining platelets more effective. All treatments for thrombocytopenia I know of are designed to reduce the destruction of platelets or increase production of platelets.

With a platelet count of 11,000 (compared with a more normal range of 140,000 to 250,000) it would be safe to say that these tretaments were not working well, regardless of what they were.

Your lack of symptoms, such as bruising, is not unusual. Often, low platelet levels do not lead to clinical problems; rather, they are picked up on a routine full blood count. Occasionally, there may be bruising, nosebleeds and/or bleeding gums - but this is not typical in thrombocytopenia. But if you received an injury, only a blood transfusion would have saved your life.


#18385 From: John Barrow <pozbod@...>
Date: Thu Aug 31, 2006 2:52 am
Subject: Re: Dr. Kaisers' vitamin study - Some hard questions and answers
johnftl59
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well, if you consider that the control group, for some reason, had more t-cells than the treatment group, I'm not sure that it's valid.

All other points examined were not statistically significant. Only when the control group and the treatment group were not comparable does a "benefit" obtain.


John Barrow




#18384 From: "Michael Mooney" <mmooney@...>
Date: Thu Aug 31, 2006 10:04 am
Subject: Jon Kaiser - a true champion to be emulated
michaelmoone...
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Norm -- you consistently assume the worst and those negative assumptions
have consistently been untrue. Please try to stick with the facts and take
at face value what is presented. None of us here are liars or deceptive or
mean or among the evil in this world  -- you can take that seriously. We all
pretty much want the best for each other.

I didn't put any words in Jon's Kaiser's mouth. I repeated the assertion you
made about him (basically being an idiot) and why he had "his patients" on
D4t, and he responded that the patients in the study were not his patients.
They were derived from several different places independent of his practice.
What they were taking was not something that he controlled. I made no
comments and did not editorialize. I simply cut and pasted Jon's answer
verbatim.

It stood on its own - as does his work.

All this negativity and personal attacks on Jon (and me) -- is a red herring
- no it's a huge red ORCA - beyond being a ridiculous waste of time when we
could all be doing something else that is positive and uplifting. Like Jon
is doing!

Jon showed that a comprehensive progressive nutrient program improved immune
response --- an increase in CD4 count of 25% overall among those receiving
the intervention over a loss among placebo recipients -this was a
statistically significant finding (p=0.01) - in a quality study. That in
itself is wonderful and all of us should be grateful that he did it and that
he continues to work diligently to answer each question that comes up as he
tries to help people with what should be the simplest and most accesible of
information. That superior nutrition can measurably benefit people with HIV.

END OF STORY.

Have a great day, filled with Marianne Williamson's words and thoughts!

Michael Mooney
www.michaelmooney.net
www.medibolics.com


Re: Jon Kaiser is a true champion
Posted by: "Norm Stuart" nspop2@...   norm_w_stuart
Wed Aug 30, 2006 4:33 pm (PST)

Michael Mooney - When you put words into Jon Kaiser's mouth claiming he
said "there weren't alternatives to d4T in 2003", that's twisted. It
made Jon Kaiser sound like a barking nutcase, which didn't sound at all
like the Jon Kaiser I have met. I knew your comments had to be wildly
incorrect.


--- In PozHealth@yahoogroups.com, "Michael Mooney" <mmooney@...> wrote:
>
> To hear people on this list tear about what Jon Kaiser did first by
assuming
> that the patients in the study were his --- which they were not ---
then by
> pursuing other means of detraction that were simply conjecture and
taking
> the most negative side of a possibility and pursuing it as if it were
true,
> I am quite simply dumbfounded and tremendously disappointed.
>
> Attacking someone through his work is notorious enough, but to attack
one of
> our own fighters, someone who is going against the mainstream to
validate
> options that he has seen work in his patients the same way Joan
Priestley
> saw them work before Kaiser did is so twisted, I wonder whether it's
worth
> it to exchange in this group at all.
>
> The negativity here is pathological.
>
> To say that he is a liar, after he answered the hardest question posed
to
> him by one of the toughest interviewers is just strange. His answers
were
> quite clear and he answered each of them with answers that showed he
had
> been working out every consideration that could come up.
>
> Thank God, we have people like Jon who devote themselves to helping
people
> regardless of what the mainstream thinks.
>
> Michael Mooney
>
>
> Tue Aug 29, 2006 1:08 pm (PST)
>

#18383 From: simon collins <simon.collins@...>
Date: Thu Aug 31, 2006 11:43 am
Subject: Re: Re: The patients in Dr. Kaiser's study were not his patients
simoninbrixt...
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d4T is more likely to sell for $50 a year, not $50 a month. The additional cost
of tenofovir puts this way out of reach for most poeple. Even the additional $50
or so a year to change form d4T to AZT is often prohibitive for people who have
neuropathy and know they are permanently damaging their nerves.

Simon

On Thursday, August 31, 2006, at 00:36AM, Norm Stuart <nspop2@...>
wrote:

>
><<Original Attached>>

When one of your many friends from India, Thailand, Zimbabwe and Nepal write to you, I wish you would stop suggesting d4T.

Since it now appears established that vitamins and micronutrients don't help prevent the mitochondrial damage from d4T, and most likely AZT as well, I hope you realize that you can no longer provide uninformed people with false hope in good conscience.

There are many better alternatives available to these people. In these nations you mentioned, Viread (tenofovir) sells for the same $50 per month that d4T (Zerit) sells for in these nations. There is no good reason for them to waste $50 a month on a dangerous drug like d4T, when they can instead spend their $50 on Viread.

Local politicians in these countries would of course like to look like they're doing something for HIV while actually doing as little as possible. Urging the purchase of expensive vitamin tablets in lieu of safer drugs, will look like a cost saving measure for local politicians, while you enrage and alienate the local population of HIV+ people - as you discovered in South Africa. Take their opposition to heart and learn from the experience. They want safer antiviral drugs, not vitamins.

 

--- In PozHealth@yahoogroups.com, "George M. Carter" <fiar@...> wrote:
>
> At 09:02 PM 8/29/2006, you wrote:
>
> For most of my friends living with HIV in India, Thailand, Zimbabwe and
> Nepal, they have NO choice.  If they can get anything, it's probably
> d4T+3TC+nevirapine or maybe efavirenz.
>
> of K-PAX.
> George M. Carter
>


#18382 From: JuLev@...
Date: Thu Aug 31, 2006 3:01 am
Subject: NATAP: Hispanics with Aggressive HCV-Liver Disease
jules72orange
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Hispanics Have More Aggressive Liver Disease in LA County Hepatitis Clinic

“More Advanced Hepatic Fibrosis in Hispanics with Chronic Hepatitis C Infection: Role of Patient Demographics, Hepatic Necroinflammation, and Steatosis”

The American Journal of Gastroenterology
Volume 101 Page 1817  - August 2006

Sumita Verma, M.D., M.R.C.P.1, Maurizio Bonacini, M.D.2, Sugantha Govindarajan, M.D.3, Gary Kanel, M.D.4, Karen L. Lindsay, M.D.1, and Allan Redeker, M.D.3
1Division of Gastrointestinal and Liver Diseases, Hepatitis Research and Treatment Center, Los Angeles, California; 2Department of Transplantation, California Pacific Medical Center, San Francisco, California; 3Rancho Los Amigos Medical Center, Downey, California; and 4Department of Pathology, University of Southern California, Los Angeles, California

“….From June 1994 to June 2004, consecutive patients with CHC were retrospectively recruited from the Los Angeles county hepatitis clinic by reviewing patient charts and personal summary records maintained by the senior author….Because of the retrospective nature and lack of serial biopsies this study had limitations. Also, the Hispanics studied were predominantly from Mexico and from the lower end of the socioeconomic spectrum. Thus, they may not have been representative of a cross section of Hispanics…..This study confirms that Hispanic ethnicity is associated with a more aggressive course of HCV infection with more than one-third having cirrhosis at the index biopsy. Compared with NHW, Hispanic patients also tended to show more NI, have a faster rate of fibrosis progression, be older at time of exposure (20 vs 23 yrs) and biopsy, and have a higher prevalence of BT as a risk factor. Furthermore, almost 50% of the Hispanics with CHC were obese with 79% having histological evidence of hepatic steatosis. Independent predictors of fibrosis stage ≥4 were presence of DM, grade 1-2 hepatic steatosis, AST/ALT >1, age at biopsy, NI grade, and serum bilirubin….”

ABSTRACT
BACKGROUND AND AIMS:  We sought to assess whether Hispanics have more advanced hepatitis C virus (HCV)-related liver disease than non-Hispanic whites (NHW) and to identify contributory factors.

PATIENTS AND METHODS:  Patients were recruited from the Los Angeles county hepatitis clinic. Liver fibrosis and necroinflammation (NI) were assessed by the Ishak scoring system. Hepatic steatosis was graded as 0-4.

RESULTS: 
A total of 232 patients were evaluated, 63 NHW and 169 Hispanic.

Hispanics were older and had a higher prevalence of blood transfusion (40% vs 21%), obesity (body mass index > 30) (47% vs 21%), diabetes mellitus (DM) (16% vs 5%), and hepatic steatosis (79% vs 47%), p< 0.02.

Independent predictors of hepatic steatosis were
-- Hispanic ethnicity (odds ratio [OR] 3.8, 95% CI 1.7-8.7, p = 0.001) and
-- obesity (OR 5.7, 95% CI 2.3-14.1, p = 0.0002).

Compared with NHW, Hispanics also had
-- higher fibrosis stage (3.3 ± 2 vs 2.3 ± 6.9, p = 0.001),
-- NI grade (6.4 ± 1.8 vs 5.6 ± 1.6, p = 0.002), and
-- faster fibrosis progression/yr (0.14 ± 0.09 vs 0.09 ± 0.07, p = 0.0002).

Presence of
-- DM (OR 2.9, p = 0.02),
-- grade 1-2 hepatic steatosis (OR 2.3, p = 0.03), AST/ALT > 1 (OR 4.3, p = 0.01),
-- NI grade (OR 1.7, p< 0.0001),
-- age at biopsy (OR 1.1, p< 0.0001), and
-- serum bilirubin (OR 5.4, p< 0.0001)
were independent predictors of fibrosis stage ≥4.

CONCLUSION: 
This study confirms that Hispanics have more advanced hepatic fibrosis than NHW. This is related to older age, higher NI grade, and greater prevalence of hepatic steatosis and DM.

Introduction
Liver disease from chronic hepatitis C virus (CHC) has now emerged as an important etiology of cirrhosis, and hepatocellular cancer and also the most frequent indication for liver transplantation in the United States. According to the National Health and Nutrition Examination Survey, there are approximately 2.7 million Americans with chronic HCV infection (1). Race/ethnicity plays an important role in modifying the natural history of CHC and a number of studies have observed attenuated HCV disease in African Americans compared with non-Hispanic whites (NHW) (2, 3).

Hispanics comprise 13% of the U.S. population and are the fastest growing minority group (4). They are also the predominant ethnic group in Los Angeles county (44%) (5).
Though chronic liver disease and cirrhosis was ranked as the eighth leading cause of death in Hispanics in the United States in 1998, it was not among the 10 leading causes of death in blacks or NHW. In fact for both genders, chronic liver disease was the third most common cause of death in Hispanics in the 45-64 age groups (6). Despite this, not only are there very few published data available on liver fibrosis in Hispanics with HCV infection, but available data are also conflicting. In an earlier study from our Unit we did observe faster fibrosis progression in Hispanics compared with NHW, though the sample size was small (7). A more recent study from Texas published in abstract form also observed higher prevalence of cirrhosis in Hispanics with CHC compared with NHW (8). Nonetheless, factors associated with this accelerated course in Hispanics were not analyzed in either of these two studies. In American veterans, Cheung et al. were unable to corroborate these findings and reported similar histology in Hispanics and NHW with CHC (9). We therefore designed this study to confirm whether Hispanics with chronic HCV have more advanced hepatic fibrosis compared with NHW and to identify contributing factors, with special emphasis on patient demographics, hepatic necroinflammation (NI), and hepatic steatosis.

RESULTS

From 1994 to 2004 there were 296 patients who were HCV RNA-positive (qualitative) by PCR, and had undergone a liver biopsy with an adequate sample (in the opinion of the reporting pathologist) available for histological analysis. All the liver biopsies had been performed as soon as possible after initial clinical evaluation. None of the patients had received interferon-based therapy prior to the biopsy. The overall patient profile (Hispanics (57%), NHW (21%), blacks (10%), Asians (9%) was consistent with the two earlier studies from our Unit (7, 10), indicating that there was no bias when selecting patients for a liver biopsy. For the purposes of the current study we included only 232 subjects (NHW, N = 63 and Hispanics, N = 169) (Table 1). The remainder (N = 64) comprising predominantly Asian and blacks were excluded. None of the 232 patients had evidence of iron overload histologically and all tested hepatitis B surface antigen (HBsAg) negative.

Table 1. Demographic and Histological Data in the Whole Group (N = 232)


Table 2 shows data in the NHW and Hispanics. Hispanics were older at HCV exposure and biopsy. They also tended to have higher ALT though the differences did not achieve statistical significance (p = 0.2). The percentage of patients with normal ALT was, however, similar among the two ethnic groups. There were no differences in serum bilirubin, albumin, and INR (data not shown). Several differences were present comparing men to women. The prevalence of obesity (BMI > 30) was greater in both NHW females (44% vs 8%, p = 0.004) and Hispanic females (54% vs 39%, p = 0.07). The prevalence of alcohol abuse was lower in women, both NHW (21% vs 57%, p = 0.01) and Hispanic (12% vs 51%, p< 0.0001) compared with men. Figure 2 shows the gender-related differences in risk factors for HCV. NHW and Hispanic males were more likely to report IDU compared with their female counterparts (86% vs 37% and 80% vs 29%, p≤ 0.001, respectively). On the other hand, both NHW and Hispanic females reported BT more frequently as compared with the males (37% vs 14%, p = 0.05 and 64% vs 16%, p< 0.0001, respectively).

Table 2. Demographic and Histological Data in the Hispanics and Non-Hispanic Whites

IDU = injection drug use; BT = blood transfusion.
*BMI and HCV viral load were unavailable in 27 and 60 patients, respectively.
Among the remaining 14 patients, risk factors included high-risk sexual behavior, body piercing, tattoos, cocaine snorting, and prior surgery.

Complete data on hepatic steatosis (i.e., presence/absence and grade) were available for 171 patients (NHW N = 45 and Hispanics N = 126). Hispanics had a significantly higher mean steatosis grade (1.2 ± 0.9) than the NHW (0.6 ± 0.8), p = 0.0001. The prevalence of any steatosis was 47% (NHW) and 79% (Hispanics), p< 0.0001 (Fig. 3). Hispanics were also more likely to have steatosis grade 1-2 compared with NHW (p = 0.0005). The prevalence of patients with grade 3-4 steatosis was also highest among the Hispanics (8%) compared with NHW (4%), p = ns (Fig. 3). On univariate analysis, the presence of any hepatic steatosis was associated with Hispanic ethnicity (79% vs 47%, p< 0.0001), female gender (81% vs 62%, p = 0.005), obesity (BMI > 30) (90% vs 56%, p< 0.0001), and presence of DM (20% vs 4%, p = 0.009). Those with any grade of hepatic steatosis had higher fibrosis stage (3.1 ± 1.9 vs 2.3 ± 1.8, p = 0.02), faster fibrosis progression (0.13 ± 0.08/yr vs 0.10 ± 0.07/yr, p = 0.04), higher alkaline phosphatase (120 ± 46.7 IU/L vs 97 ± 29 IU/L, p = 0.0007), and a lower serum albumin (3.9 ± 0.4 g/dL vs 4.1 ± 0.4 g/dL, p = 0.002). Those with any steatosis also had higher ALT (153 ± 104.3 IU/L vs 132 ± 82.2 IU/L) and grade of NI (6.3 ± 1.9 vs 5.9 ± 1.7) though the differences did not achieve statistical significance. We did not analyze association between hepatic steatosis and genotype 3 because only a small number (N = 15) had available data. A stepwise multiple logistic regression analysis was then performed including all variables that were significant on univariate analysis (p< 0.05). The following were identified to be independent predictors of hepatic steatosis: Hispanic ethnicity (odds ratio [OR] 3.8, 95% CI 1.7-8.7, p = 0.001) and obesity (BMI > 30) (OR 5.7, 95% CI 2.3-14.1, p = 0.0002).

Hispanics had the highest NI grades and also had the most advanced disease as regards fibrosis stage and fibrosis progression (Table 2). After adjusting fibrosis progression for age at biopsy, presence of DM, and alcohol abuse, it was still faster in the Hispanics (0.12/yr [95% CI 0.07-0.09]) versus NHW (0.08/yr [95% CI 0.11-0.14]), p< 0.0001. Table 3 shows the distribution of fibrosis stage (0-6) and grade of NI (0-18) in the three groups. There was a trend for higher prevalence of cirrhosis in Hispanics compared with NHW (p = 0.06) and 50% of the Hispanics had NI grades >6 (Table 3). There were no gender-related differences in NI grades, fibrosis stage, fibrosis progression, and cirrhosis in the two groups (data not shown).

Table 4 highlights the data in patients depending on those that had a fibrosis stage < or ≥4 at index biopsy. Factors that were significantly associated with fibrosis stage ≥4 on univariate analysis (p≤ 0.05) were then entered into a stepwise multiple logistic regression analysis model. A separate regression model was used for the nominal and continuous variables. Independent predictors of fibrosis stage ≥4 were age at biopsy, serum bilirubin, NI grade, presence of DM, AST/ALT >1, and presence of grade 1-2 steatosis (Table 5). Obesity (BMI > 30) was, however, not independently associated with advanced fibrosis (OR 0.9, 95% CI 0.4-1.9, p = 0.8). Because both NI grade and hepatic steatosis were independent predictors of advanced fibrosis, we analyzed probability of developing cirrhosis in those with both NI grade ≥6 (mean grade in the whole group) and hepatic steatosis versus those with either one or neither of these factors. After 30 yr of HCV exposure, the former had a significantly higher probability of developing cirrhosis (38% vs 16%, p = 0.01). It would have been useful to analyze NI and steatosis separately, but after excluding overlapping patients and those with missing data, the sample sizes generated were too small for a meaningful statistical analysis.

Table 5. Independent Predictors of Fibrosis Stage ≥4 on Multivariate Logistic Regression Analysis


This study confirms that Hispanic ethnicity is associated with a more aggressive course of HCV infection with more than one-third having cirrhosis at the index biopsy. Compared with NHW, Hispanic patients also tended to show more NI, have a faster rate of fibrosis progression, be older at time of exposure and biopsy, and have a higher prevalence of BT as a risk factor. Furthermore, almost 50% of the Hispanics with CHC were obese with 79% having histological evidence of hepatic steatosis. Independent predictors of fibrosis stage ≥4 were presence of DM, grade 1-2 hepatic steatosis, AST/ALT >1, age at biopsy, NI grade, and serum bilirubin.

Our findings of more advanced hepatic fibrosis in Hispanics with CHC compared with NHW is in variance with the recent study by Cheung et al. (9). They observed similar NI grades, fibrosis stage, and fibrosis progression in the two groups despite the former having a significantly higher prevalence of HIV coinfection (20.4% vs 3.9%). There could be a number of reasons for these differences. First, only 30% of the cohort reported by Cheung et al. underwent a liver biopsy and it was unclear as to whether they were representative of the study population. Second, in contrast with Cheung's study, our Hispanics were older and had higher BMI than the NHW. Third, because of the multicenter nature of Cheung et al.'s study, the histology was interpreted by local pathologists and therefore subject to interobserver and tissue sample variability. Ours was a single-center study, only those with adequate tissue were included, and all the biopsies had been examined by two experienced hepatopathologists (SG, GK). Most importantly, the study by Cheung described American veterans, who were therefore predominantly men, and presumably healthy enough to serve in the Armed Forces, introducing a potential bias. Ours on the other hand, was a community-based study that was conducted in a publicly funded health-care facility in which the patient population was highly representative of Hispanics in Los Angeles county (26.2% of adults aged 18-64 is uninsured, and 40% of the uninsured is Hispanic) (13).

Presence of both grade 1-2 steatosis and NI grade was independent predictor of advanced fibrosis and those who had both NI grade ≥6 and hepatic steatosis were twice as likely to develop cirrhosis (36% vs 18%, p = 0.01) compared with those with either one or neither of these features. These observations are not surprising as both hepatic steatosis and NI have been associated with fibrosis in earlier studies (14-16). Fartoux et al. showed that regardless of genotype, steatosis was a major determinant in fibrosis progression in patients with mild hepatitis C (14). Castera et al. further observed that worsening of hepatic steatosis was an independent predictor of fibrosis progression in untreated patients with CHC (15). The overall prevalence of obesity in our cohort was high (40% [82 of 205]) with 84% (173 of 205) being overweight (BMI > 25). Hispanics had the highest prevalence (47%) of obesity, this being especially true for the Hispanic females (54%). Therefore, not surprisingly hepatic steatosis was observed in 79% of the Hispanics, with almost 30% having ≥grade 2 steatosis. Others have also reported a higher prevalence of nonalcoholic fatty liver disease in Hispanics than other ethnic groups (17) and therefore the advanced hepatic fibrosis in Hispanics with CHC may be related to this factor rather than to a direct viral effect. However, we did observe that those with advanced fibrosis were less likely to have grade 3-4 steatosis (Table 4). This may be as a result of reduction or disappearance of steatosis as fibrosis progresses (18).

HCV infection is associated with increased production of inflammatory cytokines (16) and this process may be accentuated in Hispanics, resulting in more severe hepatic NI. We and others (19) have in fact observed higher NI grades in Hispanics compared with NHW. NI can worsen hepatic fibrosis as stellate cells are activated around NI lesions (20). In a study of 70 patients who had had a mean of 3.9 biopsies over an 8-yr period, Yano et al. found that cirrhosis developed within 17 yr in all patients with a high grade (>5/8) of NI on initial biopsy, whereas only 30% of those with low-level inflammation (<3.4/8) developed cirrhosis after 13 yr (16). Furthermore, there may also be an association between NI and steatosis (21). This could be explained by the fact that the HCV core protein leads to oxidative stress (22) and steatosis could result from the inflammatory changes associated with this oxidative stress (23). In this study, hepatic steatosis was associated with a higher grade of NI (6.3 vs 5.9), though the results did not achieve statistical significance.

Because of the retrospective nature and lack of serial biopsies this study had limitations. Also, the Hispanics studied were predominantly from Mexico and from the lower end of the socioeconomic spectrum. Thus, they may not have been representative of a cross section of Hispanics. Finally, the female preponderance among the Hispanics could have reflected better compliance in this group, thereby introducing a selection bias. However, this probably would not have influenced the results as no gender-related differences were observed in the histological parameters.

In conclusion, Hispanics with CHC have more advanced hepatic fibrosis compared with NHW and this appears to be related largely due to host factors such as older age and higher prevalence of obesity (47%), DM (16%), and hepatic steatosis (79%). Hispanics also have higher NI grades and whether this is also related to host characteristics or a direct viral effect is unclear. Because age at biopsy, NI grade, presence of DM, and grade 1-2 steatosis were independent predictors of advanced fibrosis in this study, it is imperative that these variables be considered when designing a treatment and management regimen for Hispanic patients with histologically mild HCV disease. Nonetheless, this important and controversial issue can only be unequivocally resolved by prospective studies recruiting a well-represented Hispanic population.

Patients & Methods
From June 1994 to June 2004, consecutive patients with CHC were retrospectively recruited from the Los Angeles county hepatitis clinic by reviewing patient charts and personal summary records maintained by the senior author (AR). There have already been two studies from our Unit assessing the demographic and biochemical differences in Hispanics with HCV infection (7, 10). Hence the main focus of this study was to assess the histological severity of CHC in this ethnic group. Only those subjects who tested HCV RNA-positive (qualitative) by PCR and had had a liver biopsy were therefore included. In this clinic, at the first visit a detailed history is taken from every patient and relevant information is recorded in the clinic summary card and patient charts including age, ethnic group, alcohol consumption, risk factors, body mass index (BMI), and presence of diabetes mellitus (DM). Pertinent labs and radiographic data are recorded at entry and at each subsequent visit. Liver biopsy results are also accordingly noted. All the liver biopsies had been assessed by either one of the two hepatopathologists (SG, GK) and the NI grade (0-18) and stage of fibrosis (0-6) were obtained using Ishak scoring system (11). Hepatic steatosis was graded depending on the percentage of hepatocytes containing fat: 0 = no fat, 1+ = <5%, 2+ = 6-33%, 3+ = 34-66%, 4+ = 67-100%. Those in whom no grade of steatosis was available but had "scanty/mild steatosis" were presumed to have 1+ steatosis. Similarly those with "mild-moderate/moderate steatosis" were graded as 2+, "moderate-severe" 3+, and severe as 4+. The estimated fibrosis progression was calculated by dividing the fibrosis stage at index biopsy with the estimated disease duration (12). HCV disease duration (in yr) was calculated as the interval from age at exposure to age at liver biopsy. Age at exposure was defined as the earliest year of (a) blood transfusion (BT), (b) initiating injection drug use (IDU), (c) surgical procedure, (d) other high-risk behavior (body piercing, tattoos).

HCV antibody status was determined by HCV-EIA 2.0 (Abbott Laboratories, Chicago, IL). HCV RNA analysis (qualitative) was performed by nested PCR (in-house method) with lower limit of 10 copies. Quantitative HCV analysis was performed using COBAS Amplicor HCV Monitor v2.0 (Roche Molecular Systems, Pleasanton, CA) from October 1999 and subsequently using TaqMan HCV Test (Focus Laboratories, Cypress, CA). Genotyping for HCV was performed by Line-probe assay (INNO-LiPA HCV II, Immunogenetics, Ghent, Belgium).

Ethnic status was classified (according to initial clinic self-classification) as NHW or Hispanics. Blacks, Asians, and patients with other racial/ethnic backgrounds were excluded from the study. Because it is difficult to accurately quantify alcohol consumption retrospectively, we only recorded presence or absence of alcohol abuse rather than the actual amount of alcohol consumed. For the purpose of this study alcohol abuse was defined as consumption of ≥40 g of alcohol per day. Study exclusion criteria were unidentifiable risk factors, presence of liver disease of another etiology (active hepatitis B infection, iron overload, autoimmune hepatitis), HCV RNA-negative by PCR, liver biopsy unavailable, coinfection with HIV, and prior treatment with interferon-based therapy.

Statistics
Data are presented as mean ± SD except the HCV viral load which is presented as median (range). Differences between continuous and nominal variables were calculated using the Mann-Whitney and χ2 test/Fisher's exact test, respectively. Multiple linear regression analysis was used to adjust fibrosis progression for age at biopsy, presence of DM, and alcohol abuse. Stepwise multiple logistic regression analysis was performed to determine independent predictors of fibrosis stage ≥4 and hepatic steatosis. Kaplan-Meier survival analysis was used to assess probability of developing cirrhosis depending on NI grade (≥6 vs<6) and presence/absence of hepatic steatosis and differences between the groups were compared using log rank test (Fig. 1). The statistical software programs used were Stat View (version 5.1) and SPSS, versions 8.2 and 13.



#18381 From: "Norm Stuart" <nspop2@...>
Date: Thu Aug 31, 2006 1:35 am
Subject: Re: Looking for Legal expertise. Ref: Patient who clearer HIV but refuses to help
norm_w_stuart
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I think Susan Diamond should talk with Dr Jay Levy at UCSF. She will learn that her patient, while a very small percentage is not that unique.

People who have a high percentage of T Regulatory Cells and CNAR CD8+ cells are able to control HIV without any additional therapy. If your levels of these cells are even higher, you don't even get infected with HIV. Interleukin-2 raises the level of these cells.

So very bright researchers are aware of this and publishing papers on their research. I don't think one more patient in this situation is even useful - although every researcher wants several of their very own to try things on.

I have a friend in Sweden who is a high T-Reg producer. His T4 count initially declined to 450 or so. Then over the next six years, his T4 count and percent returned to normal and his viral load became undetectable. The person he was infected by now has AIDS and is quite sick really. Labs tests show they still have the same viral types.

I'm not sure what is meant by immune tolerance. Immune tolerance is where the immune system does not respond to one or more antigens. An immune tolerance to HIV would result in a very elevated viral load. I'm sure what he has is a strong cellular non-cytolitic suppressive response - and that is T-Regs and CNAR cells.


--- In PozHealth@yahoogroups.com, PoWeRTX@... wrote:
>
> Dr Susan Diamond from Dallas is looking for an attorney who may want to do
> some research on legal ways to convince someone to cooperate with researchers
> for the greater good. I would appreciate if anyone can refer me to any legal
> groups that could help on this case.
>
>
> ******************************
> I am a physician in private practice in Dallas, Texas and have been taking
> care of AIDS patients for almost 20 years.
>
> Last year I came across a patient in my practice who had detectable HIV in
> his system and was treated with 3 drugs including Crixivan for a number of
> years. He then stopped his medications when he lost his job and yet remained
> undetectable for over 2 years.
>
> In collaboration with Dr. Roger Bedimo, head of Infectious Disease at the
> VAH in Dallas his blood was sent to Dr. Richard Koup's group at the NIH. Dr.
> Joe Casazza, a senior investigator at the NIH analyzed the samples and found
> that the patient had developed an immune tolerance. Although Dr. Casazza had
> seem this before he had never seen a patient with such a strong and robust
> response that was so easy to study.
>
> Unfortunately, the patient decided that he did not want to participate any
> further. He has a long history of severe mental illness and is unemployed and
> on disability.
>
> It is a shame he can choose not to participate further and that he unique
> response to HIV cannot be studied further to help elucidate the immune system's
> reaction to control HIV.
>
> *********************************************
>
>
>
>
> Regards,
>
> Nelson Vergel
> powerusa dot org
>


#18380 From: "Norm Stuart" <nspop2@...>
Date: Thu Aug 31, 2006 2:05 am
Subject: Re: drugs
norm_w_stuart
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All of these drug names can be very confusing when you're not familiar with them.

The name of the drug you mention in your other post sounds like Fuzeon. This is an injectible drug which is most often used by people whose virus has become resistant to other antiviral drugs.

If your friend's virus has not become resistant to most other drugs, Fuzeon is an odd treatment to be using, simply because of the inconvenience of twice daily injections. Perhaps there is some reason he is trying to avoid using protease inhibitors like Reyataz (atazanavir). If that's true, the twice daily injections will have them seeing the benefits of a protease inhibitor like Reyataz in a new light.

Zidovudine, Retrovir and AZT are all name for the same drug.

Truvada is a combination of Viread and Emtriva. Emtriva is an newer version of Epivir which is less likely to cause the fairly unusual side-effect of Epivir which would explain your friend's symptoms - if Epivir was the cause.

If they are taking Truvada, I can think of no good reason to also take AZT.

I think AZT (Retrovir) along with d4T (Zerit) should be removed from the market as they provide minimal viral control while over the long term causing long term damage to the energy producing structures in human cells known as the Mitochondria.


--- In PozHealth@yahoogroups.com, "wantsome_24" <wantsome_24@...> wrote:
>
> I just got better info of what my friend is going to start on.
> Zidovudine, Retrovir, and Trevada. Does this sound like a good
> combination? He was on Viread, Kalatra, And Epivir. The Epivir failed
> and they gave him something else that put him in ICU with a VERY high
> fever and Very low blood pressure. Any info would greatly be accepted.
>


#18379 From: Allan <allan2947@...>
Date: Wed Aug 30, 2006 11:50 pm
Subject: Re: drugs
allan2947@...
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You need to go back again and get better information. Zidovudine and
Retrovir are the same drug (also known as AZT).



On 8/30/06 4:18 PM, "wantsome_24" <wantsome_24@...> wrote:

>   I just got better info of what my friend is going to start on.
> Zidovudine, Retrovir, and Trevada. Does this sound like a good
> combination? He was on Viread, Kalatra, And Epivir. The Epivir failed
> and they gave him something else that put him in ICU with a VERY high
> fever and Very low blood pressure. Any info would greatly be accepted.
>
>

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