Sent from my Verizon Wireless BlackBerry

Has anyone had any experience dealing with MRSA, the multi-resistant
staph infection that's becoming increasingly common in the HIV
community? I'm writing an article on it for POZ magazine and would
love talk with anyone who has had MRSA experience.

Josh

I have started to have tremors due to the neuropathy has anyone else
had or has this problem and can you tell me what you are doing about
it. Is there some meds that can relieve this problem or something I
might be able to do for it. Thanks for your help

PoWeRTX@... wrote:
>
>   AUA 2008: Maxi-K gene transfer may prove to be safe and effective
>   erectile dysfunction treatment

Maybe I'm missing something, but how is this gene transfer accomplished?
   I see a reference to "injection" but nothing more.  Would this be a
bone-marrow injection (quite painful I understand) or a painless IV
infusion or IM injection.... or what?

I'm not familiar with "the Maxi-K channel," but I'm not an MD.  What is it?

B/

Here is the latest post from our fellow board member Thomas De Lorenzo, he has really become a key national spokesman for those of us with HIV

-al

\Universal Healthcare and hope for a New America

This is the column my parents will wish I didn't write.

I should first begin by warning you I just came home from viewing MILK. We gay people often think our history is just discos, drag queens and casual sex. But long ago, in a galaxy not so far away named San Francisco, there was a man named Harvey Milk. Milk stood up for all of us, and made this country a safer place for gays and lesbians. He made sure that discrimination against homosexuals did not occur under his watch in California by running a precise, passionate, and very well planned campaign, almost knocking on every single door of every single person in the State. Milk firmly believed that once people knew a gay person, it would be difficult to vote against us.

Where is our Harvey Milk now?

Why didn't our current gay and lesbian leaders take a page from Milk's handbook and stand in the face of those who oppose us and not back down? Why did we only preach to the choir when Proposition 8 was being campaigned around the State? Why didn't we, like Milk would have done, go to the churches that discriminated against us and show them that we count, that we are humans just like them, and convince them one at a time if we had to, that we, too, are entitled to marriage.

Instead we got a commercial that apparently went unwatched.

What happened to our leaders in the HIV community? When did it become politically correct not to stand up for what you believe in, no matter whom you pissed off? Why have HIV related health care issues seem to have become last decade's news? Why aren't our leaders kicking down doors in Washington to fight for more funding because more and more people need those precious dollars everyday? Why have we become complacent with the current status quo of holding the disease at bay, when so few can actually afford the treatments, deal with the side effects without a problem, or even begin to have the access to decent care.

Like Milk, I can point the finger at myself. There was a time when I didn't, no wait, couldn't, talk about my boyfriend, David, and his illness. We lived in fear -- fear that he would get deported, and fear that he would lose his health insurance. And I lived in fear as a gay man that I would be cut off from my family if I shared our secret. I lived with this same fear when I knew I was getting sick myself. I thought people would turn against me and would just let me die alone.

It turned out wrong - for me, at least. Plenty of people do not have anywhere to go and do die alone - from a variety of causes. I was instantly proved wrong the second I got honest with myself, and then got honest with everyone around me. For you see, after you tell your mother you have AIDS, it is truly downhill from there. Once you know you have Mom on your side, you know you will not be fighting this alone. I then made sure I told everyone that mattered in my life, for I did not want them to find out second-hand. I wanted them to hear it directly from my own mouth, and ask whatever questions they had. And you know what happened -- there was a non-stop parade of people in and out of my hospital room showing their support, so many that the nurses just started pointing and saying, "He is in there."

I realize now that in spite of whatever perceived imperfections my life may have from time to time, that I am one incredibly lucky and loved guy. I also have friends and family behind me, no matter what time is it, to help me through this crisis one calls "Living with AIDS". I also have health insurance and a family that can help me, should the need arise.

But what about my brothers and sisters with HIV that do not have this support? What about the individuals without health insurance that get forced to deal with a bankrupt and overly bureaucratic county health care program that barely works when you have the most minor of problems.

People argue that we cannot have national health insurance because they fear it will cause long lines and reduce care. God, how is wish Milk was around to help us through this one. He would have pointed to Europe, stating their high quality of care, the equal access for all, their lower infant mortality rates, and higher quality of life. The United States, in spite of our bragging about being the richest nation ever, ranks 37th on the global infant mortality rate chart - beneath France, United Kingdom, Sweden, Czech Republic, Norway, and Ireland, to name only a few.

As Thomas Jefferson stated that all men were truly created equal, then why can't all men have equal access to health care?

If we were truly pro-life, why don't we care about the life after it has been born?

Back to that comment about my Mom, since telling her my diagnosis, she has been great, amazing beyond all expectations even. She went from being a woman who never wanted to deal with this disease, to being proud of her son who speaks out on behalf of those who cannot. I am proud to say that my family are my number one fans, and, honestly, I would have not guessed that ten years ago.

In MILK, he starts to talk about his boyfriends who committed suicide because of living in the closet, how he felt he betrayed them by not being strong enough to stand up for his own lifestyle. Milk felt he had no other choice but to speak. I started speaking out, rather innocently in fact, when I was written about in the New York Times regarding a project I created for the residents of the San Antonio AIDS Foundation. I was honest with my status, and the writer included it in the piece. People who knew me but didn't "know" were amazed. I was told that it was a beautifully written story - and that "I had the balls to come out in the New York Times." Honestly, it would have taken more balls not to say it, for you see Mom already knew, and speaking freely with the Times was part of the "downhill."

I have seen too many people die because they were afraid to speak out and ask for help. I had a friend die because he was afraid to change doctors for fear of hurting that doctor's feelings. I had another friend die because his family did not accept his lifestyle.

If we want change to come to America, we must be the ones that change, not just the people that get paid to work on the Potomac. We must fight every single day for this change. We must fight for all Americans to be treated equally on every single level of their lives - and this must include health care.

Throughout the movie, Milk kept getting death threats. I had my own Milk moment recently after a radio interview. I was on the Cable Radio Networks, discussing what it was like to be a person living with AIDS in America in 2008. The very next day I received a call - it came up "private" on my caller ID. It was some woman, I believe her name was Dolores, and she said she was from the State of California Health Department. She told me that a recent sexual partner of mine tested positive and that I had to test in thirty days or she would call my employer. I laughed and said, "Well you are assuming I have an employer, for you are talking to him." She was to call in thirty days and make sure I tested. She never called back. Just to be sure, I contacted the California AIDS Department, and they backed up my fears - it was a crank call. The County makes those calls and never, ever without giving out phone numbers to call for more assistance.

My Milk moment. The part my parents did not know about until they read this, but part of the process. I now look forward to the next one, because, I know, change isn't going to happen to our health care without pissing dozens of people off.

So, to that woman named Dolores, and others just like her - I say bring it on -- I await my next Milk moment with pride.

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It's the day after. So I don't have to thank anyone now?

I sure do!! Specifically, all of the great folks here who came
through and got us the meds we put out a request for recently.
Thanks!!!

And to all of you for being here in this struggle for health and well-
being.
And for all our friends who have left us.
And lots more...
George M. Carter

From:	julev <julev@...>
Subject:	NATAP: Inflammation & AIDS Progression
Date:	November 27, 2008 12:17:21 PM EST
To:	hiv@..., nataphcvhiv@..., natapindustry@..., natapdoctors@...

Inflammation May Be Associated with AIDS Progression

"These data support a modest association between the level of inflammation as measured by CRP concentration and the degree of immunosuppression and HIV RNA levels in HIV-infected men (from Jules: progression to AIDS; it is likely that CRP is merely a mrker for inflammation, it is inflammation that causes AIDS progression) . The results indicating increasing levels of inflammation for individuals with progression to AIDS and those who remained free of AIDS may have important implications for potential cardiovascular disease within this population, especially as infected individuals are living longer with effective therapies.....

....Levels of CRP increased over time for individuals with and without progression to AIDS (Figure 3). However, individuals with progression to AIDS had higher CRP levels than those without.....

....Furthermore, the rate at which CRP concentration increased was greater for individuals with progression to AIDS, with an 8.5% change per year compared with a 4.5% change per year for individuals who remained free of AIDS....

.....The proportion of individuals with CRP of more than 3 mg/L ranged from 34% to 50% in the 2.5 years preceding AIDS development, whereas the proportion ranged from 9% to 24% when there were at least 15 individuals prior to this period.....

.......Use of ART was not significantly associated with a decrease in CRP levels when included in the random-effects model, indicating that early treatment regimens did not have an effect on CRP concentrations......To our knowledge, this is the only study that includes longitudinal CRP data from HIV-infected individuals prior to the widespread use of HAART. These results indicate increasing inflammation with disease progression, which may have implications for cardiovascular risk in HIV-infected populations......The American Heart Association and Centers for Disease Control and Prevention have recommended that the CRP concentration be used as a marker for cardiovascular disease in individuals with a Framingham risk score from 10% to 20%, considering CRP values between 1 and 3 mg/L as average risk and those of more than 3 mg/L as high risk for cardiovascular disease......the fact that the correlations of CRP concentrations with CD4 counts and HIV RNA levels were weak was somewhat surprising and may be related to the chronic immunosuppression consequent to HIV infection. Common viral infections that result in mild systemic inflammation are associated with much greater elevations in CRP levels (10-40 mg/L) than those seen in our subjects......

.....Kaplan-Meier curves of individuals categorized by CRP categories (≤0.6, 0.7-1.2, 1.3-2.3, and >2.3 mg/L) are shown in Figure 2. Individuals with higher concentrations of CRP had shorter times to AIDS (overall log-rank test, P<.001). Individuals with a CRP concentration of 0.6 mg/L or less had a median time to AIDS of 7.70 years (95% CI, 6.74 to >9.31 years). Similarly, those with a CRP level of 0.7-1.2 mg/L had a median time to AIDS of 6.87 years (95% CI, 6.22 to >9.33 years). However, those with higher levels had progression to clinical AIDS more quickly. Median times to AIDS were 5.07 years (95% CI, 4.15-7.26 years) for those with CRP levels of 1.3 to 2.3 mg/L and 4.48 years (95% CI, 3.17-5.61 years) for those with CRP levels of more than 2.3 mg/L. These results suggest a threshold effect, with accelerated progression only at CRP levels of more than 1.2 mg/L....."

C-Reactive Protein Is a Marker for Human Immunodeficiency Virus Disease Progression

Bryan Lau, PhD, MHS, ScM; A. Richey Sharrett, MD, DrPH; Larry A. Kingsley, DrPH; Wendy Post, MD, MS; Frank J. Palella, MD; Barbara Visscher, MD, DrPH; Stephen J. Gange, PhD

Arch Intern Med. 2006;166:64-70.

ABSTRACT

Background-  Limited data on acute-phase C-reactive protein (CRP) levels in human immunodeficiency virus (HIV) infection exist.

Methods-  We obtained a single measurement of CRP from 513 HIV-infected men in the Multicenter AIDS Cohort Study to examine the association between CRP and immune suppression and progression to AIDS. We estimated changes in CRP during the course of HIV infection in 81 of these individuals using specimens collected from October 1, 1984, to December 31, 1996.

Results-  The cross-sectional associations between log10 CRP were correlated inversely with CD4 lymphocyte counts (r = –0.17; P<.001) and directly with log10 HIV RNA levels (r = 0.20; P<.001). Levels of CRP of more than 2.3 mg/L were associated with a decreased time to the development of AIDS (relative time to AIDS, 0.36; P<.001) compared with individuals with CRP levels of 1.2 mg/L or less, which remained significant after adjustment for CD4 lymphocyte counts and HIV RNA and hemoglobin concentrations. Levels of CRP significantly increased over time with mean slopes of 8.5% (95% confidence interval, 4.9%-12.2%) and 4.5% (95% confidence interval CI, 2.1%-6.9%) per year for individuals with and without progression to AIDS, respectively. Individuals had a geometric mean CRP level of 2.5 mg/L in the 6-month interval before progression to AIDS, which was an increase from a nadir of 1.0 mg/L at 6.5 years before progression to AIDS.

Conclusions-  Levels of CRP were associated with HIV disease progression independent of CD4 lymphocyte counts and HIV RNA levels. In addition, regardless of progression to AIDS, HIV-infected individuals had a significant increase in CRP over time. This may have implications for cardiovascular disease among HIV-infected individuals.

INTRODUCTION

Levels of acute-phase proteins as markers of inflammation usually rise markedly during acute and chronic infections.1 This rise is particularly great for C-reactive protein (CRP), an acute-phase protein recognized as an important indicator of inflammatory conditions that are often the consequence of infection.1 Levels of CRP change in response to the proinflammatory cytokines, interleukin 1 and 6, whose expression is induced by bacterial infections and tissue necrosis. More recently, even small elevations in CRP concentrations have been shown to indicate increased risk for cardiovascular disease2 and possibly colon cancer.3

The 25th, 50th, and 75th percentiles of CRP levels have been estimated to be 0.6, 1.5, and 3.5 mg/L, respectively, in healthy middle-aged US individuals.4-5 Symptomatic mild inflammatory disease or viral infection is commonly thought to increase CRP concentrations from 10 to 40 mg/L, whereas concentrations of 40 to 200 mg/L are found in acute bacterial infections.6-8

The relationship between CRP concentration and human immunodeficiency virus (HIV) is still unclear. Lower levels of CRP have been shown to predict longer survival within HIV-infected individuals.9-11 For a population with ongoing HIV infection, the level of CRP was shown to be relatively low (median <4 mg/L), which indicates that HIV infection is not a highly inflammatory disease.11 Furthermore, it has been suggested that measurement of CRP level may be an inexpensive method for monitoring febrile episodes and opportunistic infections in individuals with AIDS.12 These studies could not examine low levels of CRP, as high-sensitivity CRP assays were not used. In addition, longitudinal evaluations of plasma CRP concentrations have not been described among HIV-infected individuals, and CRP concentrations have not been correlated with the degree of immunosuppression. Furthermore, it is unclear whether CRP remains prognostic for cardiovascular disease in HIV-infected individuals. Sklar et al13 failed to find any predictive value of CRP for cardiovascular disease in HIV-infected individuals. However, their study was limited by a small sample size.

In this study, we sought to elucidate the relationship between HIV disease and the concentration of CRP. We used a highly sensitive assay to measure the level of CRP from stored plasma specimens collected from men enrolled in the Multicenter AIDS Cohort Study (MACS). These specimens had been obtained prior to the widespread use of highly active antiretroviral therapy (HAART). We examined the relationship of CRP concentrations with markers of HIV status and time to clinical AIDS.

COMMENT

The role of inflammation as defined by CRP levels has not been fully explored in the context of HIV disease. These results indicate that elevated CRP levels were modestly correlated with low CD4 lymphocyte counts and elevated HIV RNA levels. These correlations were determined from baseline values (before June 1, 1987), and no individual had initiated any ART by their baseline visit. The association of higher CRP with progression to AIDS was independent of any HAART effects, as the specimens were collected before any ART use, and individuals were censored before the HAART era. The baseline association indicates long-term prognostic value for CRP levels, which remains after adjusting for CD4 lymphocyte counts and HIV RNA levels. These results suggest a potential role for CRP in monitoring the clinical course of HIV-infected individuals. Our data also indicated that individuals with progression to AIDS have a faster elevation in CRP concentrations over time than individuals remaining free of AIDS. It is unclear whether the underlying CRP pattern is a continuous gradual rise over time or, alternatively, an initially relatively stable level that eventually increases prior to AIDS. The random effects model on a logarithmic scale indicates an acceleration of the increase in CRP concentrations over time. Use of ART was not significantly associated with a decrease in CRP levels when included in the random-effects model, indicating that early treatment regimens did not have an effect on CRP concentrations.

An inherent difficulty in this research is the adequate exploration of the temporal relationship between the immunocompromised state induced by HIV infection and the potential for subclinical or apparent low-level infections. Although it is possible and perhaps likely that CRP elevations may result from such infectious processes, the survival models described herein used CRP concentrations assessed at the baseline visit, when CRP levels were less than 2.7 mg/L for 75.8% of the individuals with progression to AIDS. These data are perhaps the strongest to mitigate against confounding owing to chronic bacterial infection.

Because this study was restricted to individuals with prevalent HIV infection, it was impossible to examine CRP changes around the time of seroconversion. Individuals with rapid progression to AIDS after seroconversion may not have been included. Furthermore, this study population consisted of homosexual or bisexual non-Hispanic white men. Although this group constitutes a large proportion of the HIV epidemic, the demographics of the epidemic have shifted toward other populations (eg, women and injecting-drug users). Further research in these populations is warranted.

Although these results suggest that CRP concentrations may have prognostic value, such measurements clearly cannot replace CD4 lymphocyte counts and HIV RNA levels for monitoring HIV-infected individuals. In addition, in resource-poor regions where alternative markers for disease progression would be of most value, the use of high-sensitivity CRP assays could be prohibitively expensive. However, measurement of CRP concentrations may provide additional prognostic information when used in conjunction with standard markers for HIV care. Furthermore, data on CRP concentrations in HIV infection with or without antiretroviral therapy is limited.9-13,18-21 To our knowledge, this is the only study that includes longitudinal CRP data from HIV-infected individuals prior to the widespread use of HAART. These results indicate increasing inflammation with disease progression, which may have implications for cardiovascular risk in HIV-infected populations.

The fact that the correlations of CRP concentrations with CD4 counts and HIV RNA levels were weak was somewhat surprising and may be related to the chronic immunosuppression consequent to HIV infection. Common viral infections that result in mild systemic inflammation are associated with much greater elevations in CRP levels (10-40 mg/L) than those seen in our subjects.6-8 However, because this is a seroprevalent cohort of HIV-infected individuals for whom the duration of infection is unclear, it is possible that these individuals experienced a more dramatic rise in CRP concentrations during acute HIV infection that eventually diminished and assumed a relatively stable lower level of inflammation seen in this study at baseline. Just before the development of AIDS, the CRP geometric mean level approached 2.5 mg/L, which may have clinical implications for these individuals. This level of CRP has been shown to confer an increased risk for cardiovascular disease relative to those with lower CRP concentrations.4-5 The American Heart Association and Centers for Disease Control and Prevention have recommended that the CRP concentration be used as a marker for cardiovascular disease in individuals with a Framingham risk score from 10% to 20%, considering CRP values between 1 and 3 mg/L as average risk and those of more than 3 mg/L as high risk for cardiovascular disease.2 The proportion of individuals with CRP of more than 3 mg/L ranged from 34% to 50% in the 2.5 years preceding AIDS development, whereas the proportion ranged from 9% to 24% when there were at least 15 individuals prior to this period. Whether CRP predicts cardiovascular disease equally well in the presence of a chronic infection like HIV is unknown. One study of HIV-infected individuals found that CRP did not significantly add predictive value when compared with traditional risk factors for identifying cardiovascular disease, although a small sample size and lack of matching on length of follow-up time were acknowledged as limitations.13

These data support a modest association between the level of inflammation as measured by CRP concentration and the degree of immunosuppression and HIV RNA levels in HIV-infected men. The results indicating increasing levels of inflammation for individuals with progression to AIDS and those who remained free of AIDS may have important implications for potential cardiovascular disease within this population, especially as infected individuals are living longer with effective therapies.

RESULTS

The 513 individuals who were randomly selected reflected the overall MACS population.14 The sample consisted primarily of non-Hispanic white individuals (n = 453 [88.3%]), with 26 (5.1%) men who reported being Hispanic white; 21 (4.1%), non-Hispanic black; and 13 (2.5%), other race/ethnicity (Table 1). The population was well educated, with 441 (86.0%) individuals who completed at least some college. The median age of the population was 33.8 years (interquartile range [IQR], 29.9-37.8 years). The median body mass index (calculated as weight in kilograms divided by the square of height in meters) was 23.1 (IQR, 21.6-24.8). One hundred seventy-nine individuals (34.9%) reported smoking during the past 6 months. The median CD4 lymphocyte count was 532 cells/µL (IQR, 342-721 cells/µL); baseline CD4 lymphocyte counts were missing for 4 individuals. The HIV RNA data were available for 484 individuals (94.3%). The median HIV RNA level was 18 450 copies/mL (IQR, 5359-63 741 copies/mL). The median CRP concentration was 1.2 mg/L (IQR, 0.6-2.3 mg/L). Of these individuals, AIDS developed in 318 (62.0%). The median CRP concentration was 1.3 mg/L (IQR, 0.6-2.7 mg/L) for those in whom AIDS later developed and 1.0 mg/L (IQR, 0.5-1.8 mg/L) for those who remained free of AIDS (Wilcoxon rank sum test; P = .002). These individuals contributed a total of 2709 person-years of follow-up.

ASSOCIATION OF BASELINE CRP WITH HIV DISEASE MARKERS AND TIME TO CLINICAL AIDS

Figure 1 shows a scatterplot of baseline CRP concentrations with baseline CD4 lymphocyte counts and log10 HIV RNA levels. The CRP concentrations were inversely correlated with CD4 lymphocyte counts (r = –0.17; P<.001) and directly correlated with HIV RNA levels (r = 0.20; P<.001).

Kaplan-Meier curves of individuals categorized by CRP categories (≤0.6, 0.7-1.2, 1.3-2.3, and >2.3 mg/L) are shown in Figure 2. Individuals with higher concentrations of CRP had shorter times to AIDS (overall log-rank test, P<.001). Individuals with a CRP concentration of 0.6 mg/L or less had a median time to AIDS of 7.70 years (95% CI, 6.74 to >9.31 years). Similarly, those with a CRP level of 0.7-1.2 mg/L had a median time to AIDS of 6.87 years (95% CI, 6.22 to >9.33 years). However, those with higher levels had progression to clinical AIDS more quickly. Median times to AIDS were 5.07 years (95% CI, 4.15-7.26 years) for those with CRP levels of 1.3 to 2.3 mg/L and 4.48 years (95% CI, 3.17-5.61 years) for those with CRP levels of more than 2.3 mg/L. These results suggest a threshold effect, with accelerated progression only at CRP levels of more than 1.2 mg/L.

Based on these results, CRP levels were categorized into 3 groups (≤1.2, 1.3-2.3, and >2.3 mg/L) for the log-normal time-to-AIDS analyses. In unadjusted models, individuals with CRP levels in the 2 higher categories had significantly lower relative times to AIDS (Table 2). These relative times correspond to reductions of 43% and 64% in their time to AIDS for the CRP categories of 1.3 to 2.3 and more than 2.3 mg/L, respectively, compared with individuals who had CRP levels of 1.2 mg/L or less. This trend remained after adjusting for CD4 lymphocyte counts and HIV RNA and hemoglobin levels (Table 2). After controlling for these factors, individuals with CRP levels of more than 2.3 mg/L showed a relative time of 0.63 (P<.001), equivalent to a 47% reduction in time to AIDS, compared with individuals with CRP levels of 1.2 mg/L or less. Models with total lymphocyte count, body mass index, and age showed that these variables did not alter these estimates.

Similar findings were obtained using Cox proportional hazards models, despite the fact that the proportionality assumption was not always met. In the unadjusted Cox model, individuals with CRP levels of 1.3 to 2.3 mg/L and more than 2.3 mg/L had relative hazards of 1.47 (P = .008) and 1.98 (P<.001), respectively, for progression to AIDS relative to those with CRP levels of 1.2 mg/L or less. The increased hazard for the development of AIDS among higher levels of CRP remained after adjusting for CD4 lymphocyte counts and log10 HIV RNA and hemoglobin levels. However, the category of individuals with CRP concentrations from 1.3 to 2.3 mg/L was only marginally significant (relative hazard, 1.32; P = .08), whereas the highest category of CRP remained statistically significant (relative hazard, 1.57; P = .001).

LONGITUDINAL PATTERNS OF CRP

Four hundred of the 513 individuals met selection criteria for the longitudinal analyses. Of these, 81 were randomly selected and contributed 1065 visits with a median of 12 visits. These individuals were mainly non-Hispanic white (n=69, 85%), and all had finished high school. During follow-up, AIDS developed in 44 (54%). At baseline, the median age of these individuals was 34.1 years (IQR, 30.0-38.6 years). In addition, the baseline median CD4 lymphocyte count was 642 cells/µL (IQR, 511-874 cells/µL), and of the 76 individuals with baseline HIV RNA data, the median was 13 341 copies/mL (IQR, 4348-30 180 copies/mL). The median CRP concentration was 1.0 mg/L (IQR, 0.5-1.8 mg/L) overall, 1.25 mg/L (IQR, 0.80-2.65 mg/L) for those who progressed to AIDS, and 0.5 mg/L (IQR, 0.5-1.1 mg/L) for those who remained free of AIDS. During follow-up, 55 individuals (68%) initiated some antiretroviral therapy (ART) from 1987 to 1996.

Levels of CRP increased over time for individuals with and without progression to AIDS (Figure 3). However, individuals with progression to AIDS had higher CRP levels than those without. In addition, the logarithmic scale of Figure 3 indicates that individuals with progression to AIDS demonstrated more rapid increases in CRP concentrations than those without progression to AIDS (this would be visually apparent if curves were plotted on an arithmetic scale). These trends were further supported by the results from the random-effects model (Table 3), which accounts for the correlation of repeated marker measurements and provides the trajectories of CRP concentrations for individuals with and without progression to AIDS. From the random-effects model, individuals with progression to AIDS had higher initial CRP concentrations than individuals who remained free of AIDS (1.39 vs 0.91 mg/L, respectively). Furthermore, the rate at which CRP concentration increased was greater for individuals with progression to AIDS, with an 8.5% change per year compared with a 4.5% change per year for individuals who remained free of AIDS (Table 3). Models with baseline age and body mass index were assessed but not included, as these variables failed to contribute information to the model as either a confounder or a significant predictor of CRP concentration.Furthermore, because individuals initiated therapy, time-dependent ART use was assessed in the model. However, ART use was not significantly associated with a change in CRP levels (P = .36). Concentrations of CRP are shown for individuals with progression to AIDS in Figure 4. The overall trend of CRP concentration indicates a gradual rise in CRP before the development of AIDS.

METHODS

STUDY POPULATION AND LABORATORY ANALYSIS

The MACS was initiated in 1983 to study the natural history of HIV infection among homosexual and bisexual men in the United States. The design of the MACS has been previously described,14 and only aspects pertinent to this study are presented herein. From April 2, 1984, to April 8, 1985, 4954 men, who were either seropositive or seronegative for HIV, were enrolled in the Baltimore, Md/Washington, DC, area, Chicago, Ill, Los Angeles, Calif, and Pittsburgh, Pa, with an additional 625 men enrolled from April 1, 1987, to February 25, 1991. Men with clinical AIDS or who were younger than 18 years were ineligible. At semiannual visits, the men returned to the clinics to provide specimens for laboratory analyses, undergo a physical examination, and complete self-administered data forms and an interviewer-administered questionnaire. At each visit, T-cell subset levels were measured in peripheral blood samples stained with monoclonal antibodies by means of a whole-blood lysing method and analyzed by means of 2-color flow cytometry15-16 and monoclonal antibodies specific for CD3, CD4, and CD8 lymphocytes. Absolute numbers of cells per microliter of blood were calculated using the complete blood cell count with an automated 10 000-cell differential. Because the MACS began before the advent of HIV RNA assays, HIV RNA data are limited. The HIV RNA data were used in this study for the baseline analyses and included only when available within 1 year of the visit.

Individuals included in this study consisted of a random sample of 513 MACS participants who were HIV seropositive on MACS enrollment and had specimens available in the national specimen repository dating from October 1, 1984, to May 31, 1987. For this study, CRP was measured using stored specimens that had been collected from each MACS participant as part of standard visits. The earliest visit from which specimens were available is referred to as the baseline (first ever) study visit. Levels of CRP were measured by means of a highly sensitive nephelometric assay using a monoclonal antibody to CRP coated on polystyrene beads with a lower limit of detection of 0.2 mg/L (Dade Behring, Marburg, Germany). To further investigate the temporal patterns of CRP, an additional subsample of individuals was randomly selected from the men with baseline measurements who had at least 6 visits through December 31, 1996 (when HAART use in the MACS became prevalent) and who were free of clinical AIDS for a minimum of 4 visits. Furthermore, men in whom AIDS developed from October 15, 1994, to December 31, 1996, were excluded (n = 8) to enable evaluation of CRP patterns before and after an AIDS diagnosis was made but prior to the widespread use of HAART. This study was approved by the institutional review board, The Johns Hopkins Bloomberg School of Public Health, Baltimore.

STATISTICAL ANALYSIS

Pearson product moment correlations were calculated for CRP concentrations with CD4 lymphocyte counts and HIV RNA levels at the baseline visit. Concentrations of CRP and HIV RNA were logarithmically transformed such that the data was more normally distributed.

We used Kaplan-Meier product-limit estimates to measure progression to AIDS for men with differing levels of CRP. The time at risk was calculated from the first visit from which samples underwent testing for CRP and ended when the individual was lost to follow-up, clinical AIDS had developed, or the individual was administratively censored at October 15, 1994. Log-normal survival models were used to assess the relative time for progression to AIDS after adjusting for other markers of disease progression. The distribution of events was properly distributed for a log-normal model.

To describe the pattern of CRP over time, a smooth graphical depiction (locally weighted scatterplot) was computed, stratified by whether or not progression to AIDS occurred. In addition, random-effects models were used to investigate the change in CRP level over time.17 In this model, the intercepts were allowed to vary among individuals. For individuals with progression to AIDS, the geometric mean of the CRP level was determined for the 6-month intervals around the AIDS diagnosis. The geometric mean was used because it is less sensitive to extreme values that may occur in measuring CRP. The mean value was determined for an individual with multiple observations within the 6-month intervals.

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The 10th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV London, UK, 6-8 November 2008
Webcasts now available
	We are delighted to announce that the webcasts from the 10th Workshop are now available.
	In addition, view short videocasts from the Organizing Committee discussing the 10th Workshop and reviewing the history of the meeting.   Our thanks to Gilead Sciences Ltd for supporting the webcasts.
Organizing Committee
	Jacqueline Capeau Faculty of Medicine Saint Antoine, INSERM, Paris, France   Andrew Carr St Vincent's Hospital, Sydney, Australia   David Cooper University of New South Wales, Sydney, Australia   Stefan Mauss Center for HIV and Hepatogastroenterology, Düsseldorf, Germany     Kathleen Mulligan University of California at San Francisco, USA   Morrie Schambelan University of California at San Francisco, USA   Ian Weller Royal Free and University College Medical School, London, UK
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For anyone interested.
First the good news. Dr. White has secured Ryan White funding that
will allow UTMB Galveston to continue indigent HIV care through
ACCRP (the Virology Clinic). Sadly this appears to be the only
indigent care of any kind that will be available at UTMB in the
foreseeable future.
And for anyone who is a current or past client there. In ACCRP Last
week UTMB laid-off P.A. Marcia, pharmacist Bryan, Social worker
Suzanne and staffers Jackie and Anita. Pretty much the heart of the
clinic, without explanation.
One source told me ACCRP will not return to the island and that it
and Hematology/Oncology will move to UTMB's Victory Lakes facility
on the mainland. However another source (doctor) told me ACCRP will
return to the UHC building by sometime in January. Both agree it
will not be back at its(most recent)Jeanie Sealy Hospital location.
John Sealy Hospital did re-open Monday - for a few hours until mold
was re-detected in OR A/C systems after testing clean last week.
If you're still reading, John Sealy lost its blood bank, pharmacy,
cafeteria and sterilization facilities, all of which are essential
to operating a hospital in hurricane Ike.
I've got to wonder why a facility like UTMB has been left to fend
for itself after a disaster like this when so much money has been
spent to help other places after both smaller and larger disasters.
Patrick

More countries make spreading HIV a crime
By MARIA CHENG, AP Medical Writer Maria Cheng, Ap Medical Writer  Thu Nov 13,
9:18 am ET
LONDON – An increasing number of countries worldwide are making spreading HIV
a crime, according to a new report from the International Planned Parenthood
Federation.

Health officials fear the trend could undermine gains made in fighting the AIDS
pandemic and provoke a surge in cases. Globally, about 33 million people are
thought to have HIV and nearly 3 million people are newly infected
every year.
"If the law is applied badly, this could set us back and do incredible damage,"
said Paul de Lay, an AIDS expert at UNAIDS, who was not involved in the report.
De
Lay said the laws could result in forced testing and drive the epidemic
underground as people hide their HIV status, allowing the virus to
spread unnoticed.

According to Planned
Parenthood, 58 countries worldwide have laws that criminalize HIV or
use existing laws to prosecute people for transmitting the virus.
Another 33 countries are considering similar legislation.

Since 2005, seven countries in West Africa have passed HIV laws. In Benin,
simply exposing others to HIV is a crime, even if transmission doesn't
occur. And in Tanzania, intentional transmission of the virus can lead
to life imprisonment.
Many of the laws in Africa were passed after a meeting in Chad in 2004 sponsored
by the U.S. Agency for International Development, the
world's biggest funder of AIDS programs, and attended by U.N. officials.
"The
U.N. was definitely remiss to allow this to happen," said Kevin
Osborne, a senior HIV adviser at IPPF and one of the report's authors.

De Lay said UNAIDS found out about the meeting only after it happened.
But poor countries aren't the only ones using these laws.
In
the U.S., 32 states have laws criminalizing HIV transmission. Experts
estimate that thousands of people have been charged across the country
with spreading HIV.

Since 2001, 16 people in the United Kingdom have been prosecuted for spreading
HIV.
In 2005, a woman in Canada was charged with criminal negligence and aggravated
assault for passing HIV while pregnant to her baby.
She
did not tell her doctors that she had HIV and did not receive the
medications necessary to prevent the virus from infecting her child.
She was sentenced to a six-month conditional sentence followed by three years of
probation.

In countries like Britain, Canada and the U.S., which are major donors of
efforts to fight AIDS in Africa, such cases are particularly unfortunate, many
experts say.
"It
sets a poor example in the sense that other countries may then think
this is an appropriate or desirable way to deal with HIV," said Richard
Elliott, executive director of the Canadian HIV/AIDS Legal Network.

While
there might be exceptional cases where prosecuting people who are
maliciously spreading HIV makes sense, experts said those were extreme
cases.
"The criminal law is a blunt
instrument," Osborne said. "If you put everyone in prison with HIV,
then you think you've controlled it. But you haven't dealt with the
issues around the intimate behaviors that spread HIV."
___
On the Net:
http://www.ippf.org

http://news.yahoo.com/s/ap/20081113/ap_on_he_me/eu_med_hiv_laws

Overlooked Fat Loss Factors

Losing weight is about more than reducing calorie intake. Fitness expert Joel
Marion lets us in on some overlooked fat loss factors.

By Joel Marion, Fitness Expert

Page 1: Overlooked Fat Loss Factors


These overlooked fat loss factors need to be addressed
We're often told that losing weight is a simple mathematical equation of
calories in, calories out. Burn more calories than you eat and you’ll lose
fat. However, is it really that simple? The truth is that the actual
“number” of calories you consume is not the only factor that affects your
fat-loss efforts. In this article, we’ll discuss five other things that should
be considered when determining the effect of your diet on your waistline,
primarily overlooked fat loss factors. Incorporate this knowledge into your
workout and nutrition routines and soon you'll be ripped like Ryan Reynolds --
and attracting looks from fitness babes like Amy Weber and Jamie Eason for it.

1- The thermic effect of the food you eat

The thermic effect of food (TEF) measures the amount of energy that is required
to support the processes of digesting, absorbing and assimilating food nutrients
as well as the energy expended as a result of the central nervous system's
stimulatory effect on metabolism when food is ingested. Of the three
macronutrients, protein carries the highest thermic effect. Eat more protein;
burn more calories.

2- The fiber content of the food you eat

Due to its chemical makeup, fiber is classified as a carbohydrate; however, it
is unlike other carbohydrates in that it is an indigestible nutrient. Even
though each gram of fiber contains four calories, these calories will remain
undigested and will not be absorbed. Therefore, if you were to consume 300
calories of red beans (a food in which nearly 1/3 of the caloric content is from
fiber), approximately 100 of these calories would pass through your intestinal
tract undigested.

3- The glycemic and insulin indices of the food you eat

The glycemic and insulin indices are scaled numbers that refer to how quickly a
particular carbohydrate source enters the bloodstream as sugar and how much
insulin is needed to rid that sugar from the bloodstream, respectively.
Generally speaking, there is a positive relationship between the two; the
quicker sugar enters the bloodstream, the more insulin is needed to rid that
sugar from the bloodstream. When high levels of insulin are present within the
blood, fat burning is brought to a screeching halt, which is anything but
desirable for those whose goal it is to obtain a lean, muscular physique. Don't
let this be an overlooked fat loss factor.

4- The different macronutrients present in the food you eat

Although insulin's primary function is to shuttle glucose (sugar) into skeletal
muscle, it also carries many other nutrients to their respective storage sites
-- this includes lipids (fat). Since carbohydrate ingestion stimulates a large
insulin response and fat ingestion gives rise to blood lipid levels, when the
two are consumed together, they promote the greatest fat storage.

There's one more overlooked fat loss factor you need to know, along with some
other great weight loss tips...
Page 2: Fat Loss

5- The size, frequency and time of the meals you eat

Large, infrequent meals tend to promote storage of the ingested nutrients, as
the body is unsure as to when the next feeding will take place. Conversely,
consuming smaller, more frequent meals will result in an increase in metabolism
and utilization of the ingested nutrients. Also, ingesting a large amount of
carbohydrates before bed spikes insulin, deters nocturnal thermogenesis and
increases fat storage during sleep. On the contrary, consuming a great deal of
calories early in the day does not bring about this problem; rather, these
calories are likely to be used as energy to support daily activities.
fight the fat

As you can see, someone could be eating a relatively small amount of calories
daily, but at the same time be promoting a great deal of fat storage by: 1)
Making poor food choices; 2) Combining macronutrients in a nonproductive fashion
and; 3) Consuming food infrequently and at inopportune times. To illustrate this
further, let's take a look at a recent study that analyzed the diets of 38
police officers. This study discovered that although the officers were consuming
a hypocaloric diet (fewer calories than they burn), they all had unhealthy
levels of body fat and had been gaining fat mass over the past five years. If
all you had to do to lose fat was consume fewer calories than you burned, then
these individuals would be losing fat, not gaining it.

To confirm the importance of the factors that I previously mentioned, let's take
a look at some of the other things this study noted:
Only 15% of their diet consisted of protein, the macronutrient with the greatest
TEF.
Their diet contained very little fiber.
Over 50% of their carbohydrate intake was derived from simple sugars, which have
very high glycemic and insulin indices.
They didn't note this, but I'm willing to bet that they didn't avoid the
fat-carb combo.
They ate infrequently -- only 10% of their caloric intake was consumed at
breakfast and over 50% was consumed right before bed.
By now, it should be obvious that fat loss isn't just a matter of calories in,
calories out. And while it’s a little more complex than that, you can easily
use the tips in this article to ensure you’re getting the most from your
dieting efforts.

Joel Marion is an internationally recognized fitness expert and the author of
The Cheat to Lose Diet (Random House, 2007). To learn more about Joel’s
top-rated Body Transformation Coaching program and to download a free copy of
his latest fat loss report, The Secret Fat Loss Hormone, visit
www.JoelMarionCoaching.com.

http://www.askmen.com/sports/bodybuilding_200/248_fitness_tip.html

Nap without guilt: It boosts sophisticated memory


WASHINGTON - Just in time for the holidays, some medical advice most people will
like: Take a nap. Interrupting sleep seriously disrupts memory-making,
compelling new research suggests. But on the flip side, taking a nap may boost a
sophisticated kind of memory that helps us see the big picture and get creative.

"Not only do we need to remember to sleep, but most certainly we sleep to
remember," is how Dr. William Fishbein, a cognitive neuroscientist at the City
University of New York, put it at a meeting of the Society for Neuroscience last
week.

Good sleep is a casualty of our 24/7 world. Surveys suggest few adults attain
the recommended seven to eight hours a night.

Way too little clearly is dangerous: Sleep deprivation causes not just car
crashes but all sorts of other accidents. Over time, a chronic lack of sleep can
erode the body in ways that leave us more vulnerable to heart disease, diabetes
and other illnesses.

But perhaps more common than insomnia is fragmented sleep - the easy awakening
that comes with aging, or, worse, the sleep apnea that afflicts millions, who
quit breathing for 30 seconds or so over and over throughout the night.

Indeed, scientists increasingly are focusing less on sleep duration and more on
the quality of sleep, what's called sleep intensity, in studying how sleep helps
the brain process memories so they stick. Particularly important is "slow-wave
sleep," a period of very deep sleep that comes earlier than better-known REM
sleep, or dreaming time.

Fishbein suspected a more active role for the slow-wave sleep that can emerge
even in a power nap. Maybe our brains keep working during that time to solve
problems and come up with new ideas. So he and graduate student Hiuyan Lau
devised a simple test: documenting relational memory, where the brain puts
together separately learned facts in new ways.

First, they taught 20 English-speaking college students lists of Chinese words
spelled with two characters - such as sister, mother, maid. Then half the
students took a nap, being monitored to be sure they didn't move from slow-wave
sleep into the REM stage.

Upon awakening, they took a multiple-choice test of Chinese words they'd never
seen before. The nappers did much better at automatically learning that the
first of the two-pair characters in the words they'd memorized earlier always
meant the same thing - female, for example. So they also were more likely than
non-nappers to choose that a new word containing that character meant "princess"
and not "ape."

"The nap group has essentially teased out what's going on," Fishbein concludes.

These students took a 90-minute nap, quite a luxury for most adults. But even a
12-minute nap can boost some forms of memory, adds Dr. Robert Stickgold of
Harvard Medical School.

Conversely, Wisconsin researchers briefly interrupted nighttime slow-wave sleep
by playing a beep - just loudly enough to disturb sleep but not awaken - and
found those people couldn't remember a task they'd learned the day before as
well as people whose slow-wave sleep wasn't disrupted.

That brings us back to fragmented sleep, whether from aging or apnea. It can
suppress the birth of new brain cells in the hippocampus, where memory-making
begins - enough to hinder learning weeks after sleep returns to normal, warns
Dr. Dennis McGinty of the University of California, Los Angeles.

To prove a lasting effect, McGinty mimicked human sleep apnea in rats. He hooked
them to brain monitors and made them sleep on a treadmill. Whenever the monitors
detected 30 seconds of sleep, the treadmill briefly switched on. After 12 days
of this sleep disturbance, McGinty let the rats sleep peacefully for as long as
they wanted for the next two weeks.

The catch-up sleep didn't help: Rested rats used room cues to quickly learn the
escape hole in a maze. Those with fragmented sleep two weeks earlier couldn't,
only randomly stumbling upon the escape.

None of the new work is enough, yet, to pinpoint the minimum sleep needed for
optimal memory. What's needed may vary considerably from person to person.

"A short sleeper may have a very efficient deep sleep even if they sleep only
four hours," notes Dr. Chiara Cirellia of the University of Wisconsin, Madison.

But altogether, the findings do suggest some practical advice: Get apnea
treated. Avoid what Harvard's Stickgold calls "sleep bulimia," super-late nights
followed by sleep-in weekends. And don't feel guilty for napping.

---

EDITOR'S NOTE - Lauran Neergaard covers health and medical issues for The
Associated Press in Washington.


By LAURAN NEERGAARD AP Medical Writer


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Norvir (Ritonavir) is an inhibitor of Cytochrome P450 isoenzyme
CYP3A4.
Tylenol (acetaminophen, paracetamol) has a complex 3 phase liver
metabolism CYP2E1, CYP3A4, CYP1A2 which then produces NAPQI, the
cause of Tylenol Toxity. Norvir boosts acetaminophen liver toxicity
to an
unknown level. 27 Extra Strength Tylenols (27g) will destroy your
liver.

When I took norvir and vicodin (hydrocodone/acetaminophen) for
peripheral neuropathy 2 tablets per week, my liver  ALT increased to
111 over a 3 mo period. ALK PHOS was 117. I switched to Hycodan
(hydrocodone/ homotropine), and my ALT dropped back to 41 over a 3
month period. My Alk Phos also dropped back to 66.

Do not use Any tylenol containing products if you take Norvir. If you
have high liver ALT (alanine aminotransferase) and you take norvir
and any tylenol containing products, stop the tylenol and check your
ALT in 3 months.

To:
Paul C Davis

From:
WALFORD J. FESSEL MD

Received:
11/7/07 10:23 AM

Your info re the metabolism is both fascinating and clinically
relevant. It shows how extensive our knowledge gaps can be--even when
we do our best to maintain awareness!

Jeffrey Fessel MD.


----- Message -----
From: DAVIS,PAUL C
Sent: 11/7/2007 9:53 AM
To: Office of WALFORD J. FESSEL MD
Subject: RE: Paracetamol metabolism part 2

Hi Dr Fessel,

my ALT went up to 111 when I was taking vicodin and did not drop down
to 41 until we switched to hycodan for occasional peripheral
neuropathy pain.

I will no longer take paracetamol because of this. The phase 1
metabolites of paracetamol use CYP3A4 and were toxic enough to raise
my alt to 111.


Ref: O' Brian P. Biochemistry notes: Role of Glutithione
  (slide 4),2002

http://phm.utoronto.ca/~jeffh/phm%20acetaminophen.pdf

Medscape: http://www.medscape.com/viewarticle/557074