On November 26, 2012, Health Canada licensed the sale and use of a new combination of anti-HIV drugs in one pill. This combination has been nicknamed the Quad and will be sold under the brand name Stribild. The combination is a complete treatment regimen; such combinations are called single tablet regimens (STR). Stribild is approved for the treatment of people new to HIV therapy (treatment naïve). Stribild is made by the pharmaceutical company Gilead Sciences.

Stribild is already licensed in the U.S. and approval is pending in the European Union and Australia.

Inside the Quad

The Quad contains four medicines, two of which are new, as follows:

elvitegravir (150 mg) – this new drug belongs to a class of anti-HIV drugs called integrase inhibitors
cobicistat (150 mg) – this new drug is a booster and it does not have anti-HIV activity. Its purpose is to raise and maintain levels of elvitegravir in the blood. Boosters are commonly used in HIV medicine; another example of a booster is the drug ritonavir (Norvir).
The Quad also contains two older anti-HIV medicines that belong to the class commonly called nukes (nucleoside analogues):

tenofovir (300 mg) – a popular anti-HIV drug sold under the brand name Viread and found in several combinations including Truvada, Atripla and Complera
FTC (200 mg) – found in the same combinations as tenofovir
Stribild is taken once daily with food.

Studies

In clinical trials with treatment-naïve HIV-positive people, the Quad has been very effective in reducing the amount of HIV in the blood (viral load) and raising levels of CD4+ T-cells. Together these changes have resulted in improved health. Researchers have found the Quad to be roughly equivalent in effectiveness to another already licensed STR called Atripla, which consists of a fixed-dose combination of the following drugs:

efavirenz (Sustiva) + tenofovir + FTC
In HIV-positive people who are treatment experienced, researchers found the Quad to be roughly equivalent to a commonly used regimen consisting of the following anti-HIV drugs:

ritonavir + atazanavir (Reyataz) + tenofovir + FTC
Treatment issues

In clinical trials, Stribild was generally safe and effective. However, as with any regimen, there are some issues users should be aware of, including the following:

Side effects

The most common side effects associated with Stribild were nausea and diarrhea. A link to further information about possible side effects and more detailed information from clinical trials appears toward the end of this bulletin.

Kidney and liver concerns

Stribild should not be taken by people who have a moderate (or worse) degree of kidney dysfunction. The manufacturer specifies that this refers to people who have an eGFR (estimated glomerular filtration rate) of less than 70. Also, people who have severe liver damage (having Child-Pugh rating of class C) should not use Stribild.

Drug interactions

The drugs in Stribild, particularly elvitegravir and cobicistat, have the potential to interact with many other drugs and herbs. Always speak to your doctor, nurse and pharmacist about taking other drugs (both prescription and over the counter), supplements or herbs if you are taking Stribild or other anti-HIV medicines.

A drug interaction may do the following:

It can lower the level of cobicistat or elvitegravir in the blood. This can weaken the effect of Stribild and cause Stribild to fail. If this happens, you may have fewer future treatment options.
It can raise the level of cobicistat, elvitegravir or other drugs in the blood. This could cause new side effects or make pre-existing side effects worse.
Women

In clinical trials with Stribild, about 10% of participants were women. This is less than ideal. Gilead Sciences is committed to conducting further research with Stribild and HIV-positive women. Also, the safety of Stribild in pregnant women is not known.

The long and winding road

Once Health Canada approves a drug, physicians can prescribe it but patients must pay for it unless their private insurance plan provides coverage. HIV/AIDS is a catastrophic disease that can affect people’s ability to work and requires expensive care. In Canada, provincial and territorial ministries of health heavily subsidize the cost of anti-HIV medications. Each ministry has a listing of drugs for which it is prepared to pay. These listings are called formularies.

After federal approval, each HIV medicine must undergo another review process called Common Drug Review (CDR). As part of this review, recommendations are made as to whether the drug in question should be:

listed on formularies
listed on formularies with conditions, which means its use is restricted
not listed at all
The CDR may also result in no decision being made as additional information is gathered. With the exception of Quebec, all provinces and territories, the Departments of National Defence and Veterans Affairs, and the Non-Insured Health Benefits plan participate in the CDR.

Stribild will undergo the CDR process in 2013 with the results available later that year.

In Quebec

Gilead Sciences plans to submit a dossier on Stribild to L’Institut national d’excellence en santé et en services sociaux (INESSS) shortly. Stribild will hopefully be listed on the Quebec formulary—Liste des médicaments assurés du Québec—in 2013.

Cost

The wholesale price of Stribild in Canada is approximately $16,600 per person per year; this is considerably less than the wholesale price in the U.S., which is about $28,500 per person per year.

Availability

Pharmacies will be able to place orders for Stribild from December 31, 2012, and the company will ship them the drug shortly thereafter.

Resources:

Quad (Stribild) – safety and effectiveness issues in depth – TreatmentUpdate 191

The Quad (Stribild) and changes to assessments of kidney health – TreatmentUpdate 192

Cobicistat and elvitegravir – safe with methadone or buprenorphine and naloxone – TreatmentUpdate 194

A CATIE Fact Sheet on Stribild is under development.

—Sean R. Hosein

REFERENCES:

Rockstroh J, DeJesus E, Henry K, et al. Elvitegravir/cobicistat/emtricitabine/tenofovir DF (Quad) has durable efficacy and differentiated safety compared to atazanavir boosted by ritonavir plus emtricitabine/tenofovir DF at week 96 in treatment-naïve HIV-1-infected patients. In: Program and abstracts of the 11th International Congress on Drug Therapy in HIV Infection, 11–15 November 2012, Glasgow, UK. Abstract 424b.
Zolopa A, Gallant J, Cohen C, et al. Elvitegravir/cobicistat/emtricitabine/tenofovir DF (Quad) has durable efficacy and differentiated safety compared to efavirenz/emtricitabine/tenofovir DF at week 96 in treatment-naïve HIV-1-infected patients. In: Program and abstracts of the 11th International Congress on Drug Therapy in HIV Infection, 11–15 November 2012, Glasgow, UK. Abstract 424a.
DeJesus E, Felix J, Vanderwalle B, et al. Indirect treatment comparison of efficacy, safety and resistance of EVG/COBI/FTC/TDF (Quad) vs. RAL + FTC/TDF in treatment-naïve HIV patients. In: Program and abstracts of the 11th International Congress on Drug Therapy in HIV Infection, 11–15 November 2012, Glasgow, UK. Poster 265.
Lee FJ, Carr A. Tolerability of HIV integrase inhibitors. Current Opinion in HIV/AIDS. 2012 Sep;7(5):422-8.
Lepist EI, Phan TK, Roy A, et al. Cobicistat boosts the intestinal absorption of transport substrates, including HIV protease inhibitors and GS-7340, in vitro. Antimicrobial Agents and Chemotherapy. 2012 Oct;56(10):5409-13.
German P, Liu HC, Szwarcberg J, et al. Effect of cobicistat on glomerular filtration rate in subjects with normal and impaired renal function. Journal of Acquired Immune Deficiency Syndromes. 2012 Sep 1;61(1):32-40.

While these individuals might seem to be the lucky few, innate immunity has incredible potential as a research tool in finding new therapies against the virus that could benefit millions in the future!

But first, scientists need to find out how innate immunity works. Researchers are currently looking at how intrinsic mechanisms can first sense HIV entry into cells and then boost inflammation to fight the infection.

One mechanism that has been elucidated for HIV-1 (the most common strain of HIV) resistance is in plasmacytoid dendritic cells (pDCs) and involves Toll-like receptors. When infection occurs through the body’s mucous membranes, the virus needs to pass through a barrier on the surface that’s composed of epithelial cells organized into layers. Before the virus reaches the final layer, dendritic cells can stop the virus in its tracks, using sensors like Toll-like receptors that recognize intrusions by the virus. The new pCDs then start producing type I interferon, which inhibits the early stages of HIV-1 replication.

There is one catch, though – interferon and inflammatory responses can actually be used by the virus to amplify the infection. As Ploquin et al. state in their review, the inflammatory response by the immune system is a double-edged sword. Inflammation can promote adaptive responses and confine viral replication, but it can also help create viral reservoirs in T cells, and help the virus disseminate (which leads to a generalized infection of the immune system). The immune system’s inflammatory response can then become chronic and lead to progression to AIDS.

Other types of immunity might recruit macrophages, which become targeted by HIV to play roles in the viral reservoir and in the virus’ replication, but can also help fight infection by inhibiting the virus’ replication. Another contributor to natural immunity are natural killer cells, which are also present in the mucosa and become more numerous and more toxic to HIV once pDCs start releasing interferon. Natural killer and dendritic cell interactions are also very important in fostering adaptive immunity, since effective crosstalk can help the dendritic cells to specialize into their functional forms.

Resistance to progression to AIDS is unique in that the immune response has been adaptive enough so that CD8+ T-cells’ responses are unusually strong. This is thought to be related to the myeloid dendritic cells’ maturation, which is also triggered by interferon.

So what can we learn from innate immunity? Ploquin et al. believe that with more research on natural killer cells, scientists will be closer to developing an HIV vaccine. Other researchers are looking at SIV-infected macaque monkey models to see how controlling inflammation in the mucosa and lymphoid organs can help protect against the virus. So, the key now lies in discovering exactly what mechanisms allow immunity against HIV infection and against progression to AIDS, and then figuring out how to reproduce and apply the mechanisms.

Sources:
1. HIV Subtypes, Groups and Strains. Avert. http://www.avert.org/hiv-types.htm

2. Blankson, JN, D. Persaud, RF Siliciano. The challenge of viral reservoirs in HIV-1 infection. http://www.ncbi.nlm.nih.gov/pubmed/11818490. Annu Rev Med. 2002;53:557-93.

3. Ploquin, Mickaël J.-Y., Béatrice Jacquelin, Simon P. Jochems, Françoise Barré-Sinoussi and Michaela C. Müler-Trutwin. Innate immunity in the control of HIV/AIDS: recent advances and open questions. http://www.ncbi.nlm.nih.gov/pubmed/22472855. AIDS 2012; 26:1269–1279

La résistance innée – Comment ça fonctionne, et pourquoi c’est bon pour tous!

Écrit par Vivienne Walz

Peut-être vous avez déjà entendu parler des personnes qui ont une résistance naturelle contre le VIH. Pour les chercheurs qui songent trouver des nouvelle thérapies contre le virus, la résistance naturelle a le potentiel incroyable. Cette résistance est aussi appelé l’immunité innée, et il y a deux types. Le premier se présente en des personnes qui ont la résistance spontanée contre l’infection initiale. Le deuxième apparait en des personnes déjà infectés avec le VIH, et c’est une résistance contre le SIDA – ces individus sont appelés des non-progresseurs à long terme.

Au présent, les chercheurs sont en train d’investiguer les mécanismes du système immunitaire pour détecter l’entrée du virus dans les cellules et ensuite pour stimuler l’inflammation pour combattre l’infection.

Un mécanisme qui a été découvert pour le VIH-1 (la sorte de VIH la plus courante) est le résistance dans le cellules dendritiques plasmacytoïdes (pDC) et implique les récepteurs « Toll-like » (TLR). Lorsque l’infection se produit par voie muqueuse, le virus doit passer à travers une barrière de cellules épithéliales qui se compose de plusieurs couches. Avant que le virus atteint la dernière couche, les cellules dendritiques peuvent empêcher le VIH dans son élan en utilisant des capteurs comme les TLRs, qui reconnaissent les intrusions par le virus. Les pCDs commencent à produire de l’interféron de type I, qui inhibe les premiers stades de la réplication du VIH-1.

Mais, il y a un hic – l’interféron et les réactions inflammatoires peuvent aussi amplifier l’infection. Comme Ploquin et al. ont écrit, la réponse inflammatoire par le système immunitaire est une épée à double tranchant. L’inflammation peut promouvoir des réponses d’adaptation et peut contrôler la réplication virale, mais elle peut aussi aider à créer des réservoirs viraux dans les cellules T et aider à diffuser le virus, ce qui conduit à une infection généralisée du système immunitaire. La réponse inflammatoire du système immunitaire peut alors devenir chronique et entrainer la progression du sida.

Un autre type d’immunité pourrait recruter des macrophages, qui seront effectivement ciblés par le VIH à jouer un rôle dans le réservoir viral et dans la réplication du virus, mais qui peuvent aussi aider à combattre l’infection en inhibant la réplication du virus. En outre, les natural killer cells, qui sont présents dans le muqueuse, deviennent plus nombreux et plus toxiques pour le VIH une fois les pDCs commencent à libérer l’interféron. Les natural killers et les interactions des cellules dendritiques sont également très importants dans la promotion de l’immunité adaptative, car leur communication efficace permet d’optimiser le processus de le spécialisation des cellules dendritiques.

Les non-progresseurs à long terme sont uniques en ce que leur réponse immunitaire adaptative a été suffisant pour que les réponses de leurs cellules T CD8+ sont très forts. Cela ralentit considérablement la progression vers le SIDA. C’est pensé que ceci est lié à la maturation des cellules dendritiques myéloïdes, qui est déclenchée par l’interféron.

Alors, que pouvons-nous apprendre de l’immunité innée? Ploquin et al. croient qu’avec des recherches plus concentrés sur le ceullules natural killer, les chercheurs seront plus proches de l’élaboration d’un vaccin contre le VIH. D’autres chercheurs étudient les modèles de singe macaque infectés avec le VIS pour voir comment contrôler l’inflammation de la muqueuse et les organes lymphoïdes peuvent aider à protéger contre le virus. Il reste maintenant à découvrir exactement quels mécanismes permettent une immunité contre l’infection à VIH et contre la progression du sida, et ensuite réfléchir à la façon de reproduire et d’appliquer les mécanismes.

Sources:
1. HIV Subtypes, Groups and Strains. Avert. http://www.avert.org/hiv-types.htm

2. Blankson, JN, D. Persaud, RF Siliciano. The challenge of viral reservoirs in HIV-1 infection. http://www.ncbi.nlm.nih.gov/pubmed/11818490. Annu Rev Med. 2002;53:557-93.

3. Ploquin, Mickaël J.-Y., Béatrice Jacquelin, Simon P. Jochems, Françoise Barré-Sinoussi and Michaela C. Müler-Trutwin. Innate immunity in the control of HIV/AIDS: recent advances and open questions. http://www.ncbi.nlm.nih.gov/pubmed/22472855. AIDS 2012; 26:1269–1279

Vaccine development is a leading area of research within HIV/AIDS. But even after 30 years of research a working vaccine still evades us. Does something sweet hold the key? Leading researchers in the field of glycoproteins thinks it just might!

HIV is a highly variable virus with many subtypes and is prone to high rates of mutation. It is this high rate of variability that has made finding an effective vaccine so difficult. Vaccines typically are made from dead or weakened virus that forces the immune system to produce antibodies (proteins that usually seek out and attach to certain proteins on an invader marking it for removal). This approach however has not worked against HIV because the viruses proteins are hid under a sugary outer coating, which is made with the infected persons own sugars. This renders the person’s immune system unable to recognize the virus as an invader. This changeability also means that antibodies that work to deactivate one strain may not work on another.

However, the recent discovery of potent broad-spectrum antibodies (isolated from HIV positive persons) that attack this coat may just revolutionize our search for a successful vaccine. Dr. Wilson and his team at the IAVI Neutralizing Antibody Center at the Scripps Research Institute have been looking at these antibodies called PG’s and PGT’s to better understand which part of the virus they attack as they have shown the ability to render up to 80% of HIV-1 subtypes unproductive. As such, a vaccine that could prompt the body to make these antibodies would offer comprehensive protection for an immunized person.

Their research has shown that many of these antibodies are able to attach to two of the sugars as well as penetrate the sugar coat and attach to a part of a protein underneath. It is through research into how this binding occurs that may allow us to produce a vaccine that will force a healthy person’s immune system to produce antibodies similar to these. So let’s keep our fingers crossed that this sweet research might just be the answer!

Written by Vivienne Walz

Recently, the United States Food and Drug Administration (FDA) approved the OraQuick rapid HIV test for retail sale in the United States. This means that HIV tests will soon be available in pharmacies, along with pregnancy tests and condoms. Although the test has been approved in the US, there is still much debate about whether it should be sold in Canada. For some people, it’s uncertain whether the test’s benefits will outweigh its costs.

When it comes to rapid HIV testing, either blood or oral fluid can be tested. The OraQuick exam, which is a rapid oral fluid HIV test may cost between $20 and $40. Testing an oral fluid sample, which entails swabbing the gums, gives results in about 20 minutes, all in the privacy of one’s own home. Having the test widely available in pharmacies could help reduce the stigma associated with HIV. The convenience, speed and privacy could entice more people to get tested more often, which will raise awareness and could discourage risky behaviour. This regulated, government-approved home test is a better alternative to the unregulated and potentially inaccurate tests that are currently available on the internet.

However, this rapid HIV test should be only considered a preliminary test, seeing as there can be false positive and false negative results. False positives occur in around 1 per 5,000 tests – but, more alarmingly, false negatives occur in as many as 1 of 12 home tests. As a result of these false negatives, some people may be more enticed to engage in risky behaviour, such as unprotected sex, and this in turn could increase the risk of passing on the virus. False negative results can be due to improper testing technique, but they could also be due to the timeframe of testing. It can take more than 3 months after initial HIV infection for seroconversion to take place and for the body to begin forming the antibodies that the oral fluid exam detects. If an HIV+ person has not yet began producing antibodies, they may believe that they are HIV- and go on to take greater risks. This is why if someone is at risk to have contracted the virus, they should retest often, and additionally, this is why education about the test is so important – people need to be informed that the test isn’t perfect and that they still need to protect themselves.

Another problem with the home test is lack of support for people with a positive diagnosis. There is a 24 hour OraQuick Customer Support Centre with counselors on hand around the clock, but there will still be people who receive a positive diagnosis and find themselves completely alone – which, in extreme cases, could lead to more dramatic reaction. When a positive diagnosis is delivered in a clinic, there is an immediate accompanying support network, while the home test requires people to seek out support for themselves.

Selling the OraQuick exam over-the-counter in Canada will enable people to determine their HIV status with convenience and increased privacy, however, a lack of support and education may come hand in hand with the advantages.

Now to ask you – do you think that making the rapid HIV home test available in Canada is a good idea, or not?

What other issues might need to be addressed before the test is made available in Canadian pharmacies?

What can we do to make sure people with an HIV+ result still get the support and education they need?

Sources:

http://www.cdc.gov/hiv/topics/testing/resources/qa/oralfluidqandafin.htm

http://www.fda.gov/ForConsumers/ConsumerUpdates/ucm310545.htm

http://aidsetc.org/aidsetc?page=cg-209_rapid_testing

However, this approval has not come without controversy. Even though the drug has been proven to be effective for prevention through large controlled studies in both men who have sex with men (MSM) and couples who have different sero-status (one person is HIV-positive, the other HIV-negative),there are some who see it as a step backwards. Those opposed to the approval are worried that the endorsement of Truvada as a means of PrEP will lead to more risky behaviour, (i.e. forgoing condom use, engaging in riskier sexual activities etc…). Another troublesome possibility is an increase in antiretroviral resistant strains of the HIV virus due to a lack of treatment adherence (remembering to always take your pill as directed).

This increase in resistant strains could prove to be problematic as we have a limited arsenal of medications available.  Thirdly, there is always the issue of cost, at a minimum 3600$ a year not including counselling, screening and other associated costs, this is an expensive course of action for both the patient and health care system.

So while this approval is certainly a big step forward in terms of prevention possibilities, we still need to continue the research on PrEP and its associated risk and benefits so that we can move forward in the fight against AIDS.

Sources:

Cohen, J. (2012). Aids Research: FDA Panel Recommends Anti-HIV Drug for Prevention. Science , 336 (6083), 792.

Maxmen, A. (2012). Wary approval for drug to prevent HIV:US regulators seek to mitigate risks of combined pill. Nature , 487 (7407).

In the case of HIV/AIDS, managing the disease is all about consistently inhibiting viral replication. This depends on many factors that all fit together in a unique way, including the potency of the regimen, drug resistance and exposure, dosing frequency, and some physiological factors such as the absorption of the drug by the body and how much of the drug is filtered out by the kidneys. But surprisingly, one of the most difficult factors to monitor and to control is not pharmacological, nor physiological. This factor is adherence.

Adherence is such a complex factor mainly because it depends on human behaviour. But contrary to focusing on raising average adherence, to prevent viral replication the crucial factor is actually to reduce the largest interdose interval. This means that the longer the treatment interruption, the greater the HIV-RNA replication. So, the time between missed doses is a crucial factor in preventing viral replication.

The reason for this relationship is that antiretroviral drugs have long half-lives, which means that they slowly deactivate once ingested. So, interspaced missed doses can occur without letting the drug’s concentration fall below therapeutic (effective) levels, since some of the drug is still left over in the bloodstream. However if too many doses are missed in a row, then the drug’s effects fall below the level at which they inhibit viral replication.

This observation puts into question the importance given to a 95% adherence goal, and suggests that more importance should be put into making sure that less consecutive doses are missed instead of only increasing average adherence. This insight on adherence patterns will lead to better treatment counseling and therefore better treatment results for PHAs!

Source: Number of missed doses: why 1 x 7 does not make 7 x 1?. Parienti, Jean-Jacques; Paterson, David. AIDS. Volume 26(11).

KEEPING ALL YOUR MARBLES
By: Vivienne Walz
Supervision and Translation by: Gilbert Mallais June 28, 2012

In the last 15 years, treatment for HIV/AIDS has come a long way. More HIV+ adults are now living into their fifties, sixties and beyond; but with this new demographic of PHAs, comes some new challenges. Among these are serious non-AIDS related events (or SNAREs). SNAREs are linked with a low nadir (the lowest CD4 cell count ever had by a PHA), and are becoming increasingly common, as HIV+ patients are getting older.

One particular SNARE is HIV-associated dementia. Dementia is often used as a blanket term for neurocognitive impairments associated with aging. Typical symptoms of dementia include new memory impairments accompanied by language, movement-planning, learning and recognition inabilities that interfere with daily life. Alzheimer disease is one type of dementia. Another is AIDS dementia complex.

Good news: in the case of AIDS dementia complex, one’s condition can actually improve with HAART.

More good news: there are many controllable risk factors associated with cognitive decline. Consistently continuing with antiretroviral therapy is one way to reduce the risk of cognitive decline later in life. Avoiding STIs and aiming for a CD4 count of greater than 500 are also important. Large waist circumference has also been linked to development of dementia, so by eating right and exercising the risk can be decreased. Being active has the added benefit of improving cardiovascular fitness, which also helps prevent cognitive decline. By eating healthy the risk of

The published results from the HPTN 052 study as well as an increasing amount of talk around treatment as prevention have opened up a new avenue of questioning for HIV positive members of society.  Some think that having an undetectable HIV viral load means that you can’t transmit HIV to others.

Agreeing or disagreeing with this mindset is not easy and takes a lot of information.

Although it is documented that the subjects of 052 with an undetectable viral load did not transmit HIV, lets not forget that all the study participants received prevention counseling that included free condoms.

Where they used? Who knows?

Nothing in life is 100% risk free.  Getting out of bed in the morning comes with some amount risks.

A case study from Germany involving a 39-year-old man in a monogamous relationship, on ART since 2000, with a viral load <50 copies/mL over a period of over 4 years.  The patient was in good health, good treatment adherence and no other STIs.  In May of 2003, he and his partner of 3 years began having unprotected anal sex.  His partner had tested HIV negative in 2002.  In July of 2004, his partner seroconverted.  Testing ruled out that the HIV came from a 3^rd person.

So Undetectable does not necessarily mean non transmissible.

We can all agree that ART and an undetectable viral load significantly reduce the risk of HIV being transmitted; but it does not eliminate the possibility.

Shedding, (which is a spike in virus) in the male genital tract happens even in men with consistently undetectable blood viral loads.  We still don’t know the genital tract viral load needed to transmit HIV.  So risk reduction is necessary.

Recommending safer sex practices for HIV infected is the best bet to prevent HIV transmission.

Gilbert Mallais

Treatment Information Facilitator/ Info-traitement Co-coordinator

Stürmer et al. Case report:  Is transmission of HIV-1 non-viraemic serodiscordant couples possible?  Antivir Ther 2008;13:729.

Over the hill with HIV!

By:Maria Lawrynowicz

Supervised by: Gilbert Mallais (Treatment Information Facilitator)

Thanks to the incredible advances in HAART treatment during the last 30 years, those living with HIV have a much higher life expectancy and improved quality of life. This has created a relatively new area of research interest that was unheard of just 20 years ago: aging with HIV. How does infection with HIV change the progression of the normal biological processes and associated pathologies that come with aging? Research into this domain is complex because it is difficult to track subjects over long periods of time. This study, however, not only looked at 1046 HIV+ patients in France who began treatment with anti-retroviral between 1997-1999, but also followed them for 10 years!! More studies should follow this lead because in the HIV+ community, it is no longer a question of worrying IF you make it “over-the-hill”, but WHAT you will do when you get there.

Ten-year diabetes incidence in 1046 HIV+ patients started on a combination antiretroviral treatment

AIDS volume 16(30) 28 January 2012 p303-314

Capeau, Jacqueline; Bouteloup, Vincent; Katlama, Christine;Bastard, Jean-Philippe; Guiyedi, Vincent; Salmon-Ceron, Dominique;Protopopescu, Camelia; Leport, Catherine; Raffi, Francois; Chêne, Geneviève

The late 90s saw an increase in diagnosis of type II diabetes in the HIV+ community. When tested, the patients lacked certain classic risk factors for diabetes such as, high blood pressure, family history, or hepatitis C infection; however, as testing continued several pattern emerged. Researchers found that the patients who received first generation protease inhibitors such as stavudine, indinavir, or didanosine had a higher chance (12.6% in women; 14.6% in men*) of developing diabetes. Interestingly enough, this trend was restricted to those with short term exposure to the drugs (likely because those who developed diabetes ceased treatment shortly after). Since then the drugs have been taken off the market in the West and are no longer used; however, in most cases, the diabetes persisted even after the treatment was halted.

More importantly, however, the study noted that age and fat content were found to be the best markers for diabetes, even better than the use of the first generation PIs. Due to the changes in fat distribution that occur with HIV, the HIV+ community must be vigilant of risk factors for diabetes and maintain a healthy lifestyle as it ages. HIV+ individuals should also have annual checkups to test fasting glycaemia and fat parameters, such as BMI and waist: hip ratio. Early detection of risk factors may allow patients to make simple lifestyle changes before having to revolutionize their lives with another complicated disease. As the saying goes, the grass is always greener on the other side, so keep your body in the best shape on the way there!

*[Keep in mind that this study was done in Europe. Had this study been done in North America, the results would likely be even more startling.]

INFO-TRAITEMENT CONFERENCES