Modérateurs : Eric, jerome, Travis, Charlotte, marie.m, Magda Dorner, Bull
Pas exactement : c'est juste un « dommage collatéral » de la thérapie antivirale hautement active (HAART).Katioucha a écrit :Cette dénomination date des années 80. Le VIH a toute sorte d'effets, dont le plus remarquable est la destruction du système immunitaire, certes, mais pas que. Il entrainerait aussi des lipodystrophies, suppose-t-on.Eons a écrit : (SIDA = Syndrome Immuno-Déficitaire Acquis)
En fait si.Eons a écrit : je rappelle qu'en lui-même le sida ne tue pas : il se contente d'empêcher l'organisme de lutter efficacement contre d'autres envahisseurs. (SIDA = Syndrome Immuno-Déficitaire Acquis)
J Antimicrob Chemother. 2008 Jun 18.
HIV-associated lipodystrophy: a review of underlying mechanisms and therapeutic options.
Mallewa JE, Wilkins E, Vilar J, Mallewa M, Doran D, Back D, Pirmohamed M.
Department of Infectious Diseases, North Manchester General Hospital, Delaunays Road, Manchester M8 5RB, UK.
Lipodystrophy (LD) is a common adverse effect of HIV treatment with highly active antiretroviral therapy, which comprises morphological and metabolic changes. The underlying mechanisms for LD are thought to be due to mitochondrial toxicity and insulin resistance, which results from derangements in levels of adipose tissue-derived proteins (adipocytokines) that are actively involved in energy homeostasis. Several management strategies for combating this syndrome are available, but they all have limitations. They include: switching from thymidine analogues to tenofovir or abacavir in lipoatrophy, or switching from protease inhibitors associated with hyperlipidaemia to a protease-sparing option; injection into the face with either biodegradable fillers such as poly-l-lactic acid and hyaluronic acid (a temporary measure requiring re-treatment) or permanent fillers such as bio-alcamid (with the risk of foreign body reaction or granuloma formation); and structured treatment interruption with the risk of loss of virological control and disease progression. There is therefore a need to explore alternative therapeutic options. Some new approaches including adipocytokines, uridine supplementation, glitazones, growth hormone (or growth hormone-releasing hormone analogues), metformin and statins (used alone or in combination) merit further investigation.
The success of controlling HIV infection with antiretroviral drugs (ARVs) and the resultant reduction in morbidity and mortality has been marred somewhat by the development of significant adverse effects in some patients, which include metabolic and morphological changes. Lipodystrophy (LD) is a term used to embrace these changes that comprise peripheral lipoatrophy, localized fat accumulation (visceral, back of neck and lipomata), hyperlipidaemia, insulin resistance and hyperglycaemia.1 The prevalence rate of LD in patients on highly active antiretroviral therapy (HAART) is reported to be up to 40%.1,2 The frequency of LD, not unexpectedly varies with the drugs used. Nucleoside reverse transcriptase inhibitors (NRTIs), particularly thymidine analogues (zidovudine and stavudine), have been associated with morphological changes, particularly extremity fat loss,3 while protease inhibitors (PIs) have been associated with biochemical derangements of glucose and lipids as well as with localized accumulation of fat.4 NRTIs such as stavudine have also been shown to be associated with dyslipidaemia.5 Since the drugs are often used together as part of HAART, clinical data suggest that they act synergistically in causing LD. The body changes of LD are distressing and can be stigmatizing for sufferers. The metabolic effects have been associated with an increased risk of cardiovascular disease.6–9 Mitochondrial toxicity, insulin resistance, adipose gene expression derangements, genetic polymorphisms and cellular dysfunction are thought to be important pathophysiological mechanisms underlying the development of LD.8,10–16
J'ai regardé sur le site que tu as mis en lien.Katioucha a écrit :"Il y a actuellement plusieurs hypothèses physiopathologiques :
- effet secondaire des traitements
- production anormale de cytokines par les lymphocytes et monocytes infectés par le VIH etc" sur http://www.chu-limoges.fr/nutrition/cou ... a/lipo.htm, entre autres.
Moi, ce que j'en sais, c'est ce que disent les gens d'Act-Up, qui te diront qu'on ne sait pas parce qu'il faudrait arrêter les thérapies pour savoir mais dans ces cas là, on meurt, alors...
est absurde scientifiquement parlant, faisant la confusion en la prise de poids et les lipodystrophies. Ce qui n'est vraiment pas la même chose.- reprise alimentaire exagérée après mise en route de la trithérapie
Clinical features associated with HIV lipodystrophy syndrome
Fat atrophy (lipoatrophy)
• Face: sunken cheeks, hollow temples, sunken eyes, prominent zygomatic arch
• Extremities: prominent veins, skinny or muscular appearance
• Buttocks: loss of contour, loose skin folds
Fat accumulation (lipohypertrophy)
• Abdomen: increased abdominal girth with visceral fat accumulation
• Dorsocervical or supraclavicular fat pad
Related findings
• Hypertriglyceridaemia, usually with depressed high-density lipoprotein cholesterol
• Hypercholesterolaemia
• Insulin resistance, dysglycaemia progressing to glucose intolerance
• Gynaecomastia (breast enlargement)
HIV-associated dyslipidaemia was recognised for years before the widespread use of protease inhibitor-based HAART[/b]. [6] , [7] Viraemia-associated dyslipidaemia is characterised mainly by decreased plasma concentrations of total, LDL, and HDL cholesterol, [3] , [6] , [8] , [9] and later elevated plasma triglyceride.[3] Low HDL cholesterol has been correlated with immune activation early in the course of HIV infection,[10] the repercussions of which may extend beyond atherosclerosis because of HDL's numerous functions, including antioxidant and anti-inflammatory activities. [11] , [12] , [13] , [14]
Triglyceride-rich lipoproteins and HDL cholesterol are synthesised and secreted into the plasma from the liver and intestine. HIV-1 contributes to low plasma HDL cholesterol by impairing ATP-binding cassette transporter A1-dependent cholesterol efflux from macrophages.[15] Furthermore, inflammation in general stimulates endothelial lipase and phospholipase A2, which can reduce plasma HDL.[14] Additionally, HDL is triglyceride-enriched in hypertriglyceridaemia, becoming a more avid substrate for hepatic lipase-mediated clearance.[14]
HIV-associated dyslipidaemia is very similar to that observed in other chronic infections. Elevated interferon ɑ in advanced HIV disease is correlated with elevated plasma triglyceride,[16] resulting from impaired clearance of triglyceride-rich lipoproteins. [17] , [18] Similarly, tumour necrosis factor (TNF) ɑ is elevated in drug-naive HIV patients[19] and increases further during opportunistic infections. TNFɑ interferes with free fatty acid metabolism and lipid oxidation, and attenuates insulin-mediated suppression of lipolysis.[19] Finally, the nutritional state of HIV patients, including weight loss and protein depletion, [3] , [20] , [21] might contribute to reduced plasma total, HDL, and LDL cholesterol.
oué hein ?Katioucha a écrit :C'est pour ça que quand les barbaquers disent des choses comme "le Sida, aujourd'hui, c'est cool, et la capote, c'est pour les bourges", ça me met des suées.
dracosolis a écrit :surtout quand t'as suivi une bonne partie de ta génération avec une couronne dans les bras, environ une fois par an depuis tes 20 ans...
T'étais aussi au couronnement d'Albert de Monac' ? 
t'es con, rené ! 
