HIV-Associated Lipodystrophy Syndrome
Lipodystrophy
Lipodystrophy, Congenital Generalized
Lipodystrophy, Familial Partial
Antiretroviral Therapy, Highly Active
HIV Infections
Diabetes Mellitus, Lipoatrophic
Intramyocellular lipid accumulation and reduced whole body lipid oxidation in HIV lipodystrophy. (1/180)
Antiretroviral therapy in human immunodeficiency virus (HIV)-positive patients can induce a lipodystrophy syndrome of peripheral fat wasting and central adiposity, dyslipidemia, and insulin resistance. To test whether in this syndrome insulin resistance is associated with abnormal muscle handling of fatty acids, 12 HIV-1 patients (8 females/4 males, age = 26 +/- 2 yr, HIV duration = 8 +/- 1 yr, body mass index = 22.0 +/- 1.0 kg/m(2), on protease inhibitors and nucleoside analog RT inhibitors) and 12 healthy subjects were studied. HIV-1 patients had a total body fat content (assessed by dual-energy X-ray absorptiometry) similar to that of controls (22 +/- 1 vs. 23 +/- 2%; P = 0.56), with a topographic fat redistribution characterized by reduced fat content in the legs (18 +/- 2 vs. 32 +/- 3%; P < 0.01) and increased fat content in the trunk (25 +/- 2 vs. 19 +/- 2%; P = 0.03). In HIV-positive patients, insulin sensitivity (assessed by QUICKI) was markedly impaired (0.341 +/- 0.011 vs. 0.376 +/- 0.007; P = 0.012). HIV-positive patients also had increased total plasma cholesterol (216 +/- 20 vs. 174 +/- 9 mg/dl; P = 0.05) and triglyceride (298 +/- 96 vs. 87 +/- 11 mg/dl; P = 0.03) concentrations. Muscular triglyceride content assessed by means of (1)H NMR spectroscopy was higher in HIV patients in soleus [92 +/- 12 vs. 42 +/- 5 arbitrary units (AU); P < 0.01] and tibialis anterior (26 +/- 6 vs. 11 +/- 3 AU; P = 0.04) muscles; in a stepwise regression analysis, it was strongly associated with QUICKI (R(2) = 0.27; P < 0.0093). Even if the basal metabolic rate (assessed by indirect calorimetry) was comparable to that of normal subjects, postabsorptive lipid oxidation was significantly impaired (0.30 +/- 0.07 vs. 0.88 +/- 0.09 mg x kg(-1) x min(-1); P < 0.01). In conclusion, lipodystrophy in HIV-1 patients in antiretroviral treatment is associated with intramuscular fat accumulation, which may mediate the development of the insulin resistance syndrome. (+info)Incidence of morphological and lipid abnormalities: gender and treatment differentials after initiation of first antiretroviral therapy. (2/180)
OBJECTIVE: To provide population-based incidence estimates for constituent symptoms of human immundeficiency virus (HIV)-related lipodystrophy syndrome and to identify possible independent predictors of accrued cases. DESIGN: Prospective population-based cohort. Methods Study subjects were antiretroviral-naive individuals who initiated treatment between October 1998 and May 2001 and provided completed self-reported data regarding the occurrence of lipoatrophy, lipohypertrophy and increased triglyceride and cholesterol levels. Possible predictors of incident lipoatrophy, lipohypertrophy, dyslipidaemia and mixed lipodystrophy (symptoms of both lipoatrophy and lipohypertrophy) were identified using logistic regression modelling. A sub-analysis restricted to subjects retaining original treatment at study completion was conducted using similar methods. RESULTS: Among the 366 study subjects, cumulative incidence was 29% for lipoatrophy, 23% for lipohypertrophy, 9% for dyslipidaemia, and 13% for mixed lipodystrophy after a median duration of 12 months of antiretroviral therapy. In an intentto-treat analysis incident lipoatrophy and lipohypertrophy were independently associated with initiation of protease inhibitor (PI)-containing regimens, (adjusted odds ratio [AOR] = 1.94; 95% CI: 1.25-3.03 and AOR = 1.76; 95% CI: 1.09-2.85, respectively) and female gender (AOR = 2.06; 95% CI: 1.03-4.12 and AOR = 2.36; 95% CI: 1.17-4.74, respectively). Both mixed lipodystrophy and reported dyslipidaemia were associated only with PI inclusion in the initial regimen (AOR = 2.27; 95% CI: 1.14-4.53 and AOR = 2.14; 95% CI: 1.26-3.65, respectively). Similar results were obtained in analysis of individuals retained in initial treatment groups throughout follow-up. CONCLUSION: Incident morphological and lipid abnormalities are common among individuals initiating first-time antiretroviral therapy. Use of PI was consistently associated with all lipodystrophy-related abnormalities after adjustment for a broad range of patient personal, clinical and treatment characteristics. (+info)Preferential loss of omental-mesenteric fat during growth hormone therapy of HIV-associated lipodystrophy. (3/180)
Lipodystrophy with increased intra-abdominal fat in human immunodeficiency virus (HIV) infection is common in the era of highly active antiretroviral therapy. It contributes to the metabolic derangements, as it does in non-HIV-related conditions. Growth hormone administration reduces intra-abdominal fat content. This study compared the relative changes in omental-mesenteric (OMAT) and retroperitoneal adipose tissues (RPAT) during therapy with recombinant human growth hormone (rhGH) in HIV-associated lipodystrophy. Of 30 subjects who began rhGH therapy (6 mg/day), 25 completed 12 wk and 19 completed 24 wk. Fourteen subjects were followed for an additional 12 wk. Volumes of OMAT and RPAT were calculated from total body MRI scans and compared by paired t-tests. Both OMAT and RPAT significantly decreased after 12 and 24 wk of rhGH treatment (P < 0.001), but the reduction was more pronounced in OMAT than in RPAT (P < 0.001). Both OMAT and RPAT increased significantly (P < 0.001) after therapy was discontinued, but OMAT increased significantly more than did RPAT (122 vs. 37%, P < 0.001). There is preferential loss and regain of OMAT, compared with RPAT, in subjects with HIV-associated lipodystrophy undergoing growth hormone treatment. (+info)A qualitative study of the psychosocial implications of lipodystrophy syndrome on HIV positive individuals. (4/180)
OBJECTIVES: To investigate the psychosocial impact of lipodystrophy on the lifestyles of HIV positive patients on highly active antiretroviral therapy (HAART). METHODS: In-depth interviews were conducted with 14 HIV positive patients on HAART at an outpatient sexually transmitted infections (STI) and HIV clinic in central London. Qualitative data from interview transcripts were analysed using grounded theory to elicit key categories and subcategories. RESULTS: Three main themes relating to lipodystrophy emerged: effect on the individual; impact on the social world of the individual; responses of the individual. Lipodystrophy had physical and psychological effects, ranging from bodily discomfort to low self esteem and depression. Owing to its physical manifestations it was viewed as a visible marker of HIV disease. At the level of social functioning, lipodystrophy led to problems with personal and family relationships, although having a partner was protective. Individuals reported narrowing their social world, in some cases to degrees of social isolation. Individual responses included changes in diet, increased exercise regimes, steroid use and plastic surgery (mainly collagen injections to the face). For those who had experienced serious illness related to HIV, there was a more sanguine acceptance of lipodystrophy as an unfortunate consequence of longevity and drug therapy CONCLUSIONS: Health professionals need to address the psychosocial implications of lipodystrophy, including the ways in which it may affect different groups and their adherence to therapy. Formative evaluations are needed to assess the potential for targeted interventions. (+info)Alterations in lipid kinetics in men with HIV-dyslipidemia. (5/180)
Hypertriglyceridemia is common in individuals with human immunodeficiency (HIV) infection, but the mechanisms responsible for increased plasma triglyceride (TG) concentrations are not clear. We evaluated fatty acid and VLDL-TG kinetics during basal conditions and during a glucose infusion that resulted in typical postprandial plasma glucose and insulin concentrations in six men with HIV-dyslipidemia [body mass index (BMI): 28 +/- 2 kg/m2] and six healthy men (BMI: 26 +/- 2 kg/m2). VLDL-TG secretion and palmitate rate of appearance (Ra) in plasma were measured by using stable-isotope-labeled tracer techniques. Basal palmitate Ra and VLDL-TG secretion rates were greater (P < 0.01 for both) in men with HIV-dyslipidemia (1.04 +/- 0.07 micromol palmitate x kg-1 x min-1 and 5.7 +/- 0.6 micromol VLDL-TG x l plasma-1 x min-1) than in healthy men (0.67 +/- 0.08 micromol palmitate. kg-1 x min-1 and 3.0 +/- 0.5 micromol VLDL-TG x l plasma-1 x min-1). Basal VLDL-TG plasma clearance was lower in men with HIV-dyslipidemia (13 +/- 1 ml/min) than in healthy men (19 +/- 2 ml/min; P < 0.05). Glucose infusion decreased palmitate Ra (by approximately 50%) and the VLDL-TG secretion rate (by approximately 30%) in both groups, but the VLDL-TG secretion rate remained higher (P < 0.05) in subjects with HIV-dyslipidemia. These findings demonstrate that increased secretion of VLDL-TG and decreased plasma VLDL-TG clearance, during both fasting and fed conditions, contribute to hypertriglyceridemia in men with HIV-dyslipidemia. Although it is likely that increased free fatty acid release from adipose tissue contributes to the increase in basal VLDL-TG concentration, other factors must be involved, because insulin-induced suppression of lipolysis and systemic fatty acid availability did not normalize the VLDL-TG secretion rate. (+info)Psoas muscle attenuation measurement with computed tomography indicates intramuscular fat accumulation in patients with the HIV-lipodystrophy syndrome. (6/180)
The human immunodeficiency virus (HIV)-lipodystrophy syndrome is characterized by abnormalities of lipid metabolism, glucose homeostasis, and fat distribution. Overaccumulation of intramuscular lipid may contribute to insulin resistance in this population. We examined 63 men: HIV positive with lipodystrophy (n = 22), HIV positive without lipodystrophy (n = 20), and age- and body mass index-matched HIV-negative controls (n = 21). Single-slice computed tomography was used to determine psoas muscle attenuation and visceral fat area. Plasma free fatty acids (FFA), lipid profile, and markers of glucose homeostasis were measured. Muscle attenuation was significantly decreased in subjects with lipodystrophy [median (interquartile range), 55.0 (51.0-58.3)] compared with subjects without lipodystrophy [57.0 (55.0-59.0); P = 0.05] and HIV-negative controls [59.5 (57.3-64.8); P < 0.01]. Among HIV-infected subjects, muscle attenuation correlated significantly with FFA (r = -0.38; P = 0.02), visceral fat (r = -0.49; P = 0.002), glucose (r = -0.38; P = 0.02) and insulin (r = -0.60; P = 0.0001) response to a 75-g oral glucose tolerance test. In forward stepwise regression analysis with psoas attenuation as the dependent variable, visceral fat (P = 0.02) and FFA (P < 0.05), but neither body mass index, subcutaneous fat, nor antiretroviral use, were strong independent predictors of muscle attenuation (r2 = 0.39 for model). Muscle attenuation (P = 0.02) and visceral fat (P = 0.02), but not BMI, subcutaneous fat, FFA, or antiretroviral use, were strong independent predictors of insulin response (area under the curve) to glucose challenge (r2 = 0.47 for model). These data demonstrate that decreased psoas muscle attenuation due to intramuscular fat accumulation may contribute significantly to hyperinsulinemia and insulin resistance in HIV-lipodystrophy patients. Further studies are needed to assess the mechanisms and consequences of intramuscular lipid accumulation in HIV-infected patients. (+info)Exercise and vitamin E intake are independently associated with metabolic abnormalities in human immunodeficiency virus-positive subjects: a cross-sectional study. (7/180)
We investigated the relationship among habitual exercise, diet, and the presence of metabolic abnormalities (body fat redistribution, dyslipidemia, and insulin resistance) in a cross-sectional study of 120 human immunodeficiency virus (HIV)-infected subjects with use of bivariate and multivariate regression-analysis models. Total and aerobic exercise were significantly and negatively associated with fasting plasma triglyceride levels in the entire sample and in the fat redistribution group. Inverse associations between total or aerobic exercise and insulin resistance were suggestive but did not achieve statistical significance. Diastolic blood pressure was significantly and inversely associated with supplemental or total but not habitual dietary intake of vitamin E. In conclusion, exercise and vitamin E intake were independently and negatively associated with several phenotypic manifestations of HIV-associated metabolic syndrome, whereas other macro- or micronutrients did not have comparable significance. (+info)The cellular structure and lipid/protein composition of adipose tissue surrounding chronically stimulated lymph nodes in rats. (8/180)
To test the hypothesis that chronic immune stimulation of a peripheral lymph node induces the formation of additional mature adipocytes in adjacent adipose tissue, one popliteal lymph node of large male rats was stimulated by local injection of 10 microg or 20 microg lipopolysaccharide three times a week for 6 weeks. Adipocyte volumes in sites defined by their anatomical relations to the stimulated and homologous unstimulated popliteal lymph nodes were measured, plus adipocyte complement of the popliteal depot, and the lipid and protein content of adipocytes and adipose stroma. The higher dose of lipopolysaccharide doubled the mass of the locally stimulated lymph node and the surrounding adipose tissue enlarged by the appearance of additional mature adipocytes. Similar but smaller changes were observed in the popliteal adipose depot of the unstimulated leg and in a nodeless depot. The lipid content of the adipocytes decreased and that of the stroma increased dose-dependently in all samples measured but the changes were consistently greater in the depot surrounding the stimulated lymph node. The protein content of both adipocytes and stroma increased in samples surrounding the stimulated node. We conclude that chronic immune stimulation of lymphoid tissues induces the formation of more adipocytes in the adjacent adipose tissue. These findings suggest a mechanism for the selective hypertrophy of lymphoid-containing adipose depots in the HIV-associated adipose redistribution syndrome. (+info)HIV-Associated Lipodystrophy Syndrome is a term used to describe a range of body shape changes and metabolic abnormalities that can occur in some individuals receiving long-term combination antiretroviral therapy (cART) for HIV infection. The syndrome is characterized by the abnormal distribution of fat, including:
1. Lipoatrophy: Loss of subcutaneous fat from the face, limbs, and buttocks, leading to a gaunt appearance.
2. Lipohypertrophy: Accumulation of fat in the abdomen, breasts, and dorsocervical region (buffalo hump), resulting in an altered body shape.
3. Metabolic abnormalities: Insulin resistance, hyperlipidemia, and lactic acidosis, which can increase the risk of developing cardiovascular disease and diabetes mellitus.
The exact pathogenesis of HIV-Associated Lipodystrophy Syndrome is not fully understood, but it is believed to be related to a combination of factors, including the direct effects of HIV infection on adipose tissue, mitochondrial toxicity caused by certain antiretroviral medications, and chronic inflammation. The syndrome can have significant psychological and social consequences for affected individuals, and management typically involves a multidisciplinary approach that includes switching to alternative antiretroviral regimens, addressing metabolic abnormalities, and providing cosmetic interventions as needed.
Lipodystrophy is a medical condition characterized by abnormal distribution or absence of fat (adipose tissue) in the body. It can lead to metabolic complications such as insulin resistance, diabetes mellitus, high levels of fats in the blood (dyslipidemia), and liver disease. There are different types of lipodystrophy, including congenital generalized lipodystrophy, acquired generalized lipodystrophy, and partial lipodystrophy, which can affect different parts of the body and have varying symptoms and causes.
Congenital Generalized Lipodystrophy (CGL) is a rare genetic disorder characterized by the near or complete absence of body fat at birth or in early childhood. It is also known as Berardinelli-Seip congenital lipodystrophy. The condition is caused by mutations in genes responsible for the development and function of adipose tissue (fat).
Individuals with CGL typically have a lack of subcutaneous fat, which gives them a muscular appearance, but they may have excess fat accumulation in other areas such as the neck, face, and liver. This can lead to various metabolic complications, including insulin resistance, diabetes mellitus, hypertriglyceridemia (high levels of triglycerides in the blood), and hepatic steatosis (fatty liver disease).
CGL is a genetic disorder that is inherited in an autosomal recessive pattern. This means that an individual must inherit two copies of the mutated gene, one from each parent, to develop the condition. The diagnosis of CGL is typically based on clinical features and confirmed by genetic testing. Treatment for CGL focuses on managing the metabolic complications associated with the disorder.
Familial Partial Lipodystrophy (FPL) is a rare genetic disorder characterized by the selective loss of fat tissue in various parts of the body. It is caused by mutations in specific genes involved in the regulation of fat metabolism. There are several types of FPL, but the most common one is called Dunnigan-type or FPLD2, which is caused by mutations in the LMNA gene.
In FPL, there is a lack of subcutaneous fat (the fat layer beneath the skin) in certain areas of the body, such as the face, arms, legs, and buttocks, while other areas may have excess fat accumulation, such as the neck, shoulders, and abdomen. This abnormal distribution of fat can lead to a variety of metabolic complications, including insulin resistance, diabetes mellitus, high levels of triglycerides in the blood (hypertriglyceridemia), and an increased risk of cardiovascular disease.
FPL is usually inherited as an autosomal dominant trait, which means that a person has a 50% chance of inheriting the mutated gene from an affected parent. However, some cases may occur spontaneously due to new mutations in the gene. The diagnosis of FPL is typically based on clinical examination, family history, and genetic testing. Treatment usually involves lifestyle modifications, such as diet and exercise, and medications to manage metabolic complications.
Antiretroviral Therapy, Highly Active (HAART) is a medical treatment regimen used to manage HIV infection. It involves the combination of three or more antiretroviral drugs from at least two different classes, aiming to maximally suppress viral replication and prevent the development of drug resistance. The goal of HAART is to reduce the amount of HIV in the body to undetectable levels, preserve immune function, and improve quality of life for people living with HIV. Commonly used antiretroviral classes include nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), integrase strand transfer inhibitors (INSTIs), and fusion inhibitors.
HIV (Human Immunodeficiency Virus) infection is a viral illness that progressively attacks and weakens the immune system, making individuals more susceptible to other infections and diseases. The virus primarily infects CD4+ T cells, a type of white blood cell essential for fighting off infections. Over time, as the number of these immune cells declines, the body becomes increasingly vulnerable to opportunistic infections and cancers.
HIV infection has three stages:
1. Acute HIV infection: This is the initial stage that occurs within 2-4 weeks after exposure to the virus. During this period, individuals may experience flu-like symptoms such as fever, fatigue, rash, swollen glands, and muscle aches. The virus replicates rapidly, and the viral load in the body is very high.
2. Chronic HIV infection (Clinical latency): This stage follows the acute infection and can last several years if left untreated. Although individuals may not show any symptoms during this phase, the virus continues to replicate at low levels, and the immune system gradually weakens. The viral load remains relatively stable, but the number of CD4+ T cells declines over time.
3. AIDS (Acquired Immunodeficiency Syndrome): This is the most advanced stage of HIV infection, characterized by a severely damaged immune system and numerous opportunistic infections or cancers. At this stage, the CD4+ T cell count drops below 200 cells/mm3 of blood.
It's important to note that with proper antiretroviral therapy (ART), individuals with HIV infection can effectively manage the virus, maintain a healthy immune system, and significantly reduce the risk of transmission to others. Early diagnosis and treatment are crucial for improving long-term health outcomes and reducing the spread of HIV.
A syndrome, in medical terms, is a set of symptoms that collectively indicate or characterize a disease, disorder, or underlying pathological process. It's essentially a collection of signs and/or symptoms that frequently occur together and can suggest a particular cause or condition, even though the exact physiological mechanisms might not be fully understood.
For example, Down syndrome is characterized by specific physical features, cognitive delays, and other developmental issues resulting from an extra copy of chromosome 21. Similarly, metabolic syndromes like diabetes mellitus type 2 involve a group of risk factors such as obesity, high blood pressure, high blood sugar, and abnormal cholesterol or triglyceride levels that collectively increase the risk of heart disease, stroke, and diabetes.
It's important to note that a syndrome is not a specific diagnosis; rather, it's a pattern of symptoms that can help guide further diagnostic evaluation and management.
Diabetes Mellitus, Lipoatrophic is not a recognized medical term or official classification for diabetes. However, Lipodystrophy is a condition that can occur in some people with diabetes, particularly those being treated with insulin. Lipodystrophy refers to the loss of fat tissue, which can cause changes in the way the body responds to insulin and lead to difficulties controlling blood sugar levels. There are different types of lipodystrophy, including localized lipoatrophy (small areas of fat loss) and generalized lipodystrophy (widespread fat loss).
In people with Diabetes Mellitus, Lipodystrophy can lead to an increased need for insulin, as well as other metabolic complications. It is important for individuals with diabetes who notice changes in their body's response to insulin or unusual fat distribution to consult with their healthcare provider for further evaluation and management.
Lamin Type A, also known as LMNA, is a gene that provides instructions for making proteins called lamins. These proteins are part of the nuclear lamina, a network of fibers that lies just inside the nuclear envelope, which is the membrane that surrounds the cell's nucleus. The nuclear lamina helps maintain the shape and stability of the nucleus and plays a role in regulating gene expression and DNA replication.
Mutations in the LMNA gene can lead to various diseases collectively known as laminopathies, which affect different tissues and organs in the body. These conditions include Emery-Dreifuss muscular dystrophy, limb-girdle muscular dystrophy, dilated cardiomyopathy with conduction system disease, and a type of premature aging disorder called Hutchinson-Gilford progeria syndrome. The specific symptoms and severity of these disorders depend on the particular LMNA mutation and the tissues affected.
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