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PubMed2002

Lipodystrophy in a cohort of human immunodeficiency virus-infected Asian patients: prevalence, associated factors, and psychological impact.

We investigated the prevalence of and factors associated with lipodystrophy in a cohort of human immunodeficiency virus (HIV)-infected patients in Singapore. A standardized questionnaire was administered to 410 consecutive patients (mainly Chinese men), and blood samples were obtained for metabolic measurements for fasting patients. Peripheral fat loss was reported by 46% of subjects, central fat gain was reported by 32%, and 8% of patients overall had a mixed clinical presentation. Levels of total cholesterol, triglycerides, glucose, and lactate were elevated in 19%, 38%, 12%, and 16% of patients, respectively. A mixture of drug-related and non-drug-related factors was associated with these changes. The body-shape changes affected the mood of 36% of patients and the work and/or social activity of 23% of patients, but only <1% of affected subjects reported a desire to stop receipt of antiretroviral therapy because of these changes. We conclude that the prevalence of and factors associated with body-shape changes and metabolic abnormalities in HIV-infected Asian patients are similar to those reported for Western cohorts, but the changes did not appear to have a major psychosocial impact on this patient population.

Adult↗
PubMed2003

Growth hormone receptor (GH)-expressing carcinoid tumors after recombinant human GH therapy for human immunodeficiency virus-related lipodystrophy.

We describe a patient who had growth hormone receptor-expressing carcinoid tumors develop in the distal colon and rectum after he received recombinant human growth hormone therapy for human immunodeficiency virus-related lipodystrophy. This case report serves as a cautionary note regarding the use of potentially oncogenic recombinant human growth hormone therapy to treat human immunodeficiency virus-positive persons.

Adult↗
PubMed2004

Factors associated with severe impact of lipodystrophy on the quality of life of patients infected with HIV-1.

A standardized questionnaire was used to assess the impact of lipodystrophy (LD) on quality of life (QoL). Eighty-four consecutive asymptomatic human immunodeficiency virus type 1 (HIV-1)-infected outpatients with clinical LD completed a modified version of the Dermatology Life Quality Index (DLQI) survey to measure the impact of body fat changes on their QoL. Body changes influenced dressing for 55 patients (65%), produced feelings of shame for 41 (49%), and disrupted sexual life for 23 (27%). There was a greater impact on the DLQI due to body changes among women, injection drug users, patients with abdominal or breast lipoaccumulation, and patients with a high number of non-LD side effects. Multivariate proportional odds model analysis showed that the severity of non-LD-associated side effects and the presence of breast lipoaccumulation were associated with impaired psychosocial functioning. Specific characteristics of patients, antiretroviral-based side effects, and breast lipoaccumulation exert a greater impact on QoL in HIV-1-infected patients with LD.

Adult↗
PubMed2004

Suction-assisted lipectomy for lipodystrophy.

Lipodystrophy resulting from HIV disease or the antiretroviral therapy used to treat it is a common complication. We report on the treatment of cervical lipohypertrophy ("buffalo hump") with suction-assisted lipectomy in six patients.

Adult↗
PubMed2006

Ethnic variations in the prevalence of metabolic bone disease among HIV-positive patients with lipodystrophy.

A high prevalence of metabolic bone disease and osteonecrosis among HIV+ patients on highly active antiretroviral therapy (HAART) has been reported in predominantly white cohorts. We examined bone health in an ethnically diverse cohort of 23 African-Americans and 21 non-African-Americans who were mean (standard deviation) age 45 (7) years old, 66% male, and on HAART for 34 (28) months. Non-African-Americans were more likely to have osteopenia or osteoporosis (59%) compared to African-Americans (26%) (p = 0.09). The prevalence of vitamin D insufficiency (< 34 ng/ml) and elevated i-PTH (>65 pg/ml) was 79% and 20%, respectively. Higher mean urinary N-telopeptide levels were found in non-African-Americans [58 (34) nmol BCE/mmol] compared to African-Americans [41 (18) nmol BCE/mmol] (p = 0.09). Magnetic resonance imaging identified one African-American subject (3%) with bilateral asymptomatic hip osteonecrosis. Our findings suggest that the burden of metabolic bone disease in HIV+ patients with HAART-associated lipodystrophy may be greater in whites than in African-Americans. Studies to examine ethnic variations in bone metabolism are necessary to devise optimal interventions.

Absorptiometry, Photon↗
PubMed2006

Psychometric properties of a lipodystrophy scale.

Prior HIV lipodystrophy (LD) scales have been unidimensional, often combining changes of fat loss with fat accumulation with retinoid changes. Our objective was to determine the psychometric properties of a LD scale used in an outpatient LD subspecialty clinic at a university hospital HIV clinic. A patient and clinician self-administered LD scale was used to evaluate 107 patients referred to the Owen LD Clinic from March of 1999 to August of 2002. Sixteen measures of the LD syndrome were assessed on a severity scale ranging from 0 (none) to 3 (severe). SPSS was used to perform a reliability and factor analysis. A total of 150 paired patient and clinician assessments were performed. Thirty-one patients had repeat assessments. Reliability analysis of the patient and clinician self-administered LD scale revealed an alpha of 0.76 and 0.73, respectively. Factor analysis of patient self-assessment of LD identified 3 factors, which clustered in the following order: fat loss, fat accumulation, and retinoid changes. Factor analysis of clinician self-assessment of LD identified 4 factors. The first factor clustered around items of fat loss. A second cluster consisted of retinoid changes. The final 2 factors clustered around items consistent with fat accumulation. The patient and clinician self-administered Owen Clinic LD scale was found to be highly reliable and useful in the assessment of LD. Our analysis confirms clinical intuition that the evaluation of LD is a multidimensional construct and that 3 subscales may be used to evaluate dimensions of fat loss, fat accumulation, and retinoid changes.

Adult↗
PubMed2005

Severely dysregulated disposal of postprandial triacylglycerols exacerbates hypertriacylglycerolemia in HIV lipodystrophy syndrome.

BACKGROUND: The pathogenesis of hypertriacylglycerolemia, a characteristic feature of HIV lipodystrophy syndrome (HLS), is incompletely understood. One mechanism is accelerated lipolysis in the fasted state, but the severity of the hypertriacylglycerolemia suggests that additional underlying abnormalities may exist in the disposal of dietary fat. OBJECTIVE: Our objective was to investigate abnormalities in dietary fat disposal in the pathogenesis of hypertriacylglycerolemia in HLS. DESIGN: We studied 6 nondiabetic men with HLS and 6 men without HIV matched for age and body mass index as control subjects for 8 h after consumption of an isocaloric meal containing 2 g labeled [(13)C(3)]tripalmitin. Chylomicron-triacylglycerol disposal was estimated from labeled [(13)C(1)]palmitate in the plasma chylomicron fraction, and [(13)C(1)]palmitate oxidation was estimated from the (13)CO(2) enrichment in the breath and CO(2) production, over 8 h after the meal. RESULTS: HLS patients had significantly elevated concentrations of fasting plasma triacylglycerols in both chylomicron (x + SE: 100.3 +/- 49.5 compared with 29.2 +/- 2.2 mg/dL; P < 0.01) and VLDL (82.4 +/- 39.0 compared with 10.8 +/- 2.8 mg/dL; P < 0.01) fractions. Chylomicron-triacylglycerol-derived [(13)C(1)]palmitate disposal was markedly lower in the HLS patients (3.09 +/- 0.41 compared with 6.42 +/- 0.18 mmol [(13)C(1)]palmitate/8 h; P < 0.001) in the 8-h postmeal period. Further, HLS patients had lowered storage of chylomicron-triacylglycerols (0.74 +/- 0.38 compared with 5.05 +/- 0.16 mmol; P < 0.0001) and elevated plasma [(13)C(1)]palmitate concentrations (2.01 +/- 0.27 compared with 1.18 +/- 0.16 mmol; P < 0.05) 8 h after the meal. CONCLUSIONS: Patients with HLS have key defects that markedly impair postprandial disposal and storage of chylomicron-triacylglycerols. These defects contribute significantly to hypertriacylglycerolemia in HLS.

Antiretroviral Therapy, Highly Active↗
PubMed2006

Physiologic growth hormone replacement improves fasting lipid kinetics in patients with HIV lipodystrophy syndrome.

BACKGROUND: HIV lipodystrophy syndrome (HLS) is characterized by accelerated lipolysis, inadequate fat oxidation, increased hepatic reesterification, and a high frequency of growth hormone deficiency (GHD). The effect of growth hormone (GH) replacement on these lipid kinetic abnormalities is unknown. OBJECTIVE: We aimed to measure the effects of physiologic GH replacement on lipid kinetics in men with HLS and GHD. DESIGN: Seven men with HLS and GHD were studied with the use of infusions of [13C1]palmitate, [2H5]glycerol, and [2H3]leucine to quantify total and net lipolysis, palmitate and free fatty acid (FFA) oxidation, and VLDL apolipoprotein B-100 synthesis before and after 6 mo of GH replacement (maximum: 5 microg x kg(-1) x d(-1)). RESULTS: GH replacement decreased the rates of total lipolysis [FFA(total) rate of appearance (x +/- SE): from 4.80 +/- 1.24 to 3.32 +/- 0.76 mmol FFA x kg fat(-1) x h(-1); P < 0.05] and net lipolysis (FFA(net) rate of appearance: from 1.87 +/- 0.34 to 1.20 +/- 0.25 mmol FFA x kg fat(-1) x h(-1); P < 0.05). Fat oxidation decreased (from 0.28 +/- 0.02 to 0.20 +/- 0.02 mmol FFA x kg lean body mass(-1) x h(-1); P < 0.002), as did the rate of appearance of FFAs available for intrahepatic reesterification (from 0.50 +/- 0.13 to 0.29 +/- 0.09 mmol FFA x kg fat(-1) x h(-1); P < 0.03). Fractional and absolute synthetic rates of VLDL apolipoprotein B-100 were unaltered. These kinetic changes were associated with a decrease in the waist-to-hip ratio but no significant change in fasting plasma lipid concentrations. Fasting plasma glucose concentrations increased after treatment (from 5.2 +/- 0.2 to 5.8 +/- 0.3 mmol/L; P < 0.01). CONCLUSIONS: Physiologic GH replacement has salutary effects on abnormal lipid kinetics in HLS. The effects are mediated by diminished lipolysis and hepatic reesterification rather than by increased fat oxidation.

Adipocytes↗
PubMed2002

A novel interaction between lamin A and SREBP1: implications for partial lipodystrophy and other laminopathies.

The gene encoding nuclear lamins A and C is mutated in at least three inherited disorders. Two of these, Emery-Dreifuss muscular dystrophy (EDMD-AD) and a form of dilated cardiomyopathy (CMD1A), involve muscle defects, and the other, familial partial lipodystrophy (FPLD), involves loss of subcutaneous adipose tissue. Mutations causing FPLD, in contrast to those causing muscle disorders, are tightly clustered within the C-terminal domain of lamin A/C. We investigated the expression and subcellular localization of FPLD lamin A mutants and found no abnormalities. We therefore set out to identify proteins interacting with the C-terminal domain of lamin A by screening a mouse 3T3-L1 adipocyte library in a yeast two-hybrid interaction screen. Using this approach, the adipocyte differentiation factor, sterol response element binding protein 1 (SREBP1) was identified as a novel lamin A interactor. In vitro glutathione S-transferase pull-down and in vivo co-immunoprecipitation studies confirmed an interaction between lamin A and both SREBP1a and 1c. A binding site for lamin A was identified in the N-terminal transcription factor domain of SREBP1, between residues 227 and 487. The binding of lamin A to SREBP1 was noticeably reduced by FPLD mutations. Interestingly, one EDMD-AD mutation also interfered with the interaction between lamin A and SREBP1. Whilst the physiological relevance of this interaction has yet to be elucidated, these data raise the intriguing possibility that fat loss seen in laminopathies may be caused, at least in part, by reduced binding of the adipocyte differentiation factor SREBP1 to lamin A.

3T3 Cells↗
PubMed2000

Nuclear lamin A/C R482Q mutation in canadian kindreds with Dunnigan-type familial partial lipodystrophy.

Patients with Dunnigan-type familial partial lipodystrophy (FPLD) are born with normal fat distribution, but after puberty experience regional and progressive adipocyte degeneration, often associated with profound insulin resistance and diabetes. Recently, the FPLD gene was mapped to chromosome 1q21-22, which harbours the LMNA gene encoding nuclear lamins A and C. Mutations in LMNA were shown to underlie autosomal dominant Emery-Dreifuss muscular dystrophy (EDMD-AD), which is characterized by regional and progressive skeletal muscle wasting and cardiac effects. We hypothesized that the analogy between the regional muscle wasting in EDMD-AD and the regional adipocyte degeneration in FPLD, in addition to its chromosomal localization, made LMNA a good candidate gene for FPLD. DNA sequencing of LMNA in five Canadian FPLD probands indicated that each had a novel missense mutation, R482Q, which co-segregated with the FPLD phenotype and was absent from 2000 normal alleles ( P = 1.1 x 10(-13)). This is the first report of a mutation underlying a degenerative disorder of adipose tissue and suggests that LMNA mutations could underlie other diseases characterized by tissue type- and anatomical site-specific cellular degeneration.

Adipocytes↗
PubMed2003

Increasing the amount of fat in a conjugated linoleic acid-supplemented diet reduces lipodystrophy in mice.

Conjugated linoleic acid (CLA) is a naturally occurring group of dienoic derivatives of linoleic acid found in beef and dairy products. However, when 1 g CLA/100 g diet was given to mice in a low fat diet (4 g fat/100 g diet), they showed a marked decrease in fat mass, but demonstrated symptoms of lipoatrophic diabetes, i.e., marked hepatomegaly and insulin resistance. In this study, to determine whether the decrease in adipose tissue was responsible for these adverse effects, mice were fed different doses of CLA and dietary fat. In Experiment 1, mice were fed different doses of CLA (0, 0.1 and 1 g CLA/100 g diet) in a fixed 4 g fat/100 g diet; in those fed 0.1 g CLA, subcutaneous white adipose tissue (WAT) weight was 48% lower than in mice fed 0 g CLA. The mice fed 0.1 g CLA did not exhibit hepatomegaly and insulin resistance. In Experiment 2, mice were fed for 5 mo different amounts of dietary fat (4, 13 and 34 g fat/100 g diet) in 0 or 1 g CLA/100 g diet; in mice fed 1 g CLA with 34 g fat, retroperitoneal and subcutaneous WAT weights were 76 and 79% lower, respectively, than those of mice fed 0 g CLA with 34 g fat. Mice fed 1 g CLA in the diet with 34 g fat had normal plasma insulin concentrations and a 45% greater liver weight. These data suggested that the percentage of CLA in dietary fat might be a determinant of CLA-mediated lipodystrophy.

Animals↗
PubMed1993

Primary soft tissue lymphoma associated with mesenteric lipodystrophy.

Skin involvement in non-Hodgkin lymphoma is usually specific and may precede systemic manifestations of the disease by months or even years. We report the case of a man with an inguinal plaque lesion of 1 year's evolution, diagnosed as polymorphous lymphoplasmocytoid lymphoma (immunocytoma). The evaluation of spread only revealed mesenteric lipodystrophy, whose association with lymphoid processes is more common than would be expected.

Aged↗
PubMed2004

Fenofibrate is effective in treating hypertriglyceridemia associated with HIV lipodystrophy.

OBJECTIVE: To determine the effectiveness of fenofibrate in treating hypertriglyceridemia associated with highly active antiretroviral therapy-associated HIV lipodystrophy syndrome (HLS). METHODS: The authors recruited from their HIV metabolic clinic 55 adult patients with anthropomorphic changes consistent with HLS together with hypertriglyceridemia. The patients had no prior history of taking lipid-lowering medications and were free of liver and renal disease. They were on various highly active antiretroviral therapy regimens, and these regimens were not altered during the course of the study. Fenofibrate was started at 54 mg a day and the dose increased every 2 weeks to a maximum of 162 mg/day. Fasting lipid concentrations were measured at baseline and 6 months after the intervention. RESULTS: At baseline, the fasting plasma concentrations of total cholesterol, triglyceride, and high-density lipoprotein (HDL) cholesterol were 259 +/- 11, 886 +/- 172, and 35.7 +/- 2.3 (mean +/- SEM) mg/dL, respectively. After 6 months of fenofibrate treatment, the fasting plasma concentrations were as follows: total cholesterol, 243 +/- 13; triglycerides, 552 +/- 104, and HDL cholesterol, 35.7 +/- 1.8 mg/dL. The decrease in fasting plasma triglyceride concentration was statistically significant (P < 0.05). Fenofibrate was well tolerated, and no subjects dropped out of the study. CONCLUSION: Fenofibrate is an effective, well-tolerated treatment for hypertriglyceridemia associated with HLS.

Adult↗
PubMed1997

Sclerosing mesenteritis, mesenteric panniculitis and mesenteric lipodystrophy: a single entity?

We reviewed 84 cases coded as mesenteric lipodystrophy (ML), mesenteric panniculitis (MP), or retractile mesenteritis and sclerosing mesenteritis (SM), grading fibrosis, inflammation, and fat necrosis, and evaluating clinical subgroups. There was no gender or racial predominance. Patient age range was 23-87 years (average 60). Patients most often presented with abdominal pain or a palpable mass. A history of trauma or surgery was present in four of 84 patients. The most common site of involvement was the small bowel mesentery as a single mass (58 of 84) with an average size of 10 cm, multiple masses (15 of 84), or diffuse mesenteric thickening (11 of 84). All patients had some degree of fibrosis, chronic inflammation, and fat necrosis. Although a few patients showed a sufficient prominence of fibrosis, inflammation, or fat necrosis to permit a separation into SM, MP, or ML, respectively, in most patients these three components were too mixed for a clear separation. The clinical, demographic, and gross features did not help in defining these three entities. Contributors diagnosed 12 as sarcoma. Of 39 patients followed beyond the postoperative period, none died of these lesions. We conclude that SM, MP, and ML appear to represent histologic variants of one clinical entity, and in most cases "sclerosing mesenteritis" is the most appropriate diagnostic term.

Adult↗
PubMed1979

Symmetrical lipodystrophy with hypothyroidism.

We present the history and treatment of a woman who had benign symmetrical lipomatosis and hypothyroidism. We suggest full thyroid investigation of future patients. We also suggest shortening the name of the disorder to symmetrical lipodystrophy, since the syndrome seems to be related to fat deposit growth rather than lipoma, and no malignant variant has been reported.

Female↗
PubMed1982

Facial reconstruction in partial lipodystrophy.

Lipodystrophy is a rare disease characterized by progressive disappearance of the subcutaneous fat of the upper part of the body. Accompanying abnormalities of carbohydrate and lipid metabolism, diabetes, nephritis, and low levels of complement are frequent. The most striking clinical features are the extremely hollow cheeks, making the normal facial skeleton rather prominent. Very little has been reported on facial reconstruction in such patients. A 16-year-old girl is presented who was successfully reconstructed after the atrophic process arrested spontaneously. Bilateral dermal fat grafts from the buttocks were used in a one-stage procedure. Nine months later, when no more resorption of fat occurred, some trimming of the grafts was necessary. A good result was achieved.

Adipose Tissue↗
PubMed2002

Methods of assessing body shape and composition in HIV-associated lipodystrophy.

Although HIV-associated lipodystrophy can be diagnosed just from clinical examination, criteria for diagnosis and judgement of severity are not clearly defined. Clinical assessment can be systematized with questionnaires for patients and physicians. Computed tomography, nuclear magnetic imaging and dual-energy X-ray absorptiometry are objective reference methods but are expensive for routine follow-up and diagnosis. Therefore, anthropometry and other non-invasive bedside methods deserve further validation studies.

Absorptiometry, Photon↗
PubMed2000

A syndrome of lipoatrophy, lactic acidaemia and liver dysfunction associated with HIV nucleoside analogue therapy: contribution to protease inhibitor-related lipodystrophy syndrome.

BACKGROUND: Lipodystrophy (LD; peripheral lipoatrophy, central adiposity) hyperlipidaemia and insulin resistance often complicate protease inhibitor-containing antiretroviral therapy. Lipoatrophy and abdominal distension were observed in protease inhibitor-naive nucleoside analogue reverse transcriptase inhibitor (NRTI) recipients with lactic acidaemia and hepatic impairment, which are known NRTI-induced mitochondrial toxicities. DESIGN AND SETTING: Case-control study in a university-based outpatient clinic. PATIENTS AND METHODS: The patients studied included 14 NRTI recipients with lipoatrophy, 32 antiretroviral-naive patients without LD, 28 NRTI recipients without LD, 44 combined NRTI-protease inhibitor recipients without LD, and 102 NRTI-protease inhibitor recipients with LD. Data was obtained on body composition (questionnaire, physical examination, dual-energy x-ray absorptiometry and abdominal computerized tomography), with biochemical, lipid and glycaemic parameters. RESULTS: The NRTI-LD syndrome was characterized by recent onset fatigue and nausea, peripheral lipoatrophy (6 kg loss over 4 months), abdominal distension (ascites +/- hepatomegaly) and elevated lactate (4.6, 1.1, 1.2, 1.4 and 1.7 mmol/l, respectively; P< 0.0001) and liver enzymes. Cases without hepatic involvement also had lower body fat and greater lactate than unaffected controls. Metabolic disturbances and weight improved after cessation. The NRTI-LD syndrome differed from protease inhibitor-related LD syndrome by the presence of recent onset symptoms and weight loss, higher lactate and alanine aminotransferase, and lower albumin, cholesterol, triglycerides, glucose and insulin. In treated controls, current stavudine therapy, protease inhibitor duration, and lactic acidaemia were independently associated with both lipoatrophy and abdominal obesity; total NRTI duration was also associated with lipoatrophy, and lamivudine and protease inhibitor duration with buffalo hump. CONCLUSIONS: A syndrome of lipoatrophy, constitutional illness, lactic acidaemia and hepatic dysfunction can complicate NRTI therapy. Both protease inhibitor and NRTI therapies, particularly if associated with lactic acidaemia, contribute to LD syndrome, but have some distinguishable clinical and metabolic effects.

Acidosis, Lactic↗