Transient hypertriglyceridemia: a common finding during Epstein-Barr virus-induced infectious mononucleosis.

BACKGROUND: Hypertriglyceridemia can occur in lymphoproliferative disorders. Infectious mononucleosis is a self-limiting, benign lymphoproliferative disorder. This study aimed to investigate the serum triglyceride concentrations and their change over time in patients with infectious mononucleosis. METHODS: We evaluated an adult patient with severe hypertriglyceridemia (>1000 mg/dL) during infectious mononucleosis and reviewed the records of 360 patients admitted to our hospital because of infectious mononucleosis (median age, 19 years; range, 15-87 years; 51.4% male). We compared the serum triglyceride concentrations with those of a control sample from the general population (n=75). A second triglyceride measurement, obtained during convalescence (median of 30 days after the initial determination), was available for 160 patients. RESULTS: The triglyceride concentrations in the acute phase (median: 156 mg/dL) were significantly higher than those of the controls (median, 76 mg/dL; P<0.001). A total of 194 (53.9%) patients presented with hypertriglyceridemia (>150 mg/dL), which was more common in the patients older than 30 years than in the younger patients (78.6% vs. 50.6%; P<0.001). A significant correlation (P<0.005) was observed between the triglyceride levels and white blood cell counts, total cholesterol levels, and liver damage markers. The triglyceride concentrations decreased during convalescence (P<0.001) and were lower than the initial measurement in 83.7% of the cases. Conversely, the total cholesterol concentrations during the acute phase were lower than those of the controls and increased during convalescence (P<0.001). CONCLUSIONS: Patients with severe infectious mononucleosis frequently show mild, transient hypertriglyceridemia. Further studies are needed to elucidate the mechanisms underlying this finding.

Higher Risk of Abdominal Obesity, Elevated Low-Density Lipoprotein Cholesterol, and Hypertriglyceridemia, but not of Hypertension, in People Living With Human Immunodeficiency Virus (HIV): Results From the Copenhagen Comorbidity in HIV Infection Study.

Background: People living with human immunodeficiency virus (PLWH) are characterized by excess risk of cardiovascular diseases (CVD) and CVD risk factors compared to uninfected individuals. We investigated the association between HIV infection and abdominal obesity, elevated low-density lipoprotein cholesterol (LDL-C), hypertriglyceridemia, and hypertension in a large cohort of predominantly well-treated PLWH and matched controls. Methods: 1099 PLWH from the Copenhagen Co-morbidity in HIV Infection Study and 12 161 age- and sex-matched uninfected controls from the Copenhagen General Population Study were included and underwent blood pressure, waist, hip, weight, and height measurements and nonfasting blood samples. We assessed whether HIV was independently associated with abdominal obesity, elevated LDL-C, hypertriglyceridemia, and hypertension using logistic regression models adjusted for known risk factors. Results: HIV infection was associated with higher risk of abdominal obesity (adjusted odds ratio [aOR], 1.92 [1.60-2.30]) for a given body mass index, elevated LDL-C (aOR, 1.32 [1.09-1.59]), hypertriglyceridemia (aOR, 1.76 [1.49-2.08]), and lower risk of hypertension (aOR, 0.63 [0.54-0.74]). The excess odds of abdominal obesity in PLWH was stronger with older age (p interaction, 0.001). Abdominal obesity was associated with elevated LDL-C (aOR, 1.44 [1.23-1.69]), hypertension (aOR, 1.32 [1.16-1.49]), and hypertriglyceridemia (aOR, 2.12 [1.86-2.41]). Conclusions: Abdominal obesity was associated with proaterogenic metabolic factors including elevated LDL-C, hypertension, and hypertriglyceridemia and remains a distinct HIV-related phenotype, particularly among older PLWH. Effective interventions to reduce the apparent detrimental impact on cardiovascular risk from this phenotype are needed.

Relationship between chronic hepatitis B and metabolic syndrome: A structural equation modeling approach.

OBJECTIVE: Investigate the nature of the relationship between chronic hepatitis B virus (HBV) infection and metabolic syndrome among nondiabetic adults. METHODS: This was a cross-sectional analysis of 17,030 nondiabetic adults (7437 males and 9593 females; mean age, 36.0 ± 3.9 years) in northern Taiwan from 2008 to 2009. The associations of hepatitis B surface antigen (HBsAg) seropositivity with metabolic syndrome and cardio-metabolic parameters were assessed. A structural equation model was constructed to elucidate the pathways between chronic HBV infection and individual cardiometabolic risk factors. RESULTS: A total of 2982 (17.5%) participants were HBsAg-seropositive. Of the seropositive and seronegative subjects, 15.5 and 16.9% had metabolic syndrome, respectively. The HBsAg-seropositive subjects had a lower odds of having metabolic syndrome compared with the seronegative subjects irrespective of gender and age (OR: 0.76, 95% CI: 0.68-0.85). The inverse associations remained significant after adjusting for body mass index and serum alanine aminotransferase levels. HBsAg seropositivity was inversely associated with hypertriglyceridemia (OR: 0.59, 95% CI: 0.52-0.66), and low serum levels of high-density lipoprotein cholesterol (OR: 0.86, 95% CI: 0.79-0.93) after adjustments. The structural equation model revealed chronic HBV infection had a significant negative effect on dyslipidemia both in males (B = -0.054) and females (B = -0.064). CONCLUSIONS: The inverse relationship between chronic HBV infection and metabolic syndrome may be attributable to the net beneficial effects on lipid profiles.

Metabolic abnormalities and coronary heart disease risk in human immunodeficiency virus-infected adults.

BACKGROUND: Metabolic syndrome is a combination of risk factors for cardiovascular disease and diabetes, It has been reported to be increased in human immunodeficiency virus (HIV)-infected individuals. METHODS: In a cohort of HIV-infected adults we examined parameters that contribute to defining the metabolic syndrome and to estimating the 10-year risk of coronary heart disease (CHD). The study group consisted of 296 participants (217 men and 79 women) of mixed ethnicity with a mean age of 45.3 years. RESULTS: There was an appreciable prevalence of metabolic syndrome (30.0%), with the frequency increasing to 42.5% in those over 50 years of age. Those with the metabolic syndrome had a lower viral load. More women had abdominal obesity (59.5%) than men (20.7%, P < 0.001). The frequency of elevated plasma glucose was higher in females (37.2%) compared to males (16.9%, P = 0.004). High frequencies of decreased high-density lipoprotein cholesterol (HDL-C) and elevated blood pressure were seen in both sexes. Hypertriglyceridemia was less prevalent in African Americans. In those under 50 years of age, the 10-year CHD risk score for men was double that for women (6.2% vs 2.7%, P < 0.001). In older participants, the risk was similar between the sexes, with a third having scores over 10%. CONCLUSIONS: The prevalence of metabolic syndrome was higher than in most other HIV cohorts. Those with the syndrome had significantly lower viral loads. Mean 10-year Framingham Cardiovascular Risk (FCR) scores were nearly doubled for those with metabolic syndrome. Both researchers and clinicians should consider age as well as sex when assessing patients with HIV infection for risks associated with metabolic syndrome.

Impact of diabetes mellitus on prognosis of patients infected with hepatitis C virus.

Diabetes is a risk factor for the progression of liver fibrosis and development of hepatocellular carcinoma in chronic hepatitis C. However, the impact of diabetes on the long-term prognosis and the synergistic interactions of various host factors for diabetes to the progression of liver fibrosis are unknown. In the present study, we examined the host factors associated with the progression of hepatitis C in 68 patients with a posttransfusion hepatitis (PTH) and analyzed the relationships. Multivariate analysis showed that age of PTH, being male, and type 2 diabetes mellitus were risk factors for the progression of liver fibrosis. By the Kaplan-Meier method, the cirrhosis-free survival rates after the onset of PTH were significantly lower in the diabetic group than in the nondiabetic group (P < .01). Diabetes also had a great impact on the long-term prognosis of chronic hepatitis C by reducing the time from PTH to the occurrence of hepatocellular carcinoma (P < .01) and to liver-related death (P < .05). Coexistence of obesity (body mass index > or =25 kg/m(2)) or hypertriglyceridemia (> or =150 mg/dL) with diabetes had a synergistic effect on liver fibrosis progression in patients with chronic hepatitis C. Thus, the treatment of diabetes, obesity, and hypertriglyceridemia may hold the key to improving the prognosis of chronic hepatitis.

Alterations in lipid kinetics in men with HIV-dyslipidemia.

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.

Aerobic exercise training fails to lower hypertriglyceridemia levels in persons with advanced HIV-1 infection.

The purpose of this study was to determine whether blood lipid and lipoprotein concentrations varied in 5 men with advanced HIV-1 infection after 12 months of aerobic exercise training. Prior to exercise, the mean baseline cholesterol and high-density lipoprotein cholesterol (HDL-C) serum concentration were each lower, and mean baseline triglyceride concentration was higher compared to a healthy population norm. Consistent exercise training for 12 months failed to significantly (p > .05) alter cholesterol or HDL-C. Triglyceride concentration was significantly (p < .05) elevated above baseline (63 mg/dL) regardless of exercise compliance. The results suggest that long-term exercise training cannot correct lipid profile abnormality, particularly hypertriglyceridemia, common to individuals with advanced HIV-1 infection.

Severe hypertriglyceridaemia associated with human immunodeficiency virus and highly active antiretroviral therapy.

We report two cases of severe hypertriglyceridaemia associated with human immunodeficiency virus infection and highly active antiretroviral therapy (HAART). The first patient, a 39-year-old man, developed moderate hypertriglyceridaemia (5.88 mmol/L) and hypercholesterolaemia (7.0 mmol/L) after 8 months of HAART. When his therapy was altered, triglyceride and cholesterol concentrations increased further to 15.9 and 10.9 mmol/L, respectively, after 6 weeks. The second patient, a 31-year-old man, presented with triglyceride and cholesterol concentrations of 16.2 and 5.7 mmol/L, respectively, following an 8-year history of HAART. Therapy was changed, but 1 month later the triglyceride concentration had increased to 39.4 mmol/L and the cholesterol concentration to 12.1 mmol/L. Both patients were managed by a change in HAART and the introduction of a fibric acid derivative. Although neither patient displayed any clinical symptoms associated with hypertriglyceridaemia, it is important to recognize such cases because of the associated risk of pancreatitis and coronary disease.