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PubMed1976

[Antiheparin immunoglobulin in malignant lymphoma with hypertriglyceridemia, in the hamster].

A massive hypertriglyceridemia associated with low post heparin lipolytic activity, was demonstrated during the growth of a transplanted lymphoma in Hamsters. An immunoglobulin, with high anti-heparin activity, was extracted from the tumor. It could inhibit both the anti-thrombin and prolipase activity of heparin. The role of this anti-heparin immunoglobulin in triglyceride metabolism allows us to consider the hypertriglyceridemia of lymphoma-bearing Hamsters as one of the two previously described types of auto-immune hyperlipidemia.

Animals↗
PubMed2025

Pathogenicity assessment of genetic variants identified in patients with severe hypertriglyceridemia: Novel cases of familial chylomicronemia syndrome from the Dyslipidemia Registry of the Spanish Atherosclerosis Society.

PURPOSE: Genetic testing is required to confirm a diagnosis of familial chylomicronemia syndrome (FCS). We assessed the pathogenicity of variants identified in the FCS canonical genes to diagnose FCS cases. METHODS: 245 patients with severe hypertriglyceridemia underwent next-generation sequencing. Preliminary variant pathogenicity criteria and classification, based on the American College of Medical Genetics and Genomics guidelines, were obtained online and verified. Phenotype evaluation was based on lipoprotein lipase activity deficiency, a clinical score, and/or type I hyperlipoproteinemia determined in 25 patients. RESULTS: Twenty-four biallelic variants were analyzed. Evidence-based criteria allowed the reclassification of 8 likely pathogenic (LP) variants in the LPL, APOA5, and LMF1 genes into pathogenic (P) and the change of 2 variants of uncertain significance (VUS) to LP. Conversely, 2 variations in LMF1 remained as VUS. Additionally, 1 variant in LPL and 2 in GPIHBP1 were likely benign. Twenty FCS cases had biallelic P/LP variants and 1 patient, with an FCS phenotype, harbored biallelic VUS. FCS was excluded from 4 patients with pathogenic/likely benign combinations. CONCLUSION: The analysis of the clinical and biochemical features of patients with variants in the FCS canonical genes allowed a confident variant classification that helped in the diagnosis of novel FCS cases.

Humans↗
PubMed1989

The deadly quartet. Upper-body obesity, glucose intolerance, hypertriglyceridemia, and hypertension.

The contribution of obesity to cardiovascular risk has not been adequately appreciated because of a failure to recognize the involvement of upper-body predominance of body weight with hypertension, diabetes, and hypertriglyceridemia even in the absence of significant overall obesity. This article examines the evidence that upper-body obesity, as usually induced by caloric excess in the presence of androgens, mediates these problems by way of hyperinsulinemia. Because of these interrelationships, there is a need to identify and prevent upper-body obesity or, failing that, to provide therapies that will control the associated problems without aggravating hyperinsulinemia.

Adipose Tissue↗
PubMed1999

Effect of moderate alcohol consumption on hypertriglyceridemia: a study in the fasting state.

BACKGROUND: Patients with hypertriglyceridemia (HTG) are generally advised to avoid alcohol, even though moderate alcohol consumption is cardioprotective. Alcohol increases plasma triglyceride concentration transiently in normolipidemic subjects, but whether alcohol consumption per se increases triglyceride concentrations in patients with HTG is unclear. OBJECTIVE: To assess whether baseline fasting triglyceride concentration determines plasma triglyceride concentration after acute oral alcohol intake. METHODS: Twelve persons with fasting triglyceride concentrations of 2.3 to 8.5 mmol/L (200-750 mg/dL) and 12 persons as a non-HTG group were enrolled. Obesity, current smoking, and history of hypertension, diabetes, or excessive alcohol use were exclusionary. Fasted subjects consumed 38 mL of ethanol in water (equivalent, 2 alcoholic drinks); blood samples were collected at baseline and at intervals thereafter for 10 hours. No less than 1 week later, the subjects consumed water alone in a control test. RESULTS: Mean triglyceride values were 4.04+/-0.41 mmol/L (358+/-36.9 mg/dL) and 1.00+/-0.11 mmol/L (89+/-10.2 mg/dL) for the HTG and non-HTG groups, respectively. Despite similar changes with alcohol feeding in plasma ethanol, nonesterified fatty acid, and acetate concentrations, the groups differed in triglyceride response. At 6 hours (peak) compared with baseline, triglyceride concentration increased only 3% in the HTG group but 53% in the non-HTG group. The former change was not significantly different from the effect with water alone (-9.2% from baseline; P = .43), whereas the latter was (-8.0%; P = .003). CONCLUSIONS: Acute alcohol intake alone is not an important determinant of plasma triglyceride concentration in individuals with HTG. Other factors, such as the contemporaneous consumption of fat and alcohol, known to increase triglyceride concentrations synergistically in non-HTG individuals, may be more important.

Adult↗
PubMed1995

Hypertriglyceridemia may be severe in CML patients treated with interferon-alpha.

We analyzed serum triglyceride (TG) levels in 22 chronic myeloid leukemia (CML) patients treated with interferon-alpha (IFN-alpha). Hypertriglyceridemia was present in one-half of patients at diagnosis, and IFN-alpha treatment was associated with a further increase in 90% of the total group of patients. This increase was maximal during the first months of therapy. Four patients (18%) reached levels higher than 1,000 mg/dl. This is the first report describing this secondary effect in CML patients treated with IFN-alpha.

Adolescent↗
PubMed2005

Treatment of massive hypertriglyceridemia resistant to PUFA and fibrates: a possible role for the coenzyme Q10?

OBJECTIVE: To describe the effect of CoQ10 (added to either a fibrate, or PUFA or association of both) in patients affected by massive hypertriglyceridemia (MHTG) resistant to fibrates and PUFA. DESIGN: Open, sequential, comparative intervention study. SETTING: Specialised centres for dyslipidemia management. SUBJECTS: 15 subjects (mean age: 45.1 +/- 12.5 years) affected by MHTG and hyporesponsive to either fibrates, or PUFA, or fibrates-PUFA association, and 15 age-matched subjects regularly responders to PUFA and fenofibrate treatment. INTERVENTIONS: Treatment for periods of 6 weeks each with the following consecutive treatments: CoQ10 150 mg/day, PUFA 3000 mg/day, fenofibrate 200 mg/day, PUFA 3000 mg/day + fenofibrate 200 mg/day, PUFA 3000 mg/day + CoQ10 150 mg/day, fenofibrate 200 mg/day + CoQ10 150 mg/day, and finally, fenofibrate 200 mg/day + PUFA 3000 mg/day + CoQ10 150 mg/day. RESULTS: CoQ10 supplementation improved, in the control group, systolic and diastolic blood pressure, creatinine and Lp(a) plasma levels, both during fenofibrate and/or PUFA treatment. In MHTG group, CoQ10 supplementation significantly improved TG, TC, Lp(a), uric acid and blood pressure during fenofibrate treatment, but only Lp(a) and blood pressure during PUFA treatment. Fenofibrate appeared to have better effect on hsCRP and gamma-GT plasma levels than PUFA. No significant change was observed in any group and under any treatment in regards to homocysteinemia, PAI-1, or t-PA. CONCLUSION: Even though the mechanism of action through which the effects were obtained is yet to be elucidated, adding CoQ10 to fenofibrate could improve the drug's efficacy in MHTG patients not responding to fenofibrate alone.

Adult↗
PubMed1998

Lipoprotein changes in children after liver transplantation: mild hypertriglyceridemia and a decrease in HDL3/HDL2 ratio.

Hyperlipidemia is frequently observed in patients who undergo renal, cardiac, bone marrow, or liver transplantation, and its contribution to the long-term morbidity and survival of patients with organ transplants may be substantial. In the few studies that have focused on the pediatric age group, findings have been inconsistent. The lipoprotein profile of 10 children after liver transplantation was characterized and compared with those in normal population controls and 10 healthy siblings. Plasma triglyceride and cholesterol concentrations were determined, lipoprotein fractions (very-low-density lipoprotein [VLDL], low-density lipoprotein [LDL], and high-density lipoproteins [HDL2 and HDL3]) were isolated, their chemical compositions were analyzed (protein, phospholipids, triglycerides, free cholesterol, and cholesteryl ester), and the percent relative weight composition of the particles was calculated. Plasma triglyceride and VLDL cholesterol levels were higher post-liver transplantation (P < .05): triglycerides (mean +/- SD), 115.1 +/- 58.7 mg% versus 76.6 +/- 20.9 mg% in siblings and 60.0 +/- 25.0 mg% in normal population controls; very-low-density lipoprotein cholesterol (VLDL-C), 23.0 +/- 11.7 mg% versus 15.3 +/- 4.7 mg% and 13.0 +/- 8.0 mg%, respectively. Plasma triglyceride levels did not correlate with the length of the period after liver transplantation. Levels of LDL-C and total HDL-C and the relative weight composition of VLDL, LDL, HDL2, and HDL3 particles did not differ between post-liver transplantation children and controls. Posttransplantation, levels of HDL3, the normally predominant HDL subfraction, were decreased relative to HDL2 levels (HDL3, 1.3; HDL2, 2.3). Because this observed relative increase in larger cholesteryl ester-rich HDL particles (HDL2) may result from inhibition of cholesteryl ester-triglyceride transfer processes, cholesteryl ester transfer protein activity was assayed. Cholesteryl ester transfer protein activity did not differ between patients and controls. Thus, the lipoprotein changes observed in children post-liver transplantation are mild hypertriglyceridemia and a significant increase in HDL2 relative to HDL3. Because HDL2 is regarded as protective against atherosclerosis, this may be of clinical relevance.

Child↗
PubMed1995

An apolipoprotein CIII marker associated with hypertriglyceridemia in Caucasians also confers increased risk in a west Japanese population.

Polymorphisms and haplotypes at the adjacent apolipoprotein (apo) AI and CIII gene loci were investigated in 61 Japanese patients with triglycerides greater than 350 mg/dl and in 66 unrelated normolipidemic subjects. The polymorphic sites were the SstI site in the apoCIII 3' untranslated region, whose presence has previously been shown to be associated with hypertriglyceridemia (HTG) in Caucasians, and the MspI site in the third intron of the apoAI gene. The frequencies of the SstI minor allele (S2) were 0.48 in HTG patients and 0.25 in normolipidemic subjects (P < 0.00015). The frequencies of the MspI minor allele (M2) were 0.61 in HTG patients and 0.33 in normolipidemic subjects (P < 0.00001). The two polymorphic sites were in strong linkage disequilibrium, and maximum likelihood analysis supported the existence of three of the four possible haplotypes: S1-M1, S1-M2, and S2-M2. Since all S2 alleles were estimated to be present on M2-bearing chromosomes, the HTG-associated S2-M2 haplotype conferred the same approximate relative risk as the S2 allele alone when compared with the other two haplotypes (odds ratio 2.8). This study demonstrates that the S2 allele is a marker for HTG among west Japanese subjects as well as among Caucasians. The results suggest that S2-M2 chromosomes carry HTG susceptibility sequences that predate the separation of the Asian and Caucasian races.

Alleles↗
PubMed1996

Need for reduction of cyclosporin dosage in renal transplant patients with hypertriglyceridemia but not hypercholesterolemia.

Currently there is a paucity of data regarding the influence of high serum triglyceride levels on cyclosporin A (CyA) levels and dosing. We therefore undertook a retrospective study to determine the relationship of serum lipid levels to CyA levels and CyA dosages. Renal transplant patients at a 0.5-to-3-year post-transplant stage, with a stable CyA dosage, who were not on medications that affect CyA metabolism or renal function, were entered into the study. The CyA dosage was adjusted by clinicians to maintain whole blood. 12-h CyA trough levels between 200 and 250 ng/ml (monoclonal TDX method, which measures the parent compound). Forty-four patients qualified for the study. The data clearly indicated that high cholesterol levels (> 300 mg/dl and with normal triglyceride levels) did not influence the CyA levels or the dosages. Conversely, high triglyceride levels ( > 500 mg/dl) significantly reduced the amount of CyA required. A decreased clearance of CyA in the presence of hypertriglyceridemia led to high CyA levels in some patients. Reducing the CyA dosage to achieve levels between 200 and 250 ng/ml improved renal allograft function and decreased other side effects attributed to CyA toxicity. These studies indicate that high triglyceride levels, but not high cholesterol levels, increase CyA levels, which can lead to CyA toxicity.

Adolescent↗
PubMed2006

Effect of exercise on postprandial lipemia in men with hypertriglyceridemia.

We examined the effect of exercise on postprandial lipemia (PPL) and insulin resistance in individuals with metabolic syndrome. Subjects were 10 hypertriglyceridemia (HTG) males with insulin resistance [age = 40.1 +/- 2.2 years, body weight = 96.3 +/- 3.3 kg, fasting triglyceride (TG) = 263 +/- 25 mg/dl, VO(2)max = 37 +/- 1.1 ml/kg/min, and Homeostatic Model Assessment (HOMA-IR, an index of insulin resistance) = 3.05 +/- 0.40]. Each subject performed a control trial (Ctr, no exercise), and three exercise trials at 40% (40%T), 60% (60%T), and 70% (70%T) of their VO(2)max. The order of trials was randomized and there were 1-2 weeks wash-out period between the trials. All subjects had a fat-meal in each trial. In the exercise trials, subjects jogged on a treadmill for 1 h at a designated intensity 12 h prior to a fat-meal ingestion. Blood samples were taken at 0 h (before the meal), and 2, 4, 6, and 8 h after the meal. The plasma TG, area score under TG concentration curve for over an 8 h-period (TG AUC) after the meal, and HOMA-IR were analyzed. The TG AUC score in 40%T was 30% lower (P = 0.003), 60%T was 31% lower (P = 0.02), and 70%T was 39% lower (P = 0.02) than Ctr. There were no significant differences in the TG AUC scores among the exercise trials (P > 0.05). The insulin concentrations in both 60 and 70%T were lower than Ctr (P < 0.01) which did not differ from 40%T. HOMA-IR in both 60%T (P = 0.041) and 70%T (P = 0.002) were lower than Ctr, but not different from 40%T (HOMA-IR: Ctr = 3.05 +/- 0.40, 40%T = 2.67 +/- 0.35, 60%T = 2.49 +/- 0.31, 70%T = 2.21 +/- 0.27). The results suggest that for physically inactive individuals with metabolic syndrome, exercising at low to moderate intensity may be sufficient to attenuate PPL and increase insulin sensitivity, whereas higher intensity exercise may be needed to normalize blood glucose.

Adult↗
PubMed1997

Interaction between obesity and genetic polymorphisms in the apolipoprotein CIII gene and lipoprotein lipase gene on the risk of hypertriglyceridemia in Chinese.

To understand the effects of the interaction between genetic polymorphisms and obesity on the risk of hypertriglyceridemia (HTG), two polymorphisms, an SstI polymorphism on the apolipoprotein CIII gene and a HindIII polymorphism on the lipoprotein lipase gene, were analyzed in 339 Chinese subjects with (82 cases in the HTG group) or without HTG (257 cases in the control group). Our data revealed that the frequencies of obesity, the SstI minor allele (S2), and the HindIII major allele (H+) in the HTG group were significantly higher than in the control group. Subgroup analysis revealed that the association between these two polymorphisms and HTG occurred predominantly in nonobese subjects and in subjects with the less hypertriglyceridemic genotype of another polymorphism. Multivariate logistic regression analysis showed that all three risk factors (obesity, S2-containing chromosome, and H+ homozygosity) were associated with HTG, and an interaction was found between obesity and H+ homozygosity for the occurrence of HTG. The risk of HTG increased significantly with combinations of risk factors. Subjects can be divided into low or high risk groups for HTG using such combinations. These results provide evidence of interaction between obesity and the HindIII polymorphism of the lipoprotein lipase gene on the risk of HTG.

Alleles↗
PubMed2004

Population prevalence of APOE, APOC3 and PPAR-alpha mutations associated to hypertriglyceridemia in French Canadians.

Hypertriglyceridemia (HTG) is known as a common metabolic disorder associated with increased production, decrease catabolism and/or decreased hepatic uptake of triglyceride (TG)-rich particles. We assessed, in the Quebec City population, the allele frequency and haplotype distributions of mutations in genes related to HTG, such as the apolipoprotein E (APOE) (C112R and C158R), the apolipoprotein CIII (APOC3) (C-482T and C3238G) and the peroxisome proliferator-activated receptor alpha (PPARalpha) (L162V) genes. A total of 938 anonymous unlinked newborns from the metropolitan Quebec City area have been genotyped. Allele frequencies observed in the Quebec City population differed from known frequencies determined in other Caucasian populations. The co-transmitted allele distribution between the two-marker genotypes APOE/APOC3(C3238G) and APOC3(C-482T)/PPARalpha(L162V) presented a weak deviation from the assumption of genetic independence. Also, we observed a non-independent distribution of the T-482/G3238 allele combinations within the APOC3 gene, suggesting strong linkage disequilibrium between the C-482T and C3238G polymorphisms. Moreover, comparisons of allele frequencies observed in the population of Québec City to those obtained in other Caucasian populations suggested that the population of Québec City may be at a lower risk of developing HTG due to APOE, APOC3 and PPARalpha genetic variants. However, the strong linkage disequilibrium and the two-marker genotype distributions observed in the APOC3 gene suggest that these two variants may functionally interact in the Québec City population.

Amino Acid Substitution↗
PubMed2026

Comparative Efficacy of Insulin and Alternative Therapies for Hypertriglyceridemia-Associated Acute Pancreatitis: A Systematic Review and Network Meta-Analysis.

BACKGROUND AND AIMS: Hypertriglyceridemia-induced acute pancreatitis is associated with high triglyceride levels and may lead to significant clinical complications. Rapid TG-lowering strategies, including insulin, therapeutic plasma exchange (TPE), heparin, hemofiltration, and conservative management, are used in clinical practice; however, their comparative efficacy and impact on clinical outcomes remain uncertain. METHODS: Following preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines and International Prospective Register of Systematic Reviews (PROSPERO) registration (CRD420251239674), we searched PubMed, Embase, Web of Science, Scopus, CINAHL, Google Scholar, and Cochrane. Primary outcomes included TG reduction, C-reactive protein (CRP), length of stay, mortality, and organ failure. Secondary outcomes included renal and respiratory failure. Random-effects network meta-analyses estimated mean differences or relative risks with 95% confidence intervals; treatments were ranked using the Surface Under the Cumulative Ranking curve (SUCRA). Predefined sensitivity analyses were conducted according to study design (RCTs) and risk of bias (ROB). RESULTS: Across predominantly observational evidence, no intervention demonstrated statistically significant superiority over insulin-based therapy for mortality, organ failure, or length of stay, and no consistent clinical benefit was observed despite differences in biochemical TG reduction. Although some interventions showed relatively favorable SUCRA rankings across selected outcomes, these findings were not consistently supported by statistically significant or high-certainty evidence. In RCT-restricted analyses, therapeutic plasma exchange (TPE) significantly reduced TG levels versus insulin (MD&#x2009;-&#x2009;620.0; p&#x2009;=&#x2009;0.03) and CRP versus conservative therapy (MD&#x2009;-&#x2009;0.80; p&#x2009;<&#x2009;0.01), while insulin plus heparin was associated with shorter hospital stay (MD&#x2009;-&#x2009;1.60&#xa0;days; p&#x2009;<&#x2009;0.01). However, faster triglyceride reduction did not consistently translate into improved mortality, organ failure, ICU-related outcomes, or length of stay. CONCLUSION: Despite improvements in biochemical markers, the clinical significance of rapid TG reduction in HTG-AP remains uncertain, as these effects were not consistently associated with improvements in mortality, organ failure, ICU-related outcomes, or hospital length of stay. Given that most available evidence was derived from nonrandomized studies and that the certainty of evidence was predominantly low or very low, adequately powered randomized controlled trials are needed to determine whether accelerated triglyceride lowering improves clinically meaningful patient outcomes.

Humans↗
PubMed1999

Recent developments in the treatment of hypertriglyceridemia.

Hypertriglyceridemia is now recognized as an independent risk factor of coronary artery disease (CAD). A recent secondary prevention study of CAD with a statin suggested that it may be prudent to target fasting triglycerides to less than 150 mg/dL. Secondary prevention trials of CAD with drugs acting primarily on triglycerides (fibrates) have shown that reducing triglycerides and increasing high-density lipoprotein (HDL) cholesterol, without significantly affecting low-density lipoprotein cholesterol slows down coronary artery luminal narrowing (Lopid Coronary Angiography Trial [LOCAT], Bezafibrate Coronary Atherosclerosis Intervention Trial [BECAIT], Bezafibrate Infarction Prevention [BIP]). Furthermore, Veterans Administration-HDL Intervention Trial (VA-HIT) and Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto-1 (GISSI) studies recently showed that gemfibrozil and fish oils, respectively, decreased CAD mortality in secondary prevention trials. Statins are also capable of significantly reducing high triglyceride levels. Further clinical studies are necessary to confirm in terms of mortality the beneficial effect of reducing triglycerides and increasing high-density lipoprotein cholesterol in secondary CAD prevention; whereas, in primary prevention the beneficial effect of drastically reducing triglycerides by the way of pharmacology needs to be proved.

Bezafibrate↗
PubMed1999

Identification and treatment of hypertriglyceridemia as a risk factor for coronary heart disease.

Recent publications, including new population-based studies and a meta-analysis of prospective, population-based studies, provide strong evidence for an elevated triglyceride level as an independent risk factor for coronary heart disease. Pathophysiologic relationships between elevated triglyceride levels and both reduced high-density lipoprotein levels and an increase in the proportion of low density lipoproteins that are small and dense support the epidemiologic data, and suggest that an elevated triglyceride level should constitute a target for lipid-lowering therapy. There are no clear recommendations for management of patients with hypertriglyceridemia available in the current treatment guidelines. Treatment options include life-style measures and, if drug therapy is required, nicotinic acid, fibrates, more potent 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), or combination therapy with statin plus fibrate or nicotinic acid.

Cholesterol, HDL↗
PubMed2004

Major hypertriglyceridemia in HIV-infected patients on antiretroviral therapy: a role of the personal and family history.

BACKGROUND: Our aim was to identify factors predisposing HIV-infected patients on long-term antiretroviral therapy (ART) to major hypertriglyceridemia (HTG). PATIENTS AND METHODS: We conducted a retrospective, case-control study involving 76 HIV-infected patients with HTG, defined by 12-hour fasting plasma triglyceride (TG) > 4.5 mmol/l on at least one occasion, and 150 HIV-infected matched control patients with TG consistently below 1.8 mmol/l. RESULTS: Patients coinfected by the hepatitis C virus appeared to be protected from HTG. In addition to known predisposing factors for HTG in HIV-infected patients (ART and immune/viral status), patients with a history of excess body weight were twice as likely to have HTG (odds ratio [OR] 2.8, 95% confidence interval [CI]: 1.1-6.9); HTG was also more frequent in patients who had a first-degree relative with cardiovascular disease (CVD) or a major risk factor for CVD (OR = 3.6, CI: 1.3-9.9). CONCLUSION: By identifying subgroups of highly predisposed patients, appropriate lifestyle and dietary measures could be recommended on ART initiation.

Adult↗