OBJECTIVE: TPE drastically reduces serum triglyceride (sTG), but its role in the treatment of hypertriglyceridemia-induced acute pancreatitis (HTG-AP) or at risk of developing it, is not well established. The objectives were to assess the effectiveness and safety of TPE in the treatment of severe HTG (sHTG), as well as to evaluate the severity of HTG-AP treated with TPE.
METHODS: Observational-retrospective-single-center study, in which a descriptive analysis of sHTG treated with TPE was conducted, with the aim of treating HTG-AP or preventing its recurrence. TPE was performed if sTG≥ 1000 mg/dL after 24 hours of admission.
RESULTS: 42 TPE were performed to treat 35 sHTG in 23 patients: 29 HTG-AP, and 6 sHTG with previous HTG-AP. Among the patients, 37% (13/55) were women, with 37 ± 14 years-old, 74.3% had normal BMI (25/35), 34% (12/35) were drinking > 40 g/alcohol/day and 54% (19/35) were diabetics. TPE significantly reduced the baseline sTG (4425 ± 2782 mg/dL vs. 709 ± 353 mg/dL, p < 0.001) in a single session, achieving a mean percentage reduction of 79 ± 13%; 20% (7/35) of sHTG cases required two TPE sessions to reduce sTG to < 1000 mg/dL. Adverse effects were reported in 4/42 TPE sessions (9,5%). sHTG-AP was observed in 3% of cases (1/29), and there were no deaths. sTG at 24 hours of admission showed no relation with the severity of APs.
CONCLUSIONS: The treatment of sHTG with TPE, with the aim of treating HTG-AP or preventing its recurrence, reduces sTG quickly and safety.

Hypertriglyceridemia encompasses a set of lipid disorders common in clinical practice, generally defined as a fasting concentration above 150mg/dL. There are various classifications of the severity of hypertriglyceridaemia based on serum values, with levels generally considered moderate when below 500mg/dL and severe when above 1000mg/dL. Its importance lies in its association with other alterations in the lipid profile, contributing to increased cardiovascular risk and increased risk of acute pancreatitis, mainly with concentrations above 500mg/dL.

BACKGROUND: Acute pancreatitis is a frequent inflammatory gastrointestinal disorder with high mortality rates in severe forms. An early evaluation of its severity is key to identify high-risk patients. This study assessed the influence of waist circumference together with hypertriglyceridemia on the severity of acute pancreatitis.
METHODS: A retrospective study was performed, which included patients admitted with acute pancreatitis from March 2014 to March 2021. Patients were classified into four phenotype groups according to their waist circumference and triglyceride levels: normal waist circumference and normal triglycerides; normal waist circumference and elevated triglycerides; enlarged waist circumference and normal triglycerides; and enlarged waist circumference and triglycerides, namely hypertriglyceridemic waist (HTGW) phenotype. Clinical outcomes were compared among the groups.
RESULTS: 407 patients were included. Systemic inflammatory response syndrome (SIRS) and intensive care unit admission were most frequent among patients in the HTGW phenotype group, at 44.9% and 8.2%, respectively. The incidence of local complications was higher in the normal waist circumference with elevated triglycerides group (27%). On multivariable analysis, an enlarged waist circumference was related to an increase of 4% and 2% in the likelihood of developing organ failure and SIRS, respectively. Hypertriglyceridemia was an independent risk factor for both organ failure and local complications.
CONCLUSIONS: HTGW phenotype was significant related to developing of SIRS. It seems that an enlarged waist circumference has a greater role than hypertriglyceridemia in the development of SIRS. Obesity and hypertriglyceridemia were both independent risk factors for organ failure. Patients with hypertriglyceridemia were more likely to develop local complications.

The Working Groups of Cardiovascular Pharmacotherapy of the Sociedad Española de Cardiología and Cardiovascular Disease of the Sociedad Española de Diabetes have prepared a consensus document on the treatment of hypertriglyceridaemia in patients with high/very-high-cardiovascular risk with icosapent ethyl, a highly purified and stable eicosapentaenoic acid ethyl ester. This document is necessary since there are differences among the three main omega-3 fatty acids and there is large-scale clinical evidence with icosapent ethyl that demonstrates that in addition to its efficacy in lowering triglyceridaemia, it reduces the risk of cardiovascular events in both patients with atherosclerotic cardiovascular disease and in those with type 2 diabetes, with a good safety profile. The number needed to treat to avoid a major cardiovascular event is analysed, comparing it with other pivotal studies of pharmacological intervention in cardiovascular prevention, and an estimate of the Spanish population likely to be treated with ethyl icosapent is carried out. These recommendations are of interest to all clinicians who manage patients with lipid metabolism disorders, cardiovascular disease and diabetes.

The incorporation of a healthy diet, regular physical exercise and smoking cessation are the initial measures to reduce cardiovascular risk in patients with atherogenic dyslipidemia. In these patients, the nutritional quality of their diet should be improved, replacing foods with a greater atherogenic effect for others with a healthier effect. There is strong evidence that plant-based dietary patterns, low in saturated fatty acids, cholesterol and sodium, with a high content of fiber, potassium and unsaturated fatty acids, are beneficial and reduce the expression of cardiovascular risk factors. This document focuses on the role of nutrition in the prevention and treatment of atherogenic dyslipidemia, providing current evidence to serve as a tool for health professionals in its clinical management. To facilitate the reading of these recommendations, they are presented in a user-friendly table format, with a hierarchy of different levels of evidence.

Familial chylomicronemia syndrome (FCS) is a genetic entity with autosomal recessive inheritance. Mutations in genes (such as APOC2, APOAV, LMF-1, GPIHBP-1) that code for proteins that regulate the maturation, transport, or polymerization of lipoprotein lipase-1 are the most common causes, but not the only ones. The objective of this study was to report the first documented case in Ecuador. CLINICAL CASE: A 38-year-old man presented with chronic hepatosplenomegaly, thrombocytopenia, pancreatic atrophy, and severe hypertriglyceridemia refractory to treatment. A molecular analysis was performed by next generation sequencing that determined a deficiency of Lipoprotein Lipase OMIM #238600 in homozygosis. Genetic confirmation is necessary in order to establish the etiology of HTGS for an adequate management of this pathology.

OBJECTIVE: Triglycerides are the initiators of the metabolic changes that lead to atherogenic dyslipidemia (AD). The APOA5 and APOA1 genes are involved in the response and metabolism of serum lipids and lipoproteins, where single nucleotide polymorphisms (SNP) rs662799 (promoter region) and rs5070 (intronic region) have been associated with the susceptibility to dyslipidemia. Until now, few studies evaluate the association of these polymorphisms with the presentation of hypertriglyceridemia and AD among Mexican children. Therefore, the objective was to determine the association between rs662799 and rs5070 with hypertriglyceridemia and AD in a pediatric population of southeastern Mexico.
METHODS: A case-control analysis was performed including 268 infants aged 2-16 years, anthropometric, clinical variables, and serum lipid profiles were analyzed. DNA was extracted from blood samples and genotyping of polymorphisms was executed with the TaqMan SNP genotyping assay. Allele and genotypic frequencies were calculated. For genetic association analysis, logistic regression models were fitted according to models of inheritance.
RESULTS: The SNP rs662799 (C) was significantly associated with hypertriglyceridemia in the overdominant model (OR=3.89, p=0.001) and AD in the dominant model (OR=4.01, p=0.001). The SNP rs5070 (T) has a protective effect against hypertriglyceridemia in the additive risk model (OR=0.68, p=0.03).
CONCLUSIONS: Polymorphism rs662799 was significantly associated with cases of hypertriglyceridemia and AD in minors in southeastern Mexico. On the other hand, rs5070 polymorphism was not associated with cases of hypertriglyceridemia or AD.

BACKGROUND: In its initial stages, nonalcoholic fatty liver disease presents hypertriglyceridemia and accumulation of lipids in the liver (hepatic steatosis). Bempedoic acid is an ATP:citrate lyase inhibitor that promotes a dual inhibition of the synthesis of cholesterol and fatty acids. However, its effect in the prevention / treatment of hepatic steatosis and hypertriglyceridemia has not been investigated. The aim of our work has been to elucidate whether bempedoic acid, through a mechanism other than ATP:citrate lyase inhibition, reverses these metabolic alterations.
METHODS: The study was carried out in female Sprague-Dawley rats fed, for three months, with a high fat diet supplemented with fructose (10% w/v) in drinking water. During the last month, bempedoic acid (30mg/kg/day) was administered to a group of animals. Zoometric and plasmatic parameters were analyzed, gene and protein expression analysis were performed in liver samples and PPAR-PPRE binding activity was determined.
RESULTS: Our interventional model developed hepatic steatosis and hypertriglyceridemia. Despite an increase in total caloric intake, there was no increase in body weight of the animals. The administration of bempedoic acid significantly reduced hepatic steatosis and promoted a marked hepatocyte hypertrophy. There was a 66% increase in the liver weight of the animals treated with the drug that was not accompanied by modifications in the markers of inflammation, oxidative stress, or endoplasmic reticulum stress. Bempedoic acid activated the peroxisome proliferator activated nuclear receptor (PPARα) and its target genes.
CONCLUSIONS: Bempedoic acid could be an effective therapy for the treatment of fatty liver and associated cardiovascular risk. Bempedoic acid has other mechanisms of action besides the inhibition of ATP: citrate lyase, such as the activation of PPARα, which could explain the reduction in hepatic steatosis and the increase in liver weight observed in animals treated with the drug.

BACKGROUND: Low-density lipoprotein cholesterol (LDL) is essential in managing cardiovascular disease risk. Since 1972, the Friedewald formula has been used to estimate LDL concentration, although with some limitations. In 2013, Martin et al. proposed a similar but more accurate formula for calculating LDL.
OBJECTIVE: To assess the applicability of the new formula, which we have named the Martin-Hopkins formula, in the Portuguese population and compare it with the Friedewald formula using direct LDL.
METHODS: Cross-sectional study, including 1689 participants from the e_COR study. We applied the Martin-Hopkins and Friedewald formulas for estimated LDL (LDL-M and LDL-F). The Friedewald formula was not applied in 12 cases due to triglycerides ≥400mg/dL. Direct LDL was measured and the accepted significance level was p<0.05.
RESULTS: Of the total subjects, 50.2% were male and had a median age of 51 (34) years. LDL-D was 117.0 (44.0) mg/dL, LDL-M was 114.6 (43.7) mg/dL and LDL-F was 113.8 (43.2) mg/dL. The Spearman coefficient (ρ) between LDL-M/LDL-D was 0.987 and between LDL-F/LDL-D was 0.983, p=0.001. This strong correlation was maintained in the group with diabetes (LDL-M/LDL-D ρ=0.987; LDL-F/LDL-D ρ=0.978, p=0.001) and hypertriglyceridemia (LDL-M/LDL-D ρ=0.983; LDL-F/LDL-D ρ=0.982, p=0.001). In terms of agreement, the highest value of κ=0.90 was obtained for LDL-M when LDL-D <100mg/dL.
CONCLUSIONS: The Martin-Hopkins formula performed well and had good applicability, showing superiority in relation to the Friedewald formula, especially for LDL-D values <100mg/dL, diabetes, and hypertriglyceridemia.

BACKGROUND: Low-density lipoprotein cholesterol (LDL) is essential in managing cardiovascular disease risk. Since 1972, the Friedewald formula has been used to estimate LDL concentration, although with some limitations. In 2013, Martin et al. proposed a similar but more accurate formula for calculating LDL.
OBJECTIVE: To assess the applicability of the new formula, which we have named the Martin-Hopkins formula, in the Portuguese population and compare it with the Friedewald formula using direct LDL.
METHODS: Cross-sectional study, including 1689 participants from the e_COR study. We applied the Martin-Hopkins and Friedewald formulas for estimated LDL (LDL-M and LDL-F). The Friedewald formula was not applied in 12 cases due to triglycerides ≥400mg/dL. Direct LDL was measured and the accepted significance level was p<0.05.
RESULTS: Of the total subjects, 50.2% were male and had a median age of 51 (34) years. LDL-D was 117.0 (44.0) mg/dL, LDL-M was 114.6 (43.7) mg/dL and LDL-F was 113.8 (43.2) mg/dL. The Spearman coefficient (ρ) between LDL-M/LDL-D was 0.987 and between LDL-F/LDL-D was 0.983, p=0.001. This strong correlation was maintained in the group with diabetes (LDL-M/LDL-D ρ=0.987; LDL-F/LDL-D ρ=0.978, p=0.001) and hypertriglyceridemia (LDL-M/LDL-D ρ=0.983; LDL-F/LDL-D ρ=0.982, p=0.001). In terms of agreement, the highest value of κ=0.90 was obtained for LDL-M when LDL-D <100 mg/dL.
CONCLUSIONS: The Martin-Hopkins formula performed well and had good applicability, showing superiority in relation to the Friedewald formula, especially for LDL-D values <100 mg/dL, diabetes, and hypertriglyceridemia.