Acute pancreatitis due to severe hypertriglyceridemia in the COVID-19 era: The role of therapeutic plasma exchange.

The psychosocial consequences of the COVID-19 pandemic caused multifaceted challenges in clinical and therapeutic practices. This was the case at the Therapeutic Apheresis Unit of the Padua University Hospital too. Several published reports describe the increase in alcohol and food addiction diseases. In this context, during the last months, the Padua Therapeutic Apheresis Unit treated many more patients with acute pancreatitis due to severe hypertriglyceridemia with therapeutic plasma exchange than in the previous ten years. Furthermore, retrospective cohort studies have been recently published describing the onset of acute pancreatitis during the COVID-19 infection even if, to date, there is still insufficient evidence to estabilish a direct causality. Anyway, the COVID-19 pandemic translated into changes of the overall disease prevalence scenario and therefore the Padua Therapeutic Apheresis Unit will need to reorganise its Therapeutic Apheresis activity.

Postprandial endothelial dysfunction and CIMT after oral fat challenge in patients with type 2 diabetes mellitus with and without macrovascular disease - A preliminary study.

BACKGROUND: Very few studies have reported on association of postprandial lipids and endothelial dysfunction among patients with diabetes. Whether endothelial dysfunction particularly postprandial FMD is worse in patients with T2DM with macrovascular disease compared to those without and whether this difference is related to postprandial hypertriglyceridemia (PPHTg) is unclear. Therefore, present study was aimed to assess the relationship between PPHTg and endothelial function in patients with T2DM with and without macrovascular disease. METHOD: Endothelial dysfunction by FMD and CIMT were compared in patients with T2DM with and without macrovascular disease (n = 13 each group) and 13 age, sex and BMI matched healthy individuals after an oral fat challenge. RESULTS: There was significant postprandial deterioration of FMD 4-hr after fat challenge in patients with diabetes (P < 0.001) as well as healthy individuals (P = 0.004). Patients with diabetes with macrovascular disease had significantly lower fasting (5.7 ± 6.1% vs. 22.7 ± 10.0% and vs. 24.7 ± 5.3%) as well as postprandial (4-hr) (3.1 ± 5.0% vs. 15.3 ± 8.1% and vs. 15.4 ± 5.7%) FMD compared to other two groups. Fasting, postprandial as well as change in FMD and CIMT in patients with diabetes correlated significantly with fasting as well as postprandial triglycerides with stronger correlation in those with macrovascular disease. CONCLUSION: Study found significant endothelial dysfunction by FMD that shows substantial further deterioration postprandially following high fat meal in patients with diabetes with macrovascular disease compared to patients with diabetes without macrovascular disease and healthy individuals. Study also indicates that PPHTg is a contributor to endothelial dysfunction. However, more studies are required to corroborate these findings.

Hypertriglyceridemia during hospitalization independently associates with mortality in patients with COVID-19.

BACKGROUND: Alteration in blood triglyceride levels have been found in patients with coronavirus disease 2019 (COVID-19). However, the association between hypertriglyceridemia and mortality in COVID-19 patients is unknown. OBJECTIVE: To investigate the association between alteration in triglyceride level and mortality in hospitalized COVID-19 patients. METHODS: We conducted a retrospective study of 600 hospitalized patients with COVID-19 diagnosis (ICD10CM:U07.1) and/or SARS-CoV-2 positive testing results between March 1, 2020 and December 21, 2020 at a tertiary academic medical center in Milwaukee, Wisconsin. De-identified data, including demographics, medical history, and blood triglyceride levels were collected and analyzed. Of the 600 patients, 109 patients died. The triglyceride value on admission was considered the baseline and the peak was defined as the highest level reported during the entire period of hospitalization. Hypertriglyceridemia was defined as greater than 150 mg/dl. Logistic regression analyses were performed to evaluate the association between hypertriglyceridemia and mortality. RESULTS: There was no significant difference in baseline triglyceride levels between non-survivors (n = 109) and survivors (n = 491) [Median 127 vs. 113 mg/dl, p = 0.213]. However, the non-survivors had significantly higher peak triglyceride levels during hospitalization [Median 179 vs. 134 mg/dl, p < 0.001]. Importantly, hypertriglyceridemia independently associated with mortality [odds ratio=2.3 (95% CI: 1.4-3.7, p = 0.001)], after adjusting for age, gender, obesity, history of hypertension and diabetes, high CRP, high leukocyte count and glucocorticoid treatment in a multivariable logistic regression model. CONCLUSIONS: Hypertriglyceridemia during hospitalization is independently associated with 2.3 times higher mortality in COVID-19 patients. Prospective studies are needed to independently validate this retrospective analysis.

Incidence, predictors and patterns of care of patients with very severe hypertriglyceridemia in Ontario, Canada: a population-based cohort study.

BACKGROUND: The incidence of severe (S-HTG) and very severe hypertriglyceridemia (VS-HTG) among Canadians is unknown. This study aimed to determine the incidence, characteristics, predictors and care patterns for individuals with VS-HTG. METHODS: Using linked administrative healthcare databases, a population-based cohort study of Ontario adults was conducted to determine incidence of new onset S-HTG (serum triglycerides (TG) > 10-20 mmol/L) and VS-HTG (TG > 20 mmol/L) between 2010 and 2015. Socio-demographic and clinical characteristics of those with VS-HTG were compared to those who had no measured TG value > 3 mmol/L. Univariable and multivariable logistic regression were used to determine predictors for VS-HTG. Healthcare patterns were evaluated for 2 years following first incidence of TG > 20 mmol/L. RESULTS: Incidence of S-HTG and VS-HTG in Ontario was 0.16 and 0.027% among 10,766,770 adults ≥18 years and 0.25 and 0.041% among 7,040,865 adults with at least one measured TG, respectively. Predictors of VS-HTG included younger age [odds ratios (OR) 0.64/decade, 95% confidence intervals (CI) 0.62-0.66], male sex (OR 3.83; 95% CI 3.5-4.1), diabetes (OR 5.38; 95% CI 4.93-5.88), hypertension (OR 1.69; 95% CI 1.54-1.86), chronic liver disease (OR 1.71; 95% CI 1.48-1.97), alcohol abuse (OR 2.47; 95% CI 1.90-3.19), obesity (OR 1.49; 95% CI 1.13-1.98), and chronic kidney disease (OR 1.39; 95% CI 1.19-1.63). CONCLUSION: The 5-year incidence of S-HTG and VS-HTG in Canadian adults was 1 in 400 and 1 in 2500, respectively. Males, those with diabetes, obese individuals and those with alcohol abuse are at highest risk for VS-HTG and may benefit from increased surveillance.

A rare case of diabetic ketoacidosis presenting with severe hypertriglyceridemia requiring plasmapheresis in an adult with type-2 diabetes mellitus: Case report.

INTRODUCTION: Severe hypertriglyceridemia (HTG) is a rare complication of insulin resistance. Its presentation with diabetic ketoacidosis (DKA) has been reported in a few cases, where most patients have type-1 diabetes mellitus (DM). Our case represents a unique presentation of DKA associated with severe HTG above 10,000 mg/dL in an adult with type-2 DM. PATIENT CONCERNS AND DIAGNOSIS: Case Report: A 51-year-old man with no prior illnesses presented to the emergency department with abdominal pain and nausea. He was found to have DKA with a blood glucose level of 337 mg/dL, pH of 7.17, beta-hydroxybutyrate of 7.93 mmol/L, and anion gap of 20 mmol/L. His triglyceride levels were >10,000 mg/dL. His serum was found to be lipemic. Computerized tomography scan of the abdomen demonstrated mild acute pancreatitis. Negative GAD65 antibodies supported the diagnosis of type-2 DM. INTERVENTIONS AND OUTCOMES: Endocrinology was consulted and one cycle of albumin-bound plasmapheresis was administered. This therapy significantly improved his HTG. DKA gradually resolved with insulin therapy as well. He was discharged home with endocrinology follow-up. CONCLUSION: This unique case highlights an uncommon but critical consequence of uncontrolled DM. It brings forth the possibility of severe HTG presenting as a complication of uncontrolled type-2 DM. Severe HTG commonly presents with acute pancreatitis, which can be debilitating if not managed promptly. Most patients with this presentation are managed with insulin infusion. The use of plasmapheresis for management of severe HTG has not been well studied. Our case supports the use of plasmapheresis as an effective and rapid treatment for severe HTG.

Association between Tumor Prognosis Marker Visfatin and Proinflammatory Cytokines in Hypertensive Patients.

Visfatin has been reported as a risk factor and a potential diagnostic marker in cancer. It is an adipokine, secreted by visceral fat and associated with the pathogenesis of arterial hypertension. We investigated the circulatory levels of visfatin in hypertensive patients with hypertriglyceridemia, which are the risk factors for various cancers and its association with proinflammatory cytokines. A total of 81 (male/female: 33/48) subjects with or without hypertension were enrolled for this study. Group 1 was normotensive, Group 2 hypertensive, and Group 3 with hypertension with hypertriglyceridemia. Data on anthropometric and biochemical data were recorded. Plasma visfatin levels were measured using an ELISA kit. The plasma inflammatory cytokines were estimated using a multiplex bead-based assay. The results revealed that the hypertension with hypertriglyceridemia group has the highest levels of visfatin compared to the hypertension and control groups with a significant difference (p < 0.001). Besides, circulatory visfatin showed the strongest possible correlation with proinflammatory cytokines among hypertensive patients with hypertriglyceridemia. We found a positive correlation between visfatin and diastolic blood pressure as well as high-density lipoproteins. In conclusion, the outcomes of the present study demonstrate that plasma visfatin levels were found to be elevated in hypertensive patients with hypertriglyceridemia and associated with proinflammatory cytokines. Since hypertension has been documented as the most common comorbidity observed in cancer patients, visfatin may be a novel potential therapeutic target for hypertension in cancer patients and survivors.

Soluble guanylate cyclase chronic stimulation effects on cardiovascular reactivity in cafeteria diet-induced rat model of metabolic syndrome.

Metabolic syndrome is linked to an increased risk of cardiovascular complications by a mechanism involving mainly decreased nitric oxide (NO) bioavailability and impaired NO-soluble guanylate cyclase (sGC)- cyclic guanosine monophosphate (cGMP) signalling (NO-sGC-cGMP). To further develop this scientific point, this study aimed to investigate the effects of long-term treatment with BAY 41-2272 (a sGC stimulator) on cardiovascular reactivity of spontaneously hypertensive rats (SHR) as a model of metabolic syndrome. SHR were randomly divided into 3 groups: control group, cafeteria diet (CD)-fed group and CD-fed group treated daily with BAY 41-2272 (5 mg/kg) by gastric gavage for 12 weeks. In vivo measurements of body weight, abdominal circumference, blood pressure and glucose tolerance test were performed. At the end of the feeding period, ex vivo cumulative concentration-response curves were performed on isolated perfused heart (isoproterenol (0.1 nM - 1 µM)) and thoracic aorta (phenylephrine (1 nM-10 µM), acetylcholine (1 nM-10 µM), and sodium nitroprusside (SNP) (0.1 nM-0.1 µM)). We showed that chronic CD feeding induced abdominal obesity, hypertriglyceridemia, glucose intolerance and exacerbated arterial hypertension in SHR. Compared to control group, CD-fed group showed a decrease in ß-adrenoceptor-induced cardiac inotropy, in coronary perfusion pressure and in aortic contraction to phenylephrine. While relaxing effects of acetylcholine and SNP were unchanged. BAY 41-2272 long-term treatment markedly prevented arterial hypertension development and glucose intolerance, enhanced the α1-adrenoceptor-induced vasoconstriction, and restored cardiac inotropy and coronary vasodilation. These findings suggest that BAY 41-2272 may be a potential novel drug for preventing metabolic and cardiovascular complications of metabolic syndrome.

Association of lipoprotein levels with sleep apnea: role of autonomic dysfunction.

Objectives. Although multiple mechanisms, including autonomic dysfunction, seem to link sleep-disordered breathing (SDB) with dyslipidemia in animal studies, the data in clinical studies are limited. The aim of this study was to explore the association of lipoprotein levels with SDB measures in healthy habitual snorers. We supposed that autonomic dysfunction is the linking mechanism.Methods. We enrolled 110 previously healthy subjects with complaints of habitual snoring. To assess SDB, polysomnography was performed. Blood samples for the analysis of total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein cholesterol (LDL), and triglycerides (TG) were obtained in a fasting condition after the polysomnography. Baroreflex sensitivity (BRS) was used to assess the autonomic dysfunction.Results. In stepwise multiple linear regression analysis, minimal nocturnal blood oxygen saturation (beta=-0.240, p=0.020) and neck circumference (beta=0.224, p=0.03) were the only significant contributors in model predicting TG. SDB measures were not identified as significant contributors in models predicting TC, LDL, and HDL. We failed to find any significant difference in BRS in SDB subjects when compared according to the presence or absence of hypercholesterolemia/ hypertriglyceridemia. In SDB subjects, the area under the curve in a receiver operating curve to predict hypercholesterolemia and hypertriglyceridemia by BRS was 0.468 (95% CI: 0.328-0.608) and 0.425 (95% CI: 0.304-0.546), respectively.Conclusions. Our results suggest that minimal nocturnal blood oxygen saturation is significant contributor in model predicting TG. No significant decrease in BRS was found in SDB subjects with hypercholesterolemia and hypertriglyceridemia. In SDB subjects, the role of autonomic dys-function in the development of dyslipidemia remains controversial.

Factores cardiometabólicos asociados y prevalencia de concentraciones bajas de colesterol HDL y de dislipidemia aterogénica. Estudio SIMETAP-DA / Related cardiometabolic factors and prevalence of low HDL-cholesterol levels and atherogenic dyslipidemia. SIMETAP-AD study

OBJETIVO: Determinar las prevalencias ajustadas por edad y sexo de concentraciones bajas de colesterol HDL (cHDL-bajo) y de dislipidemia aterogénica (DA), y valorar sus asociaciones con factores de riesgo cardiovascular, enfermedad renal crónica, enfermedades cardiovasculares y cardiometabólicas. MÉTODOS: Estudio observacional transversal de base poblacional realizado en atención primaria, con sujetos adultos seleccionados aleatoriamente. Se consideró DA si los pacientes tenían hipertrigliceridemia (triglicéridos≥150mg/dL) y cHDL-bajo (<40mg/dL [hombres],<50mg/dL [mujeres]). Se determinaron las tasas de prevalencia crudas y ajustadas por edad y sexo, y se realizó análisis univariado y multivariante para evaluar los factores cardiometabólicos relacionados. RESULTADOS: Población de estudio con 6.588 adultos (55,9% mujeres) con edad media de 55,1 (±17,5) años. Las medias de cHDL fueron 49,2 (±12,6) mg/dL en hombres y 59,2 (±14,7) mg/dL en mujeres. Las prevalencias crudas de cHDL-bajo y de DA fueron 30,8% (IC95%: 29,7-31,9), y 14,3% (IC95%: 13,5-15,2), respectivamente. Las prevalencias ajustadas de cHDL-bajo fueron 28% en hombres y 31% en mujeres, y de DA fueron 16,4% en hombres y 10,6% en mujeres. El 73% de la población con DA tenía riesgo cardiovascular alto o muy alto. Los factores independientes asociados con cHDL-bajo o con DA fueron diabetes, tabaquismo, obesidad abdominal y obesidad. Los principales factores asociados con cHDL-bajo y con DA fueron hipertrigliceridemia y diabetes, respectivamente. CONCLUSIONES: Casi un tercio de la población adulta presentaba cHDL-bajo y la mitad de ellos cumplía criterios de DA. Los factores cardiometabólicos se asociaban con cHDL-bajo y DA, destacando la hipertrigliceridemia con el cHDL-bajo, y la DM con la DA

AIM: To determine the crude and sex- and age-adjusted prevalence rates of atherogenic dyslipidemia (AD) and low HDL-cholesterol levels (low-HDLc), and to assess their associations with cardiovascular risk factors, chronic kidney disease, cardiovascular and cardiometabolic diseases. METHODS: Population-based cross-sectional study conducted in Primary Care, with randomly selected adult subjects. The AD was considered if the patients had hypertriglyceridemia (triglycerides≥150mg/dL) and low-HDLc (<40mg/dL [men];<50mg/dL [women]). Crude and sex- and age-adjusted prevalence rates were determined, and univariate and multivariate analysis were performed to assess related cardiometabolic factors. RESULTS: Study population with 6,588 adults (55.9% women) with mean age 55.1 (±17.5) years. The mean HDLc levels were 49.2 (±12.6) mg/dL in men and 59.2 (±14.7) mg/dL in women. The crude prevalence rates of low-HDLc and AD were 30.8% (95%CI: 29.7-31.9), and 14.3% (95%CI: 13.5-15.2), respectively. The adjusted prevalence rates of low-HDLc were 28.0% in men and 31.0% in women, and AD were 16.4% in men and 10.6% in women. Seventy-three percent of the population with AD had high or very high cardiovascular risk. The independent factors associated with low HDLc or with AD were diabetes, smoking, abdominal obesity, and obesity. The major factors associated with low HDLc and AD were hypertriglyceridemia and diabetes, respectively. CONCLUSIONS: Almost a third of the adult population had low HDL-C and half of them met AD criteria. Cardiometabolic factors were associated with low HDL-C and AD, highlighting hypertriglyceridemia with low HDLc, and DM with AD

Dysregulated SREBP1c/miR-153 signaling induced by hypertriglyceridemia worsens acute pancreatitis and delays tissue repair.

Severe acute pancreatitis (AP) is a life-threatening disease with up to 30% mortality. Therefore, prevention of AP aggravation and promotion of pancreatic regeneration are critical during the course and treatment of AP. Hypertriglyceridemia (HTG) is an established aggravating factor for AP that hinders pancreatic regeneration; however, its exact mechanism remains unclear. Using miRNA sequencing and further verification, we found that miRNA-153 (miR-153) was upregulated in the pancreas of HTG animal models and in the plasma of patients with HTG-AP. Increased miR-153 aggravated HTG-AP and delayed pancreatic repair via targeting TRAF3. Furthermore, miR-153 was transcriptionally suppressed by sterol regulatory element-binding transcription factor 1c (SREBP1c), which was suppressed by lipoprotein lipase malfunction-induced HTG. Overexpressing SREBP1c suppressed miR-153 expression, alleviated the severity of AP, and facilitated tissue regeneration in vivo. Finally, therapeutic administration of insulin also protected against HTG-AP via upregulating SREBP1c. Collectively, our results not only provide evidence that HTG leads to the development of more severe AP and hinders pancreatic regeneration via inducing persistent dysregulation of SREBP1c/miR-153 signaling, but also demonstrate that SREBP1c activators, including insulin, might be used to treat HTG-AP in patients.

Uncovering the role of apolipoprotein C-III in insulin resistance.

Apolipoprotein C-III (apoC-III) is a small protein that is predominantly synthesized in the liver and mainly resides at the surface of triglyceride-rich lipoproteins. Its expression is upregulated by glucose and reduced by insulin, with enhanced apoC-III promoting hypertriglyceridemia and inflammation in vascular cells. The protein is also elevated in patients with diabetes, suggesting that enhanced apoC-III levels might contribute to the development of type 2 diabetes mellitus. The present review focuses on the key mechanisms by which apoC-III could promote type 2 diabetes mellitus, including exacerbation of insulin resistance in skeletal muscle, activation of ß-cell apoptosis, promotion of weight gain through its effects on white adipose tissue and hypothalamus, and attenuation of the beneficial effects of high-density lipoproteins on glucose metabolism. Therapeutic strategies aimed at reducing apoC-III levels may not only reduce hypertriglyceridemia but also might improve insulin resistance, thus delaying the development of type 2 diabetes mellitus.

DGAT1 mutations leading to delayed chronic diarrhoea: a case report.

BACKGROUND: Early-onset chronic diarrhoea often indicates a congenital disorder. Mutation in diacylglycerol o-acyltransferase 1 (DGAT1) has recently been linked to early-onset chronic diarrhoea. To date, only a few cases of DGAT1 deficiency have been reported. Diarrhoea in those cases was severe and developed in the neonatal period or within 2 months after birth. CASE PRESENTATION: Here, we report a female patient with DGAT1 mutations with delayed-onset chronic diarrhoea. The patient had vomiting, hypoalbuminemia, hypertriglyceridemia, and failure to thrive at early infancy. Her intractable chronic diarrhoea occurred until she was 8 months of age. A compound heterozygous DGAT1 mutation was found in the patient, which was first found in the Chinese population. Her symptoms and nutrition status improved after nutritional therapy, including a fat restriction diet. CONCLUSIONS: This case expanded our knowledge of the clinical features of patients with DGAT1 mutations. Intractable diarrhoea with delayed onset could also be a congenital disorder.

Association of 25-hydroxyvitamin D levels and metabolic syndrome in Thai postmenopausal women.

BACKGROUND AND AIMS: Low serum 25-hydroxyvitamin D [25(OH)D] levels have been reported to be associated with metabolic syndrome (MetS). In this study, we aimed to investigate the association between serum 25(OH)D levels and MetS in Thai postmenopausal women. METHODS: A total of 340 postmenopausal women were enrolled in the study. The concentration of 25(OH)D, lipid profiles, fasting blood glucose (FBG) levels, blood pressure, and demographic and anthropometric parameters were measured. Subjects were divided into the hypovitaminosis D and vitamin D sufficiency groups. The association of serum 25(OH)D levels with MetS in postmenopausal women was analyzed using multivariate regression analysis. RESULTS: Waist circumference, total cholesterol levels, and triglyceride levels were significantly higher in hypovitaminosis D than in vitamin D sufficiency (p < 0.05). The prevalence of MetS, central obesity, and hypertriglyceridemia in hypovitaminosis D was significantly higher than in vitamin D sufficiency (p < 0.05). In the multivariable logistic regression model, hypovitaminosis D was associated with MetS (OR 1.85; 95% CI 1.12-3.04, p = 0.015), central obesity (OR 2.41; 95% CI 1.20-4.85, p = 0.014), and hypertriglyceridemia (OR 1.91; 95% CI 1.12-3.26, p = 0.018) compared with vitamin D sufficiency after adjusting for covariates. Serum vitamin D concentrations were significantly lower in the MetS group than in the non-MetS group (p = 0.016) and decreased with an increasing number of MetS components (p for trend = 0.034). CONCLUSIONS: Hypovitaminosis D was associated with an increased risk of MetS, central obesity, and hypertriglyceridemia in Thai postmenopausal women.

The Impact of Dietary Glycemic Index and Glycemic Load on Postprandial Lipid Kinetics, Dyslipidemia and Cardiovascular Risk.

Many recent studies have acknowledged postprandial hypetriglyceridemia as a distinct risk factor for cardiovascular disease. This dysmetabolic state is the result of the hepatic overproduction of very low-density lipoproteins (VLDLs) and intestinal secretion of chylomicrons (CMs), which leads to highly atherogenic particles and endothelial inflammation. Postprandial lipid metabolism does not only depend on consumed fat but also on the other classes of nutrients that a meal contains. Various mechanisms through which carbohydrates exacerbate lipidemia have been identified, especially for fructose, which stimulates de novo lipogenesis. Glycemic index and glycemic load, despite their intrinsic limitations, have been used as markers of the postprandial glucose and insulin response, and their association with metabolic health and cardiovascular events has been extensively studied with contradictory results. This review aims to discuss the importance and pathogenesis of postprandial hypertriglyceridemia and its association with cardiovascular disease. Then, we describe the mechanisms through which carbohydrates influence lipidemia and, through a brief presentation of the available clinical studies on glycemic index/glycemic load, we discuss the association of these indices with atherogenic dyslipidemia and address possible concerns and implications for everyday practice.

Associations between high triglycerides and arterial stiffness in a population-based sample: Kardiovize Brno 2030 study.

BACKGROUND: The term arterial stiffness (ArSt) describes structural changes in arterial wall related to the loss of elasticity and is known as an independent predictor of cardiovascular diseases (CVD). The evidence relating to ArSt and triglycerides (TG) shows contradictory results. This paper means to survey the association between high TG and ArSt, utilizing the cardio-ankle vascular index (CAVI). METHODS: Subjects aged between 25 and 64 years from a random population-based sample were evaluated between 2013 and 2016. Data from questionnaires, blood pressure, anthropometric measures, and blood samples were collected and analyzed. CAVI was measured using VaSera VS-1500 N devise. Subjects with a history of CVD or chronic renal disease were excluded. RESULTS: One thousand nine hundred thirty-four participants, 44.7% of males, were included. The median age was 48 (Interquartile Range [IQR] 19) years, TG levels were 1.05 (0.793) mmol/L, and CAVI 7.24 (1.43) points. Prevalence of high CAVI was 10.0% (14.5% in males and 6.4% in females; P <  0.001) and prevalence of hypertriglyceridemia was 20.2% (29.2% in males and 13% in females, P <  0.001). The correlation between TG and CAVI was 0.136 (P <  0.001). High CAVI values were more prevalent among participants with metabolic syndrome (MetS), high blood pressure, dysglycemia, abdominal obesity, high LDL-cholesterol (LDL-c), and high total cholesterol. Using binary regression analysis, high TG were associated with high CAVI, even after adjustment for other MetS components, age, gender, smoking status, LDL-c, and statin treatment (ß = 0.474, OR = 1.607, 95% CI = 1.063-2.429, P = 0.024). CONCLUSION: TG levels were correlated with ArSt, measured as CAVI. High TG was associated with high CAVI independent of multiple cardiometabolic risk factors. Awareness of the risks and targeted treatment of hypertriglyceridemia could further benefit in reducing the prevalence of CVD and events.

Acute effects of oral triglyceride load on dynamic changes in peripheral endothelial function in heart failure patients with reduced ejection fraction and healthy controls.

BACHGROUND: Postprandial hyperlipaemia impairs endothelial function, possibly via oxidative-stress-mediated mechanisms. The aim of this study was to evaluate the acute effects of an oral triglyceride load (OTGL) on peripheral endothelial function in heart failure patients with reduced ejection fraction (HFrEF) compared to healthy controls. DESIGN: Prospective cross-sectional. METHODS: We enrolled 47 patients with HFrEF and 20 healthy controls. Peripheral endothelial function was assessed with EndoPAT2000 technology using a reactive hyperaemia index (RHI) and pulse wave amplitude (PWA) at baseline (after 8-h overnight fasting) as well as 1, 2, 3 and 4-h post-OTGL consumption (250-ml cream drink). Pulse wave amplitude index (PWAI) was calculated as a ratio of PWA at each time point to the baseline PWA. RESULTS: RHI at baseline was lower in HFrEF patients compared to controls (1.7 ± 0.3 and 2.3 ± 0.6, respectively; P = 0.001). The OTGL accounted for a physiologic increase in PWA in healthy controls (p = 0.01), but this change was not observed in HFrEF patients. After 4 h, vasodilator response was significantly increased in healthy controls but not patients with HFrEF (2.3 ± 1.3 vs. 1.3 ± 0.8 respectively, P < 0.05). CONCLUSIONS: The main finding of this study was the impaired postprandial dynamic changes in peripheral endothelial function in patients with HFrEF compared to healthy controls. A high-fat load that caused acute hypertriglyceridaemia significantly increased resting blood flow and peak flow at reactive hyperaemia in healthy subjects. By contrast, patients with HFrEF exhibited impaired dynamic changes in peripheral endothelial function after oral triglyceride load.

The Efficacy of Intravenous Insulin Infusion in the Management of Hypertriglyceridemia-Induced Pancreatitis in a Rural Community Hospital.

A 28-year-old female presented to the emergency room with epigastric pain, nausea, and vomiting; her lipase was elevated, and computed tomography of abdomen showed evidence of acute pancreatitis. Her past medical history was significant for poorly controlled insulin requiring type 2 diabetes mellitus and 2 previous admissions for hypertriglyceridemia-induced pancreatitis. Due to the severity of her pancreatitis presentation, she was admitted to the intensive care unit. She received aggressive intravenous fluid hydration and was started on an insulin drip. Apheresis was strongly considered given the degree of her hypertriglyceridemia (11 602 mg/dL), but there was no timely access to this treatment option. She, however, significantly improved with insulin therapy alone. Her triglyceride levels decreased rather quickly to 4783 mg/dL within 24 hours and by the fourth day of admission were comfortably <1000 mg/dL with insulin infusion along with clinical improvement. She was discharged on niacin and insulin therapy along with her home medications of statin and fenofibrate.

Fish oil reduces subclinical inflammation, insulin resistance, and atherogenic factors in overweight/obese type 2 diabetes mellitus patients: A pre-post pilot study.

OBJECTIVE: Insulin resistance-associated obesity and type 2 diabetes mellitus (T2DM) are commonly accompanied with metabolic lipid abnormalities and are characterized by hypertriglyceridemia and low HDL-c levels (atherogenic index plasma, AIP). The primary molecular mechanism that is known to cause insulin resistance is chronic low-grade inflammation. Considering that omega-3 fatty acid reduces subclinical inflammation, we hypothesized that fish oil could affect insulin resistance and AIP. Therefore, the present study evaluated the effects of fish oil supplementation on the inflammatory, insulin resistance, and atherogenic factors in overweight/obese T2DM patients. RESEARCH DESIGNS AND METHODS: In this study, we recruited 32 overweight and/or obese patients diagnosed with T2DM for over one year and who exhibited hypertriglyceridemia. These patients received fish oil supplementation (4.0 g/day) for eight weeks. Anthropometric and body composition measurements were obtained. In addition, blood samples were collected before and after omega-3 supplementation for the evaluation of lipid profile, glycemia, insulin, and inflammation. RESULTS: As expected, patients showed reduction in the TNFα, IL-1ß, and Il-6 levels after fish oil supplementation and showed improved insulin sensitivity (HOMA-IR) without observed alterations in anthropometric and body composition. These observations were followed by reduction in the levels of triglycerides and non-esterified fatty acids, increase in HDL cholesterol levels, and a significant reduction in triglycerides/HDL-c ratio, and total cholesterol/HDL-c ratio. CONCLUSION: Fish oil supplementation is effective in reducing the levels of proinflammatory cytokines, improving insulin resistance, and reducing atherogenic factors in overweight/obese and T2DM patients independent of weight loss.