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Fasting chylomicronaemia appears in type V (multifactorial chylomicronaemia syndrome, MCS), and in type I (familial chylomicronaemia syndrome, FCS). MCS needs to be treated as in any general hypertriglyceridaemia low-calorie diet, avoid sugar and alcohol, reduce body weight, control of diabetes and, in some cases, common lipid lowering-drugs, such as fibrates or omega-3 fatty acids. For type I HLP, FCS, patients should adhere to a strict very low fat diet, usually less than 15-20 g per day. In spite of this, many patients with FCS suffer from recurrent abdominal pain and/or acute pancreatitis. Volanesorsen, an antisense oligonucleotide against apolipoprotein C-III, is the only drug approved to control the disease. As shown in the APPROACH study, the administration of volanesorsen at a weekly dose of 285 mg induced at three month a reduction of triglycerides of 77% (primary end-point) and a reduction of 1712 mg/dL from the baseline. Among patient receiving volanesorsen, 77% reached a fasting triglyceride value below 750 mg/dL. The most frequent side effects were a skin reaction at injection site and low platelet levels, which should be monitored.Based on the most recent scientific evidence, in this chapter we describe the relation of levels of triglycerides and risk of cardiovascular diseases. Particularly, we describe the prevalence of hypertriglyceridemia based on studies published at national and international reports; the relation between hypertriglyceridemia and cardiovascular diseases according to results of cohort studies; and finally, we describe the most recent evidence from clinical trials, meta-analysis and systematic reviews that have shown data on the efficacy of lowering triglyceride levels and reducing cardiovascular diseases.The atherogenic role of triglycerides (TG) as an independent cardiovascular risk factor has been discussed for many years, largely because hypertriglyceridaemia (HTG) is a complex metabolic entity of multiple aetiology involving processes of diverse nature. In this chapter, a discussion will be presented on the current recommendations for the management of mild-moderate hypertriglyceridaemia (150-880mg/dL). The aim of the interventions used is to decrease the LDL-cholesterol (c-LDL) and control the HTG. This entails reducing apoprotein B (ApoB) levels, the number of remaining TG-rich lipoproteins (LRP), non-HDL-cholesterol (c-non-HDL), and increasing HDL-cholesterol (c-HDL). The management strategy includes healthy lifestyle recommendations, and subsequent use of lipid-lowering drugs, including statins, fibrates, n-3 fatty acids and PCSK9 inhibitors.Hypolipoproteinemias are characterized by a decrease in the plasma concentration of lipoproteins. Within them, we find two groups hypobetalipoproteinemias (HBL), due to a decrease in the plasma concentration of lipoproteins containing apolipoprotein B, and hypoalphalipoproteinemias. Hypolipoproteinemias can be classified according to their origin, into primary and secondary. Primary HBLs are rare entities produced by mutations in different genes. So far, more than 140 mutations have been identified in the APOB, PCSK9, ANGPTL3, MTTP, and SAR1 genes. Early diagnosis and treatment are essential to avoid the development of serious complications. In this review we address the diagnosis and treatment of HBL, especially those in which there is hypotriglyceridemia.The accumulation of chylomicrons in plasma beyond the postprandial period is a pathological event secondary to the partial or complete lack of activity of lipoprotein lipase that can lead to recurrent episodes of abdominal pain and acute pancreatitis. This article reviews the pathophysiology of this syndrome and the differential characteristics depending on whether it is due to congenital monogenic causes or acquired on a polygenic basis in which multiple factors may inluence.Dysbetalipoproteinaemia (or type III hyperlipoproteinaemia) is a severe mixed hyperlipidaemia resulting from the accumulation of remnant chylomicron and VLDL particles in plasma, also called β-VLDL. It is caused by a defect in the recognition by hepatic LDL and lipoprotein receptor-related protein (LRP) of β-VLDL. Mutations in the APOE gene, especially in subjects homozygous for the ɛ2/ɛ2 allele, are responsible for this lack of receptor recognition. Dysbetalipoproteinaemia represents 2-5% of the mixed dyslipidaemias seen in Lipid Units, is highly atherogenic and predisposes to diffuse atheromatosis, either coronary, peripheral vascular, or carotid, so early diagnosis and treatment is necessary. The presence of hypertriglyceridaemia, with non-HDL cholesterol/apolipoprotein B ratios>1.43 (in mg/dL) followed by APOE genotyping is the method of choice in the diagnosis of dysbetalipoproteinaemia. It is a dyslipidaemia that responds well to hygienic-dietary treatment, although the combination of statin and fenofibrate is often necessary to achieve optimal control.Familial combined hyperlipidaemia (FCH) is the most prevalent form of familial hyperlipidaemia with a multigenic origin and a complex pattern of inheritance. In this respect, FCH is an oligogenic primary lipid disorder due to interaction of genetic variants and mutations with environmental factors. Patients with FCH are at increased risk of cardiovascular disease and often have other associated metabolic conditions. Despite its relevance in cardiovascular prevention, FCH is frequently underdiagnosed and very often undertreated. In this review, emphasis is placed on the most recent advances in FCH, in order to increase its awareness and ultimately contribute to improving its clinical control.For decades, familial hypertriglyceridemia (HTG) has been considered a specific entity characterized by an increase in VLDL particles and an autosomal dominant inheritance pattern. In the genomics era, it has been proven that familial HTG, although it could be grouped in families, had a polygenic inheritance in which the phenotype would be determined by concomitant environmental factors. Hence its inclusion in the group of polygenic HTGs. Clinically, they are characterized by moderate HTG, with the consequent increase in cardiovascular risk, and in rare cases, by severe HTG with risk of acute pancreatitis. Treatment will be based on controlling environmental factors, implementing hygienic-dietetic measures and sometimes drugs, to reduce cardiovascular risk in moderate HTGs and acute pancreatitis risk in severe HTGs.Secondary hypertriglyceridemia (HTG) are the most common cause of excess triglyceride rich particles in plasma. Faced with HTG, the first thing to do is rule out if there is a secondary cause since it can interact with genetic susceptibility and further aggravate the HTG. The most common causes are diet with high fat and high glycemic index, obesity, diabetes mellitus, alcohol consumption, renal disease like nephrotic syndrome, hepatic disorders and medications. The most important medications that can influence in HTG are oestrogen, isotretinoin, immunosuppressant therapy, L-asparaginase and with less effect thiazides, beta blockers, atypical antipsychotics and glucocorticoids. Other causes less frequent are endocrinological diseases such as Cushing's syndrome, acromegaly, hypothyroidism; pregnancy, lipodystrophies and autoimmune diseases. Lastly, the identifications and treatment or correction of secondary causes is a corner stone in the treatment of this disease.Hypertriglyceridaemia has been associated with cardiovascular disease risk in humans for several decades. However, only recently, data from basic research, as well as from genetic and observational studies, have suggested triglyceride-rich lipoproteins (TRLs) as causal factors for atherosclerotic cardiovascular disease. Novel findings highlighting the relevance of TRL-derived lipolytic products (remnant lipoprotein particles "RLPs"), rather than plasma triglycerides or TRL themselves, as the true mediators in atherosclerosis, have contributed to explain a causal relationship through a number of direct and indirect mechanisms. Thus, experimental studies in animal models and in vitro cell culture methods reveal that RLPs, having sizes below 70-80nm, enter the arterial wall and accumulate within the sub-endothelial space. They then become involved in the cholesterol deposition of cholesterol in the intima in addition to several pro-inflammatory and pro-apoptotic pathways. In this review, a summary is presented of current understanding of the pathophysiological mechanisms by which TRLs and their lipolytic derived RLP induce the formation and progression of atherosclerotic lesions, and actively contribute to cardiovascular disease.Diagnosis and treatment of triglyceride metabolism disorders from pathophysiology to clinical practice. Hypertriglyceridaemia (HTG) affects 15%-20% of the world's population, and is frequently discovered as an incidental finding in a laboratory test. Selleck Ferrostatin-1 Disorders of triglyceride (TG) metabolism have a complex genetic basis. New genetic tools that allow a more precise approach to the disorders have made it possible to redefine and classify HTG into two groups monogenic HTG (TG>10 mmol/L) and polygenic HTG (2 mmol/L less then TG less then 10 mmol/L) with a milder phenotype, but with a clear genetic influence. In approximately 50% of patients with severe HTG a genetic cause has not yet been found. In addition to the inclusion of ever more genes in studies, statistical models are now also being examined that consider complex gene-environment interactions that could explain why the presence of a set of apparently benign variants may cause HTG in the presence of a triggering factor such as adiposity. Knowledge of the genetic nature of HTG has also helped identify targets for pharmacological treatments, thus avoiding a strict diet with a fat content of less than 20%, which is difficult to maintain. link2 Accurate diagnosis of these disorders is essential for correct treatment according to the inherent risk of each HTG, since, as has been shown in multiple studies, high fasting and postprandial TG concentrations are an independent risk factor for cardiovascular disease.Triglycerides (TG) are the most important molecules for the energy reserve of our body. After their hepatic or intestinal synthesis from fatty acids, they are carried by chylomicrons (QM (intestinal origin) or VLDL (hepatic origin) in plasma. Their catabolism is determined by the action of the lipoprotein lipase protein complex (LPL) and the hepatic receptors (RLDL and LRP-1) are responsible for their clearance are. Changes in the production or catabolism leads to hypertriglyceridaemia (HTG). The HTG are classified according to severity as, mild-moderate (150-885mg/dl), severe (>885mg/dl), or very severe (>1770mg/dl). link3 They can be primary and secondary depending on origin. In the main primary form is highlighted Familial Chylomicronaemia Syndrome (CFS), a very severe form due to mutations in the LPL gene or associated proteins. Most HTG are due to a combination of genetic and environmental predisposing factors.Background We examined links among face visibility on dating-profile pictures, self-perceived attractiveness, condom use self-efficacy, and unprotected receptive anal intercourse (URAI) in 223 young men who have sex with men (YMSM; ages 18-24 years) using online dating applications (e.g. Grindr).

Participants reported their face visibility on their main dating-profile picture, attractiveness, condom use self-efficacy, and frequency of URAI in the past 3 months. Number of casual sex partners and pre-exposure prophylaxis (PrEP) use were statistically controlled in all analyses.

Using a mediated moderation model, we found that a significant attractiveness-by-face-visibility interaction for URAI was fully mediated by condom use self-efficacy. Specifically, lower face visibility on profile pictures related to lower condom use self-efficacy, which in turn related to higher URAI, but only among highly attractive YMSM.

Our findings suggest that attractive YMSM who show less-visible faces on their dating profiles could be at particularly high risk for sexually transmissible infections.