Hypertriglyceridemia is the presence of high amounts of triglycerides in the blood. Triglycerides are the most abundant fatty molecule in most organisms. Hypertriglyceridemia occurs in various physiologic conditions and in various diseases, and high triglyceride levels are associated with atherosclerosis, even in the absence of hypercholesterolemia (high cholesterol levels) and predispose to cardiovascular disease.
Hypertriglyceridemia itself is usually symptomless, although high levels may be associated with skin lesions known as xanthomas.[1]
Signs and symptoms
Most people with elevated triglycerides experience no symptoms. Some forms of primary hypertriglyceridemia can lead to specific symptoms: both familial chylomicronemia and primary mixed hyperlipidemia include skin symptoms (eruptive xanthoma), eye abnormalities (lipaemia retinalis), hepatosplenomegaly (enlargement of the liver and spleen), and neurological symptoms. Some experience attacks of abdominal pain that may be mild episodes of pancreatitis. Eruptive xanthomas are 2–5 mm papules, often with a red ring around them, that occur in clusters on the skin of the trunk, buttocks and extremities.[2]Familial dysbetalipoproteinemia causes larger, tuberous xanthomas; these are red or orange and occur on the elbows and knees. Palmar crease xanthomas may also occur.[1][2]
The diagnosis is made on blood tests, often performed as part of screening. Once diagnosed, other blood tests are usually required to determine whether the raised triglyceride level is caused by other underlying disorders ("secondary hypertriglyceridemia") or whether no such underlying cause exists ("primary hypertriglyceridemia"). There is a hereditary predisposition to both primary and secondary hypertriglyceridemia.[1]
Triglyceride, which cause hypertriglyceridemia at high level
Acute pancreatitis may occur in people whose triglyceride levels are above 1000 mg/dL (11.3 mmol/L).[1][2][3] Hypertriglyceridemia is associated with 1–4% of all cases of pancreatitis. The symptoms are similar to pancreatitis secondary to other causes, although the presence of xanthomas or risk factors for hypertriglyceridemia may offer clues.[3]
The diagnosis is made on blood tests, often performed as part of screening. The normal triglyceride level is less than 150 mg/dL (1.7 mmol/L).[1][5] Once diagnosed, other blood tests are usually required to determine whether the raised triglyceride level is caused by other underlying disorders ("secondary hypertriglyceridemia") or whether no such underlying cause exists ("primary hypertriglyceridaemia"). There is a hereditary predisposition to both primary and secondary hypertriglyceridemia.[1]
Lifestyle changes including weight loss, exercise and dietary modification may improve hypertriglyceridemia.[12][1][13][14] This may include dietary changes such as restriction of fat and carbohydrates (specifically fructose[13][15] and sugar-sweetened beverages[1]) and increased consumption of omega-3 fatty acids from algae, nuts, and seeds.[16][17]
The decision to treat hypertriglyceridemia with medication depends on the levels and on the presence of other risk factors for cardiovascular disease. Very high levels that would increase the risk of pancreatitis is treated with a drug from the fibrate class. Niacin and omega-3 fatty acids as well as drugs from the statin class may be used in conjunction, with statins being the main drug treatment for moderate hypertriglyceridemia where reduction of cardiovascular risk is required.[18][1] Medications are recommended in those with high levels of triglycerides that are not corrected with lifestyle modifications, with fibrates being recommended first.[1][19][20]Epanova (omega-3-carboxylic acids) is another prescription drug used to treat very high levels of blood triglycerides.[21]
Epidemiology
As of 2006, the prevalence of hypertriglyceridemia in the United States was 30%.[5]
Research
Analysis of the genes in depression and anxiety showed those linked solely to depression were also linked to hypertriglyceridemia.[22]
^ abTsuang W, Navaneethan U, Ruiz L, Palascak JB, Gelrud A (April 2009). "Hypertriglyceridemic pancreatitis: presentation and management". The American Journal of Gastroenterology. 104 (4): 984–991. doi:10.1038/ajg.2009.27. PMID19293788. S2CID24193233.
^Garg A, Grundy SM, Unger RH (October 1992). "Comparison of effects of high and low carbohydrate diets on plasma lipoproteins and insulin sensitivity in patients with mild NIDDM". Diabetes. 41 (10): 1278–1285. doi:10.2337/diabetes.41.10.1278. PMID1397701.
^Chou R, Dana T, Blazina I, Daeges M, Bougatsos C, Jeanne TL (October 2016). "Screening for Dyslipidemia in Younger Adults: A Systematic Review for the U.S. Preventive Services Task Force". Annals of Internal Medicine. 165 (8): 560–564. doi:10.7326/M16-0946. PMID27538032. S2CID20592431.
^Gill JM, Herd SL, Tsetsonis NV, Hardman AE (February 2002). "Are the reductions in triacylglycerol and insulin levels after exercise related?". Clinical Science. 102 (2): 223–231. doi:10.1042/cs20010204. PMID11834142.
^European Association for Cardiovascular Prevention & Rehabilitation; Reiner, Zeljko; Catapano, Alberico L.; De Backer, Guy; Graham, Ian; Taskinen, Marja-Riitta; Wiklund, Olov; Agewall, Stefan; Alegria, Eduardo; Chapman, M. John; Durrington, Paul; Erdine, Serap; Halcox, Julian; Hobbs, Richard; Kjekshus, John (July 2011). "ESC/EAS Guidelines for the management of dyslipidaemias: the Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS)". European Heart Journal. 32 (14): 1769–1818. doi:10.1093/eurheartj/ehr158. ISSN1522-9645. PMID21712404.
^Davidson MH, Cannon CP, Armani AM (28 January 2008). "Pharmacological Therapy for Cardiovascular Disease". In Davidson MH, Toth PP, Maki KC (eds.). Therapeutic Lipidology. Contemporary Cardiology. Totowa, New Jersey: Humana Press, Inc. pp. 141–142. ISBN978-1-58829-551-4.
^Abourbih S, Filion KB, Joseph L, Schiffrin EL, Rinfret S, Poirier P, et al. (October 2009). "Effect of fibrates on lipid profiles and cardiovascular outcomes: a systematic review". The American Journal of Medicine. 122 (10): 962.e1–962.e8. doi:10.1016/j.amjmed.2009.03.030. PMID19698935.
^Jun M, Foote C, Lv J, Neal B, Patel A, Nicholls SJ, et al. (May 2010). "Effects of fibrates on cardiovascular outcomes: a systematic review and meta-analysis". Lancet. 375 (9729): 1875–1884. doi:10.1016/S0140-6736(10)60656-3. PMID20462635. S2CID15570639.
^Blair HA, Dhillon S (October 2014). "Omega-3 carboxylic acids (Epanova): a review of its use in patients with severe hypertriglyceridemia". American Journal of Cardiovascular Drugs. 14 (5): 393–400. doi:10.1007/s40256-014-0090-3. PMID25234378. S2CID23706094.
^Thorp JG, Campos AI, Grotzinger AD, Gerring ZF, An J, Ong JS, et al. (October 2021). "Symptom-level modelling unravels the shared genetic architecture of anxiety and depression". Nature Human Behaviour. 5 (10): 1432–1442. doi:10.1038/s41562-021-01094-9. PMID33859377. S2CID233259875.