Hypertriglyceridemia Explained

Hypertriglyceridemia
Synonyms:Elevated levels of triglycerides
Field:Endocrinology
Complications:Heart disease, pancreatitis
Risks:Metabolic dysfunction-associated steatotic liver disease, atherosclerosis, alcoholism, metabolic syndrome
Differential:Hyperlipidemia, atheroma, hypercholesterolemia, hypercalcemia

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.

Chronically elevated serum triglyceride levels are a component of metabolic syndrome and metabolic dysfunction-associated steatotic liver disease, both of which typically involve obesity and contribute significantly to cardiovascular mortality in industrialised countries as of 2021. Extreme triglyceride levels also increase the risk of acute pancreatitis.

Hypertriglyceridemia itself is usually symptomless, although high levels may be associated with skin lesions known as xanthomas.

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 (lipemia 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.[1] Familial dysbetalipoproteinemia causes larger, tuberous xanthomas; these are red or orange and occur on the elbows and knees. Palmar crease xanthomas may also occur.[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.[2]

Acute pancreatitis may occur in people whose triglyceride levels are above 1000 mg/dL (11.3 mmol/L).[2] [1] [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]

Causes

Diagnosis

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).[2] [6] 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.[2]

Guidelines

The National Cholesterol Education Program has set guidelines for triglyceride levels:[7] [8]

LevelInterpretation
(mg/dL)(mmol/L)
< 150< 1.70Normal range – low risk
150–1991.70–2.25Slightly above normal
200–4992.26–5.65Some risk
500 or higher> 5.65Very high – high risk
These levels are tested after fasting 8 to 12 hours. Triglyceride levels remain temporarily higher for a period after eating.

The AHA recommends an optimal triglyceride level of 100mg/dL (1.1mmol/L) or lower to improve heart health.[9]

Screening

In 2016, the United States Preventive Services Task Force concluded that testing the general population under the age of 40 without symptoms is of unclear benefit.[10] [11]

Treatment

Lifestyle changes including weight loss, exercise and dietary modification may improve hypertriglyceridemia.[12] [2] [13] [14] This may include dietary changes such as restriction of fat and carbohydrates (specifically fructose[13] [15] and sugar-sweetened beverages[16]) and increased consumption of omega-3 fatty acids from algae, nuts, and seeds.[17] [18]

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.[2] Medications are recommended in those with high levels of triglycerides that are not corrected with lifestyle modifications, with fibrates being recommended first.[2] [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%.[6]

Research

Analysis of the genes in depression and anxiety showed those linked solely to depression were also linked to hypertriglyceridemia.[22]

Etymology

The word hypertriglyceridemia uses combining forms of hyper- + triglyceride + -emia, thus corresponding to "high triglyceride levels in the blood" or "too many triglycerides in the blood".

See also

External links

Notes and References

  1. Yuan G, Al-Shali KZ, Hegele RA . Hypertriglyceridemia: its etiology, effects and treatment . CMAJ . 176 . 8 . 1113–1120 . April 2007 . 17420495 . 1839776 . 10.1503/cmaj.060963 .
  2. Berglund L, Brunzell JD, Goldberg AC, Goldberg IJ, Sacks F, Murad MH, Stalenhoef AF . Evaluation and treatment of hypertriglyceridemia: an Endocrine Society clinical practice guideline . The Journal of Clinical Endocrinology and Metabolism . 97 . 9 . 2969–2989 . September 2012 . 22962670 . 3431581 . 10.1210/jc.2011-3213 .
  3. Tsuang W, Navaneethan U, Ruiz L, Palascak JB, Gelrud A . Hypertriglyceridemic pancreatitis: presentation and management . The American Journal of Gastroenterology . 104 . 4 . 984–991 . April 2009 . 19293788 . 10.1038/ajg.2009.27 . 24193233 .
  4. Garg A, Grundy SM, Unger RH . 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 . October 1992 . 1397701 . 10.2337/diabetes.41.10.1278 .
  5. Beigneux AP, Miyashita K, Ploug M, Blom DJ, Ai M, Linton MF, Khovidhunkit W, Dufour R, Garg A, McMahon MA, Pullinger CR, Sandoval NP, Hu X, Allan CM, Larsson M, Machida T, Murakami M, Reue K, Tontonoz P, Goldberg IJ, Moulin P, Charrière S, Fong LG, Nakajima K, Young SG . 6 . Autoantibodies against GPIHBP1 as a Cause of Hypertriglyceridemia . The New England Journal of Medicine . 376 . 17 . 1647–1658 . April 2017 . 28402248 . 5555413 . 10.1056/NEJMoa1611930 .
  6. Pejic RN, Lee DT . Hypertriglyceridemia . Journal of the American Board of Family Medicine . 19 . 3 . 310–316 . May–Jun 2006 . 16672684 . 10.3122/jabfm.19.3.310 . free .
  7. Web site: Triglycerides . https://web.archive.org/web/20140228062757/http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/Triglycerides_UCM_306029_Article.jsp . 28 February 2014 . 2015-04-23 . MedlinePlus.
  8. Crawford, H., Micheal. Current Diagnosis & Treatment Cardiology. 3rd ed. McGraw-Hill Medical, 2009. p19
  9. Web site: 28 September 2012 . What's considered normal? . Triglycerides: Why do they matter? . Mayo Clinic.
  10. Chou R, Dana T, Blazina I, Daeges M, Bougatsos C, Jeanne TL . 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 . October 2016 . 27538032 . 10.7326/M16-0946 . 20592431 .
  11. Bibbins-Domingo K, Grossman DC, Curry SJ, Davidson KW, Epling JW, García FA, Gillman MW, Kemper AR, Krist AH, Kurth AE, Landefeld CS, LeFevre M, Mangione CM, Owens DK, Phillips WR, Phipps MG, Pignone MP, Siu AL . 6 . Screening for Lipid Disorders in Children and Adolescents: US Preventive Services Task Force Recommendation Statement . JAMA . 316 . 6 . 625–633 . August 2016 . 27532917 . 10.1001/jama.2016.9852 . free .
  12. Koneru SC . 2022-03-01 . Fellow's voice: Hypertriglyceridemia: Understanding the current guideline . American Journal of Preventive Cardiology . en . 9 . 100322 . 10.1016/j.ajpc.2022.100322 . 35243465 . 2666-6677 . 8885448.
  13. Nordestgaard BG, Varbo A . Triglycerides and cardiovascular disease . Lancet . 384 . 9943 . 626–635 . August 2014 . 25131982 . 10.1016/S0140-6736(14)61177-6 . 33149001 .
  14. Gill JM, Herd SL, Tsetsonis NV, Hardman AE . Are the reductions in triacylglycerol and insulin levels after exercise related? . Clinical Science . 102 . 2 . 223–231 . February 2002 . 11834142 . 10.1042/cs20010204 .
  15. 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 . 10.1093/eurheartj/ehr158 . 1522-9645 . 21712404.
  16. Berglund . Lars . Brunzell . John D. . Goldberg . Anne C. . Goldberg . Ira J. . Sacks . Frank . Murad . Mohammad Hassan . Stalenhoef . Anton F. H. . Endocrine society . September 2012 . Evaluation and treatment of hypertriglyceridemia: an Endocrine Society clinical practice guideline . The Journal of Clinical Endocrinology and Metabolism . 97 . 9 . 2969–2989 . 10.1210/jc.2011-3213 . 1945-7197 . 3431581 . 22962670.
  17. Book: Davidson MH, Cannon CP, Armani AM . Davidson MH, Toth PP, Maki KC . Therapeutic Lipidology . limited . Pharmacological Therapy for Cardiovascular Disease . 141–142 . Contemporary Cardiology. 28 January 2008 . Humana Press, Inc. . Totowa, New Jersey. 978-1-58829-551-4.
  18. Anagnostis P, Paschou SA, Goulis DG, Athyros VG, Karagiannis A . Dietary management of dyslipidaemias. Is there any evidence for cardiovascular benefit? . Maturitas . 108 . 45–52 . February 2018 . 29290214 . 10.1016/j.maturitas.2017.11.011 . free .
  19. Abourbih S, Filion KB, Joseph L, Schiffrin EL, Rinfret S, Poirier P, Pilote L, Genest J, Eisenberg MJ . 6 . Effect of fibrates on lipid profiles and cardiovascular outcomes: a systematic review . The American Journal of Medicine . 122 . 10 . 962.e1–962.e8 . October 2009 . 19698935 . 10.1016/j.amjmed.2009.03.030 .
  20. Jun M, Foote C, Lv J, Neal B, Patel A, Nicholls SJ, Grobbee DE, Cass A, Chalmers J, Perkovic V . 6 . Effects of fibrates on cardiovascular outcomes: a systematic review and meta-analysis . Lancet . 375 . 9729 . 1875–1884 . May 2010 . 20462635 . 10.1016/S0140-6736(10)60656-3 . 15570639 .
  21. Blair HA, Dhillon S . Omega-3 carboxylic acids (Epanova): a review of its use in patients with severe hypertriglyceridemia . American Journal of Cardiovascular Drugs . 14 . 5 . 393–400 . October 2014 . 25234378 . 10.1007/s40256-014-0090-3 . 23706094 .
  22. Thorp JG, Campos AI, Grotzinger AD, Gerring ZF, An J, Ong JS, Wang W, Shringarpure S, Byrne EM, MacGregor S, Martin NG, Medland SE, Middeldorp CM, Derks EM . 6 . Symptom-level modelling unravels the shared genetic architecture of anxiety and depression . Nature Human Behaviour . 5 . 10 . 1432–1442 . October 2021 . 33859377 . 10.1038/s41562-021-01094-9 . 233259875 .

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