Hypertriglyceridemia
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 | |
|---|---|
| Other names | Elevated levels of triglycerides |
| Blood samples of a young patient with extreme hypertriglyceridemia | |
| Specialty | Endocrinology |
| Complications | Heart disease, pancreatitis |
| Risk factors | Non-alcoholic fatty liver disease, atherosclerosis, alcoholism, metabolic syndrome |
| Differential diagnosis | Hyperlipidemia, atheroma, hypercholesterolemia, hypercalcemia |
Chronically elevated serum triglyceride levels are a component of metabolic syndrome and non-alcoholic fatty liver disease (NAFLD), 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.[1]
Signs and symptoms edit
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.[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]
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]
Causes edit
- Overeating[4][5]
- Obesity
- Diabetes mellitus and insulin resistance - it is one of the defined components of metabolic syndrome (along with central obesity, hypertension, and hyperglycemia)
- Excess alcohol consumption
- Kidney failure, nephrotic syndrome
- Genetic predisposition; some forms of familial hyperlipidemia such as familial combined hyperlipidemia i.e. Type II hyperlipidemia
- Lipoprotein lipase deficiency - Deficiency of this water-soluble enzyme, that hydrolyzes triglycerides in lipoproteins, leads to elevated levels of triglycerides in the blood.
- Lysosomal acid lipase deficiency or Cholesteryl ester storage disease
- Certain medications e.g. isotretinoin, hydrochlorothiazide diuretics, beta blockers, protease inhibitors
- Hypothyroidism (underactive thyroid)
- Lupus and associated autoimmune responses [6]
- Glycogen storage disease type 1.
- Propofol
- HIV medications
Diagnosis edit
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]
Screening edit
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.[7][8]
Treatment edit
Lifestyle changes including weight loss, exercise and dietary modification may improve hypertriglyceridemia.[9][1][10][11] This may include dietary changes such as restriction of fat and carbohydrates (specifically fructose),[10] and increased consumption of omega-3 fatty acids from algae, nuts, and seeds.[12][13]
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.[1] Medications are recommended in those with high levels of triglycerides that are not corrected with lifestyle modifications, with fibrates being recommended first.[1][14][15] Epanova (omega-3-carboxylic acids) is another prescription drug used to treat very high levels of blood triglycerides.[16]
Epidemiology edit
As of 2006, the prevalence of hypertriglyceridemia in the United States was 30%.[5]
Research edit
Analysis of the genes in depression and anxiety showed those linked solely to depression were also linked to hypertriglyceridemia.[17]
Etymology edit
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 edit
References edit
- ^ a b c d e f g h i Berglund L, Brunzell JD, Goldberg AC, Goldberg IJ, Sacks F, Murad MH, Stalenhoef AF (September 2012). "Evaluation and treatment of hypertriglyceridemia: an Endocrine Society clinical practice guideline". The Journal of Clinical Endocrinology and Metabolism. 97 (9): 2969–2989. doi:10.1210/jc.2011-3213. PMC 3431581. PMID 22962670.
- ^ a b c Yuan G, Al-Shali KZ, Hegele RA (April 2007). "Hypertriglyceridemia: its etiology, effects and treatment". CMAJ. 176 (8): 1113–1120. doi:10.1503/cmaj.060963. PMC 1839776. PMID 17420495.
- ^ a b Tsuang 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. PMID 19293788. S2CID 24193233.
- ^ 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. PMID 1397701.
- ^ a b c Pejic RN, Lee DT (May–Jun 2006). "Hypertriglyceridemia". Journal of the American Board of Family Medicine. 19 (3): 310–316. doi:10.3122/jabfm.19.3.310. PMID 16672684.
- ^ Beigneux AP, Miyashita K, Ploug M, Blom DJ, Ai M, Linton MF, et al. (April 2017). "Autoantibodies against GPIHBP1 as a Cause of Hypertriglyceridemia". The New England Journal of Medicine. 376 (17): 1647–1658. doi:10.1056/NEJMoa1611930. PMC 5555413. PMID 28402248.
- ^ 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. PMID 27538032. S2CID 20592431.
- ^ Bibbins-Domingo K, Grossman DC, Curry SJ, Davidson KW, Epling JW, García FA, et al. (August 2016). "Screening for Lipid Disorders in Children and Adolescents: US Preventive Services Task Force Recommendation Statement". JAMA. 316 (6): 625–633. doi:10.1001/jama.2016.9852. PMID 27532917.
- ^ Koneru SC (2022-03-01). "Fellow's voice: Hypertriglyceridemia: Understanding the current guideline". American Journal of Preventive Cardiology. 9: 100322. doi:10.1016/j.ajpc.2022.100322. ISSN 2666-6677. PMC 8885448. PMID 35243465.
- ^ a b Nordestgaard BG, Varbo A (August 2014). "Triglycerides and cardiovascular disease". Lancet. 384 (9943): 626–635. doi:10.1016/S0140-6736(14)61177-6. PMID 25131982. S2CID 33149001.
- ^ 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. PMID 11834142.
- ^ 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. ISBN 978-1-58829-551-4.
- ^ Anagnostis P, Paschou SA, Goulis DG, Athyros VG, Karagiannis A (February 2018). "Dietary management of dyslipidaemias. Is there any evidence for cardiovascular benefit?". Maturitas. 108: 45–52. doi:10.1016/j.maturitas.2017.11.011. PMID 29290214.
- ^ 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. PMID 19698935.
- ^ 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. PMID 20462635. S2CID 15570639.
- ^ 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. PMID 25234378. S2CID 23706094.
- ^ 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. PMID 33859377. S2CID 233259875.
External links edit
- Lowering Triglycerides (EMedicineHealth.com; October 2020)