Primary hypertriglyceridemia
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]
Overview
Primary hypertriglyceridemia i.e type 4 hyper lipidemia is due to high concentration of triglycerides in the blood. It is also known as hypertriglyceridemia (or pure hypertriglyceridemia). According to the NCEP-ATPIII definition of high triglycerides (>200 mg/dl), prevalence is about 16% of adult population.[1] Elevated levels of triglycerides can be detrimental for the normal cardiac functioning.[2]
Historical Perspective
- A study conducted in 1964 explained the post carbohydrate rise in triglycerides and the difference in the levels in patients with cirrhosis and metastasis.[3]
Classification
Hypertriglyceridemia can be classified in two ways
- As primary or secondary to another cause that can be obesity, diabetes type 2 or excessive alcohol consumption[4] and
- Depending on the concentration [5] of triglyceride levels
- Normal <150 mg/dL
- Borderline-high triglycerides 150-199 mg/dL
- High triglycerides 200-499 mg/dL
- Very high triglycerides >500
Pathophisiology
Causes
Differentiating Primary hypertriglyceridemia from Other Diseases
Epidemiology and Demographics
Type 4 hyperlipidemia i.e hypertriglyceridemia has a population prevalence of 5%–10%[4]
Risk Factors
Screening
Natural History, Complications, and Prognosis
A large number of people in the US (approximately one fourth of the total population) have a high level of triglycerides (>150mg/dl) that can predispose and lead to numerous complications[6] including
- Cardiovascular diseases
- Non Alcoholic Fatty Liver Disease (NAFLD)
- Pancreatitis
Diagnosis
Hypertriglyceridemia is preferably diagnosed by estimating fasting triglyceride levels as compared to non-fasting levels.[2]
History and Symptoms
Physical Examination
Laboratory Finding
Imaging Findings
Biopsy
Medical Therapy
Non Pharmacological
The mainstay of therapy for hypertriglyceridemia includes life style modifications to lower the triglyceride levels to below 150 mg/dl. A reduction of weight by 5-10 % can help decrease the triglyceride levels by 20%.[6] Other measure include reduction of fat content of food and high glycemic index foods.[7] Appropriate dietary changes and increase in aerobic activity can decrease triglyceride content in the body. Diet adjustment and weight loss can curtail the triglycerides by unto 25% [8] 4 grams daily of Omega 3 Fatty acids when taken along with these measures can also be helpful in reducing plasma levels by upto 20%.[9]
Pharmacological Treatment
If the triglyceride levels are excessively increased, control of blood levels can be achieved by various medical therapies varying according to the level of triglycerides found in the body. Moderate increase i.e >500 can be treated by statins while severe increase that is >1000 need to be treated by using a fibrate as the primary treatment.[6]
Emerging treatment options
- Rimonabant a cannabinoid-1 (CB1) receptor antagonist works by decreasing appetite and consumption of food.[10] [11]
- Glitazar drugs have dual agonists on peroxisome proliferator-activated receptor-α (like fibrates) and -γ (like thiozolidinidiones).[12]
- LPL Gene Therapy can be helpful by treating monogenic LPL (lipoprotein lipase) deficiency[13].
Surgery
Prevention
References
- ↑ Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report. Circulation 2002; 106; page 3240
- ↑ 2.0 2.1 Berglund L, Brunzell JD, Goldberg AC, Goldberg IJ, Sacks F, Murad MH; et al. (2012). "Evaluation and treatment of hypertriglyceridemia: an Endocrine Society clinical practice guideline". J Clin Endocrinol Metab. 97 (9): 2969–89. doi:10.1210/jc.2011-3213. PMC 3431581. PMID 22962670.
- ↑ LEVERTON RM (1964). "CARBOHYDRATE INDUCED HYPERTRIGLYCERIDEMIA". Nutr Rev. 22: 328–30. PMID 14223171.
- ↑ 4.0 4.1 Yuan G, Al-Shali KZ, Hegele RA (2007). "Hypertriglyceridemia: its etiology, effects and treatment". CMAJ. 176 (8): 1113–20. doi:10.1503/cmaj.060963. PMC 1839776. PMID 17420495.
- ↑ National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) (2002). "Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report". Circulation. 106 (25): 3143–421. PMID 12485966.
- ↑ 6.0 6.1 6.2 Kushner PA, Cobble ME (2016). "Hypertriglyceridemia: the importance of identifying patients at risk". Postgrad Med. doi:10.1080/00325481.2016.1243005. PMID 27710158.
- ↑ Jenkins DJ, Kendall CW, Augustin LS, Franceschi S, Hamidi M, Marchie A; et al. (2002). "Glycemic index: overview of implications in health and disease". Am J Clin Nutr. 76 (1): 266S–73S. PMID 12081850.
- ↑ Gerhard GT, Ahmann A, Meeuws K, McMurry MP, Duell PB, Connor WE (2004). "Effects of a low-fat diet compared with those of a high-monounsaturated fat diet on body weight, plasma lipids and lipoproteins, and glycemic control in type 2 diabetes". Am J Clin Nutr. 80 (3): 668–73. PMID 15321807.
- ↑ Hooper L, Thompson RL, Harrison RA, Summerbell CD, Ness AR, Moore HJ; et al. (2006). "Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review". BMJ. 332 (7544): 752–60. doi:10.1136/bmj.38755.366331.2F. PMC 1420708. PMID 16565093.
- ↑ Boyd ST, Fremming BA (2005). "Rimonabant--a selective CB1 antagonist". Ann Pharmacother. 39 (4): 684–90. doi:10.1345/aph.1E499. PMID 15755787.
- ↑ Gelfand EV, Cannon CP (2006). "Rimonabant: a cannabinoid receptor type 1 blocker for management of multiple cardiometabolic risk factors". J Am Coll Cardiol. 47 (10): 1919–26. doi:10.1016/j.jacc.2005.12.067. PMID 16697306.
- ↑ Nissen SE, Wolski K, Topol EJ (2005). "Effect of muraglitazar on death and major adverse cardiovascular events in patients with type 2 diabetes mellitus". JAMA. 294 (20): 2581–6. doi:10.1001/jama.294.20.joc50147. PMID 16239637.
- ↑ Rip J, Nierman MC, Sierts JA, Petersen W, Van den Oever K, Van Raalte D; et al. (2005). "Gene therapy for lipoprotein lipase deficiency: working toward clinical application". Hum Gene Ther. 16 (11): 1276–86. doi:10.1089/hum.2005.16.1276. PMID 16259561.