Hypertriglyceridemia: Difference between revisions
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***[[Hypothyroidism]], ESRD, nephrotic syndrome, [[HIV]], anti-HIV meds | ***[[Hypothyroidism]], ESRD, nephrotic syndrome, [[HIV]], anti-HIV meds | ||
*TG levels > 2000mg/dL almost always have both secondary and genetic form<ref>Yuan et al. Hypertriglyceridemia: its etiology, effects and treatment. CMAJ 2007;176:1113-1120.</ref> | *TG levels > 2000mg/dL almost always have both secondary and genetic form<ref>Yuan et al. Hypertriglyceridemia: its etiology, effects and treatment. CMAJ 2007;176:1113-1120.</ref> | ||
*1.7% of US estimated to have [TG] between 500-2000<ref>Brown, Virgil W. Et al. “Clinical Lipidology Roundtable Discussion: Severe Hypertriglyceridemia.” Journal of Clinical Lipidology 2012; 6:397-408</ref> | |||
[[File:hypertriglyceridemia_green_top.jpg|thumbnail]] | [[File:hypertriglyceridemia_green_top.jpg|thumbnail]] | ||
*May present with normal serum lipase levels | *May present with normal serum lipase levels | ||
==Pathophysiology== | |||
*Excess TG hydrolyzed by increased concentration of pancreatic lipase | |||
*Produces increased concentration of free fatty acids that exceeds binding capacity of albumin | |||
*Micelles are formed that attack platelets, vascular endothelium and acinar cells | |||
*Ischemia and pancreatic injury result | |||
*An acidic environment potentiates free fatty acid toxicity | |||
==Management of Pancreatitis== | ==Management of Pancreatitis== | ||
Revision as of 15:08, 23 August 2017
Background
- ~5% of acute pancreatitis caused by high triglycerides[1]
- Etiologies
- Familial hypertriglyceridemia, autosomal dominant with variable penetrance
- Secondary forms
- DM, obesity, EtOH, estrogen therapy
- Hypothyroidism, ESRD, nephrotic syndrome, HIV, anti-HIV meds
- TG levels > 2000mg/dL almost always have both secondary and genetic form[2]
- 1.7% of US estimated to have [TG] between 500-2000[3]
- May present with normal serum lipase levels
Pathophysiology
- Excess TG hydrolyzed by increased concentration of pancreatic lipase
- Produces increased concentration of free fatty acids that exceeds binding capacity of albumin
- Micelles are formed that attack platelets, vascular endothelium and acinar cells
- Ischemia and pancreatic injury result
- An acidic environment potentiates free fatty acid toxicity
Management of Pancreatitis
- Evidence for management based on case series and reports[4][5]
- Insulin drip - most dramatic and rapid intervention, with reduction within 24 hrs
- 5-10 units/hr with or without dextrose infusion to maintain BSs ~150mg/dL
- May require higher dosages for diabetics, 0.1–0.3 U/kg/hr
- Titrate to BS 140–180mg/dL[6]
- Treat concurrent hypothryoidism if present
- Niacin 500mg QD
- Gemfibrozil or fenofibrate
- Max dose statin, 81mg ASA
- Heparin q8 SC, effect short-lived
- NPO initially
- May advance diet starting at TG level < 1000mg/dL with resolution of abdominal pain/pancreatitis symptoms
- No fat diet
- Low calorie diet
- Follow TG levels, goal < 500-1000mg/dL by discharge
Plasma exchange
- Therapeutic plasma exchange, for 1-3 days
- For euglycemic patients, not routine first line
- Requires central venous access
Disposition
- ICU or step-down for frequent labs, insulin drip
References
- ↑ Yadav D, Pitchumoni CS. Issues in hyperlipidemic pancreatitis. J Clin Gastroenterology 2003;36:54-62.
- ↑ Yuan et al. Hypertriglyceridemia: its etiology, effects and treatment. CMAJ 2007;176:1113-1120.
- ↑ Brown, Virgil W. Et al. “Clinical Lipidology Roundtable Discussion: Severe Hypertriglyceridemia.” Journal of Clinical Lipidology 2012; 6:397-408
- ↑ Santana YR et al. Treatment of severe hypertriglyceridemia with continuous insulin infusion. Case Reports in Critical Care. June 2011.
- ↑ Poonuru S et al. Rapid Reduction of Severely Elevated Serum Triglycerides with Insulin Infusion, Gemfibrozil and Niacin. Clin Med Res. 2011 Mar; 9(1): 38–41.
- ↑ Schaefer EW. Management of Severe Hypertriglyceridemia in the Hospital: A Review. Journal of Hospital Medicine Vol 7|No 5|May/June 2012.