Diferencia entre revisiones de «Hypertriglyceridemia»
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==Background== | ==Background== | ||
*~5% of acute [[pancreatitis]] caused by high triglycerides<ref>Yadav D, Pitchumoni CS. Issues in hyperlipidemic pancreatitis. J Clin Gastroenterology 2003;36:54-62.</ref> | |||
*~5% of acute [[Special:MyLanguage/pancreatitis|pancreatitis]] caused by high triglycerides<ref>Yadav D, Pitchumoni CS. Issues in hyperlipidemic pancreatitis. J Clin Gastroenterology 2003;36:54-62.</ref> | |||
*Etiologies | *Etiologies | ||
**Familial hypertriglyceridemia, autosomal dominant with variable penetrance | **Familial hypertriglyceridemia, autosomal dominant with variable penetrance | ||
**Secondary forms | **Secondary forms | ||
***[[DM]], obesity, [[EtOH]], estrogen therapy | ***[[Special:MyLanguage/DM|DM]], obesity, [[Special:MyLanguage/EtOH|EtOH]], estrogen therapy | ||
***[[Hypothyroidism]], ESRD, nephrotic syndrome, [[HIV]], anti-HIV meds | ***[[Special:MyLanguage/Hypothyroidism|Hypothyroidism]], ESRD, nephrotic syndrome, [[Special:MyLanguage/HIV|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> | *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> | ||
*May present with normal serum lipase levels | *May present with normal serum lipase levels | ||
===Pathophysiology=== | ===Pathophysiology=== | ||
*Excess TG hydrolyzed by increased concentration of pancreatic lipase | *Excess TG hydrolyzed by increased concentration of pancreatic lipase | ||
*Produces increased concentration of free fatty acids that exceeds binding capacity of albumin | *Produces increased concentration of free fatty acids that exceeds binding capacity of albumin | ||
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*Ischemia and pancreatic injury result | *Ischemia and pancreatic injury result | ||
*An acidic environment potentiates free fatty acid toxicity | *An acidic environment potentiates free fatty acid toxicity | ||
==Clinical Features== | ==Clinical Features== | ||
===General=== | ===General=== | ||
[[File:Xanthoma.jpg|thumb|A pediatric patient's knee showing multiple xanthoma tuberosum (i.e. xanthoma located over a joint).]] | [[File:Xanthoma.jpg|thumb|A pediatric patient's knee showing multiple xanthoma tuberosum (i.e. xanthoma located over a joint).]] | ||
*Most are generally asymptomatic until sequelae present | *Most are generally asymptomatic until sequelae present | ||
*Eruptive xanthoma may be found on dermatologic exam | *Eruptive xanthoma may be found on dermatologic exam | ||
===Hypertriglyceridemic Pancreatitis=== | ===Hypertriglyceridemic Pancreatitis=== | ||
''Signs/symptoms of pancreatitis'' | ''Signs/symptoms of pancreatitis'' | ||
*[[Epigastric pain|Pain]] is the most common symptom and is often characterized by: | *[[Special:MyLanguage/Epigastric pain|Pain]] is the most common symptom and is often characterized by: | ||
**Persistent | **Persistent | ||
**Localizes to epigastric area, around waist, RUQ, or occasionally LUQ | **Localizes to epigastric area, around waist, RUQ, or occasionally LUQ | ||
**Radiates to back | **Radiates to back | ||
**The onset may be less abrupt and the pain poorly localized | **The onset may be less abrupt and the pain poorly localized | ||
*[[Nausea/vomiting]] noted in most | *[[Special:MyLanguage/Nausea/vomiting|Nausea/vomiting]] noted in most | ||
*Abdominal distention is frequent complaint | *Abdominal distention is frequent complaint | ||
*[[Eponyms_(C-E)#Cullen.27s_sign|Cullen sign]] (ecchymosis of periumbilical region) - intrabdominal hemorrhage | *[[Special:MyLanguage/Eponyms_(C-E)#Cullen.27s_sign|Cullen sign]] (ecchymosis of periumbilical region) - intrabdominal hemorrhage | ||
*Turner sign (ecchymosis of flanks) - retroperitoneal hemorrhage | *Turner sign (ecchymosis of flanks) - retroperitoneal hemorrhage | ||
*Pulmonary Findings | *Pulmonary Findings | ||
**[[Hypoxemia]], [[ARDS]], tachypnea | **[[Special:MyLanguage/Hypoxemia|Hypoxemia]], [[Special:MyLanguage/ARDS|ARDS]], tachypnea | ||
**Indicates severe pancreatitis | **Indicates severe pancreatitis | ||
***Diaphragmatic inflammation, pancreatico-pleural fistula | ***Diaphragmatic inflammation, pancreatico-pleural fistula | ||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
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{{Abdominal Pain DDX Epigastric}} | {{Abdominal Pain DDX Epigastric}} | ||
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==Evaluation== | ==Evaluation== | ||
[[File:hypertriglyceridemia_green_top.jpg|thumbnail]] | [[File:hypertriglyceridemia_green_top.jpg|thumbnail]] | ||
*Triglycerides; Severely elevated (at least >500 mg/dL, generally >1,000 mg/dL) | *Triglycerides; Severely elevated (at least >500 mg/dL, generally >1,000 mg/dL) | ||
**Lipids in serum may interfere with other lab tests | **Lipids in serum may interfere with other lab tests | ||
***Falsely low Na+, amylase | ***Falsely low Na+, amylase | ||
===Pancreatitis workup=== | ===Pancreatitis workup=== | ||
*Rule out other causes of pancreatitis (e.g. [[gallstone pancreatitis]]) | |||
*Rule out other causes of pancreatitis (e.g. [[Special:MyLanguage/gallstone pancreatitis|gallstone pancreatitis]]) | |||
*In general, if triglycerides >1000, can assume this is cause of pancreatitis | *In general, if triglycerides >1000, can assume this is cause of pancreatitis | ||
*Lipase level >3x upper limit of normal | *Lipase level >3x upper limit of normal | ||
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**Negative lipase does not exclude pancreatitis in chronic/recurrent disease | **Negative lipase does not exclude pancreatitis in chronic/recurrent disease | ||
**Absolute value not associated with prognosis or severity | **Absolute value not associated with prognosis or severity | ||
*Characteristic findings on [[ultrasound]] or CT | *Characteristic findings on [[Special:MyLanguage/ultrasound|ultrasound]] or CT | ||
==Management== | ==Management== | ||
===Management of [[acute pancreatitis]] in the setting of hypertriglyceridemia=== | |||
===Management of [[Special:MyLanguage/acute pancreatitis|acute pancreatitis]] in the setting of hypertriglyceridemia=== | |||
*Evidence for management based on case series and reports<ref>Santana YR et al. Treatment of severe hypertriglyceridemia with continuous insulin infusion. Case Reports in Critical Care. June 2011.</ref><ref>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.</ref> | *Evidence for management based on case series and reports<ref>Santana YR et al. Treatment of severe hypertriglyceridemia with continuous insulin infusion. Case Reports in Critical Care. June 2011.</ref><ref>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.</ref> | ||
*[[Insulin]] drip - most dramatic and rapid intervention, with reduction within 24 hrs | *[[Special:MyLanguage/Insulin|Insulin]] drip - most dramatic and rapid intervention, with reduction within 24 hrs | ||
**Initiate at 0.1 units/kg/hr (similar to treatment for DKA) | **Initiate at 0.1 units/kg/hr (similar to treatment for DKA) | ||
**Goal is to reduce triglycerides to < 500 | **Goal is to reduce triglycerides to < 500 | ||
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***K > 5 no extra potassium | ***K > 5 no extra potassium | ||
*IVF as for standard pancreatitis treatment, add potassium as per above | *IVF as for standard pancreatitis treatment, add potassium as per above | ||
*Treat concurrent [[hypothyroidism]] if present | *Treat concurrent [[Special:MyLanguage/hypothyroidism|hypothyroidism]] if present | ||
*Pain control | *Pain control | ||
*[[Niacin]] 500mg QD | *[[Special:MyLanguage/Niacin|Niacin]] 500mg QD | ||
*[[Gemfibrozil]] or [[fenofibrate]] | *[[Special:MyLanguage/Gemfibrozil|Gemfibrozil]] or [[Special:MyLanguage/fenofibrate|fenofibrate]] | ||
*Max dose statin, 81mg [[ASA]] | *Max dose statin, 81mg [[Special:MyLanguage/ASA|ASA]] | ||
*[[Heparin]] q8 SC, effect short-lived | *[[Special:MyLanguage/Heparin|Heparin]] q8 SC, effect short-lived | ||
*NPO initially | *NPO initially | ||
*May advance diet starting at TG level < 1000mg/dL with resolution of abdominal pain/pancreatitis symptoms | *May advance diet starting at TG level < 1000mg/dL with resolution of abdominal pain/pancreatitis symptoms | ||
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**Low calorie diet | **Low calorie diet | ||
====[[Plasma exchange]]==== | |||
====[[Special:MyLanguage/Plasma exchange|Plasma exchange]]==== | |||
*Therapeutic plasma exchange, for 1-3 days (sickest patients) | *Therapeutic plasma exchange, for 1-3 days (sickest patients) | ||
**Generally indicated for hypocalcemia, persistent elevated lactic acidosis, other signs of worsening organ dysfunction | **Generally indicated for hypocalcemia, persistent elevated lactic acidosis, other signs of worsening organ dysfunction | ||
*For euglycemic patients, not routine first line | *For euglycemic patients, not routine first line | ||
*Requires central venous access | *Requires central venous access | ||
==Disposition== | ==Disposition== | ||
*Asymptomatic hypertriglyceridemia is treated as an outpatient | *Asymptomatic hypertriglyceridemia is treated as an outpatient | ||
*For acute pancreatitis, ICU or step-down for frequent labs, insulin drip | *For acute pancreatitis, ICU or step-down for frequent labs, insulin drip | ||
==See Also== | ==See Also== | ||
*[[Acute pancreatitis]] | |||
*[[Special:MyLanguage/Acute pancreatitis|Acute pancreatitis]] | |||
==External Links== | ==External Links== | ||
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==References== | ==References== | ||
<references/> | <references/> | ||
[[Category:GI]] | [[Category:GI]] | ||
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Revisión actual - 23:09 4 ene 2026
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
Clinical Features
General
- Most are generally asymptomatic until sequelae present
- Eruptive xanthoma may be found on dermatologic exam
Hypertriglyceridemic Pancreatitis
Signs/symptoms of pancreatitis
- Pain is the most common symptom and is often characterized by:
- Persistent
- Localizes to epigastric area, around waist, RUQ, or occasionally LUQ
- Radiates to back
- The onset may be less abrupt and the pain poorly localized
- Nausea/vomiting noted in most
- Abdominal distention is frequent complaint
- Cullen sign (ecchymosis of periumbilical region) - intrabdominal hemorrhage
- Turner sign (ecchymosis of flanks) - retroperitoneal hemorrhage
- Pulmonary Findings
Differential Diagnosis
Epigastric Pain
- Gastroesophageal reflux disease (GERD)
- Peptic ulcer disease with or without perforation
- Gastritis
- Pancreatitis
- Gallbladder disease
- Myocardial Ischemia
- Splenic Infarctionenlargement/rupture/aneurysm
- Pericarditis/Myocarditis
- Aortic dissection
- Hepatitis
- Pyelonephritis
- Pneumonia
- Pyogenic liver abscess
- Fitz-Hugh-Curtis Syndrome
- Hepatomegaly due to CHF
- Bowel obstruction
- SMA syndrome
- Pulmonary embolism
- Bezoar
- Ingested foreign body
Evaluation
- Triglycerides; Severely elevated (at least >500 mg/dL, generally >1,000 mg/dL)
- Lipids in serum may interfere with other lab tests
- Falsely low Na+, amylase
- Lipids in serum may interfere with other lab tests
Pancreatitis workup
- Rule out other causes of pancreatitis (e.g. gallstone pancreatitis)
- In general, if triglycerides >1000, can assume this is cause of pancreatitis
- Lipase level >3x upper limit of normal
- Sensitivity 82-100%, specificity 82-100%[4]
- Negative lipase does not exclude pancreatitis in chronic/recurrent disease
- Absolute value not associated with prognosis or severity
- Characteristic findings on ultrasound or CT
Management
Management of acute pancreatitis in the setting of hypertriglyceridemia
- Evidence for management based on case series and reports[5][6]
- Insulin drip - most dramatic and rapid intervention, with reduction within 24 hrs
- Initiate at 0.1 units/kg/hr (similar to treatment for DKA)
- Goal is to reduce triglycerides to < 500
- Add D5NS if glucose drops < 200 [7]
- Monitor BMP q2 hr
- Manage potassium
- K < 3.2 stop insulin and replete K
- K 3.3 to 5 add 20 mEq K/Lto IVF
- K > 5 no extra potassium
- IVF as for standard pancreatitis treatment, add potassium as per above
- Treat concurrent hypothyroidism if present
- Pain control
- 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
Plasma exchange
- Therapeutic plasma exchange, for 1-3 days (sickest patients)
- Generally indicated for hypocalcemia, persistent elevated lactic acidosis, other signs of worsening organ dysfunction
- For euglycemic patients, not routine first line
- Requires central venous access
Disposition
- Asymptomatic hypertriglyceridemia is treated as an outpatient
- For acute pancreatitis, ICU or step-down for frequent labs, insulin drip
See Also
External Links
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
- ↑ Yadav D, Agarwal N, Pitchumoni CS. A critical evaluation of laboratory tests in acute pancreatitis. Am J Gastroenterol. 2002 Jun;97(6):1309-18.
- ↑ 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.
