Hypertriglyceridemia induced pancreatitis

#Hypertriglyceridemia-induced pancreatitis:

- Keep NPO while on insulin drip

- F/u HbA1c

- continue insulin drip at 0.1 units/kg/hour without titration

- continue dextrose containing fluids (D5 1/2NS at 250 cc hr or D10 150 cc/hr) titrated to maintain glucoses between 150-200

- check fingersticks hourly while on insulin drip

- Trend triglycerides q12-24h. Continue insulin drip until triglycerides <500

- Continue atorvastatin 80mg daily

- Continue fenofibrate 145mg daily

- Fish Oil/vascepa ***

- On discharge, patient should take fish oils/lovaza as non-formulary here

- Indications to discuss apheresis SIRS, hypocalcemia, end organ dysfunction, worsening abdominal pain

- Replete elecrolytes to goal of K>4, Magnesium 2, Phosph 3. Would replete K, Mg and Phosph before repleting calcium (as Mg needs to be releted for Calcium repletion to work).

- Additionally, would use caution with repletion of calcium, as excess calcium can cause pancreatic acinar cell death. If patient with symptoms of hypocalcemia or prolonged QTc on EKG not improving with magnesium then can replete Ca. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4810896/)

- Signs/Symptoms of Hypocalcemia include: periorbital numbness/tingling, AMS, QTc prolongation, bradycardia, paresthesia (perioribtal or extremities), muscle spasms, cramps, tetany, circumoral numbness, and seizures.

Hypertriglyceridemia Induced Pancreatitis in Pregnant Patients ***

- Will hold off on fenofibrates ***, and atorvastatin, as patient pregnant***. Can start *** Fish oil ***

1. What is HTGP, and why is it important to recognize?

Question: What is hypertriglyceridemia-induced pancreatitis (HTGP), and why is early recognition important?
Answer: HTGP is a form of acute pancreatitis triggered by extremely high triglyceride levels, often above 1,000 mg/dL. Early recognition is crucial to provide appropriate therapy, reduce triglyceride levels, and prevent further episodes and complications, such as organ failure.

2. What are common causes of HTGP?

Question: What are the primary and secondary causes of hypertriglyceridemia leading to HTGP?
Answer: HTGP can be caused by primary (genetic) disorders like familial hypertriglyceridemia, or secondary factors like uncontrolled diabetes, obesity, hypothyroidism, nephrotic syndrome, alcohol abuse, or as an adverse effect of medications (e.g., tamoxifen, beta blockers, corticosteroids, antiretrovirals).

3. At what triglyceride levels does the risk of pancreatitis increase?

Question: At what serum triglyceride levels does the risk of developing acute pancreatitis increase, and what levels are considered critical?
Answer: The risk of acute pancreatitis begins to increase at triglyceride levels above 500 mg/dL, and the risk becomes significant when levels exceed 1,000 mg/dL.

4. What are the clinical signs of HTGP?

Question: What are the typical symptoms and physical findings associated with HTGP?
Answer: HTGP presents similarly to other forms of acute pancreatitis, with severe epigastric pain often radiating to the back, nausea, and vomiting. Physical findings may include eruptive xanthomas (small, yellowish skin nodules) and hepatosplenomegaly in cases of chronic hypertriglyceridemia.

5. What are worrisome features in HTGP, and why are they significant?

Question: What are worrisome features in patients with HTGP, and what do they indicate?
Answer: Worrisome features include hypocalcemia, lactic acidosis, signs of systemic inflammation (e.g., high or low temperature, tachycardia, tachypnea, elevated or low WBC count), and organ dysfunction per the Modified Marshall scoring system. These features indicate a severe case with a higher risk of complications, warranting aggressive treatment.

6. When is plasmapheresis indicated in HTGP?

Question: When is plasmapheresis indicated for patients with HTGP?
Answer: Plasmapheresis is indicated in HTGP patients with very high triglyceride levels (typically >1,000 mg/dL) and worrisome features, such as hypocalcemia, lactic acidosis, signs of systemic inflammation, or multi-organ failure, as it can rapidly reduce triglyceride levels.

7. What is the role of dietary fat restriction in HTGP management?

Question: How is dietary fat restriction used in the management of HTGP?
Answer: Once patients with HTGP can tolerate oral intake, dietary fat is restricted to less than 5 percent of total calories until triglyceride levels are below 1,000 mg/dL. This helps to reduce triglyceride production and stabilize the condition.

8. What is the initial management approach for HTGP?

Question: What is the initial management approach for patients with HTGP?
Answer: Initial management includes supportive care, such as fluid resuscitation and pain control, dietary fat restriction, and cessation of any medications that may increase triglycerides. In severe cases, plasmapheresis or intravenous insulin may be used to lower triglycerides quickly.

9. Why are fibrates used in HTGP, and in what cases?

Question: What is the role of fibrates in the treatment of HTGP, and when are they indicated?
Answer: Fibrates, such as gemfibrozil or fenofibrate, are effective for lowering triglycerides and are typically used in patients with severe hypertriglyceridemia (levels >500 mg/dL) to reduce the risk of recurrent pancreatitis.

10. What role does insulin therapy play in HTGP?

Question: How is insulin therapy used in the management of HTGP?
Answer: Insulin therapy, particularly intravenous insulin, may be used to lower triglyceride levels in HTGP patients with worrisome features when plasmapheresis is unavailable. Insulin enhances lipoprotein lipase activity, helping to clear triglycerides from the blood.

11. What are the long-term management strategies for HTGP?

Question: What are the long-term management strategies for preventing HTGP recurrence?
Answer: Long-term management includes lifestyle modifications (e.g., diet low in fat and simple sugars, weight loss, exercise) and pharmacologic therapy like fibrates or omega-3 fatty acids to maintain triglyceride levels below 500 mg/dL. Managing underlying conditions, such as diabetes, and avoiding medications that elevate triglycerides are also crucial.

12. What is the Modified Marshall scoring system, and why is it used in HTGP?

Question: What is the Modified Marshall scoring system, and how does it help in managing HTGP?
Answer: The Modified Marshall scoring system assesses organ failure in patients with acute pancreatitis. A score of 2 or more in any system (cardiovascular, renal, or respiratory) indicates organ failure and helps guide the need for intensive management in HTGP patients.

1. What is the cornerstone of managing elevated triglyceride levels?

Answer: Therapeutic lifestyle changes are the cornerstone of managing hypertriglyceridemia. This includes reducing sugar, total fat, and alcohol intake, along with decreasing caloric intake to achieve a weight loss of 5-10%.

2. What dietary changes are recommended to manage hypertriglyceridemia?

Answer: Dietary recommendations include reducing sugar, total fat, and alcohol consumption, as well as incorporating omega-3 fatty acids from fish. Omega-3 supplements may help lower triglyceride levels, although they do not reduce heart disease, stroke, or death risk.

3. What medications should be avoided in hypertriglyceridemia due to their potential to elevate triglyceride levels?

Answer: Medications like estrogens, β-blockers, and glucocorticoids can increase triglyceride levels and should be avoided if possible in patients with hypertriglyceridemia.

4. When should statin therapy be considered for patients with elevated triglyceride levels?

Answer: Statin therapy can be considered for adults without ASCVD or diabetes who have a 10-year ASCVD risk of 5% to less than 20% and a fasting triglyceride level of 150–499 mg/dL (1.69–5.64 mmol/L) or a nonfasting level of 175 mg/dL or higher (≥1.98 mmol/L), especially if lifestyle changes alone are insufficient.

5. When is statin therapy recommended based on ASCVD risk?

Answer: Statin therapy is recommended if the 10-year ASCVD risk is 20% or greater, regardless of triglyceride levels, as part of a strategy to lower cardiovascular risk.

6. What additional therapy may be beneficial for patients with persistently elevated triglycerides despite statin use and who have ASCVD or diabetes?

Answer: For patients with persistently elevated triglycerides despite statin therapy, established cardiovascular disease or diabetes, age 50 or older, and at least one other ASCVD risk factor, adding icosapent ethyl, a highly purified fish oil, may decrease the risk of cardiovascular events.

7. What role do omega-3 fatty acids play in triglyceride management?

Answer: Omega-3 fatty acids, found in fish and available as supplements, can help lower triglyceride levels. Pharmacologic doses (4 g/day) of omega-3 fatty acids can be effective in decreasing triglyceride levels, although they do not have established benefits for reducing heart disease, stroke, or mortality.

8. What is the role of fibrates in hypertriglyceridemia management?

Answer: Fibrates, particularly fenofibrate, are the most effective pharmacologic therapy for reducing triglyceride levels, resulting in a 30–50% reduction. They are particularly indicated in patients with severe hypertriglyceridemia (≥500 mg/dL, and especially ≥1,000 mg/dL) to prevent acute pancreatitis.

9. What are the indications for using icosapent ethyl in hypertriglyceridemia?

Answer: Icosapent ethyl is indicated in patients with persistently high triglycerides despite statin use, especially those with ASCVD or diabetes who are at least 50 years old and have an additional ASCVD risk factor, as it may help reduce cardiovascular events.

10. What triglyceride levels are considered critical for preventing pancreatitis?

Answer: Triglyceride levels above 500 mg/dL (5.65 mmol/L), and especially levels exceeding 1,000 mg/dL (11.30 mmol/L), are considered critical, as they significantly increase the risk of acute pancreatitis.

1. What is HTGP, and why is it important to recognize?

Question: What is hypertriglyceridemia-induced pancreatitis (HTGP), and why is early recognition important?
Answer: HTGP is a form of acute pancreatitis triggered by extremely high triglyceride levels, often above 1,000 mg/dL. Early recognition is crucial to provide appropriate therapy, reduce triglyceride levels, and prevent further episodes and complications, such as organ failure.

2. What are common causes of HTGP?

Question: What are the primary and secondary causes of hypertriglyceridemia leading to HTGP?
Answer: HTGP can be caused by primary (genetic) disorders like familial hypertriglyceridemia, or secondary factors like uncontrolled diabetes, obesity, hypothyroidism, nephrotic syndrome, alcohol abuse, or as an adverse effect of medications (e.g., tamoxifen, beta blockers, corticosteroids, antiretrovirals).

3. At what triglyceride levels does the risk of pancreatitis increase?

Question: At what serum triglyceride levels does the risk of developing acute pancreatitis increase, and what levels are considered critical?
Answer: The risk of acute pancreatitis begins to increase at triglyceride levels above 500 mg/dL, and the risk becomes significant when levels exceed 1,000 mg/dL.

4. What are the clinical signs of HTGP?

Question: What are the typical symptoms and physical findings associated with HTGP?
Answer: HTGP presents similarly to other forms of acute pancreatitis, with severe epigastric pain often radiating to the back, nausea, and vomiting. Physical findings may include eruptive xanthomas (small, yellowish skin nodules) and hepatosplenomegaly in cases of chronic hypertriglyceridemia.

5. What are worrisome features in HTGP, and why are they significant?

Question: What are worrisome features in patients with HTGP, and what do they indicate?
Answer: Worrisome features include hypocalcemia, lactic acidosis, signs of systemic inflammation (e.g., high or low temperature, tachycardia, tachypnea, elevated or low WBC count), and organ dysfunction per the Modified Marshall scoring system. These features indicate a severe case with a higher risk of complications, warranting aggressive treatment.

6. When is plasmapheresis indicated in HTGP?

Question: When is plasmapheresis indicated for patients with HTGP?
Answer: Plasmapheresis is indicated in HTGP patients with very high triglyceride levels (typically >1,000 mg/dL) and worrisome features, such as hypocalcemia, lactic acidosis, signs of systemic inflammation, or multi-organ failure, as it can rapidly reduce triglyceride levels.

7. What is the role of dietary fat restriction in HTGP management?

Question: How is dietary fat restriction used in the management of HTGP?
Answer: Once patients with HTGP can tolerate oral intake, dietary fat is restricted to less than 5 percent of total calories until triglyceride levels are below 1,000 mg/dL. This helps to reduce triglyceride production and stabilize the condition.

8. What is the initial management approach for HTGP?

Question: What is the initial management approach for patients with HTGP?
Answer: Initial management includes supportive care, such as fluid resuscitation and pain control, dietary fat restriction, and cessation of any medications that may increase triglycerides. In severe cases, plasmapheresis or intravenous insulin may be used to lower triglycerides quickly.

9. Why are fibrates used in HTGP, and in what cases?

Question: What is the role of fibrates in the treatment of HTGP, and when are they indicated?
Answer: Fibrates, such as gemfibrozil or fenofibrate, are effective for lowering triglycerides and are typically used in patients with severe hypertriglyceridemia (levels >500 mg/dL) to reduce the risk of recurrent pancreatitis.

10. What role does insulin therapy play in HTGP?

Question: How is insulin therapy used in the management of HTGP?
Answer: Insulin therapy, particularly intravenous insulin, may be used to lower triglyceride levels in HTGP patients with worrisome features when plasmapheresis is unavailable. Insulin enhances lipoprotein lipase activity, helping to clear triglycerides from the blood.

11. What are the long-term management strategies for HTGP?

Question: What are the long-term management strategies for preventing HTGP recurrence?
Answer: Long-term management includes lifestyle modifications (e.g., diet low in fat and simple sugars, weight loss, exercise) and pharmacologic therapy like fibrates or omega-3 fatty acids to maintain triglyceride levels below 500 mg/dL. Managing underlying conditions, such as diabetes, and avoiding medications that elevate triglycerides are also crucial.

12. What is the Modified Marshall scoring system, and why is it used in HTGP?

Question: What is the Modified Marshall scoring system, and how does it help in managing HTGP?
Answer: The Modified Marshall scoring system assesses organ failure in patients with acute pancreatitis. A score of 2 or more in any system (cardiovascular, renal, or respiratory) indicates organ failure and helps guide the need for intensive management in HTGP patients.

Pathogenesis involves toxic that are released from via breakdown by . Associated with primary (e.g., type V hyperlipidemia) as well as secondary (e.g., due to medications) forms of .

How does hypertriglyceridemia lead to acute pancreatitis?

{{c1::inc production of free fatty acids by pancreatic lipase -> exceeds binding capacity of albumin -> DIRECT TISSUE TOXICITY to pancreatic ACINAR cells}}

How does hypertriglyceridemia lead to acute pancreatitis?

{{c1::inc production of free fatty acids by pancreatic lipase -> exceeds binding capacity of albumin -> DIRECT TISSUE TOXICITY to pancreatic ACINAR cells}}

HTGP: hypertriglyceridemic pancreatitis; TG: triglycerides; WBC: white blood cell; PaCO2: partial pressure of carbon dioxide.
* Signs of worsening inflammation include:

Temperature >38.5°C or <35.0°C
Heart rate of >90 beats/min
Respiratory rate of >20 breaths/min or PaCO2 of <32 mmHg
WBC count of >12,000 cells/mL, <4000 cells/mL, or >10% immature (band) forms

¶ As defined by the modified Marshall scoring system for organ dysfunction. Refer to UpToDate topic on hypertriglycerdemia-induced acute pancreatitis.

Which thyroid abnormality is associated with hyperlipidemia (eg. hypercholesterolemia, hypertriglyceridemia)?

- Most patients have high cholesterol (due to decreased LDL receptors) +/- high triglycerides (due to decreased LPL activity)

- Secondary causes of high cholesterol include diabetes, hypothyroidism, obstructive liver disease, and chronic renal failure

Patients with type IV familial dyslipidemia often have triglyceride levels around {{c2::200}} to {{c1::500}} mg/dL, which typically is not enough to cause pancreatitis

When TG > 1000 mg/dL, this causes acute pancreatitis

Which serum lipid is elevated in type IV familial dyslipidemia?

{{c1::Triglycerides}}

hence why it is also known as hypertriglyceridemia

Which Familial dyslipidemias present with increased triglycerides in the serum?

Hyperchylomicronemia
Hypertriglyceridemia

Familial hypercholesterolemia
Hypertriglyceridemia

Hypothyroidism may contribute to development of {{c1::atherosclerosis}} due to dyslipidemia and endothelial dysfunction

* Hypothyroidism causes decreased LDL turnover due to decreased expression and activity of LDL receptors → increased total cholesterol and LDL
* It also causes decreased activity of lipoprotein lipase → hypertriglyceridemia

What thyroid abnormality (hyper- or hypothyroidism) is associated with hyperlipidemia (e.g. hypercholesterolemia, hypertriglyceridemia)?

{{c1::Hypothyroidism}}

most patients have high cholesterol (due to decreased LDL receptors) with or without high trigylcerides (decreased LPL activity); patients may also develop hyponatremia and asymptomatic elevations in CK and AST/ALT

To calculate the corrected sodium concentration in cases of hypertriglyceridemia-induced hyponatremia, we use the following equation:
$\text{Corrected Na}^+ = \text{Measured Na}^+ + \left[\left(0.21 \times \text{triglycerides (g/L)}\right) - 0.6\right] \times \frac{\text{Na}^+}{100}$
Let’s go through the calculation for a sample with:
Triglyceride concentration: 1500 mg/dL (or 15 g/L, since 1 g/L = 100 mg/dL)
Measured sodium concentration: 130 mmol/L
Step-by-Step Calculation:
Convert triglycerides to g/L:
Triglycerides are already given as 15 g/L.
Calculate the correction factor:
$0.21 \times \text{triglycerides} - 0.6 = 0.21 \times 15 - 0.6 = 3.15 - 0.6 = 2.55$
Apply the correction factor to sodium:
$\text{Correction term} = 2.55 \times \frac{130}{100} = 2.55 \times 1.3 = 3.315$
Add the correction to the measured sodium:
$\text{Corrected Na}^+ = 130 + 3.315 = 133.315 \approx 133.3 \text{ mmol/L}$
So, with a triglyceride concentration of 1500 mg/dL and a sodium concentration of 130 mmol/L, the corrected sodium concentration is approximately 133.3 mmol/L.

SamuelYHuang

Search This Blog