Compassion•Accountability•Effectiveness

Hypertriglyceridemic pancreatitis-a case report
黃博彥 陳欽明 陳志金 廖家德 許鄭億
奇美醫學中心加護醫學部
Department of Intensive Care Medicine,
Chi Mei Medical Center, Tainan, Taiwan
Case presentation
A 47-year-old man was admitted to intensive care unit for the management of acute pancreatitis and acute renal insufficiency
with hyponatremia, hyperkalemia and hypocalcemia. He had a medical history of recurrent pancreatitis for two times and
hypertension, poor controlled diabetes mellitus but no urolithiasis. He had a family history of hypertriglyceridemia (HTG) and he
was not a heavy drinker. Endotracheal intubation was performed due to acute respiratory failure. After drawing his blood, a
lactescent (milky-white) appearance of supernatant was noted (figure 1a). Biochemistry laboratory data revealed high triglyceride
(TG) level (5655 mg/dL). Continuous venous venous hemofiltration (CVVH) was set up for acute renal failure with metabolic
acidosis and hyperkalemia. Double filtration plasmapheresis (DFPP) for 3000ml was performed for hypertriglyceridemia after
consulted nephrologist. The lactescent plasma became clearer after DFPP (fig. 1b, c). The triglyceride level dropped to 313 mg/dL
after DFPP. Adequate fluid hydration, pain control and imipenam were used. The CVVH was removed 4 days later. The patient was
extubated 12 days later and was transferred to ordinary ward.
Discussion/Conclusion
Lactescent blood was a clinical sign of severe hypertriglyceridemia (TG >10 mmol/L). The risk of pancreatitis increased as a
function of the plasma creamy white collar and was the greatest among nonobese individuals with early-onset lactescence not
responding to current TG-lowering drugs (familial hyperchylomicronemia). Patients with lactescent plasma and yellowish palmar
xanthomas (dysbetalipoproteinemia) responded significantly better to fibrates than the other severe hyperTG phenotypes but were
at greater risk of peripheral atherosclerosis [1]. The mechanism for hypertriglyceridemic pancreatitis (HTGP) is postulated to
involve hydrolysis of TG by pancreatic lipase and release of free fatty acids that induce free radical damage. Early initiation of
treatment with HTGP is likely to be beneficial but establishment of indications for apheresis and guidelines for its timing still
require further investigation. When serum is grossly lipemic or TG is >1,000 mg/dl, the clinician should prepare for acute HTG
management with a goal TG < 500 mg / dl [2]. But the American Society for Apheresis (ASFA) Apheresis Applications Committee
guidelines currently only suggest DFPP or plasma exchange for familial hypertriglyceridemia instead of hypertriglyceridemic
pancreatitis [3]. The relationship between cause and effect of hypertriglyceridemia and acute pancreatitis still controversial and
clinically had no consensus of recommendation of reduce hypertriglyceridemia for acute hypertriglyceridemic pancreatitis yet.
References
1. Karine Tremblay, PhD, Julie Méthot, BPharm, PhD, Diane Brisson, PhD, Daniel Gaudet, MD, PhD. Etiology and risk of lactescent
plasma and severe hypertriglyceridemia. Journal of Clinical Lipidology. Volume 5, Issue 1 , Pages 37-44, January 2011
2. Wayne Tsuang , MD1, Udayakumar Navaneethan , MD, Luis Ruiz, MD, Joseph B. Palascak, MD and Andres Gelrud, MD, MMSc.
Hypertriglyceridemic Pancreatitis: Presentation and Management. Am J Gastroenterol 2009; 104:984-991.
3. Zbigniew M. Szczepiorkowski, Jeffrey L. Winters, Nicholas Bandarenko, Haewon C. Kim, Michael L. Linenberger, Marisa B.
Marques, Ravindra Sarode, Joseph Schwartz, Robert Weinstein, and Beth H. Shaz. Guidelines on the Use of Therapeutic
Apheresis in Clinical Practice-Evidence-Based Approach from the Apheresis Applications Committee of the American Society for
Apheresis. Journal of Clinical Apheresis 25:83-177 (2010)
Figure Legends
(a)
(b)
(c)
Figure 1. (a)Lactescent supernatant was noted of his blood sample.
(b)lactascent plasma(yellow arrow) during DFPP,
(c)Lactescent part became clear after double filtration plasmapheresis(DFPP).
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