Plasma exchange treatment for acute hyperlipidemic pancreatitis with falsely low levels of serum triglycerides – a case report

Plasma exchange treatment for acute hyperlipidemic pancreatitis with falsely low levels of serum triglycerides – a case report

Transfusion and Apheresis Science 51 (2014) 178–180 Contents lists available at ScienceDirect Transfusion and Apheresis Science j o u r n a l h o m ...

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Transfusion and Apheresis Science 51 (2014) 178–180

Contents lists available at ScienceDirect

Transfusion and Apheresis Science j o u r n a l h o m e p a g e : w w w. e l s e v i e r. c o m / l o c a t e / t r a n s c i

Case Report

Plasma exchange treatment for acute hyperlipidemic pancreatitis with falsely low levels of serum triglycerides – a case report A. Markota a, M. Knehtl b,*, A. Sinkovic a, R. Ekart c, R. Hojs b, S. Bevc b a

Department of Internal Intensive Medicine, Clinic for Internal Medicine, University Medical Centre Maribor, Ljubljanska 5, SI-2000 Maribor, Slovenia Department of Nephrology, Clinic for Internal Medicine, University Medical Centre Maribor, Ljubljanska 5, SI-2000 Maribor, Slovenia c Department of Dialysis, Clinic for Internal Medicine, University Medical Centre Maribor, Ljubljanska 5, SI-2000 Maribor, Slovenia b

A R T I C L E

I N F O

Article history: Received 12 May 2014 Accepted 19 August 2014 Keywords: Acute pancreatitis Plasma exchange Serum triglycerides

A B S T R A C T

Hypertriglyceridemia is a well-recognized cause of acute pancreatitis. We present a patient with acute hypertriglyceridemic pancreatitis. At presentation serum triglycerides were severely elevated (104 mmol/l) and were decreasing the next day (11 mmol/l). However, based on increasing levels of serum lipase, worsening respiratory failure and evidently lipemic serum, we decided to perform plasma exchange, and patient’s condition improved dramatically. Repeated laboratory test of the serum obtained before the first plasma exchange revealed that the actual value of serum triglycerides was 57 mmol/l. A clinically-driven decision is crucial when treating patients with hypertriglyceridemic acute pancreatitis as the serum triglyceride levels can be falsely low. © 2014 Elsevier Ltd. All rights reserved.

Introduction Acute pancreatitis is a common condition with several possible etiologies. Mortality rate of severe acute pancreatitis is around 50% [1]. Ethanol and gallstones are the most common etiologies; however, metabolic, drug-related and iatrogenic causes are responsible for around 20% of cases [2]. Hypertriglyceridemia (HTG) is the cause of about 5% of all cases of acute pancreatitis and is the most common cause of acute pancreatitis not due to gallstones or ethanol [1,2]. HTG-induced acute pancreatitis usually occurs when serum triglyceride levels exceed 20 mmol/l [2,3]. HTG can cause multiple spurious laboratory results, which can make a diagnosis of acute pancreatitis difficult. Moreover, HTG can produce falsely low triglyceride levels, making appropriate treatment decisions also difficult [2,4,5].

* Corresponding author. University Medical Centre Maribor, Clinic for Internal Medicine, Department of Nephrology, Ljubljanska 5, SI-2000 Maribor, Slovenia. Tel.: +386 2 321 28 71; fax: +386 2 331 23 93. E-mail address: [email protected] (M. Knehtl). http://dx.doi.org/10.1016/j.transci.2014.08.015 1473-0502/© 2014 Elsevier Ltd. All rights reserved.

We present a patient who was diagnosed with acute hypertriglyceridemic pancreatitis and transferred to our hospital. At presentation serum triglycerides were severely elevated, the repeated laboratory tests showed decreasing serum triglyceride levels. However, based on clinical deterioration, increasing levels of serum lipase, worsening respiratory failure and evidently lipemic serum, we decided to perform plasma exchange. Our patient improved dramatically after the treatment.

Case presentation Fifty-five-year-old man with a history of arterial hypertension and hyperlipidemia was transferred to our facility because of HTG-induced acute pancreatitis. His past history included acute biliary pancreatitis and cholecystectomy 4 years before present admission. His therapy regimen consisted of bisoprolol, ramipril/hydrochlorothiazide and rosuvastatin. Severe abdominal pain and nausea appeared 2 days before present admission. The diagnosis of HTGinduced acute pancreatitis was made in the peripheral

A. Markota et al./Transfusion and Apheresis Science 51 (2014) 178–180

hospital without plasma exchange capability. Laboratory tests in peripheral hospital revealed leukocytosis (11.0 × 109/l), elevated serum glucose (14.8 mmol/l), elevated serum lipase (4.7 mckat/l) and amylase (1.9 mckat/l), elevated C-reactive protein (41 mg/l), severely elevated serum triglycerides (104 mmol/l) and serum cholesterol (20.1 mmol/l). Patient was fasted and treated with insulin and glucose infusion. On admission to our hospital he was afebrile, his blood pressure was 146/88 mmHg, heart rate 110/min and peripheral oxygen saturation was 96% without supplemental oxygen. His body mass index was 35.5 kg/m2. Abdominal examination was diffusely painful, especially in the epigastrium. Repeated laboratory results revealed decreasing levels of serum triglycerides (11 mmol/l) and cholesterol (3.5 mmol/l), elevated serum glucose (16.5 mmol/l) and lipase (20.8 mckat/l). Abdominal ultrasound showed acute edematous pancreatitis with no signs of necrosis and liver steatosis. As the level of serum triglycerides seemed to decrease, we decided not to perform plasma exchange. However, during the following 12 hours abdominal tenderness became more pronounced, tachycardia worsened (heart rate 125/min), patient became febrile (body temperature 38.6 °C), pancreatic enzyme levels continued to increase (serum lipase increased to 62.8 mckat/l, serum amylase to 2.0 mckat/l) and C-reactive protein increased to 390 mg/l. Respiratory failure developed and supplemental oxygen (via non-rebreather mask) was required to maintain peripheral oxygen saturation at 95%. Based on clinical deterioration, laboratory tests (especially increasing levels of serum lipase), worsening respiratory failure and evidently lipemic serum (Fig. 1) we decided to perform plasma exchange in-spite of decreasing levels of serum triglycerides. Vascular access was established via right internal jugular vein. One calculated plasma volume was processed during each session of plasma exchange with blood flow rate of 100 ml/min. Two plasma exchange procedures were performed on 2 consecutive days. Plasma was substituted with a solution of 20% human albumin. Coagulation was prevented with heparin infusion. Procedures lasted 5.6 and 6.6 hours. There were

Fig. 1. Hyperlipemic serum of the patient suggested that the actual value of serum triglycerides was higher.

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no side-effects of plasma exchange. Already during the first plasma exchange procedure patient’s respiratory function improved and abdominal tenderness decreased. Because of macroscopically visible lipemic serum and waste fluid we decided to repeat laboratory tests for hyperlipidemia. Laboratory staff were contacted and notified regarding the discrepancy between clinical course and laboratory results. Repeated laboratory tests of the serum obtained before the first plasma exchange procedure revealed that the actual value of serum triglycerides was 57.0 mmol/l and not 11.1 mmol/l. After the first plasma exchange procedure serum triglyceride levels decreased to 18.9 mmol/l and serum lipase decreased to 29.1 mckat/l. Fraction of inspired oxygen could be decreased immediately after the first plasma exchange session (to oxygen via 28% Venturi mask) and supplemental oxygen could be withdrawn after the second session. Three days after admission to our hospital serum lipase decreased to 8.9 mckat/l, serum triglyceride levels decreased to 6.0 mmol/l and physical examination was unremarkable. Treatment with statin and gemfibrozil was initiated along with fat- and sugar-restricted diet. The patient was discharged home after 17 days of treatment. Discussion HTG-induced acute pancreatitis is defined by the presence of elevated triglyceride levels (>11.3 mmol/l) and lactescent serum in the absence of other etiologic factors [6,7]. Failure to investigate lipid levels as the cause of acute pancreatitis can lead to clinical deterioration. HTG-induced acute pancreatitis with serum triglyceride levels >20 mmol/l must be distinguished from mildly elevated triglycerides (up to 10 mmol/l), which can be present in about 50% of patients with acute pancreatitis associated with other etiologies. Serum triglyceride levels of less than 5.7 mmol/l should not be incriminated as a factor in the etiology of pancreatitis [8,9]. Mildly elevated levels of serum triglycerides can remain for about 2 weeks after presentation. In a patient with acute pancreatitis and mildly elevated triglyceride levels false conclusions about pancreatitis etiology can be made. Apart from acute pancreatitis, elevated serum triglyceride levels can be associated with xanthomas, lipemia retinalis, abdominal pain (“hyperlipemic abdominal crisis”), hepatosplenomegaly and neuropathy [2,10]. Elevated serum triglyceride levels can cause multiple spurious laboratory results. Measurements of serum sodium, serum and urine amylase and hemoglobin, are most often affected. Excess triglycerides in serum can displace sodium diluted in water and cause pseudo-hyponatremia. Laboratory determination of amylase levels is affected by triglycerides interfering with amylase calorimetric determination [11]. Patients with acute severe hyperlipidemic pancreatitis usually have falsely normal amylase levels [2]. Increased plasma turbidity may be associated with falsely high hemoglobin levels [4]. Triglyceride assays can be subject to interference at triglyceride levels >20 mmol/l. The interference is caused by anaerobic conditions associated with grossly/high lipemic plasma. Anaerobic conditions can alter enzymatic reactions performed during triglyceride assay and may markedly underestimate final values of triglyceride concentrations.

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Decreased oxygen content that occurs in serum samples with highly elevated lipid levels is a result of rapid utilization of oxygen during enzymatic reaction cascade. The solution for samples with surprisingly low results and at the same time evidently lipemic plasma is to re-assay after diluting or using a smaller volume of sample [5]. Use of plasma exchange in the setting of HTG-induced acute pancreatitis has been described in case reports, case series, and one nonrandomized controlled trial. Reductions in triglyceride levels of 46–80% have been reported with improvement in symptoms of pancreatitis following one to three plasma exchange procedures [12,13]. Plasma exchange was usually implemented early in the course of the HTG-induced acute pancreatitis, although some authors recommended its use only if there is no improvement with standard therapy [12]. The only nonrandomized trial performed by Chen et al. showed that plasma exchange cannot ameliorate the overall mortality or morbidity of HTGinduced acute pancreatitis. They found no difference between standard therapy and therapeutic plasma-exchange with regard to mortality, systemic complications, and local complications in patients with severe pancreatitis [14]. The time of plasma exchange might be crucial. If plasma exchange is performed as soon as possible, better result may be expected. Further studies are needed to clarify the role of plasma exchange in the treatment of HTG-induced acute pancreatitis [12,14]. We decided to perform plasma exchange because of clinical and laboratory deterioration and evident discrepancy between grossly lipemic serum and laboratory results that were released initially. Additionally, we were aware of development of systemic inflammatory response syndrome (SIRS) in our patient. SIRS can be treated with plasma exchange as well. Plasma exchange in the setting of SIRS was studied mostly in associated with sepsis, where it can be used as an adjuvant to conventional therapy. SIRS is associated with multiorgan failure and imbalance in the levels of various proteins associated with inflammatory response. It is thought that plasma exchange therapy acts by bringing the levels of inflammatory mediators closer to normal homeostatic levels [15,16]. Conclusions In conclusion, this paper highlights that careful clinicaldriven decision is crucial when treating patients with

HTG-induced acute pancreatitis. Clinicians need to consider the possibility of spurious laboratory results caused by HTG that may affect diagnosis and treatment of acute pancreatitis.

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