hypertriglyceridemia induced pancreatitis

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HYPERTRIGL LYCERIDE MIA INDUC CED PANC CREATITIS

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PERTRIGL

      

LYCERIDEMIA INDUC

  

CED PANCCREATITIS 

Case Report

CASE REPORT

A 32 year-old female presented to the emergencydepartment complaining of 12 hour upper abdominal painaccompanied by 2-3 episodes of vomiting. She was aknown diabetic for 4 years and had 2 episodes ofpancreatitis in past. She was on oral hypoglycaemic agentsand statins for the same. She had no history of gallstonedisease or alcohol intake. The patient’s physicalexamination revealed a mild upper abdominal tenderness.There were no signs of peritonitis. The rest of the clinicalexamination was normal. Her vital signs were: BloodPressure: 120/80 mmHg, Heart rate: 86 bpm. RespiratoryRate: 26 breaths/min, Temperature: 99ºF, Pulse Oximetry:95% (on air). Routine laboratory examinations revealedleukocytosis (WBC: 13,3 K/μL), hyperglycemia (378 mg/dL) and hyperamylasemia (serum amylase: 336 mg/dL).BMI was 33.75 kgr/m2. The lipid profile revealed animpressive elevation of triglycerides (4240 mg/dL) andcholesterol (325 mg/dL) levels. The serum was extremelylipemic (Fig 1). The abdomen computed tomographyconfirmed the diagnosis of pancreatitis. The patient wasadmitted for further evaluation and treat-ment.She wasmanaged conservatively with iv hydration and dietaryrestriction. Moreover, she was admitted to the ICU for 3days as she developed severe acidosis and respiratorycompromise. The patient was treated with rapid actinginsulin for 2 days during admission and underwent twosessions of plasmapheresis, in order to achieve quickimprovement of triglyceride levels. She was restarted onlipid-lowering medications (atorvastatin, fenofibrate). Herclinical condition improved significantly with NIV andplasmapheresis and the patient was discharged in goodhealth 15 days later, with a triglyceride level of 324 mg/dL.Uncontrolled diabetes with hypertriglyceridemia was

313 Apollo Medicine, Vol. 7, No. 4, December 2010

HYPERTRIGLYCERIDEMIA INDUCED PANCREATITIS

Bhavesh Thakkar, V Seshadri and KR PalaniswamyDepartment of Gastroenterology, Apollo Hospitals, Greams Road, Chennai 600 006, India.

Correspondence: Dr K R Palaniswamy, Senior Consultant, Department of Gastroenterology, Apollo Hospitals,Greams Road, Chennai 600 006, India.

Background: A 32 year-old female presented to the emergency department complaining of 12 hours upperabdominal pain accompanied by 2-3 episodes of vomiting.Case report: The patient had a heavy meal a fewhours before. There were no signs of peritonitis. Routine laboratory examinations revealed leukocytosis,hyperglycemia and hyperamylasemia (serum amylase: 336 mg/dL).Conclusion:The lipid profile revealed animpressive elevation of triglycerides (4240 mg/dL). The serum was extremely lipemic. The abdomencomputed tomography confirmed the diagnosis of pancreatitis.

Fig 1 Lipemic serum- picture after plasmapheresis.

probably the cause of this episode of acute pancreatitis.

Hypertriglyceridemia is a relatively uncommon causeof pancreatitis [1]. Pancreatitis secondary tohypertriglyceri-demia typically presents as an episode ofacute pancreatitis (AP) or recurrent pancreatitis and rarelyas chronic pancreatitis [1,2]. An important and usuallyidentifiable risk factor is a serum triglycerides level of1000-2000 mg/dL in a patient with an already known typeI, IV or V hyperlipidemia (Fredrickson’s classification).The typical clinical profile is a patient presenting with apreexisting lipid abnormality in combination with asecondary co-releasing factor, such as poorly controlled

Apollo Medicine, Vol. 7, No. 4, December 2010 314

Case Report

diabetes mellitus, medications related to induction of AP oralcohol consumption. In addition to the usual findings inAP, in Hyperlipidemic Pancreatitis (HLP), the serumpancreatic enzymes may be normal or slightly elevated [3],even in the presence of severe AP that has been confirmedby imaging techniques [2,4]. The diagnostic hallmarkconsists of a mildly elevated amylase with interestingly lowurine amylase levels along with the presence of lipemicserum in a patient with a family history of disturbed lipidprofile [1]. As far as it concerns the clinical course of HLP,it does resemble to that of AP derived from other causes,with similar complications but not in a higher rate than inother types of AP. Routine management should not differmuch, aiming at a reduction of triglyceride levels to lessthan 1000 mg/dL, through dietary restriction of fat andlipid-lowering medications (mainly fibric acid derivatives:fenofibrate). Such a reduction has been proved to preventfrom recurrent episodes of AP, whereas there are anecdotalreports of other therapies, such as plasmapheresis.

CONSENT

Written informed consent was obtained from the patientfor publication of this case report and accompanyingimages.

REFERENCES

1. Linares LC, Pelletier AL, Czernichow S, Vergnaud AC,Bonnefont-Rousselot D, Levy P, et al. Acute pancreatitis ina cohort of 129 patients referred for severehypertriglyceridemia. Pancreas. 2008; 37(1):13.

2. Tsuang W, Navaneethan U, Ruiz L, Palascak JB, GelrudA: Hypertriglyceridemic pancreatitis: presentation andmanagement. Am J Gastoenterol. 2009; 104(4): 984-991

3. Frank B, Gottlieb K. Amylase normal, lipase elevated: Is itpancreatitis? A case series and review of the literature. AmJ Gastroenterol. 1999; 94(2): 463-469.

4. Yadav D, Pitchumoni CS. Issues in Hyperlipidemicpancreatitis. J Clin Gastroenterol; 2003; 261(1): 54-62.

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