Lipemic serum in hyperlipidemic pancreatitis
© Michalakis et al; licensee BioMed Central Ltd. 2009
Received: 19 September 2009
Accepted: 18 November 2009
Published: 18 November 2009
A 37 year-old man presented to the emergency department complaining of six hour diffuse abdominal pain accompanied by persistent vomiting.
The patient had a heavy meal a few hours before. There were no signs of peritonitis. Routine laboratory examinations revealed leukocytosis, hyperglycemia and hyperamylasemia (serum amylase: 380 mg/dl, urinary amylase: 1150 mg/dl).
The lipid profile revealed an impressive elevation of triglycerides (4800 mg/dl) and cholesterol (1009 mg/dl) levels. The serum was extremely lipemic. The abdomen computed tomography confirmed the diagnosis of pancreatitis.
Hypertriglyceridemia is a relatively uncommon cause of pancreatitis . Pancreatitis secondary to hypertriglyceridemia typically presents as an episode of acute pancreatitis (AP) or recurrent pancreatitis and rarely as chronic pancreatitis [1, 2]. An important and usually identifiable risk factor is a serum triglycerides level of 1000-2000 mg/dl in a patient with an already known type I, IV or V hyperlipidemia (Fredrickson's classification). The typical clinical profile is a patient presenting with a preexisting lipid abnormality in combination with a secondary co-releasing factor, such as poorly controlled diabetes mellitus, medications related to induction of AP or alcohol consumption. In addition to the usual findings in AP, in Hyperlipidemic Pancreatitis (HLP), the serum pancreatic enzymes may be normal or slightly elevated , even in the presence of severe AP that has been confirmed by imaging techniques [2, 4]. The diagnostic hallmark consists of a mildly elevated amylase with interestingly low urine amylase levels along with the presence of lipemic serum in a patient with a family history of disturbed lipid profile . 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 in other types of AP. Routine management should not differ much, aiming at a reduction of triglyceride levels to less than 1000 mg/dl, through dietary restriction of fat and lipid-lowering medications (mainly fibric acid derivatives). Such a reduction has been proved to prevent from recurrent episodes of AP, whereas there are anecdotal reports of other therapies, such as plasmapheresis.
Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
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