Steroid Induced Hyperlipidemic

Bhavini Bhavsar
, Archit Bhatt
Department of Adult Medicine, Michigan State University. East Lansing, MI, USA.
St. Barnabas Hospital. Bronx, NY, USA
Dear Sir:
Acute pancreatitis had been a known
complication of hypertriglyceridemia. Very
high levels of triglycerides (greater than 1,000
mg/dL) are usually associated with
pancreatitis. It is usually a challenge to treat
this fatal condition. We describe a case of
hypertriglyceridemia related pancreatitis in a
patient with new onset diabetes mellitus,
which was successfully treated with
A 40-year-old female with history of severe
asthma on oral prednisone 5 mg once a day
for 4 months presented with a two-day history
of nausea, vomiting, epigastric abdominal
pain, and increased thirst. There was no
history of hyperlipidemia. Patient did any
history of drug or alcohol abuse. Family
history was non-contributory. Review of
systems revealed no history of bloody
diarrhea and tenesmus. Clinical exam
revealed epigastric tenderness. The serum
amylase level was 8 times the reference
limits. Serum lipase was 7 times the normal
limits. Liver function tests were normal.
Urine analysis was normal. Coagulation
studies were normal. Patient was found to
have high serum glucose 700 mg/dL
(reference range: 70-105 mg/dL) but there
was no evidence of diabetic ketoacidosis.
Complete blood count was normal. Initial
serum triglyceride level was 3,500 mg/dL
(reference range: 50-250 mg/dL). CT scan
with contrast on day 3 revealed edematous
pancreas suggesting acute pancreatitis. There
was no evidence of dilated common bile duct
or stones. In addition to aggressive hydration
and supportive therapy, plasmapheresis and
continuous insulin drip were initiated. After
two sessions of plasmapheresis and intensive
blood glucose control for 48 hours, plasma
triglyceride levels improved to 650 mg/dL.
There was also improvement in abdominal
pain and appetite. Prednisone was
discontinued. Patient recovered by day 5 and
was discharged on long acting insulin and
gemfibrozil and simvastatin. According to
Atlanta criteria our patient had severe
pancreatitis. His Ranson`s score was 3. His
BUN rose from 13 to 23 mg/dL (reference
range: 8-20 mg/dL); his calcium was 7.9
mg/dL (reference range: 5-10.5 mg/dL), CRP
level was 3.6 mg/dL (reference range: 0-1
mg/dL); hematocrit fall was 15% in the first
48 hours. Plasmapheresis was done to rapidly
reduce the levels of circulating triglyceride
levels to prevent inflammation of the
Acute pancreatitis is a known complication of
severe hypertriglyceridemia, which is mostly
in related to uncontrolled diabetes mellitus or
type V hyperlipidemia. Elevated triglyceride
levels greater than 1,000 mg/dL are usually
associated with pancreatitis. The exact
pathologic mechanism is by which high
triglycerides cause pancreatitis is unknown.
However, it is postulated that elevated levels

Page 2
JOP. J Pancreas (Online) 2008; 9(5):664-665.
JOP. Journal of the Pancreas - - Vol. 9, No. 5 - September 2008. [ISSN 1590-8577]
of triglycerides and chylomicrons obstruct
capillaries and induce local ischemia. The
local inflammatory damage can lead to
cytotoxic injury perpetuated further by free
fatty acids. This inflammatory cascade results
in pancreatitis [1]. Other risk factors for
alcoholism, pregnancy, diet and anti-retroviral
drugs. Chronic steroid therapy is known to
cause hyperlipidemia and diabetes mellitus
[2]. Preclinical studies have shown that high
lipid content due to cholesterol rich diet
aggravates necrotizing pancreatitis [3].
Acute treatment of hyperlipidemic
pancreatitis includes aggressive insulin
therapy, heparin and plasmapheresis.
Plasmapheresis is reserved for severe cases of
pancreatitis especially in acute phase.
Plasmapheresis is a safe and highly effective
method for removing triglycerides [3]. Low
fat diet and aggressive treatment of
hyperlipidemia and diabetes is a key in
preventing pancreatitis. Rarely plasma-
pheresis is required to prevent
hypertriglyceridemia if there is failure of
conservative therapy [4, 5, 6].
On rare occasions, acute pancreatitis, as in our
case, is due to steroid induced hyper-
triglyceridemia and diabetes mellitus.
Our case emphasizes the two key aspects.
First, chronic steroid therapy is uniquely
implicated in development of hyperlipidemia
and diabetes mellitus leading to pancreatitis.
Secondly, hyperlipidemic pancreatitis once
recognized can be treated with plasma-
Received May 8
, 2008 - Accepted August
, 2008
Keywords Hypertriglyceridemia; Pancreatitis;
Conflict of interest The authors have no
potential conflicts of interest
Bhavini Bhavsar
Department of Adult Medicine
Michigan State University
East Lansing
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