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Therapeutic Apheresis and Dialysis 2015; 19(4):405410
doi: 10.1111/1744-9987.12286
2015 The Authors
Therapeutic Apheresis and Dialysis 2015 International Society for Apheresis
Extracorporeal Treatment in Severe
Hypertriglyceridemia-Induced Pancreatitis
Heike Zeitler, Zeynep Balta, Burkhard Klein, and Christian P. Strassburg
Internal Medical Clinic I, Centre of Extracorporeal Therapy and Autoimmunity (CETA), University of Bonn,
Bonn, Germany
Abstract: Plasmapheresis is a well-accepted treatment
option in severe hypertriglyceridemia-induced pancreatitis
(HTGP). The rationale behind this approach is the deple-
tion of triglycerides and the reduction of inflammatory
cytokines. The time span between onset of clinical symp-
toms and start of plasmapheresis might have an important
impact on mortality. Hyperviscosity of patients plasma
represents another special challenge for the applied sepa-
ration technology. The procedures can be performed either
by centrifugal device (CFD) or membrane based (MBS)
units. The present study reports the outcome of 10 patients
Hypertriglyceridemia (HTG) is, beside gallstones
and alcohol, the third major cause of pancreatitis
(HTGP) and occurs in about 1.33.8% of cases in
acute pancreatitis (1). HTGP mainly occurs in fasting
triglyceride (TG) levels of >1000 mg/dL. TG eleva-
tion can result from increased production and/or a
reduced catabolism due to a defective hydrolysis of
TG enriched particles. Defective lipolysis can be
caused by a variety of genetic defects such as muta-
tions of the lipoprotein lipase (LPL) resulting in a
reduced activity of this a key enzyme of TG metabo-
lism (2). In a case study reported by Watts et al. a
deficiency of the lecithin-cholesterol acyltransferase
resulted in an acute period of HTGP and was treated
successfully with plasma infusion to correct the
dyslipidemia (3,4). Besides enzyme defects, muta-
tions of apolipoproteins can impair LPL function.
The deficiency of apolipoprotein CII can result in a
minor LPL activity decreasing the hydrolysis of TG
enriched particles in patients plasma (4).An increase
Received May 2014; revised September 2014.
Address correspondence and reprint requests to Dr Heike
Zeitler, Senior Physician, Internal Medical Clinic I, CETA, Uni-
versity of Bonn, Sigmund Freud Str. 27, 53127 Bonn, Germany.
Email: heike.zeitler@ukb.uni-bonn.de
These authors contributed equally to the work.
405
suffering from HTG. The expected mortality of the collec-
tive was 25%. Plasmapheresis was started after an average
16.3 h (SD 6.7 h) after onset of symptoms. No mortality
occurred. Apheresis was statistically equally effective with
both devices. A median of 3 sessions reduced the TG level
to normal and correlated with patients improvement.
During follow up, three patients developed a pancreatic
pseudocyst requiring surgical intervention without further
complication. Key Words: Hypertriglyceridemia, Pan-
creatitis, Plasmapheresis.
of apolipoprotein CIII, as it is described in metabolic
syndrome and diabetes mellitus type II, causes an
inhibition of the LPL activity and blocks the lipopro-
tein uptake by the liver. In contrast to apolipoprotein
CII deficiency the apolipoprotein CIII induced HTG
is linked with an increased risk of atherosclerosis
mediated by the activation of proinflammatory signal
transduction of vascular cells (5,6). In most cases
other exacerbating factors like diabetes mellitus,
alcohol intake, fatty and carbohydrate-rich nutrition
can trigger HTGP. In all cases the TG clearance
is insufficient, leading to an accumulation of
chylomicrons and/or very low density lipoproteins
(VLDL) (7). The accumulation of large lipoproteins
with diameters varying from 50 nm (VLDL) to
1000 nm (chylomicrons) increases plasma viscosity
and finally impairs blood flow in all organs. Another
cause of HTGP may be a breakdown of TG to free
fatty acids by pancreatic lipase, inducing a severe
toll-like receptor 2 and 4 mediated inflammatory
response followed by pancreatic autodigestion
(8,9). Therefore HGTP is considered to cause a
higher morbidity and mortality than other types of
pancreatitis (10). Plasmapheresis is an accepted
treatment option allowing a fast reduction of TG and
pro-inflammatory cytokines. The American Society
406 H Zeitler et al.

for Apheresis (ASFA) therefore suggests it as a
Grade 2C indication (10,11). The procedure can be
performed either with centrifugal device (CFD) or
with membrane based separation (MBS) units. The
hyperviscous plasma in HTGP represents a special
challenge for the applied separation technology.
Data comparing both methods with respect to treat-
ment efficacy and patient outcome are therefore of
great interest. The present study retrospectively
analyzes the results for 10 patients suffering from
HTGP who underwent either CFD or MBS based
plasmapheresis.
PATIENTS AND METHODS
Patients
This observational retrospective study analyzes 10
patients admitted at the Emergency Unit, Medical
Clinic I University of Bonn from 2009 to 2014. All
patients experienced the diagnosis of HTGP and
were treated by plasmapheresis. The diagnosis of
HTGP was based on patients clinical symptoms
(upper abdominal pain, nausea, vomiting) and was
confirmed by biochemical and radiological examina-
tions. Biochemical analyses performed were: choles-
terol, triglycerides, lipase, alpha amylase, CRP, GOT,
GPT, yGT, calcium, potassium, magnesium, red blood
cell counts, creatinine, glucose and HbA1c. The diag-
nosis was confirmed by ultrasonic and abdominal
computer tomography (CT) according to the Atlanta
classification (12). CT was performed in general
within 72 h after onset of symptoms to diagnose the
complexity of pancreatic damage.
All patients were classified for disease severity
according to the APACHE II (13) and the Ranson
score (14). The grade of pancreatitis was verified
by computer tomography severity index based on
the Balthazar score (15) as defined; Grade A: Normal
pancreasnormal size, sharply defined, smooth
contour, homogeneous enhancement, retroperitoneal
peripancreatic fat without enhancement; Grade
B: Focal or diffuse enlargement of the pancreas,
contour may show irregularity, enhancement may
be inhomogeneous but there is no peripancreatic
inflammation; Grade C: Peripancreatic inflammation
with intrinsic pancreatic abnormalities; Grade D:
Intrapancreatic or extrapancreatic fluid collection;
Grade E: Two or more large collections of gas in the
pancreas or retroperitoneum.
Information was gathered on demographic data,
patients family history of dyslipidemia, and patients
history of dyslipidemia, medical treatment, diabetes,
arterial hypertension, alcohol consumption, smoking
and former episodes of pancreatitis. Patients charac-
teristics on admission are summarized in Table 1.
Plasmapheresis was performed either with a centrifu-
gal device using a Cobe Optia (Gambro, Lund,
Sweden) or as a membrane plasma separation (MPS)
performed by Octonova (Diamed Medizintechnik,
Cologne, Germany) using a Plasmaflo filter OP-05W
(L), a polyethylene hollow fiber membrane. The
filter allows blood flow rates of 80130 mL/min,
with plasma filtration rates of 2040 mL/min, and a
transmembranous pressure (TMP) maximum of
45 mm Hg. The anticoagulation of the centrifugal
procedure was performed with a combination of acid
citrate monohydrate solution (Fenwal ACD-A
Fenwal Europe sprl, Mont Saint Guibert, Belgium)/
heparin combination. The extracorporeal system was
primed with ACD-A and 2500 IU heparin. When
apheresis started, another bolus of 2500 IU heparin
was given into the arterial inflow line. The ratio of
ACD-A to plasma was in general a maximum of 1:8
1:10, and could be adapted to the blood flow with

TABLE 1. Patients characteristics on admission

ID Age Apa Ran Balt BMI Chol TG Lip CRP Ca BG HDL A1 LDL B100 Assoc. Dis
1 39 16 6 E 28 779 11 103 795 206 1.65 145 36 na 121 na DF DM RI DL
2 59 13 6 D 26 662 4 597 2 696 375 1.60 281 33 na 90 na NODM DL
3 36 10 6 E 35 787 8 540 2 831 370 1.28 553 32 na 115 na NODM DL
4 36 12 8 E 35 490 6 186 2 567 200 1.68 260 48 1.7 159 1.4 DM DF DL
5 34 8 5 D 29 304 1 630 1 856 2.6 1.77 360 47 1.6 122 1.3 DM DF DL
6 45 8 5 D 30 521 4 945 550 42 1.78 106 39 1.4 91 1.4 DL DF
7* 44 10 6 E 28 233 671 828 19 1.18 233 31 1.3 86 1.4 Alcohol DM DL
7 44 10 6 E 28 297 2 703 1 289 205 1.12 152 na na na na Alcohol DM DL
8 21 16 7 E 24 315 2 329 14 583 181 1.10 104 30 1.3 145 1.2 DF DL
9 34 6 3 C 25 510 10 817 916 45 0.98 78 34 1.2 161 1.5 Alcohol DL
10 42 6 6 E 30 627 10 000 972 184 1.81 98 41 1.6 130 1.2 Alcohol DL

Apa, APACHE II score; Assoc. Dis., associated disorder; Balt, Balthazar score; BG, blood glucose mg/dL; Ca, serum calcium mmol/L; Chol,
cholesterol mg/dL; CRP, C reactive protein mg/L; DF, diet failure; DL, dyslipidemia; DM, diabetes mellitus; Lip, lipase U/L; na, not available;
NODM, new onset of diabetes mellitus; Ran, Ranson score; RI, renal impairment; TG, Triglycerides mg/dL.

2015 The Authors

Ther Apher Dial, Vol. 19, No. 4, 2015 Therapeutic Apheresis and Dialysis 2015 International Society for Apheresis
 Plasmapheresis For Hypertriglycerdemia-Induced Pancreatitis 407

TABLE 2. Patients plasmapheresis data

ID Treatment Time to PE hours Unit TG before TG after TG % PV % PP time AE
1 1 12 1 11 103 2153 81% 80% 104 BP
2 1 2 153 794 63% 79% 98 BP
3 1 800 240 70% 79% 99 BP
2 1 12 1 4 597 1860 60% 77% 88
2 1 1 860 556 70% 77% 88
3 1 563 198 65% 87% 45
3 1 18 1 8 540 2815 67% 79% 85
2 1 2 815 712 75% 80% 85
3 1 760 130 83% 79% 83
4 1 8 1 6 186 4594 26% 79% 103
2 1 1 565 268 83% 79% 103
5 1 24 1 1 630 835 49% 88% 67
2 1 835 530 37% 88% 67
3 1 530 198 63% 86% 74
6 1 24 1 4 945 1480 70% 82% 91 BP
2 1 1 510 950 37% 82% 37
3 1 950 148 84% 82% 54
7 1 48 2 1 195 827 31% 84% 100
2 2 1 037 507 51% 84% 95
3 2 671 408 39% 84% 144 BP
4 2 814 297 64% 84% 110
7* 1 12 2 2 703 1800 33% 112% 150
2 2 1 800 710 61% 112% 127
3 2 710 98 86% 112% 130
8 1 12 2 2 329 720 69% 107% 135
2 2 820 370 55% 107% 110
9 1 12 2 10 817 4514 58% 96% 165
2 2 4 514 1472 67% 96% 120
3 2 1 472 410 72% 96% 120
10 1 12 2 10 000 3587 64% 87% 220
2 2 3 587 1481 59% 87% 190
1 481 490 67% 87% 120

Time from onset of symptoms until start of plasmapheresis in hours, numbers of plasmapheresis sessions; AE, adverse events of
plasmapheresis; BP, low blood pressure; PV%, percentage part of the exchanged plasma volume per treatment; TG%, percentage decrease
of triglyceride level per treatment; Unit 1, centrifugal device (CFD); Unit 2, membrane based plasma separation (MBS).

lower rates of 1:151:20. To protect the patient from
hypocalcemia, continuous 10% calcium gluconate
infusion was added to the venous bloodline. As vas-
cular access a Shaldon catheter was used in all MPS
treated patients, whereas five patients of the CFD
group could be treated by peripheral vascular access.
CFD allows lower blood flow rates of 5080 mL/min
and, depending on inflow rate, plasma flow rates of
2040 mL/min. In MPS the extracorporeal system
was primed with 5000 IU heparin. During treatment
a heparin based continuous infusion of 600
1000 IU/h depending on blood/plasma flow rates and
TMP (<45 mm Hg), was performed. The exchanged
plasma volume was adapted to the patients clinical
situation. In general, 0.71.0 equivalents of the calcu-
lated plasma volume was intended to be exchanged.
As a replacement solution 5% albumin was chosen.
The TG levels were measured before and after each
procedure. Plasmapheresis was continued until a TG
level below 500 mg/dL was achieved. Clinical data of
plasmapheresis treatment are summarized in Table 2.
For each patient, data were recorded concerning time
to onset of apheresis and the clinical symptoms, the
number of plasmapheresis sessions the exchanged
volume, the replacement procedures, complications
and adverse effects of apheresis, hospitalization
days, as well as any other clinical events during the
hospitalization.
Data analysis
All statistical analyses were performed using the
Statistical Package for Social Sciences, version 22.0
(SPSS, Chicago, IL, USA). Descriptive statistics have
been used to characterize the study population. Non-
parametric statistics, the Spearmans-Rho rank corre-
lation (rs) and the MannWhitney U-test were used.
The clinical and technical parameters related to
extracorporeal treatment groups were compared
using the MannWhitney U-test. A P-value of 0.05 or
less was considered statistically significant.

2015 The Authors

Therapeutic Apheresis and Dialysis 2015 International Society for Apheresis Ther Apher Dial, Vol. 19, No. 4, 2015
408 H Zeitler et al.
RESULTS
Ten patients (six males/four females) suffering
from severe HTGP underwent plasmapheresis.
Patients characteristics at initial presentation were
summarized in Table 1. Their median age was 39
years (range: 2159 years). The median BMI was
28 kg/m2 (range: 2435), therefore diabetes mellitus
(DM) was the most usual personal history beside
alcoholism and dietary failures (DF). The family
history of lipid disorders and HTGP was negative in
all patients. None of the patients had received a
regular lipid lowering medical treatment prior to
HTGP. One patient (patient 10) had a history of
HTGP and had undergone gastrojejunostomy in
another hospital 4 years before. In two patients
(patients 2 and 3) a new onset of diabetes mellitus
(NODM) resulted in a metabolic decompensation
with HTGP. At initial presentation the mean choles-
terol level was 502 mg/dL (SD 197 mg/dL) the
mean triglyceride level was 5774 mg/dL (SD
3822 mg/dL). An elevation of the lipase (normal
range: 73393 U/L) was found in all patients with in
mean 2716 U/L (SD 5076 U/L).
Seven patients suffered from Type E pancreatitis as
diagnosed by contrast enhanced computer tomogra-
phy. Severe hypocalcemia was seen in nearly all
patients with a mean calcium concentration of
1.45 mmol/L (SD 0.31 mmol/L). The mean Ranson
score of 5.8 (SD 1.2, expected mortality 40%) and
an average APACHE II score of 10 (SD 3.5,
expected mortality 11%) corresponded to an
expected median mortality of 25% for both scores.
The disease severity Ranson score correlated signifi-
cantly with the APACHE (rs = 0.702, P = 0.016) and
Balthazar score (rs = 0.787, P = 0.004).
The mean CRP level at initial presentation was
166 mg/L (SD 129.8 mg/L, normal range: <3 mg/L).
HTG and CRP levels were not correlated to the clini-
cal scores.
All patients underwent plasmapheresis for an
average of 16.3 h (SD 6.7 h) after onset of clinical
symptoms. Altogether, 30 plasmapheresis sessions
were performed without severe complications. Treat-
ment interruption due to patients discomfort or to
failure of the apheresis device did not occur.
In 80% of patients three apheresis sessions were
required to decrease TG below 500 mg/dL, one
patient received four sessions, and another patient
two sessions. The median TG decreases per plasma-
pheresis session in the Cobe Optia treated group
were at 63% (range: 2684%) statistically not signifi-
cantly higher than in the MPS group with 60% (range
3186%). In the MPS group an average of 96% (SD
Ther Apher Dial, Vol. 19, No. 4, 2015
11.5%) calculated plasma volume was exchanged
compared to the CFD (81% 3.5%). Hypotension
occurred in six patients mainly at the end of treat-
ment. It could be controlled by substitution with
calcium and saline infusions. Bleeding complications,
symptoms of severe hypocalcemia or allergic reac-
tions were not seen. There were no statistically rel-
evant differences between the MPS and the CFD
treated group concerning patients characteristics,
disease severity scores, the laboratory parameters
before/ after treatment and patients outcome.
All patients received an adjacent medical treat-
ment consisting of fenofibrate and atorvastatin
to reduce the de novo synthesis of TG. In case
of diabetes mellitus, adjacent intravenous insulin
treatment was started. All patients were under food
abstinence until TG levels decreased below 500 mg/
dL. Due to hypotension most patients required
intensive hydration with isotonic crystalline solution
at a mean 510 mL/kg per hour. Pain control was
achieved in most patients with intravenous
pethidine. One patient (patient 8) required peridural
anesthesia.
Outcome and follow up
Despite the expected mortality of 25% all patients
survived. After an average of 11.4 hospitalization
days (range: 725 days) all patients were discharged
with slightly elevated TG levels of in mean 163 mg/dL
(SD 40 mg/dL). During long term follow up of in
median 30 months (range: 648 months) one patient
(patient 7) relapsed due to medical incompliance, and
required two more plasmapheresis sessions. This
patient developed a pancreatic pseudocyst during
follow up. Twelve months after HTGP patient 1 suf-
fered from duodenal stenosis due to three pancreatic
pseudocyst and underwent surgical pancreatico-
jejunostomy. Patient 8 developed a superinfection
with pancreatic necrosis 10 days after plasmapher-
esis, which was resolved with a percutaneous drain-
age and systemic antibiotic treatment.
DISCUSSION AND CONCLUSIONS
Ten patients admitted at the Emergency Unit
experienced the diagnosis of HTGP. In this high risk
collective of HTGP patients no fatalities were seen.
Although the applied score systems predicted a mor-
tality of 25% the prompt initiation of plasmapheresis
after a median of 16 h seemed to have a beneficial
effect. A delay between onset of symptoms and plas-
mapheresis could have a negative impact on patients
outcome and has been seen by other authors (16,17).
Treatment within 48 h has been recommended after
2015 The Authors
Therapeutic Apheresis and Dialysis 2015 International Society for Apheresis
 Plasmapheresis For Hypertriglycerdemia-Induced Pancreatitis
onset of symptoms (18).The decrease of TG results in
a rapid lowering of the abdominal pain and patients
nausea. In our collective a reduction of TG to
<500 mg/dL required three apheresis sessions in
nearly all patients. An increased rate of plasma
exchange volume results in a progressive loss of
coagulation factors when the chosen substitute is 5%
albumin and not fresh frozen plasma. In our experi-
ence an exchange of 7080% of patients plasma
results in a 50% reduction of coagulation factors.
Hence, patients bleeding risk increases, especially
since the initial treatment requires intensive
anticoagulation to avoid system clotting. Gubensek
et al. described intestinal bleedings as a side effect of
apheresis (19). Bleeding into the inflamed pancreatic
tissue leads to additional organ damage, which can
cause the formation of pancreatic pseudocysts. In our
collective the clinical outcome was not different
between the MBS patients and the CFD group.
As mentioned above the chosen substitute during
plasmapheresis in our collective was 5% albumin. In
rare cases of patients with genetically proven Apo
CII or LCAT deficiency the substitution of fresh
frozen plasma during or after plasmapheresis might
be beneficial as it corrects the dyslipidemia (3,4).
Due to the potential infection risk of fresh frozen
plasma, its use should be reserved for rare clinical
conditions where lipid disorders are genetically
proven. In the future, genetic testing of lipid disorders
might allow a better individualized treatment deci-
sion. In the absence of genetic testing our study
therefore has some clinical limitations. Plasmapher-
esis in HTGP is a special challenge because it
requires adequate anticoagulation due to plasma
hyperviscosity, especially during the first apheresis
session, when the excessive TG levels can occlude the
extracorporeal system. Gubensek et al. reported that
in 10% of procedures the plasma filter had to be
replaced and in up to 3% the filter was clotted (19). In
our collective the combined ACDA/heparin during
CFD, as well as the continuous anticoagulation with
heparin, prevented system clotting sufficiently. Com-
paring CFD with MBS, no statistical differences con-
cerning efficacy and safety of therapy were seen.
Therefore, a treatment decision can be made based
on the availability of the apheresis device in the
medical center. Episodes of low blood pressure at the
end of apheresis sessions were seen in four patients
treated with CFD compared to only one patient in
the MBS group. Hypotonic blood pressure might
be triggered by the ACDA anticoagulation enhanc-
ing hypocalcemia that already pre-exists due to pan-
creatitis. The symptoms subsided promptly under
additional calcium gluconate infusion and fluid sub-
2015 The Authors
Therapeutic Apheresis and Dialysis 2015 International Society for Apheresis
409
stitution. The advantage of CFD is that lower blood
flow rates allow treatment via peripheral veins.
Avoiding a central venous access might be preferable
for some patients, especially since only two to three
sessions have to be performed. The role of heparin in
the treatment of HTGP is controversial (20). Heparin
stimulates the release of endothelial lipoprotein
lipase into the circulation and causes a rapid reduc-
tion of the TG level by converting them into free fatty
acids. Recently published data from Nasstrm et al.
show that flesh frozen plasma (FFA) are involved in
the inflammatory process of HTGP (21,22). Heparin
may worsen the condition and is not recommended
as a mono-treatment of HTGP (23). A rapid deple-
tion of the lipoprotein lipase storage retards the TG
clearing rate and has been reported in patients under
hemodialysis (22). These effects of heparin were not
seen under TG depletion during plasmapheresis.
Although early start of plasmapheresis leads to a fast
control of the acute clinical situation, the late onset
complications like pancreatic pseudocyst formation
were not prevented in three patients. These patients
underwent successful surgical interventions. The
benefit of apheresis was questioned by one study
published in 2004 by Chen et al. where an improved
outcome among HTGP patients treated with plasma-
pheresis vs. conventional treatment was not seen
(24). Finally, the answer to this question requires
randomized double blind controlled studies, which
might be, in our opinion, ethically problematic
according to recent published data supporting the
benefit of plasmapheresis in this high risk patient
collective (7,1619,23,25).
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2015 The Authors
Therapeutic Apheresis and Dialysis 2015 International Society for Apheresis