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Managing Hypertriglyceridaemia-Associated Acute Pancreatitis
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*This study demonstrated that patients with both
pathogenic variants and high polygenic risk score of
triglyceride-rich lipoprotein metabolism had signicantly increased risk for very severe hypertriglyceridemia and acute pancreatitis, highlighting an important
role for genetic testing to identify individuals who can
maximally benet from novel triglyceride- lowering
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99. *Rosenson RS, Gaudet D, Ballantyne CM, et al.
Evinacumab in severe hypertriglyceridemia with
or without lipoprotein lipase pathway mutations: a
phase 2 randomized trial. Nat Med 2023;29:729–737.
*A phase 2 clinical trial which demonstrated that
evinacumab, a novel angiopoietin-like 3 inhibitor,
reduced serum triglyceride levels of patients with
severe hypertriglyceridaemia and a past history of
acute pancreatitis except for those who had familial
chylomicronemia syndrome without functional lipoprotein lipase.
Managing Idiopathic Pancreatitis
https://t.me/med1917
RowanW.Parks andElizabethGleeson
Key Points
1. “Idiopathic” pancreatitis is a diagnosis of
exclusion, and true idiopathic cases should
account for ≤20% of all acute pancreatitis etiologies after meticulous investigation.
2. Initial management of idiopathic acute pancreatitis is similar to management of other etiologies of pancreatitis.
3. Extensive workup should be performed to
identify the cause of pancreatitis in order to
provide adequate and appropriate treatment
which will, in turn, reduce recurrence. These
studies include serum IgG4 testing, genetic
testing in appropriate patient populations,
EUS, ERCP with biliary analysis, contrastenhanced CT, and MRCP.
4. Laparoscopic cholecystectomy should be performed if microlithiasis is found.
5. Further studies should be conducted to investigate multiple, or interacting, factors leading
to idiopathic acute pancreatitis.
R. W. Parks (*)
Royal Inrmary of Edinburgh, University of
Edinburgh, Edinburgh, UK
e-mail: r.w.parks@ed.ac.uk
E. Gleeson
University of North Carolina, Chapel Hill, NC, USA
e-mail: elizabeth_gleeson@med.edu.edu
1 Introduction
The term “idiopathic pancreatitis” has long been
dened as pancreatitis when the etiology cannot
be explained by thorough history, physical examination, laboratory studies, and imaging including transabdominal ultrasound and computed
tomography (CT). Previously, the prevalence of
idiopathic pancreatitis was reported to be as high
as 40% [1–3]. However, with advances in genetic
testing, computed tomography (CT), magnetic
resonance cholangiopancreatography (MRCP),
endoscopic retrograde cholangiopancreatography (ERCP), and endoscopic ultrasound (EUS),
79–80% of cases previously dened as idiopathic
now have a dened etiology [4–6]. Overall, the
mortality rate of acute pancreatitis is 2–11% but
is reportedly higher (14%) when the etiology is
idiopathic, or miscellaneous [2, 7]. Likewise,
recurrence of acute pancreatitis is also higher
when the etiology is idiopathic [3].
Patients for whom a diagnosis cannot be determined using conventional workup often undergo
multiple, expensive, and invasive procedures, as
early diagnosis and etiology-based therapy are
critical to achieve best outcomes and prevention
of recurrence [8]. Patients with true idiopathic
pancreatitis generally have had a comprehensive
assessment and the most common causes (Fig.1)
have been eliminated [6]. Table 1 shows an
exhaustive list of possible etiologies for idiopathic pancreatitis. After exclusion of other diagnoses, generally only 10% of cases persist as
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024
J. A. Windsor et al. (eds.), Acute Pancreatitis, https://doi.org/10.1007/978-981-97-3132-9_15
203
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Fig. 1 Causes of idiopathic pancreatitis
Category Etiology
Toxin Alcohol-related (>5 drinks
daily)
Scorpion venom
Organophosphorus insecticides
Cannabis
Cocaine
Opiates
Mechanical Gallstones
Microlithiasis/biliary sludge
Sphincter of Oddi dysfunction
Pancreas divisum
Autoimmune pancreatitis
Annular pancreas
Pancreatobiliary tumors
Choledochocele
Duodenal stricture or
obstruction
Ascariasis
Metabolic Hypertriglyceridemia
Hypercalcemia
Hyperparathyroidism
Trauma Blunt or penetrating abdominal
injury
Post-ERCP pancreatitis
ERCP sphincterotomy
Sphincter of Oddi manometry
Iatrogenic surgical
complication
Viral Mumps
Coxsackievirus type B
R. W. Parks and E. Gleeson
Table 1 (continued)Table 1 Possible etiologies of idiopathic pancreatitis
Category Etiology
Hepatitis B
Cytomegalovirus
Herpes simplex
Varicella zoster
HIV
Rubella
SARS-CoV-2
Bacterial Legionella
Leptospira
Salmonella
Mycoplasma
Brucella
Salmonella typhi
Fungal Aspergillus
Parasites Toxoplasma
Cryptosporidium
Ascaris lumbricoides
Antimicrobial
medications
HIV medications Didanosine
Diuretics Furosemide
GI medications 5-ASA
Metronidazole
Stibogluconate
Sulfonamides
Tetracycline
Nitrofurantoin
Erythromycin
Isoniazid
Pentamidine
Thiazides
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Table 1 (continued)
Category Etiology
Sulfasalazine
Cimetidine
Ranitidine
Mercaptopurine
Proton pump inhibitors
Cardiac medications Procainamide
Immunosuppressives L-asparaginase
Azathioprine
Cytosine
Arabinoside
Dexamethasone
Neuropsychiatric
medications
Other medications Acetaminophen
Autoimmune Sjogren’s syndrome
Genetic CFTR
Vascular Atheroembolism
Miscellaneous Renal transplant
Refs. [6, 40, 41, 58]
Valproic acid
Alpha-methyl dopa
Salicylates
Sulindac
Calcium
Ethinylestradiol
Norethindrone
Primary biliary cirrhosis
Renal tubular acidosis
Hyper IgG4 disease
Celiac disease
Serine protease inhibitor Kazal
type 1
Cationic trypsinogen gene
PRSS1
Intraoperative hypotension
Hemorrhagic shock
Vasculitis (lupus and
polyarteritis nodosa)
truly idiopathic, and multiple guidelines state
that no more than 20% should be classied as
idiopathic [9–11].
sia, nutritional support, antibiotics (if indicated),
additional procedures (if indicated), workup for
causes, and treatment of any identied cause.
Patients should be asked about previous gallstones, alcohol intake, family history of pancreatitis, pancreatic cancer, recurrent undiagnosed
abdominal pain or type 1 diabetes, drug intake,
exposure to known viral causes, or whether they
have prodromal symptoms. Laboratory tests
including plasma pancreatic enzymes and liver
function tests should be performed. As the vast
majority of patients with idiopathic pancreatitis
are due to undiagnosed stones or microlithiasis
[12], high-quality transabdominal ultrasound
should be conducted at least twice prior to determination of idiopathic pancreatitis [10].
Serum triglyceride and calcium levels should
be drawn at admission since these will need to be
corrected at the outset. In the recovery phase following an episode of pancreatitis, investigations
should include viral antibody titers (mumps,
Coxsackie B4, and others), repeat biliary ultrasound, MRCP, and contrast-enhanced CT (helical
or multi-slice with pancreas protocol). If these
investigations do not yield a diagnosis, then further investigations are necessary and include an
additional transabdominal ultrasound, endoscopic ultrasound (EUS), immunoglobulin
gamma-4 (IgG4), antinuclear antibodies (ANA),
MRCP with secretin stimulation (MRCP-S),
ERCP—bile for cytology, ERCP—bile and pancreatic cytology, and sphincter of Oddi manometry. Pancreatic function tests, including breath
tests, may also be performed to exclude chronic
pancreatitis. These tests include noninvasive
fecal fat measurements, fecal elastase or invasive
tests that require endoscopy, injection of secretin,
and analysis of pancreatic uid production.
2 Initial Management
Initial management of idiopathic pancreatitis is
similar to acute pancreatitis due to other causes.
As discussed previously in this book, management should include uid resuscitation, analge-
3 Subsequent Management
If the cause of acute pancreatitis cannot be treated
because it is not identied, patients can develop
idiopathic recurrent acute pancreatitis (IRAP).
IRAP has a much higher risk for chronic pancreatitis than a single episode of acute pancreatitis.
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R. W. Parks and E. Gleeson
Furthermore, chronic pancreatitis puts patients at
risk for the development of pancreas cancer [9].
Thus, clinicians must determine whether the
patient has true idiopathic pancreatitis or if this
has an identiable and potentially treatable cause.
3.1 Hereditary Pancreatitis
andGenetic Testing
If there is any family history of pancreatitis,
patients should be referred for, as a minimum,
genetic counseling [10]. Hereditary pancreatitis
(HP) is dened as two, or more, individuals in a
family developing pancreatitis in two, or more,
generations, or pancreatitis associated with
mutation of the serine protease 1 gene, PRSS1,
p.N29I, and p.R122H variants [13]. The PRSS1
gene encodes cationic trypsinogen, and mutation
in this gene leads to premature activation of trypsin in the acinar cell leading to pancreatic parenchymal destruction [9]. Interestingly, loss of
function of anionic trypsinogen, coded by PRSS2
gene, affords a protective effect against pancreatitis [14]. Loss of function variants in two trypsinogen inhibitor genes, serine protease inhibitor
Kazal type 1 (SPINK1) [15] and chymotrypsin C
(CTRC) [16], are also associated with acute pancreatitis. Lastly, a variant of the cystic brosis
transmembrane conductance regulator gene
(CFTR) leads to impaired bicarbonate secretion
and, thus, impaired ushing out of trypsinogen
from the pancreatic duct [17, 18].
The median age of patients with HP is 10years
[19, 20]. Genetic testing should be offered to all
young patients with RAP who have undergone a
cholecystectomy or sphincterotomy (thus ruling
out a biliary etiology) and who do not binge drink
alcohol (<5 drinks per day) [9]. The rationale for
genetic testing is to (1) ascertain the etiology and
limit the need for further investigation; (2) dene
an etiologic-based pathway; (3) foresee any
potential complications; (4) develop management plans; and (5) enable counseling of patients
about the cause and prognosis of their disease
[9]. Patients should be advised to cease smoking
and avoid alcohol, as both substances increase
the risk of pancreatitis and smoking increases the
risk of pancreatic cancer. Pancreatic cancer risk
increases with increasing age in these patients
and is 40% by age 70years in these patients [21].
A total pancreatectomy with islet autotransplantation (TPIAT) is and option to be considered
in patients with unremitting chronic pain who have
failed medical and/or endoscopic treatments with
ongoing recurrent pancreatitis. However, it is
advisable to consider TPAIT before the onset of
central sensitization.However, postoperative glucose control is dependent on the islet cell yield,
and the majority of patients ultimately develop
diabetes. TPIAT should not be offered if the only
concern is of developing pancreatic cancer [9, 22].
3.2 Autoimmune Pancreatitis
Autoimmune pancreatitis (AIP) is primarily a histologic diagnosis although it can be diagnosed
using clinical (obstructive jaundice, abdominal
pain), radiologic (diffusely enlarged pancreas or
“sausage-shaped” pancreas), and serologic (elevated serum immunoglobulin gamma-4 [IgG4])
markers. Diagnosis of AIP also requires the exclusion of pancreatic cancer. International consensus
guidelines categorize AIP into type 1, type 2, and
not otherwise specied (NOS) [23]. Type 2 AIP is
often referred to as idiopathic duct- centric pancreatitis [9]. Both types are found in adults with a
median age between 40 and 50years. However,
patients with type 1 AIP are diagnosed at a mean
age of about 10–15years older than those with
type 2 AIP [24]. AIP has a sex predilection for
males at a ratio of 2.94:1 [25].
The basis of treatment of AIP is corticosteroids
followed by immunomodulators, or, if patients
are unable to tolerate corticosteroids, they can be
started on rituximab as a single agent [23]. In a
randomized controlled trial of prednisolone taper
followed by long-term maintenance therapy
(3 years) vs. short-term maintenance therapy
(26 weeks), patients who underwent long-term
maintenance therapy experienced almost 50%
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fewer recurrent pancreatitis episodes (3-year follow-up period) [26]. The combination of corticosteroids and immunomodulators has not been
well studied, and guidelines lack detail regarding
dosing and duration of treatment. When imaging
suggests a mass, the patient should be presented at
a multidisciplinary tumor board for discussion. In
certain cases, when the mass is concerning for
cancer, surgery may be recommended.
3.3 Sphincter ofOddi Dysfunction
(SOD)
Sphincter of Oddi dysfunction (SOD) is dened
as the presence of biliary pain, elevation of liver
enzymes or dilated bile duct (but not both), and
absence of biliary stones or other structural
abnormalities [27]. SOD is thought to cause pancreatitis by obstructing outow of pancreatic
juices or by causing reux of bile into the pancreatic duct. Sphincter of Oddi manometry (SOM) is
the gold standard for diagnosing SOD.SOM is
performed via ERCP and cannulation of the biliary and pancreatic ducts with a water-perfused
catheter system to measure the pressure [28].
SOD is identied as the cause of idiopathic pancreatitis in up to 31% of cases [4].
In a randomized controlled trial of
ERCP+SOM for patients with recurrent acute
pancreatitis, 69 patients with pancreatic SOD
were assigned biliary endoscopic sphincterotomy
(BES) or dual (biliary and pancreatic) endoscopic
sphincterotomy (DES). There was no difference
in incidence of recurrent episodes of acute pancreatitis after a median follow-up of 78months.
Those with normal SOM were randomized to
BES or sham surgery with no difference in recurrent episodes of acute pancreatitis. However, the
analysis of normal SOM patients was underpowered as the authors did not meet their target sample size. Overall, patients with pancreatic SOD
were more likely to develop recurrent acute pancreatitis than patients with normal SOM (HR 3.5,
95% 1.07–11.4, p<0.04) [29].
SOM is not performed as a standard of care as
outcomes are dependent on the technical skill of
the proceduralist and there is still a risk for postERCP pancreatitis. To avoid post-ERCP complications, asecretin stimulated MRCP (MRCP-S)
can be performed. It shows the anatomy and
function of the pancreatic ducts at the same time
[30, 31]. The pancreatic duct size is measured at
baseline and at 15min after secretin stimulation.
The difference in the pancreatic duct size serves
as a marker for sphincter of Oddi function
[32–34], with dilation of the main pancreatic duct
reecting a functional obstruction at the ampulla.
In a study by Testoni and colleagues, 37 consecutive patients with unexplained recurrent
acute pancreatitis, who also had a nondiagnostic
EUS, underwent MRCP-S to identify the cause
of pancreatitis. In patients in whom this MRCP-S
did not identify a cause or in those for whom an
ERCP was required for treatment, an ERCP was
performed. The positive and negative predictive
values of the MRCP-S for diagnosing pancreatic
outow obstruction were 100% and 64%, respectively. The positive and negative predictive values
of the test for SOD were 92% and 64%, respectively [30].
3.4 Pancreatic Divisum (PD)
Pancreatic divisum (PD) comprises 25–50% of
idiopathic pancreatitis cases [35, 36]. PD is the
absence of fusion of the dorsal and ventral pancreatic ducts that develop as pancreatic buds during embryology. Thus, two separate ducts drain
the pancreas through two papillae: the dorsal duct
into the minor and the ventral duct with the main
bile duct into the major papilla [35]. Patients with
PD are considered to be more at risk for acute
pancreatitis. In the presence of risk factors (i.e.,
sludge, alcohol use, minor elevations in serum
triglycerides) that would not ordinarily trigger an
episode of pancreatitis in patients with normal
anatomy, it is felt that the minor papilla may be
“too small” in patients with PD to accommodate
adequate ow of pancreatic juice and this may
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R. W. Parks and E. Gleeson
predispose to an episode of pancreatitis [35, 37].
Treatment is case specic and may consist of
cholecystectomy for biliary sludge, abstinence
from alcohol if alcohol is the trigger, control of
serum triglycerides in cases of hypertriglyceridemia, and, sometimes, improving drainage through
the minor papilla using endoscopic techniques(papillotomy ± stenting).
In a trial by Lans etal., 19 patients with PD
and at least 2 episodes of pancreatitis were randomized to prophylactic dorsal stent placement,
or no intervention. One of the ten patients (10%)
in the intervention group developed pancreatitis
compared to seven of nine (78%) in the control
group (p < 0.05, mean follow-up 28.6 and
31.5months, respectively). Based on the results
of this study, the authors recommended dorsal
pancreatic duct stent placement for patients with
PD to prevent recurrent pancreatitis and improve
quality of life [37]. However, these numbers are
exceptionally small and the context with which
the patient with PD developed pancreatitis must
be taken into account. Counseling should be
directed toward prevention of pancreatitis based
on the triggering events.
3.5 Microlithiasis
Biliary stones <3mm are unlikely to be detected
by transabdominal ultrasound, or CT, and are
termed “microlithiasis.” Although technically
incorrect, microlithiasis has also been used to
describe sludge, biliary sediment, biliary “sand,”
microcrystalline disease, and pseudolithiasis
[38]. Given that many patients with biliary
sludge eventually develop gallstones, many clinicians believe that sludge is a precursor to
microlithiasis, and thus the terms are used interchangeably [12]. Microlithiasis is responsible
for about half of all idiopathic pancreatitis
cases.
Identication of microlithiasis is done by
either EUS or ERCP with bile sampling (Fig.2).
EUS has the advantage over transabdominal
ultrasound in that it minimizes interference of
bowel gas and peripheral fat on image quality,
leading to a high diagnostic yield [38]. EUS has a
sensitivity of 95% for microliths, whereas biliary
uid analysis via ERCP detects with a sensitivity
of 65–95% [38]. If microlithiasis is diagnosed,
the patient should undergo cholecystectomy as
Fig. 2 Endoscopic techniques. EUS endoscopic ultrasound, ERCP endoscopic retrograde cholangiopancreatography,
SOM sphincter of Oddi manometry, SOD sphincter of Oddi dysfunction
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the mechanism of microlithiasis in causing pancreatitis is thought to be obstruction of the pancreatic duct.
3.6 Combination ofEtiologies
In a study that compared the frequency of PD in
a cohort of patients with idiopathic pancreatitis
and a control cohort, no differences in rates of PD
were observed. These results suggest that another
etiology may be at play. Potentially, the combination of PD and microlithiasis led to pancreatitis
[39]. Future research should focus on the combination of etiologies in identifying and treating
idiopathic pancreatitis.
3.7 SARS-CoV-2
With the recent COVID−19 pandemic (caused by
SARS-CoV-2), authors from the United Kingdom
have reported a high percentage of COVID-19positive patients with idiopathic pancreatitis
(25%) [40]. Furthermore, those with pancreatitis
and COVID-19 have worse outcomes than those
with acutepancreatitis alone [41]. These patients
were more likely to require ICU admission,
develop local complications, have persistent
organ failure, and have a prolonged length of stay
and increased 30-day mortality [41].
3.8 EUS
There are multiple reasons why EUS is critical in
the workup of patients with idiopathic pancreatitis. The diagnosis of microlithiasis can be
detected with greater sensitivity on EUS when
compared to transabdominal ultrasound.
Additionally, EUS can identify masses within the
pancreas causing obstruction where MRCP and
CT cannot. In a systematic review and metaanalysis of EUS compared to MRI/MRCP, EUS
had a diagnostic yield of >60% in patients with
idiopathic acute pancreatitis and was statistically
better at detecting biliary sludge or microlithiasis
[42, 43]. It is technically feasible to perform
sphincterotomy in addition to stone extraction
using EUS. As the technology improves, EUS
will become the primary tool for therapy and
should minimize or eliminate post-ERCP pancreatitis risks [44].
While rare, pancreatitis is the presenting symptom in 5–11% of patients with pancreatic ductal
adenocarcinoma (PDAC) [45, 46]. Although
PDAC generally occurs in only 1–5% of patients
with acute pancreatitis, this rate is higher than the
rate of PDAC in the general population [47, 48].
The possibility of an unidentied pancreatic ductal adenocarcinoma (PDAC) causes great distress
among patients who present with idiopathic pancreatitis. In a retrospective study of 565 patients
who had no discrete mass identied on imaging
(CT, MRI, and/or US) performed after an episode
of acute pancreatitis, EUS with biopsy identied a
pancreatic cancer in 30 (5.3%) patients [48]. More
than 50% of patients with a pancreatic mass were
stage I–II, consistent with previous studies showing that EUS is particularly accurate in identifying tumors <2 cm in size [49]. EUS should be
performed at ≥6weeks following the episode of
pancreatitis [50].
Because EUS has increased the diagnostic
yield so greatly in patients with idiopathic pancreatitis, many believe that EUS should be utilized
routinely [51]. However, all invasive procedures
come with risk. In order to avoid patients undergoing an unnecessary procedure, Cortés and colleagues have created a risk score for identifying
patients who are most likely to have a positive
EUS.They identied the criteria of delayed EUS,
obesity, repeat transabdominal ultrasound, male
sex, and age over 65years as risk factors and have
named this score DORM65 (Table 2). This risk
score has a positive predictive value of 86% (sensitivity 35% and specicity 92%) with an AUC of
0.77 [52]. While further validation is needed, this
score may be used to rule out patients who would
unlikely benet from an EUS.
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R. W. Parks and E. Gleeson
Table 2 DORM65 risk score and point assignment for
likelihood of positive EUS
Factor Points
Delayed EUS +0.5
Obesity +1.5
Repeat transabdominal ultrasound
Male sex +1
Age≥65
−1
+1.5
3.9 Laparoscopic
Cholecystectomy
In a prospective trial in Finland, 85 patients with
a rst episode of idiopathic acute pancreatitis
were randomized to either laparoscopic cholecystectomy (LC) or observation. During the
24-month follow-up, 30% (14/46) of the patients
in the control group developed recurrent pancreatitis compared to 10% (4/39) of the patients in
the LC group (p = 0.016). Examination of the
gallbladders during surgery revealed that 59%
(23/39) contained biliary stones or sludge [53].
In general, utilization of LC during admission
for idiopathic pancreatitis has been low. In a
study from the US National Inpatient Sample, of
all patients with idiopathic pancreatitis between
2015 and 2018 (62,305 patients), only 1% had
LC performed during the index admission.
Hispanics, those on total parenteral nutrition
(TPN), and those with private insurance were
more likely to undergo LC during the index
admission [54].
4 Medical Therapies
Since microlithiasis is one of the most common
causes of idiopathic pancreatitis, use of ursodeoxycholic acid (UDCA) has the potential to
reduce recurrence. Multiple small, non-
randomized studies of patients with idiopathic
pancreatitis have reported success with UDCA
[55, 56]. However, in a randomized, controlled
trial of UDCA vs. placebo for patients with
highly symptomatic gallstones awaiting cholecystectomy, no reduction in biliary symptoms,
including pancreatitis, was seen in the UDCA
group compared to controls [57]. This study was
not powered to focus on pancreatitis events but
suggests that UDCA may not be as effective as
previously thought.
Pancreatic enzyme therapy has long been used
to treat symptoms from pancreatitis, namely,
abdominal pain and steatosis. However, there is
limited research on whether it treats the underlying cause of idiopathic pancreatitis. Likewise,
octreotide has been prescribed in order to reduce
the severity of acute pancreatitis, and the same
principles would be applied in the acute setting of
idiopathic pancreatitis. Octreotide has also been
used to reduce output of postoperative pancreatic
stulas, but no data exist on its use for treating
underlying causes of idiopathic pancreatitis. In
summary, the role of medical therapy in idiopathic pancreatitis lacks a signicant evidence
base.
5 Management Algorithm
Based on evidence from several studies, a proposed algorithm for working up patients with
idiopathic pancreatitis is presented (Fig.3) [58,
59]. Additional diagnostic testing in a modern
retrospective study from the Netherlands revealed
the etiology of idiopathic pancreatitis in 36%
(64/176) of patients. These authors recommend,
as a minimum, a repeat ultrasound followed by
either EUS or MRCP in all patients with a rst
episode of idiopathic pancreatitis [59].
Managing Idiopathic Pancreatitis
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Initial Investigations:
• History and physical
• Biochemistry (including serum triglycerides,
calcium, and lgG4)
• Abdominal US
• Viral titers (if history concordant)
211
Etiology Evident?
Subsequent Workup:
• Repeat Abdominal US
Contrast Enhanced CT
• MRCP
• EUS
• MRCP-S
Etiology Evident?
No
Genetic counseling
Etiology Evident?
No
Yes
Treatment
(including ERCP & LC)*
Yes
Fig. 3 Recommended algorithm forthe diagnosis of idiopathic pancreatitis. *If clinically indicated. IgG4 immunoglobulin G4, US ultrasound, CT computed tomography,
MRCP magnetic resonance cholangiopancreatography,
No
Idiopathic Pancreatitis
Yes
Hereditary
Pancreatitis
EUS endoscopic ultrasound, ERCP endoscopic retrograde
cholangiopancreatography, MRCP-S magnetic resonance
cholangiopancreatography with secretin stimulation, LC
laparoscopic cholecystectomy
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