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Drug
-induced acute pancreatitis
Maria Cristina Conti Bellocchi, Pietro Campagnola, Luca Frulloni.
Department of Medicine, Pancreas Center, University of Verona, Verona, Italy.
e-mail:
luca.frulloni@univr.it
Version 1.0, August
8, 2015 [DOI:
10.3998/panc.2015.32
] 1.
Introduction
Acute
pancreatitis (AP) is a
heterogeneous
disease
ranging
from a clinically mild form to a
more severe forms associated with high morbidity
and mortality
(78). A correct diagnosis of AP
should b
e made within 48 h of admis
sion.
Understanding of the
etiology and severity
assessment are essential, as they may affect the
acute management of the disease
(8). The most common etiology for AP are gallstones
and alcohol abuse. Other causes include
iatrogenic injury (i.e. post
-ERCP), metabolic and
autoimmune disorders, inherited disorders,
neoplasia (even intraductal papillary mucinous
neoplasia
– IPMN), anatomical
abnormalities,
infections, ischaemia, trauma and drugs
(87). Additional investigations after recovery from the
acute episode are recommended
in patients with
an episode of AP classified as idiopathic
(68). Drugs may be considered a potential cause of the
disease in patients who take medications that
have been associated with AP.
Drug
-induced pancreatitis (DIP) is assumed to be
a relative rare entity, and
its incidence is reported
between 0.1 and 2% of AP cases
(62). However,
the true incidence of DIP is still unknown since
little e
vidence has been obtained from clinical
trials, and most incidences have been
documented as case reports
(62) gene
rally limited
by the absence or
inadequacy of diagnos
tic
criteria for AP, failure to
rule out common
etiologies of AP, and lack of a re
-challenge test.
The main problem in the identification of DIP is
the absence of a clear and largely accepted
definitio
n of the disease. The diagnosis of DIP is
difficult to establish since it is rarely accompanied
by clinical or laboratory evidence of a drug
reaction and the large proportion of patients
admitted for AP are already taking a medication.
Therefore, criteria
to diagnose DIP should include
the evidence for drug intake shortly preceding AP,
an increased risk for AP in patients taking the
drug, direct correlation between increased risk
and dose, presence of a plausible biological
mechanism, evidence in clinical t
rials using the
specific drug and a re
-challenge test. However,
we lack a definition for each of these potential
diagnostic criteria for DIP (i.e. elapsed time
between drug intake and AP).
Five
-hundred and
twenty
-five
different drugs
suspected to caus
e acute pancreatitis are
reported in the
database
of
World Health
Organization (WHO)
(61). The majority of the data
are derived from case reports, case series or
summaries of them. Furthermore, the causality for
many of these drugs remains elusive and for only
about thirty of these 525 dug
s has
a definite
causality be
en established
(61). Another
methodological problem is the evaluation of other
potential cause of AP. Some definitions exclude
the presence of other etiologies of AP, primarly
biliary lithi
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