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abstrakt gastrodagarna
1 Karolinska Universitetssjukhuset, Sekt. för pediatrisk Gastroenterologi,
Hepatologi och Nutrition, Huddinge, Sverige; 2 Karolinska Universitetssjukhuset,
Gastro Center Surgery, Huddinge, Sverige; 3 Karolinska Universitets
Sjukhuset.Huddinge, Sekt. för pediatrisk Gastroenterologi,Hepatologi och
Nutrition, Hälsovägen, Sverige
Background: The Pancreas is poorly described in pediatric inflammatory
bowel disease (IBD). We characterized pancreatic involvement in children
with IBD at our center.
Methods: Retrospective chart review of pediatric IBD patients investigated/treated
at our center 2000-2011. IBD-patients with associated
autoimmune liver disease (AILD)were excluded. Pancreatic amylase
(0,15-1,10 microkat/L), lipase (0,36-0,85microkat/L) and fecal elastase
(>200 microg/g) outside the normal range at any time before, at initial
diagnosis or follow-up of IBD were included. Apart from symptoms and
enzymes, MRI with secretin stimulation and a modified Lundh’s test were
used in suspicious cases to diagnose pancreatitis or exocrine pancreas
insuffiency (EPI).
Results: 131/136 IBD patients were included in the study; 77 Crohn’s
(CD), 34 ulcerative colitis (UC) and 20 indeterminate colitis (IC).
65/131(50%), 36 boys,had abnormal pancreatic enzymes at any time;
35 (45%) of the CD-, 20 (59%) of the UC- and 10 (50%) of the IC- patients.
Median age at IBD-diagnosis, in the group with abnormal enzymes was
13.3 (2.3 – 17.9) years. Elevated enzymes in 39/131 (30%); CD 21
(54%), UC 11 (28%) and IC 7 (18%). 25 had only elevated enzymes. Possible
causes were pharmacological drugs in 14 (eg. steroids,5-ASA and
azathioprin), infections 5, at diagnosis of IBD 2, after colectomy 1, hyperamylasemia
1, and 2 unknown causes.14 (11%) patients had pancreatitis.
11/14 pts had acute or recurrent pancreatitis: (5 due to pharmacological
therapy, 2 due to possible auto-immune pancreatitis (AIP), 2 with severe
EBV-infection and 2 with pancreatitis preceding IBD-diagnosis. Chronic
pancreatitis in 3: Possible AIP in 2 girls with UC and CD and one boy with
UC, gallstones/possible AIP.Low enzymes in 41/131(31%),23 boys, CD
21/41 (51%) ,14 (34%) with UC and 6 (15%) with IC. 15 of these 41 pts
also had elevated enzymes at any time, and 13/15 showed elevated
enzymes preceding low enzyme levels. 5 (3.8%) of 131 pts; CP in 3 and
pancreatic atrophy in 2,had definite EPI. 3 pts (2.3%) had suspected EPI
with low enzymes and low fecal elastase.
Conclusion: Elevated and/or low pancreatic enzymes was seen in 50%
and pancreatitis in 11%. Pharmacotherapy and suspected AIP were the
most common causes of pancreatitis. Definite/possible EPI were seen
in 6%. Elevated pancreatic enzymes can sometimes precede low enzyme
levels, which may be a sign of pancreatic injury. Pancreas should be continousely
evaluated in pediatric IBD
Inflammatorisk tarmsjukdom
PO-15
Metotrexat vid budesonidrefraktär kollagen kolit
Münch, A. 1 ; Bohr, J. 2 ; Vigren, L. 3 ; Tysk, C. 2 ; Ström, M. 1
1 Universitetssjukhus, EM-kliniken, Linköping, Sverige; 2 Universitetssjukhus,
Gastroenterologi, Örebro, Sverige; 3 Universitetssjukhus, Gastroenterologi,
Malmö/Trelleborg, Sverige
Bakgrund: Kollagen kolit (KK) är en inflammatorisk tarmsjukdom som
vanligtvis kan behandlas effektivt med budesonid. Det finns dock patienter
som utvecklar intolerans eller har kvarvarande aktiv sjukdom trots underhållsbehandling
med högdos budesonid. Vi har genomfört en prospektiv
sammanställning av patienter med budesonidrefraktär KK som erhöll
metotrexat (MTX, 15-25 mg) subkutant en gång per vecka.
Metod/Patienter: Nio patienter (7 kvinnor, medelålder 56 år) inkluderades.
Avföringsfrekvens/dag beräknades under en veckas symtomregistrering
innan, efter 6 och 12 veckors behandling. Koloskopi med biopsitagning
genomfördes hos alla patienter för att bekräfta diagnosen. MTX gavs
15 mg s.c. i 6 veckor och ökades till 25 mg s.c. om patienten inte svarade
på behandling efter vecka 6. Andelen patienter i klinisk remission (definierad
som