Incidence, etiology and prognosis of first-time acute pancreatitis in young patients: a population-based cohort study.
OBJECTIVE
The etiology of acute pancreatitis (AP) seems to have changed during the last two decades, and since detection of mutations in the gene for cationic trypsinogen(PRSS1) causing hereditary pancreatitis some patients formerly diagnosed with idiopathic AP (IAP) turn out to have a genetic cause.


METHODS
Data on patients <30 years of age, diagnosed with AP identified in the Danish National Registry of Patients, were retrieved. Patients previously diagnosed with IAP were offered genetic counseling and testing for mutations in the PRSS1, the Serine Protease Inhibitor Kazal type1 (SPINK1) and the Cystic Fibrosis Transmembrane Conductance Regulator gene (CFTR).


RESULTS
The standardized incidence ratio (SIR) of AP increased from 3.56 per 100,000 person-years in the period 1980-1984 to 6.43 in 2000-2004 (p < 0.01). The SIR of women surpassed that of men in 1999. Among patients with former IAP, 3 had hereditary pancreatitis, 3 CFTR and 4 SPINK1 mutations after re-evaluation.


CONCLUSIONS
The incidence of AP, especially in women, increased over time. More patients had gallstone-related and less alcohol-related AP in the period 1999-2004 compared to 1980-1999. Genetic causes of AP were found in 32% of those tested with IAP and as a minimum estimation in 4% of the total cohort. and IAP.
Joergensen
Maiken
M
Department of Medical Gastroenterology, Odense University Hospital, University of Southern Denmark, Odense, Denmark. maiken.t.joergensen@ouh.regionsyddanmark.dk
Brusgaard
Klaus
K
Crüger
Dorthe Gylling
DG
Gerdes
Anne-Marie
AM
Schaffalitzky de Muckadell
Ove B
OB
D000208:Acute Disease; D000328:Adult; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D015331:Cohort Studies; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000235:genetics / Q000378:metabolism; D005260:Female; D006801:Humans; D015994:Incidence; D008297:Male; D050500:Pancreatitis, Chronic / Q000453:epidemiology* / Q000209:etiology* / Q000235:genetics; D011159:Population Surveillance; D011379:Prognosis; D015996:Survival Rate; D014357:Trypsin / Q000235:genetics / Q000378:metabolism; D014359:Trypsin Inhibitor, Kazal Pancreatic; D055815:Young Adult
C505032:CFTR protein, human; D002352:Carrier Proteins; C486642:SPINK1 protein, human; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D014359:Trypsin Inhibitor, Kazal Pancreatic; C489303:PRSS1 protein, human; D014357:Trypsin