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Volume 8
Journal of Gastrointestinal & Digestive System
ISSN: 2161-069X
Gastro Congress 2018
August 20-21, 2018
Page 57
conference
series
.com
August 20-21, 2018 | Rome, Italy
13
th
Euro-Global
Gastroenterology Conference
Bashar Attar, J Gastrointest Dig Syst 2018, Volume 8
DOI: 10.4172/2161-069X-C5-075
Subclinical exocrine pancreatic insufficiency (EPI): A disease that merits treatment
Introduction:
Exocrine pancreatic insufficiency (EPI) is one of the long-term consequences of chronic pancreatitis (CP). Majority
of patients with EPI are undiagnosed or undertreated.
Study Design:
We prospectively evaluated 200 consecutive individuals seen in a pancreatic outpatient practice. These individuals
were screened on 2 occasions to determine their baseline stool elastase excretion. The 200 individuals were segmented into 4
distinct groups: a)“Normals” (n=105) with stool elastase >500 ug/g stool, received no treatment; b) “Minimal EPI” (n=60) with
stool elastase >200 to <500 ug/g stool, received 3000 IU of a standard pancreatic enzyme preparation (Creon) with their 2 ingested
meals; c) “Moderate EPI” (n=23) with stool elastase >100 to 200 ug/g stool, received 12,000 IU of the same pancreatic enzyme
preparation with each meal; d) “Severe/Overt EPI” (n=12) with stool elastase <100 ug /g stool, received 24,000 IU of the same
pancreatic enzyme preparation with each meal and with a bedtime snack.
Results:
These groups presented with abdominal pain, bloating, flatulence, diarrhea, large bulky stools, and greasy stools.
Symptoms were graded (1-10) at entry and monthly for 3 months. Symptom scores decreased in all groups. The response to
therapy was maximal in those with most severe disease identified by their greatest reduction in stool elastase at entry. Lesser
responses were seen in the other groups and mired the severity of the disease at entry as defined by their stool elastase levels.
Conclusions:
We conclude that 1) pancreatic elastase in stool enable the segmentation of individuals into distinct subgroups
of EPI. 2) pancreatic elastase in stool enables identification of not only overt EPI but those with minimal and moderate EPI. 3)
therapy with pancreatic enzyme preparations can be individualized based upon the concentration of pancreatic elastase in stools.
4) individuals with “subclinical” EPI with stool elastase level of 100-500 improve with treatment.
Recent Publications:
1. Wang Y and Attar B M (2017) Comment on Comparison of BISAP, Ranson, MCTSI, and APACHE II in predicting
severity and prognoses of hyperlipidemic acute pancreatitis in Chinese patients. Gastroenterol. Res. Pract.
2017:1426486. Doi:10.1155/2017/1426486.
2. Wang Y et al. (2017) Evaluation of the prognostic value of neutrophil to lymphocyte ratio in patients with
hypertriglyceridemia-induced acute pancreatitis. Pancreatology. 17(6):893-897. Doi:10.1016/j.pan.2017.10.001.
3. Wang Y et al. (2017) Concurrent diabetic ketoacidosis in hypertriglyceridemia-induced pancreatitis: how does it affect
the clinical course and severity scores? Pancreas. 46(10):1336-1340. Doi:10.1097/MPA. 0000000000000937.
4. Walter R J et al. (2012) Newcastle disease virus LaSota strain kills human pancreatic cancer tumor cells
in vitro
with
high selectivity. Journal of Pancreas,.13(1):45-53.
5. Walter R J (2012) Two avirulent, lentogenic strains of Newcastle disease virus are cytotoxic for some human pancreatic
tumor lines
in vitro
. Journal of Pancreas. 13(5):502-513. Doi: 10.6092/1590-8577/977.
Bashar Attar
Cook County Health and Hospitals System, USA