Is Endogenous Cortisol Excess Really Associated with Peptic Ulcer Disease ?

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SAT 26-40-Glucocorticoid Actions & Disease
Translational
Saturday, June 15, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SAT-38
Esra Hatipoglu*, Asli Sezgin Caglar, Erkan Caglar, Murat Tuncer, Ahmet Sadi Gundogdu and Pinar Kadioglu
Cerrahpasa Medical School, University of Istanbul, Istanbul, Turkey
Purpose:Despite the well-known association of exogenous corticosteroid replacement and peptic ulcer disease, ulcerogenic and other upper gastrointestinal system (GIS) effects of endogenous hypercortisolism has not been based on an evidence from a study, yet. There is not a controlled study to represent the exact frequency of peptic ulcer disease (PUD)  and helicobacter pylori infection in presence of high endogenous cortisol levels. The objective of the current study is to evaluate the relationship of endogenous cushing syndrome with  H.pylori infection and PUD.

Methods: In this cross-sectional, comparative study 20 active cases with ACTH dependent Cushing syndrome (CS) (19 with pituitary Cushing disease and 1 with ectopic CS; 13 with new diagnosis and 7 with recurrence) were included in the study. Gender and age matched 100 non-cushingoid dispeptic patients composed the control group (CG). All cases were questionned about secondary causes of PUD, including their medications and upper GI endoscopy was performed to all. Biopsy was taken from 5 different points ; 2 samples from antrum, 2 samples from from corpus and 1 sample from fundus.

Results: In patients with CS median time of diagnosis was 2 [IQR:1-24] monthes,time between the onset of symptoms to the diagnosis of CS was 24 [IQR:12-51] monthes, basal cortisol levels was 21 [IQR:13.6-26.55] µg/dL and basal ACTH levels was 49.9 [IQR:21.31-93.17] pg/mL. Usage of proton pump inhibitor was not different between the groups (p=0.21). Candida esophagitis was present in 10% of patients CS and none of  the CG (p=0.001). Frequency of pangastritis was higher in CS than it was in CG (55% vs 5%, p<0.001). Antral gastritis was higher in CG ( 45% in CS and 81% in CG, p=0.001). Frequency of stomach ulcer, and bulbitis were not different between two groups (peptic ulcer 0% in CS and 3% in CG, p=0.43; bulbitis 20% in CS and 11% in CG, p=0.26). Duedonal ulcer (0% vs 2%, p=0.52) and duodenitis (0% vs 3%, p=0.43) were also not different. Biopsy results showed no difference for active gastritis (55% vs 67.7%, p=0.27), atrophic gastritis (0% vs 5%, p=0.3) and H.pylori infection (60% vs 68%, p=0.48) between CS and CG.  Inactive gastritis was higher in CS (40% vs 17%, p=0.02).

Conclusion: Despite the increased pangastritis in endoscopy of patients with CS, biopsy confirmation of active gastritis did not accompany this finding so in case of increased endogenous cortisol, endoscopic appearence of Upper GIS may not be parallel to the  histopathologic changes. Although endoscopic finding of pangastritis and histologic verification of inactive gastritis were higher in CS, peptic ulcer frequency was not increased on the contrary to what was expected. Endogenous cortisol excess may have different effects on GIS from  exogenously taken glucocorticoids.

Nothing to Disclose: EH, ASC, EC, MT, ASG, PK

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