Canine Gallbladder Erosion/Ulcer and Hemocholecyst: Clinicopathological Characteristics of 14 Cases.

(1) Background: Gallbladder mucosal erosion and/or ulceration are illnesses associated with unexpected gallbladder intra-cystic bleeding (hemocholecyst), an under-reported problem in dogs. (2) Methods: Clinicopathological characteristics of 14 dogs with gallbladder erosion/ulcer were investigated in this single-center retrospective study using clinical data and archived gallbladder tissues of client-owned dogs. (3) Results: Canine gallbladder erosion/ulcer tends to occur in older, neutered dogs of various breeds. Vomiting, lethargy, and anorexia are common. Concurrent gallbladder rupture occurred in 5/14 cases (35.7%), while rupture was absent in 6/14 cases (42.8%) and undetermined in 3/14 (21.4%) cases. Histologically, the gallbladder wall was markedly thickened due to mucosal hyperplasia, inflammatory infiltrates, fibrosis, edema, hemorrhage, and smooth muscle hyperplasia/hypertrophy. Twelve out of fourteen cases (85.7%) had concurrent cholecystitis of varying severity. Bacteria were detected by Giemsa or Warthin-Starry stain in 8/14 (57.1%) cases. Bacterial rods immunoreactive to the anti- Helicobacter antibody were present in one case. Mucosal epithelial cells of the gallbladder erosion/ulcer cohort were immunopositive for the cyclooxygenases COX-1 or COX-2 in only 5/14 (35.7%) cases. In contrast, COX-1 and COX-2 were more frequently expressed in a reference pool of cases of gallbladder mucocele ( n = 5) and chronic cholecystitis ( n = 5). COX-1 was expressed in 9/10 cases (90.0%) of gallbladder mucocele and chronic cholecystitis and in 10/10 cases (100%) for COX-2. (4) Conclusions: Canine gallbladder erosion/ulcer is an under-reported condition which requires active clinical intervention. Based on the clinicopathological information reported in this study in addition to the COX-1 and COX-2 IHC results, we suggest that canine gallbladder erosion/ulcer may be related to decreased cytoprotection physiologically provided by arachidonic acid, but which is decreased or absent due to reduced COX expression because of yet undetermined etiologies.