Choledochoduodenostomy combined with Billroth II procedure for extrahepatic biliary obstruction and duodenal perforation in a cat.

Case summary: A 5-year-old neutered Somali cat presented with a 2-week history of icterus. Diagnostic imaging revealed extrahepatic biliary obstruction (EHBO) due to a common bile duct (CBD) mass. During exploratory laparotomy, a duodenal perforation was discovered incidentally. Choledochoduodenostomy combined with the Billroth II procedure was performed after resection of the CBD mass and the proximal duodenum to treat the EHBO and duodenal perforation. Based on histological and immunohistochemical findings, the CBD mass was diagnosed as a neuroendocrine carcinoma with gastrin-producing cell differentiation. The cat recovered almost uneventfully and was discharged 11 days after surgery. The cat survived for nearly 100 days without recurrence of EHBO or duodenal perforation; however, intermittent vomiting and weight loss persisted despite supportive medications. Relevance and novel information: To the best of our knowledge, there is no detailed report on the application of choledochoduodenostomy combined with the Billroth II procedure in cats, as we used to treat the EHBO and duodenal perforation in the present case. As serum gastrin concentrations were elevated on the first day of hospitalisation, the CBD mass was diagnosed as a neuroendocrine carcinoma with gastrin-producing cell differentiation, which seemed to have caused not only EHBO but also duodenal perforation (Zollinger-Ellison syndrome). The cat survived for almost 100 days without any perioperative complications. However, this combined procedure might be considered as only a salvage option and not as a definitive treatment option in cats requiring simultaneous biliary and gastrointestinal reconstruction because postoperative supportive care could not improve the cat's condition or maintain its quality of life.

The proteasome inhibitor bortezomib inhibits the growth of canine malignant melanoma cells in vitro and in vivo.

Canine malignant melanomas are highly aggressive and fatal neoplasms. In the present report, 21 drugs that target specific signalling pathways were screened for their growth inhibitory activity on three canine malignant melanoma cell lines. The proteasome inhibitor bortezomib inhibited the growth of these cell lines. The growth inhibitory properties of bortezomib were then examined using nine canine malignant melanoma cell lines. Bortezomib demonstrated potent growth inhibitory activity in all cell lines with calculated IC50 values of 3.5-5.6 nM. Because suppression of the NF-κB pathway by preventing proteasomic degradation of I κB is an important mechanism of the anti-tumour activity of bortezomib, the activation status of and the effect of bortezomib on the NF-κB pathway were examined using a canine malignant melanoma cell line, CMM-1. The NF-κB pathway was constitutively activated in CMM-1 cells and bortezomib efficiently suppressed this activated pathway. Using a CMM-1 xenograft mouse model, bortezomib also significantly inhibited tumour growth via suppression of tumour cell proliferation. Collectively, these findings suggest that bortezomib has growth inhibitory activity against canine malignant melanomas potentially through suppression of the constitutively activated NF-κB pathway. Targeted therapy using bortezomib could therefore be beneficial in the management of canine malignant melanomas.