Cystic endometrial hyperplasia (CEH)-pyometra syndrome is one of the most common diseases of noncastrated female dogs. However, determination of etiological mechanisms and differential diagnosis of CEH-pyometra syndrome are undefined. The aim of this study is to compare immunohistochemically the expression of cyclooxygenase-2 (COX-2) inflammatory mediator, Ki-67 antigen proliferation marker, vascular endothelial growth factor (VEGF-A) angiogenesis mediator and its FLT-1 and KDR receptors, and correlate with Doppler velocimetry of uterine artery and endometrial vascularization in bitches with CEH-pyometra syndrome. Bitches were allocated into CEH-mucometra Group (n = 13), Pyometra Group (n = 11), and Control Group (n = 8). Pyometra Group presented cytoplasmatic staining intensity for COX-2, VEGF-A, and FLT-1 and KDR receptors in luminal epithelium cells significantly higher compared to CEH-mucometra and Control groups. For the glandular epithelium, Pyometra Group had higher immunostaining score for VEGF-A and its receptors (FLT-1 and KDR). Hemodynamic indexes showed negative correlation with VEGF-A and its receptors as well as with COX-2. On the other hand, uterine vascularization score showed positive correlation in relation to immunostaining of COX-2, VEGF-A, and receptors in the endometrium luminal epithelium. In conclusion, uterus of bitches with CEH-pyometra syndrome show inflammatory process characterized by COX-2 expression, resulting in greater expression of proliferative Ki-67 marker as tissue response against the infectious agent. Furthermore, the increased VEGF-A expression and its receptors in CEH-pyometra reflect the increased blood flow and lower vascular resistance. Therefore, canine pyometra is characterized by an inflammatory, proliferative, and vascular disorder.

Primary hepatobiliary tumors have low prevalence in dogs and are usually observed in nine to 12-year-old animals. This article reports a case of acute clinical cholangiocarcinoma in a three-year-old Labrador Retriever bitch. The animal had a clinical history of emesis and hyporexia. Physical and laboratory examinations disclosed hyperthermia, jaundice, hypoglycemia, leukocytosis, anemia, thrombocytopenia and coagulopathy. Abdominal ultrasound revealed an enlarged liver of heterogeneous echotexture with hyperechoic and hypoechoic irregular areas. The animal developed severe hemolysis and came to die. Necropsy revealed hepatomegaly and irregular appearance of the liver; metastasis were found in the bone marrow, kidneys and spleen, and neoplastic pulmonary embolism was also observed. Cholangiocarcinoma was identified microscopically. The aim of this report was to describe an atypical case of cholangiocarcinoma because of the precocity of its occurrence.