Protein-Losing Enteropathy in a 7 year old Mixed Breed Dog

Our patient is a 7-year-old male castrated mixed breed dog that presented to the Cornell University Hospital for Animals Emergency Service on 11/27/17 for a 3-week history of persistent diarrhea, lethargy, inappetance, and weight loss. The owner reported that prior to showing these signs, he had access to a dead deer carcass in his backyard. Blood chemistry from the referring veterinarian indicated severe panhypoproteinemia (albumin 0.9; rr. 3.1-4.2, globulins 1.4; rr. 1.9-3.6). At presentation, our patient was bright, alert and responsive. His hindlimbs, prepuce, and ventral neck had moderate subcutaneous edema. The remainder of his physical examination was unremarkable. A complete blood count (CBC) revealed mild neutrophilia and low total proteins (2.8, rr. 5.3-7.0). A chemistry panel disclosed hypocalcemia (5.8; rr. 9.4-11.1), hypomagnesemia (0.6; rr. 1.5-2.1), hypoalbuminemia (1.3; rr. 3.2-4.1), hypoglobulinemia (1.4; rr. 1.9-3.7), and hypocholesterolemia (103; rr. 136-392). Urinalysis was unremarkable with a urine specific gravity of 1.043 and trace proteinuria. A Disseminated Intravascular Coagulation panel revealed low normal antithrombin. Abdominal ultrasound showed a mild to moderate diffuse gastroenteropathy with mild peritoneal effusion, which was sampled at intake and characterized as a transudate. A baseline cortisol ruled out hypoadrenocorticism, and vitamin B12 level was less than 150 (rr. 175 – 800). Fecal qualitative analysis revealed Neospora caninum or Isospora heydorni (Hammondia), and Sarcocystis sp. Aerobic, Clostridium perfingens, Campylobacter jejuni, and Salmonella bacteriological cultures of a duodenal biopsy sample were negative. A clinical diagnosis of protein-losing enteropathy (PLE) was made based on the patient's history, clinical signs, physical examination findings, and ancillary diagnostic test results. Differential diagnoses for PLE include inflammatory bowel disease, intestinal lymphangiectasia, neoplasia, hookworm, and histoplasmosis. The diagnosis of PLE was confirmed by endoscopic biopsies of the duodenum and histopathologic findings consistent with PLE secondary to inflammatory bowel disease (IBD) and intestinal lymphangiectasia. This presentation will address the clinical diagnosis, histopathology, treatment, and prognosis of PLE.