Background Gastric wall edema has not been reported as a complication of acute pancreatitis in dogs. Objective To describe the ultrasonographic features of gastric wall thickening in dogs with acute pancreatitis. Animals Fourteen dogs with ultrasonographic evidence and clinical diagnosis of acute pancreatitis, with ultrasonographic evidence of increased gastric wall thickness (>5 mm). Methods A retrospective search in the medical records from 2014 to 2016 was performed to identify dogs that had ultrasonographic evidence of acute pancreatitis, that had increased thickness of the gastric wall and that were diagnosed with acute pancreatitis clinically. The gastric wall changes such as thickness, layering appearance, echogenicity, distribution of lesions, and perigastric changes were recorded. Serial ultrasonographic examination and histopathological findings were recorded if available. Results Mean gastric wall thickness was 9.9 ± 4.0 mm (SD). A complete loss of wall layering was observed in 2 dogs. Thickening of the submucosal layer was observed in 12 dogs, and 5 of them had concurrent muscularis layer thickening. The echogenicity of thickened submucosal layer was intermediate hyperechoic. Lacy appearances were present within the thickened submucosal layer in 7 dogs and in the muscularis layer of 1 dog. Thickening was focal in 12 dogs and adjacent to the diseased pancreas. Subsequent resolution of gastric wall thickening was observed in 3 dogs (range 3‐28 days) via follow‐up ultrasound. One dog underwent necropsy, and gastric wall edema was confirmed histopathologically. Conclusions and Clinical Importance Findings indicated that gastric wall thickening presumably because of edema could be a complication of acute pancreatitis.

Malakoplakia in humans most often affects the urinary bladder and is characterized by inflammation with von Hansemann–type macrophages, with or without Michaelis-Gutmann bodies, and is frequently associated with Escherichia coli infection. We describe the microscopic features of malakoplakia in the urinary bladder of 4 puppies. In all cases, the lamina propria of the urinary bladder was markedly expanded by sheets of large, round to polygonal macrophages with intracytoplasmic, periodic acid-Schiff-positive granules and granular inclusions, and rare Prussian blue–positive inclusions. Macrophages were positive for CD18 and Iba1. In 2 cases, Michaelis-Gutmann bodies were detected with hematoxylin and eosin stain and were best demonstrated with von Kossa stain. E. coli infection was confirmed in 2 cases with bacterial culture or polymerase chain reaction (PCR) and sequencing of the bacterial 16S ribosomal RNA gene. Transmission electron microscopy of one case demonstrated macrophages with abundant lysosomes, phagolysosomes, and rod-shaped bacteria. Microscopic features were similar to human cases of malakoplakia. In dogs, the light microscopic characteristics of malakoplakia closely resemble granular cell tumors and histiocytic ulcerative colitis.

Galectin-3 demonstrated to be a robust independent marker of cardiovascular mid-term (18-month) outcome in heart failure (HF) patients. The objective of this study was to analyze the value of a predischarged determination of plasma galectin-3 alone and with plasma brain natriuretic peptide (BNP) in predicting mid-term outcome in frequent-flyers (FF) HF (≥2 hospitalization for HF/year)/dead patients discharged after an acute decompensated HF (ADHF) episode.All FF chronic HF subjects discharged alive after an ADHF were enrolled. All patients underwent a determination of BNP and galectin-3, a 6-minute walk test, and an echocardiogram within 48 hours upon hospital discharge. Death by any cause, cardiac transplantation, and worsening HF requiring readmission to hospital were considered cardiovascular events.Eighty-three patients (67 males, age 73.2 ± 8.6 years old) were analyzed (mean follow-up 11.6 ± 5.2 months; range 4–22 months). During the follow-up 38 events (45.7%) were scheduled: (13 cardiac deaths, 35 rehospitalizations for ADHF). According to medical history, in 33 patients (39.8%) a definition of FF HF patients was performed (range 2–4 hospitalization/year). HF patients who suffered an event (FF or death) demonstrated more impaired ventricular function (P = 0.037), higher plasma BNP (P = 0.005), and Gal-3 at predischarge evaluation (P = 0.027). Choosing adequate cut-off points (BNP ≥ 500 pg/mL and Gal-3 ≥ 17.6 ng/mL), the Kaplan–Meier curves depicted the powerful stratification using BNP + Gal-3 in predicting clinical course at mid-term follow-up (log rank 5.65; P = 0.017).Adding Gal-3 to BNP, a single predischarge strategy testing seemed to obtain a satisfactorily predictive value in alive HF patients discharged after an ADHF episode.

Background: Ultrasonographic features of gastric wall edema have not been reported in dogs with hypoalbuminemia. Objectives: To describe the prevalence and ultrasonographic features of gastric wall thickening in dogs with hypoalbuminemia and analyze correlation with serum albumin concentrations. Animals: Forty-two dogs with abdominal ultrasound and diagnosis of hypoalbuminemia (<2.3 g/dL). Methods: Retrospective search in the medical records from 2018 to 2019 was performed. Ultrasound studies were reviewed and >5 mm were considered gastric wall thickening. The gastric wall changes such as thickness, layering appearance, echogenicity, echotexture, distribution of lesions, and presence of peritoneal effusion were recorded. Serial ultrasonographic examination and histopathological findings were recorded if available. Mean serum albumin concentration of dogs with and without gastric wall thickening was compared. Results: Prevalence of gastric wall thickening in dogs with hypoalbuminemia was 21.4% (95% confidence intervals 7.4-35.4%). Mean gastric wall thickness was 10.0 ± 2.0 mm. Preserved mucosal layer and thickening of submucosal layer were observed in all 9 dogs. Five dogs had 3-layer appearance in thickened submucosal layer. Diffuse wall thickening was observed in 6 dogs. All 9 dogs had peritoneal effusion. Subsequent changes of gastric wall thickening were observed in 3 dogs (range 4-70 days). Gastric wall edema was confirmed histopathologically in 2 dogs via necropsy. There was no correlation between serum albumin concentration of the dogs and gastric wall thickness. Conclusions and clinical importance: Findings indicated that gastric wall edema is a common finding in dogs with hypoalbuminemia. However, serum albumin concentrations did not correlate with the gastric wall thickness.

Angiogenesis is a common feature of pathological processes including wound healing, tumor formation, and chronic inflammation. Chronic inflammation can also be associated with dilation or proliferation of lymph vessels. We examined blood vessels and lymphatics and the expression of pro- and antiangiogenic genes in the skin of SHARPIN-deficient mice which spontaneously develop a chronic proliferative dermatitis (cpdm). The number of blood vessels in the dermis of cpdm mice increased with age as the inflammation progressed. Lymphatics identified by labeling for LYVE1 and podoplanin were moderately dilated, but they were not increased in number. The expression of proangiogenic Vegfa, Flt1 and anti-angiogenic Sema3a mRNA was increased. VEGFA was primarily localized in keratinocytes of cpdm skin. There was also increased expression of Ece1 and Pdpn mRNA. Podoplanin was restricted to lymphatic endothelial cells in normal skin, but fibroblasts in cpdm skin also reacted with anti-podoplanin antibodies indicating that they were activated. The expression of other angiogenic and lymphangiogenic factors was not altered or decreased. These results indicate that cpdm mice may be a useful model to study the pathogenesis of angiogenesis in chronic inflammation.