BackgroundThrombocytosis is a hematologic abnormality in dogs that has been associated with various neoplastic, metabolic, and inflammatory conditions.ObjectiveTo classify thrombocytosis in dogs based on severity and evaluate whether there are associations between severity and underlying disease processes.AnimalsSeven hundred and fifteen dogs with thrombocytosis and 1,430 dogs with normal numbers of platelets.MethodsRetrospective study. Medical records of dogs with increased (>500 × 103/μL; thrombocytosis group) and normal (300–500 × 103/μL; control group) platelet counts between 2011 and 2015 were reviewed. Dogs were characterized by severity of platelet increase and diagnosis. Diagnostic categories included neoplasia, endocrine disease, inflammatory disease, or miscellaneous.ResultsA total of 1,254 complete blood counts with thrombocytosis from 715 dogs were included in the study. Median platelet count in this population was 582 × 103/μL (500–1,810 × 103/μL). No correlation between severity of thrombocytosis and diagnosis was identified. Causes of secondary thrombocytosis included neoplasia (55.7%), endocrine disease (12.0%), and inflammatory disease (46.6%). Immune‐mediated disease was common (22.2%), associated with frequent glucocorticoid administration, and had a significantly higher median platelet count (636 × 103/μL [500–1,262 × 103/μL] versus 565 × 103/μL [500–1,810 × 103/μL]) when compared to the other inflammatory processes (P < 0.001). The diagnoses in the thrombocytosis dogs differed significantly from the control population (P < 0.001).Conclusions and Clinical ImportanceThrombocytosis is commonly associated with carcinoma and immune‐mediated disease in dogs.

Background: Sepsis is associated with ascorbic acid (AA) depletion and critical illness-related corticosteroid insufficiency (CIRCI) in humans. Hypotheses: Intravenous infusion of lipopolysaccharide (LPS) would (a) decrease endogneous AA concentrations, (b) induce CIRCI and (c) administration of a combination of AA and hydrocortisone (HC) would have decreased indices of inflammation compared to either drug alone. Animals: Thirty-two healthy horses. Methods: Randomized placebo-controlled experimental trial. Horses were assigned to 1 of 4 groups (saline, AA and HC, AA only, or HC only). Treatments were administered 1 hour after completion of LPS infusion. Clinical signs, clinicopathological variables, pro-inflammatory cytokine gene expression and production, and plasma AA concentrations were assessed at various time points. Serum cortisol concentrations and ACTH stimulation tests were used to detect CIRCI. Results: There was no effect of drug on clinical signs or pro-inflammatory cytokine gene expression or production compared to controls at any time point. Administration of AA was associated with higher blood neutrophil counts 6 hours after LPS infusion (11.01 ± 1.02 K/μl) compared to other groups (8.99 ± 0.94 K/μL; P < .009).

BackgroundOxidative stress plays a role in the pathophysiology of several diseases and has been documented as a contributor to disease in both the human and veterinary literature. One at‐risk cell is the erythrocyte, however, the role of oxidative stress in anemia in dogs has not been widely investigated.Hypothesis/ObjectiveAnemic dogs will have an alteration in the activity of glutathione peroxidase (GPx), a decrease in of total antioxidant capacity (TAC), and an increased concentration of urinary 15‐F2‐isoprostanes (F2‐IsoP) when compared to healthy dogs.Animals40 client‐owned dogs with anemia (PCV <30%) age‐matched to 40 client‐owned healthy control dogs.MethodsProspective, cross‐sectional study. Whole blood GPx activity, plasma TAC, and urinary F2‐isoprostane concentrations were evaluated in each dog and compared between groups.ResultsAnemic dogs had significantly lower GPx activity (43.1 × 103 +/‐ 1.6 × 103 U/L) than did dogs in the control group (75.8 × 103 +/‐ 2.0 × 103 U/L; P < 0.0001). The GPx activity in dogs with hemolysis (103 +/‐ 0.8 × 103 U/L) was not significantly different (P = 0.57) than in dogs with nonhemolytic anemia (43.5 × 103 +/‐ 1.1 × 103 U/L). The TAC concentrations (P = 0.15) and urinary F2‐isoprostanes (P = 0.73) did not significantly differ between groups.Conclusions and Clinical ImportanceGlutathione peroxidase activity was significantly decreased in anemic dogs indicating oxidative stress. Additional studies are warranted to determine if antioxidant supplementation would improve survival and overall outcome as part of a therapeutic regimen for anemic dogs.

The use of mycophenolate mofetil (MMF) for a variety of immune‐mediated diseases in veterinary medicine has been described. However, there is only a small number of cases documenting its use in dogs with meningoencephalomyelitis of unknown aetiology (MUE). We hypothesized that the use of MMF and corticosteroids in dogs with MUE results in comparable survival data to other published treatment protocols and is associated with limited adverse effects. A retrospective study of medical case records of dogs clinically diagnosed with MUE recorded signalment, neuroanatomic localization, magnetic resonance imaging findings, cerebrospinal fluid analysis results, medications administered, follow‐up neurologic examinations, survival and adverse events. Variables were compared between dogs which were treated with MMF within 30 days of diagnosis (immediate group) vs. dogs in which MMF therapy was started >30 days after diagnosis (delayed group). Twenty‐five cases of MUE were identified. The overall median survival time from diagnosis was 731 days (range 43–1672 days). After 1 month of MMF treatment, 92% of dogs showed improvement on a neurological examination. There was no significant effect of any recorded parameter on survival, including delayed vs. immediate initiation of MMF treatment. Dogs with delayed treatment had significantly lower clinical remission rates than dogs with immediate treatment at 6 months after starting MMF. Adverse events were identified in two cases (8%) and were characterized by mild gastrointestinal signs (vomiting and decreased appetite). Administration of MMF appears safe in dogs with MUE. The use of MMF results in comparable survival times to alternate immunosuppressive protocols.

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Background/objectivesDiet-induced obese (DIO) rats have altered stress (HPA) axis activity compared to diet-resistant (DR) rats when chronically exposed to a high-fat (HF) diet. Since stress axis is tightly regulated by leptin, an adipocyte-secreted hormone that is important for controlling body weight, we hypothesized that leptin action is impaired in DIO rats leading to alterations in HPA axis activity.Subjects/methodsWe intraperitoneally injected selectively bred DIO and DR rats with either saline or recombinant rat leptin. HPA axis activity was assessed by measuring norepinephrine (NE) in the paraventricular nucleus (PVN), corticotropin-releasing hormone (CRH) in the median eminence, and serum corticosterone (CORT). To test if HF exposure duration and the corresponding increase in leptin differentially affects HPA axis activity, we placed animals on a chow or HF diet for 1 or 6 weeks.ResultsLeptin injection significantly increased serum leptin levels in both DIO and DR animals. It also reduced PVN NE in both groups, indicating that noradrenergic neurons in both groups remain responsive to leptin. HF diet duration-dependently increased serum leptin only in DIO animals whereas PVN NE increased in both groups. While DR rats responded to HF diet by increasing CRH and CORT at both time-points, responses in DIO rats varied, suggesting that they have altered HPA axis activity that may be dependent on HF-induced leptin levels and/or signaling. To understand the underlying mechanisms, we measured pSTAT-3, a marker of leptin signaling, in brainstem noradrenergic neurons and found reduced pSTAT-3 in A1 region of HF-fed DIO rats. We also found higher serum free fatty acids (FFAs) and a pro-inflammatory cytokine, IL-1β.ConclusionsCollectively, these findings reveal that DIO rats have inherent neuroendocrine impairment in NE-HPA axis circuitry that worsens with the extent of HF diet exposure, possibly due to brainstem leptin resistance and/or elevated circulating FFAs and IL-1β.

Case summary A 4-year-old neutered male cat was presented with a 2-month history of intermittent constipation that progressed to obstipation. Primary clinical findings included a large, multi lobulated mass in the caudodorsal abdomen, peripheral eosinophilia and hyperglobulinemia. Abdominal imaging revealed a multilobulated, cavitated mass in the sublumbar region. Exploratory celiotomy revealed multiple firm masses in the sublumbar retroperitoneal space causing ventral displacement and compression of the descending colon with extension of the masses into the pelvic canal. Histopathology was consistent with feline gastrointestinal eosinophilic sclerosing fibroplasia (FGESF). Aerobic culture was positive for Staphylococcus aureus. The cat was treated with prednisolone (2 mg/kg PO q24h), lactulose (0.5 g/kg PO q8h), amoxicillin/clavulanic acid (62.5 mg/cat PO q12h for 1 month) and fenbendazole (50 mg/kg PO q24h for 5 days). Six months postoperatively, the cat had no recurrence of clinical signs. Repeat evaluation and imaging at day 732 postoperatively revealed marked improvement of the abdominal mass, resolution of peripheral eosinophilia and no clinical signs with continued prednisolone therapy (0.5 mg/kg PO q24h). Relevance and novel information This is a report of a primary extramural FGESF lesion, and the first description of characteristics of FGESF on CT. Previous evidence suggests that the most favorable outcomes require immunosuppressive therapy and complete surgical excision; however, this case demonstrates a favorable outcome with medical management alone.

Background: Oxidative stress refers to the accumulation of reactive oxygen species (ROS). Most assays for ROS detection are costly, laborious, and usually use indirect markers. The use of 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) is a possible alternative. This substance becomes a fluorochrome when oxidized by ROS, with the resultant fluorescence proportional to ROS concentration. Erythrocytes are highly exposed to ROS, resulting in cell damage and consequently impaired oxygen delivery. The effects of this exposure in physiologic and pathologic conditions necessitate an improvement in ROS detection methods. Objective: We aimed to validate intraerythrocytic ROS detection by flow cytometry using DCHF-DA in healthy horses. Methods: Erythrocytes from 31 healthy horses were isolated, incubated with DCFH-DA, and either left unstimulated or stimulated with hydrogen peroxide (H 2 O 2). For specificity, each cellular component of blood was separated and plotted according to its size and complexity. Samples were run in triplicate for intra-assay precision and five consecutive times for inter-assay repeatability. Stability was determined by analyzing the same sample up to 48 hours after blood collection. The acceptable coefficient of variation (CV) was ≤20%. Results: The intra-assay CV was 1.7% and 13.3%, and the inter-assay CV was 4.8% and 17.8% for unstimulated and stimulated samples, respectively. Unstimulated and stimulated samples were stable for up to 48 and 24 hours, respectively. Stimulated samples had greater fluorescence than unstimulated samples (P < .0001). Conclusions: This flow cytometric assay demonstrated adequate specificity, precision, and stability and is, therefore, a promising technique with multiple applications for studying oxidative stress in horses.