Background: Neurofilament light chain (NfL) is a neuron-specific cytoskeletal protein expressed in axons. Damaged axons of the central nervous system release NfLs into the cerebrospinal fluid (CSF) and the blood. In humans with neurologic diseases, NfL is used as a biomarker.Objectives: To identify the potential of NfL as a supportive tool for the diagnosis, prognosis, and monitoring of meningoencephalitis of unknown etiology (MUE) in dogs.Animals: Twenty-six client-owned healthy dogs, 10 normal Beagle dogs, and 38 client-owned MUE dogs.Methods: Cohort study. The concentrations of NfL in serum and CSF were measured using single-molecule array technology.Results: Median NfL concentration was significantly higher in MUE dogs (serum, 125 pg/mL; CSF, 14 700 pg/mL) than in healthy dogs (serum, 11.8 pg/mL, P < .0001; CSF, 1410 pg/mL, P = .0002). The areas under the receiver operating characteristic curves of serum and CSF NfL concentrations were 0.99 and 0.95, respectively. The cut-off values were 41.5 pg/mL (serum) and 4005 pg/mL (CSF) for differentiating between healthy and MUE dogs, with sensitivities of 89.19% and 90%, respectively, and specificities of 96.97% and 100%, respectively. The NfL concentration showed a significant decrease (pretreatment, 122 pg/mL; posttreatment, 36.6 pg/mL; P = .02) in the good treatment-response group and a significant increase (pretreatment, 292.5 pg/mL; posttreatment, 1880 pg/mL, P = .03) in the poor treatment-response group.Conclusions and Clinical importance: Neurofilament light chain is a potential biomarker for diagnosing MUE and evaluating response to treatment.

OBJECTIVE To investigate the neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), and platelet-to-lymphocyte ratio (PLR) in dogs with myxomatous mitral valve disease (MMVD). ANIMALS 106 dogs with MMVD and 22 healthy dogs were included in the study. PROCEDURES CBC data were obtained retrospectively, and NLR, MLR, and PLR were compared between dogs with MMVD and healthy dogs. The ratios were also analyzed according to MMVD severity. RESULTS NLR and MLR were significantly higher in dogs with MMVD C and D (NLR of 4.99 [3.69–7.27]; MLR of 0.56 [0.36–0.74]) than in healthy dogs (NLR: 3.05 [1.82–3.37], P < .001; MLR: 0.21 [0.14–0.32], P < .001), MMVD stage B1 (NLR: 3.15 [2.15–3.86], P < .001; MLR: 0.26 [0.20–0.36], P < .001), and MMVD stage B2 dogs (NLR: 3.22 [2.45–3.85], P < .001; MLR: 0.30 [0.19–0.37], P < .001). The area under the receiver operating characteristic curves of the NLR and MLR to distinguish dogs with MMVD C and D from those with MMVD B were 0.84 and 0.89, respectively. The optimal cutoff value for NLR was 4.296 (sensitivity, 68%; specificity, 83.95%), and the MLR value was 0.322 (sensitivity, 96%; specificity, 66.67%). NLR and MLR were significantly decreased after treatment in dogs with congestive heart failure (CHF). CLINICAL RELEVANCE NLR and MLR can be used as adjunctive indicators of CHF in dogs.

Background: The neutrophil-to-lymphocyte ratio (NLR) has been identified as a biomarker in several inflammatory and autoimmune diseases. Multiple sclerosis (MS) has been found to be associated with changes in the NLR in humans.Objectives: To examine the diagnostic value of the NLR in meningoencephalitis of unknown etiology (MUE) in dogs.Animals: Thirty-eight MUE dogs, 20 hydrocephalic dogs, 10 brain tumor (BT) dogs, 32 idiopathic epilepsy (IE) dogs, and 41 healthy dogs.Methods: Retrospective study. Medical records were reviewed to identify dogs with a diagnosis of neurologic disease. The NLR was determined in all dogs.Results: The median NLR was significantly higher in MUE dogs (6.08) than in healthy (1.78, P < .001), IE (2.50, P < .05), and hydrocephalic dogs (1.79, P < .05). The area under the receiver operating characteristic curve of the NLR for differentiation between MUE and healthy dogs was 0.96, and between the MUE dogs and dogs with other forebrain diseases was 0.86. An optimal cutoff of 4.16 for the NLR had a sensitivity of 71.1% and specificity of 83.9% to differentiate the MUE dogs from the dogs with other forebrain diseases.

Background Inflammatory bowel disease (IBD) commonly occurs in dogs, but there is lack of information about potential biomarkers of clinical and histopathologic severity. Objective To examine the role of serum C‐reactive protein (CRP) and high‐mobility group box 1 (HMGB1) concentrations in dogs with IBD. Animals Seventeen dogs with IBD and 25 healthy dogs. Methods In this prospective study, duodenal histopathologic severity was graded, and the clinical severity of IBD was assessed by the canine IBD assessment index (CIBDAI) score in dogs with IBD. Serum CRP and HMGB1 concentrations were compared between IBD and healthy dogs and analyzed according to histopathologic grade in dogs with IBD. The correlations between serum CRP and HMGB1 concentrations and the CIBDAI score were evaluated. Results Dogs with IBD had higher serum CRP (median [range] = 20.39 [1.53‐67.69] μg/mL vs 2.31 [0.17‐11.49] μg/mL; P < .001) and HMGB1 concentrations (0.44 [0.07‐1.58] ng/mL vs 0.05 [0.01‐0.25] ng/mL; P < .001) than healthy dogs. The serum HMGB1 concentration was higher in IBD dogs with a moderate to severe histopathologic grade (0.51 [0.30‐1.58] ng/mL, P = .03) than in those with a mild histopathologic grade (0.17 [0.07‐0.75] ng/mL). Serum CRP concentrations and CIBDAI score were positively correlated in dogs with IBD (rs = .49, P = .05). Conclusions and Clinical Importance Serum HMGB1 could be a potential biomarker for diagnosing IBD and might be indicative of histopathologic severity in dogs, whereas serum CRP might be an indicator of clinical severity.

Background: High-mobility group box 1 (HMGB1) is a key mediator of neuroinflammation and there are increased HMGB1 levels in laboratory animal models of epilepsy and human patients with epilepsy. Objectives: To determine serum HMGB1 levels in dogs with epilepsy. Animals: Twenty-eight epileptic dogs, 12 dogs with nonepileptic brain diseases, and 26 healthy dogs. Methods: In this case-control study, serum HMGB1 concentrations were estimated using the canine-specific enzyme-linked immunosorbent assay kit. Diagnosis of dogs with epilepsy was based on medical history, physical and neurological examination findings, laboratory test results, magnetic resonance image, and cerebrospinal fluid analysis. Results: Serum HMGB1 levels were significantly higher in epileptic dogs (median = 0.41 ng/mL; range, 0.03-5.28) than in healthy dogs (median = 0.12 ng/mL; range, 0.02-1.45; P = .002). In contrast, serum HMGB1 levels of dogs with non-epileptic brain diseases (median = 0.19 ng/mL; range, 0.03-1.04) were not significantly increased compared to those of healthy dogs (P = .12). Regarding idiopathic epilepsy, dogs with an epilepsy course of >3 months showed a higher serum HMGB1 concentration (median = 0.87 ng/mL; range, 0.42-2.88) than those with that of ≤3 months (median = 0.26 ng/mL; range, 0.03-0.88; P = .02). Conclusions and Clinical Importance: Serum HMGB1 could be a biomarker of epilepsy.