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A 6‐year‐old spayed female domestic short‐hair cat was presented for primary complaints of anorexia and lethargy. The cat was being treated with cyclosporine (25 mg/cat, PO q24h) and prednisolone (1 mg/kg, PO q12h) for feline hypersensitivity dermatitis and inflammatory bowel disease for 1 year, wherein prednisolone was withdrawn 2 weeks prior to presentation. At presentation, dehydration, hyperglycaemia, ketonaemia, increased fructosamine, glucosuria, ketonuria and metabolic acidosis were observed. The cat was diagnosed with diabetic ketoacidosis (DKA). Immediate treatments with insulin continuous‐rate infusion and intravenous fluid therapy were initiated. A serum cyclosporine concentration was >2100 ng/mL, indicating cyclosporine toxicity. Cyclosporine was discontinued immediately. The cat's acidosis and ketonaemia were resolved within a week, allowing a switch from insulin continuous‐rate infusion to subcutaneous glargine (1 IU/cat), which was eventually discontinued due to persistent normoglycaemia 12 days after initial presentation. Hyperglycaemia was not observed for 28 days thereafter without insulin, indicating remission of diabetes mellitus. This report suggests that using prednisolone, particularly immune suppressive doses, could be problematic in cats receiving long‐term cyclosporine therapy. Additionally, diabetic cats receiving immune‐suppressive agents can possibly achieve diabetic remission after surviving DKA through regular monitoring of blood glucose concentration, elimination of prednisolone and intensive blood glucose management. [ABSTRACT FROM AUTHOR]

Background: Neurofilament light chain (NfL) is released into the peripheral circulation by damaged axons. Objective s : To evaluate the diagnostic value of serum NfL concentration in dogs with intracranial diseases. Animals: Study included 37 healthy dogs, 31 dogs with idiopathic epilepsy (IE), 45 dogs with meningoencephalitis of unknown etiology (MUE), 20 dogs with hydrocephalus, and 19 dogs with brain tumors. Methods: Cohort study. Serum NfL concentrations were measured in all dogs using single‐molecule array technology. Results: Serum NfL concentration in dogs with each structural disease was significantly higher than in healthy dogs and dogs with IE (P =.01). The area under the receiver operating characteristic curve of NfL for differentiating between dogs with structural diseases and IE was 0.868. An optimal cutoff value of the NfL 27.10 pg/mL had a sensitivity of 86.67% and a specificity of 74.19% to differentiate the dogs with IE from those with structural brain diseases. There were significant correlations between NfL concentrations and lesion size: (1) MUE, P =.01, r = 0.429; (2) hydrocephalus, P =.01, r = 0.563. Conclusions and Clinical Importance: Serum NfL could be a useful biomarker for distinguishing IE from structural diseases in dogs and predicting the lesion sizes of MUE and hydrocephalus. [ABSTRACT FROM AUTHOR]

Copyright of Veterinary Dermatology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

A 2‐year‐old neutered male Bengal cat presented with solid food dysphagia and chronic regurgitation for >5 months. There were no clinical abnormalities on haematological or radiographic examinations. Thoracic radiography revealed a soft tissue opacity mass adjacent to the diaphragm in the caudoventral thorax. Ultrasonography revealed a protruding liver lobe surrounded by a hyperechoic lining from the diaphragm towards the thorax, and a pleuroperitoneal hernia was diagnosed. An endoscopy was performed to examine the cause of regurgitation, and an oesophageal stricture was observed. Endoscopic balloon dilation of the oesophageal stricture was performed, and the regurgitation was resolved immediately. However, regurgitation relapsed 2 months later, and computed tomography was performed to ascertain the cause. Computed tomography revealed oesophageal mural thickening and true pleuroperitoneal hernia with partial liver lobe herniation. A second endoscopy with balloon dilation was performed to treat the relapsing oesophageal stricture, and the clinical signs resolved without the need for herniorrhaphy. Nevertheless, oesophageal stricture could occur due to gastroesophageal reflux related to a pleuroperitoneal hernia; however, a definite link could not be elucidated in this case. This report describes a case of oesophageal stricture and concurrent true pleuroperitoneal hernia in a cat. [ABSTRACT FROM AUTHOR]

Background: High concentrations of complement factors are presented in serum of animal epilepsy models and human patients with epilepsy. Objectives: To determine whether complement dysregulation occurs in dogs with idiopathic epilepsy (IE). Animals: The study included 49 dogs with IE subgrouped into treatment (n = 19), and nontreatment (n = 30), and 29 healthy dogs. Methods: In this case‐control study, the serum concentrations of the third (C3) and fourth (C4) components of the complement system were measured using a canine‐specific ELISA kit. Results: Serum C3 and C4 concentrations were significantly higher in dogs with IE (C3, median; 4.901 [IQR; 3.915‐6.673] mg/mL, P <.001; C4, 0.327 [0.134‐0.557] mg/mL, P =.03) than in healthy control dogs (C3, 3.550 [3.075‐4.191] mg/mL; C4, 0.267 [0.131‐0.427] mg/mL). No significant differences were observed in serum C3 and C4 concentrations between dogs in the treatment (C3, median; 4.894 [IQR; 4.192‐5.715] mg/mL; C4, 0.427 [0.143‐0.586] mg/mL) and nontreatment groups (C3, 5.051 [3.702‐7.132] mg/mL; C4, 0.258 [0.130‐0.489] mg/mL). Dogs with a seizure frequency >3 times/month had significantly higher serum C3 (6.461 [4.695‐8.735] mg/mL; P <.01) and C4 (0.451 [0.163‐0.675] mg/mL; P =.01) concentrations than those with a seizure frequency ≤3 times/month (C3, 3.859 [3.464‐5.142] mg/mL; C4, 0.161 [0.100‐0.325] mg/mL). Conclusions and Clinical Importance: Dysregulation of classical complement pathway was identified in IE dogs. Serum C3 and C4 concentrations could be diagnostic biomarkers for IE in dogs with higher seizure frequency. [ABSTRACT FROM AUTHOR]

This report describes the clinical presentation and progression of a Serratia marcescens‐associated subcutaneous abscess in a dog with hypothyroidism, hyperadrenocorticism and diabetes mellitus. The S. marcescens isolate was resistant to several antibiotics. Treatment with antibiotics and topical antiseptics was not successful. [ABSTRACT FROM AUTHOR]

It has been reported that hypertriglyceridemia can partially mediate between diabetes mellitus (DM) and pancreatitis in dogs, implying that another mediator, such as chronic hyperglycemia, might exist. Therefore, this study aimed to evaluate the relationship between hyperglycemia and serum canine pancreatic lipase immunoreactivity (cPLI) concentration in diabetic dogs. This retrospective cohort study included 26 client-owned diabetic dogs, divided according to their serum fructosamine levels (<500 μmol/L = well-controlled DM group; ≥500 μmol/L = untreated or poorly controlled DM group). Five of the 26 DM dogs (19.2%) had serum cPLI concentrations consistent with pancreatitis, among which two showed ultrasonographic evidence of pancreatitis without clinical signs. The serum cPLI concentrations (median [interquartile range]) were significantly higher in the untreated or poorly controlled group (520 μg/L [179.76–1000 μg/L]) than in the well-controlled group (77 μg/L [32.22–244.6 μg/L], P = 0.0147). The serum fructosamine concentration was positively correlated with the serum cPLI concentration (r = 0.4816; P = 0.0127). Multivariate analysis revealed serum triglyceride and fructosamine concentrations were associated with the serum cPLI concentration. In conclusion, this study suggests that chronic hyperglycemia may induce pancreatic inflammation in diabetic dogs; however, the clinical significance of increased cPLI concentration is unknown. [ABSTRACT FROM AUTHOR]

Background: Previous studies have documented vitamin D imbalance in dogs with acute pancreatitis (AP), but no studies have investigated serum vitamin D receptor (VDR) and vitamin D‐binding protein (VDBP) concentrations. Objectives: Compare serum 25‐hydroxyvitamin D (25[OH]D), VDR, and VDBP concentrations in healthy dogs and dogs with AP and identify correlations between these concentrations with ionized calcium, C‐reactive protein (CRP), and canine‐specific pancreatic lipase (Spec cPL) concentrations. Animals: Twenty‐two dogs with AP and 20 healthy control dogs. Methods: Prospective cross‐sectional study. Serum 25(OH)D concentrations were measured using a chemiluminescence immunoassay, and VDR and VDBP concentrations were measured using a ELISA kit designed for dogs. Results: Serum concentrations of 25(OH)D were lower in dogs with AP (mean ± SD, 66.1 ± 39.2 ng/mL) than in controls (96.8 ± 30.4 ng/mL; P =.01), and VDR concentrations were lower in dogs with AP (5.3 ± 3.5 ng/mL) than in controls (7.4 ± 2.5 ng/mL; P =.03). No difference was observed in serum VDBP concentrations between the groups. Serum VDR concentrations differed between survivors (median [interquartile range] = 6.6 [4.3‐8.2] ng/mL) and nonsurvivors (2.7 [0.5‐3.5] ng/mL; P =.01). Negative correlations were observed among serum VDR, CRP (rs = −0.55), and Spec cPL (rs = −0.47) concentrations in dogs with AP. Conclusions and Clinical Importance: Dogs with AP had lower serum 25(OH)D and VDR concentrations than controls. Additionally, our study suggests a potential role of VDR expression in the inflammatory process of AP in dogs. [ABSTRACT FROM AUTHOR]

Background: Neurofilament light chain (NfL) is an axonal cytoplasmic protein in neurons. Recently, NfL has shown potential as a diagnostic biomarker in dogs with meningoencephalitis of unknown origin (MUO). However, there have been no studies on the biomarkers of lesion progression and resolution in MUO. Objectives: To identify the potential of NfL as a biomarker for predicting changes in lesions. Methods: Seven dogs with MUO who had undergone two magnetic resonance imaging (MRI) scans were included. The serum NfL levels were measured using a single‐molecule array. The relationship between the rate of change in lesion size and the rate of change in serum NfL level was analysed using simple linear regression. To investigate the effect of changes in lesion size on NfL levels, the dogs were divided into two groups depending on the change in lesion size: decreased lesion size group (n = 5) and increased lesion size group (n = 2). Trends in lesion size change were identified in the second MRI compared with the first MRI. Results: A significant positive relationship between the rate of lesion size change and the rate of NfL level change was identified (R2 = 0.9239, p = 0.0006). In the decreased lesion size group (n = 5), all NfL levels in each dog decreased, and in the increased lesion size group (n = 2), all NfL levels in each dog increased. Conclusions: This preliminary study showed a positive relationship between the rate of change in lesion size and rate of change in serum NfL levels. Therefore, the serum NfL level may be a promising biomarker of lesion progression and resolution in MUO. [ABSTRACT FROM AUTHOR]

A 3‐year‐old, 3.5 kg, female spayed Pomeranian was referred due to persistent vomiting, anorexia, polyuria and polydipsia, 7 days after receiving general anaesthetic for a medial patellar luxation correction. Physical examination revealed lethargy, tachypnoea and 7% dehydration. Complete blood count and serum chemistry results were unremarkable, and venous blood gas analysis revealed hypokalaemia and hyperchloraemic metabolic acidosis with a normal anion gap. Urinalysis revealed a urine specific gravity (USG) of 1.005, pH of 7.0 and proteinuria, and the bacterial culture was negative. Based on these results, the dog was diagnosed with distal renal tubular acidosis, and potassium citrate was prescribed to correct metabolic acidosis. In addition, concurrent diabetes insipidus (DI) was suspected because the dog showed persistent polyuria, polydipsia and a USG below 1.006 despite dehydration. After 3 days of initial treatment, acidosis was corrected, and vomiting resolved. Desmopressin acetate and hydrochlorothiazide were also prescribed for DI, but the USG was not normalized. Based on the insignificant therapeutic response, nephrogenic DI was highly suspected. DI was resolved after 24 days. This case report describes the concomitant presence of RTA and DI in a dog after general anaesthesia. The manuscript describes a clinical case of both transient distal renal tubular acidosis and nephrogenic diabetes insipidus in a dog showing repetitive vomiting after general anaesthesia. The aetiology of repetitive vomiting was a compensatory mechanism for metabolic acidosis caused by distal renal tubular acidosis. The clinical course and diagnostic approach for transient distal renal tubular acidosis with concurrent nephrogenic diabetes insipidus are described. Furthermore, suspected mechanisms for this clinical sequelae are discussed. [ABSTRACT FROM AUTHOR]

Thyroid nodules are common in older cats and are mostly benign; however, carcinomas may occur infrequently. In cats, thyroid carcinomas tend to be highly metastatic. The role of 18F‐2‐deoxy‐2‐fluoro‐D‐glucose (FDG) positron emission tomography (PET)/computed tomography (CT) in human thyroid carcinoma has been well established. However, guidelines have not yet been established for veterinary medicine. Metastasis assessment has typically been performed using CT in veterinary medicine; however, it is poorly sensitive in detecting regional lymph nodes or distant metastases if these lesions are not abnormally contrast‐enhanced, enlarged or cause overt mass effects. This case suggested that FDG PET/CT may be used for staging feline thyroid carcinoma, and the results contributed to treatment recommendations. [ABSTRACT FROM AUTHOR]

An 8‐year‐old Miniature Poodle presented with chronic sneezing and unilateral epistaxis. A left‐sided intranasal mass was identified on computed tomography. 18F‐fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed to evaluate the metabolic activity of the mass. The intranasal mass showed mildly increased 18F‐FDG uptake. The maximal and mean standardized uptake values (SUVs) of the mass were 3.4 and 2.6, respectively. The maximal SUV of the mass/mean SUV of the normal liver was 2.5. The 7‐cm soft, pink mass was easily removed through rhinoscopy, with subsequent dramatic improvement in clinical signs. Histopathological and immunohistochemical analyses determined that the mass was an intermediate‐grade malignant peripheral nerve sheath tumour (PNST). This is the first report of 18F‐FDG PET findings in a PNST in dogs. [ABSTRACT FROM AUTHOR]

Background: Serum microRNAs have emerged as biomarkers of various diseases. Overexpression of serum miR‐216a and miR‐375 occurs in dogs with experimentally induced acute pancreatitis (AP). Objectives: To identify the possibility of using serum miR‐216a and miR‐375 as biomarkers for the diagnosis and evaluation of treatment response in dogs with naturally occurring AP. Animals: Twenty‐one dogs with AP and 20 healthy dogs. Methods: Cross‐sectional study. The relative expression of serum hsa‐miR‐216a‐5p, cfa‐miR‐216a, and cfa‐miR‐375 were analyzed using reverse transcription and real‐time PCR. Results: A significant difference in the serum expression of cfa‐miR‐375 was found between dogs with AP (median [interquartile range] 3.59 [1.55‐24.52]‐fold) and healthy dogs (0.81 [0.54‐2.21]‐fold, P <.001), and no significant differences were observed in hsa‐miR‐216a‐5p and cfa‐miR‐216a (P >.05). The area under the receiver operating characteristic curve of serum cfa‐miR‐375 for differentiating between AP dogs and healthy dogs was 0.84 (95% confidence interval [CI]: 0.71‐0.96). The expressions of hsa‐miR‐216a‐5p and cfa‐miR‐375 were positively correlated with the concentrations of serum C‐reactive protein (rs =.46, rs =.48, respectively), but not with the serum specific canine pancreatic lipase. The expression of cfa‐miR‐375 was significantly less after treatment in dogs with AP (P =.02). Conclusions and Clinical Importance: Serum cfa‐miR‐375 could be a potential biomarker for the diagnosis and evaluation of treatment response of AP in dogs. In addition, miR‐216a and miR‐375 could be associated with inflammatory processes in dogs with AP. [ABSTRACT FROM AUTHOR]

Copyright of Veterinary Dermatology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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. Conclusions and Clinical Importance: The NLR could be a biomarker for diagnosing MUE and distinguishing it from other intracranial diseases in dogs. [ABSTRACT FROM AUTHOR]

Background: An imbalance in adipokines is associated with the progression of chronic kidney disease (CKD) in humans. However, alterations in adipokines in dogs with CKD remain unclear. Objectives: To examine whether adipokine concentrations in serum differ between healthy dogs and dogs with CKD and to determine the correlation between serum adipokine concentrations and CKD severity in dogs. Animals: Twenty dogs with CKD and 10 healthy dogs. Methods: In this cross‐sectional study, serum concentrations of leptin, adiponectin, interleukin (IL)‐6, IL‐10, IL‐18, and tumor necrosis factor (TNF)‐α were measured in healthy dogs and dogs with CKD, which were classified according to the International Renal Interest Society guidelines. Results: Serum leptin concentrations were positively correlated with systolic arterial blood pressure (r =.41), creatinine concentrations (r =.39), and symmetric dimethylarginine concentrations (r =.73). Serum adiponectin concentrations (median [range]) in CKD dogs with borderline or non‐proteinuric (20.25 [14.9‐45.8] ng/mL) were significantly higher than those in proteinuric CKD dogs (13.95 [6.4‐22.1] ng/mL; P =.01). Serum IL‐6 (median [range]; 43.27 [24.30‐537.30] vs 25.63 [6.83‐61.03] pg/mL; P =.02), IL‐18 (median [range]; 25.98 [11.52‐280.55] vs 10.77 [3.53‐38.45] pg/mL; P =.01), and TNF‐α (median [range]) concentrations (11.44 [8.54‐38.45] vs 6.105 [3.97‐30.68] pg/mL; P =.02) were significantly different between proteinuric and borderline or non‐proteinuric CKD dogs. Conclusions and Clinical Importance: leptin and adiponectin concentrations in serum might be associated with severity of CKD and proteinuria in dogs with CKD, respectively. [ABSTRACT FROM AUTHOR]

Inflammatory mammary carcinoma is known to be aggressive, which makes thorough evaluation of the severity of tumour infiltration and metastasis important in determining a recommended treatment course. This case report describes the use of 18F‐2‐deoxy‐2‐fluoro‐d‐glucose positron emission tomography/computed tomography for evaluating the invasiveness and metastasis of inflammatory mammary carcinoma in a dog. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

A 16-year-old castrated male Persian cat was presented with weight loss, anorexia and dyspnoea. Tachycardia and tachypnoea were observed upon presentation. The cat was previously diagnosed with hyperthyroidism and left ventricular hypertrophy and received methimazole, but was subsequently not followed up and treated appropriately. Thoracic radiography revealed mild pleural effusion, interstitial lung pattern, moderate cardiomegaly and moderate-to-severe dilation of the pulmonary artery and pulmonary vein. On echocardiography, the left ventricular hypertrophy, identified earlier, shoed partial regression. Therefore, the previous myocardial hypertrophy was diagnosed as a hypertrophic cardiomyopathy phenotype related to hyperthyroidism. ST-segment elevation was identified on electrocardiography, and the thyroid profile examination revealed increased total thyroxine and free thyroxine and decreased thyroid-stimulating hormone levels, suggesting myocardial injury and uncontrolled hyperthyroidism, respectively. In addition, normal N-terminal pro-B-type natriuretic peptide and high cardiac troponin I levels were found. Based on these findings, the observed congestive heart failure was considered as a sequel of myocardial injury caused by uncontrolled hyperthyroidism. Clinical signs resolved after intravenous administration of furosemide and butorphanol, oxygen supply and thoracocentesis. Furosemide and pimobendan were additionally administered, and the cat was discharged. This case demonstrates that myocardial damage due to chronic uncontrolled hyperthyroidism may cause heart failure in cats. [ABSTRACT FROM AUTHOR]

• Hyperglycemia and eosinopenia are well-known characteristics of hypercortisolism in dogs. • Eosinophils can affect glucose metabolism in hypercortisolism, like in humans. • Eosinophil percentage was negatively correlated with fasting blood glucose in dogs with hypercortisolism. • Eosinophil percentage was associated with the presence of hyperglycemia in dogs with hypercortisolism. Hyperglycemia and eosinopenia are well-known characteristics of hypercortisolism (HC) in humans, however, their association in dogs with HC has rarely been reported. This study aimed to evaluate the association between eosinophils and serum fasting glucose concentration in dogs with HC. Forty-seven dogs with HC and 43 dogs with non-adrenal illness were included. In this retrospective cohort study, the complete blood count, blood chemistry profile, and pre- and post-adrenocorticotropic hormone (ACTH) cortisol concentrations were analyzed. Significant differences were found in neutrophil, monocyte, eosinophil, and platelet counts; eosinophil percentage; neutrophil-to-lymphocyte ratio; aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transferase activities (P < 0.05) between the groups. In dogs with HC, the eosinophil percentage was inversely correlated with fasting blood glucose (r = –0.3515, P = 0.0154) and post-ACTH cortisol concentrations (r = –0.6509, P < 0.0001). The neutrophil-to-lymphocyte ratio was inversely correlated with the eosinophil percentage (r = –0.4573, P = 0.0012) and count (r = –0.3688, P = 0.0108), but positively correlated with the fasting blood glucose level (r = 0.3888, P = 0.0069). Such correlations were not identified in dogs with non-adrenal illness. A multivariate analysis showed that only eosinophil percentage was associated with the presence of hyperglycemia in dogs with HC (odds ratio = 2.100, 95% confidence interval = 1.051–4.199, P = 0.0360). Therefore, eosinopenia induced by excess cortisol might be associated with altered glucose metabolism in dogs with HC. A better understanding of this correlation could be valuable to predict and prevent the complications of HC. [ABSTRACT FROM AUTHOR]

A 9-year-old, neutered male, domestic short-haired cat was referred for recurrent ascites of unknown etiology over a week. Physical examination revealed abdominal distension and ultrasonography revealed a large volume of ascites throughout the abdominal cavity; this was interpreted as modified transudate. The mesentery and abdominal fat were hyperechoic and edematous. Fat tissue was assessed using fine-needle aspiration cytology, and adipocytes, fat-phagocytizing macrophages, and neutrophils were identified. Computed tomography revealed a pancreatic mass connected to the left pancreatic leg. Exploratory laparoscopy confirmed nodular masses and organ adhesions, leading to a tentative diagnosis of sclerosing encapsulating peritonitis. The cat was administered prednisolone, vitamin E, and tamoxifen but died 22 days after the initial therapy. Necropsy revealed a multi-lobulated pancreatic tumor (10 × 10 cm) tightly attached to the stomach and intestine, with a large amount of ascites. The peritoneum, stomach, intestine, and mesentery were covered with numerous disseminated nodules of various sizes (1-5 mm diameter). Microscopically, the tumor consisted of extensive adipose tissue, locally extensive inflammatory infiltrates, fibrous connective tissue, and small invasive proliferative glands. Well-defined small irregular glands composed of single-layered epithelial cells that appear to be of ductal origin were surrounded by an abundant desmoplastic stroma. Neoplastic nodules were widespread in the liver, stomach, peritoneum, mesentery, mesenteric lymph nodes, lungs, and urinary bladder. Immunohistochemistry revealed that the neoplastic glands were positive for pan-cytokeratin, confirming the pancreatic epithelial origin of the tumor. This is the first report of sclerosing encapsulating peritonitis accompanied by aggressive pancreatic adenocarcinoma of presumed ductal origin and extensive metastasis in a cat., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Kim, Kim, Park, Lee, Chae, Yun, Chang, Kang, Lee, Kim and Kim.)

Objective: To evaluate the relationships between the severity of myxomatous mitral valve disease (MMVD) and pulmonary hypertension (PH) and serum angiopoietin (Ang)-1 and Ang-2 concentrations in dogs with MMVD., Animals: 74 dogs (control, n = 12; MMVD, n = 62) were included., Methods: Serum Ang-1 and Ang-2 concentrations were estimated using the canine-specific ELISA kit. The concentrations were compared between dogs with MMVD and healthy dogs, and they were analyzed according to the severity of MMVD and PH., Results: The median serum Ang-1 concentration did not differ among the study groups. The median serum Ang-2 concentration was higher in dogs with stage B2 MMVD (P = .041) and acute congestive heart failure (P = .002) than in control dogs. In addition, the median serum Ang-2 concentration was higher in MMVD dogs with PH than in those without PH (P = .031). Serum Ang-2 concentration was correlated with vertebral heart score (rs = 0.36, P = .004) and vertebral left atrial score (r = 0.50, P < .001) in dogs with MMVD, and correlated with vertebral heart score (r = 0.63, P = .01), maximum E wave amplitude of the diastolic transmitral flow (rs = 0.61, P = .018), ejection fraction (rs = -0.77, P < .001) and fractional shortening (rs = -0.56, P = .032) in dogs with acute congestive heart failure., Clinical Relevance: Circulating Ang-2 levels increase in dogs with the severity of MMVD and the presence of PH.

Neurofilament light chain (NfL) is a neuroaxonal protein in the nervous system. NfL has recently been demonstrated to be a biomarker for various neurological diseases. In this study, we investigated the potential role of NfL in hypoxia-induced neuronal injury in dogs. Serum NfL levels were determined using a single-molecule array. Serum NfL concentrations were significantly higher in hypoxemic dogs without neurological signs ( n  = 6, 175.5 pg/mL) than in healthy dogs ( n  = 15, 15.9 pg/mL; p  < 0.0001). Therefore, neuronal injury should be considered in dogs with hypoxemia caused by cardiopulmonary diseases, even in the absence of neurological signs., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Yun, Chae, Koo, Lee, Kim, Yang and Kang.)

Vitamin D plays a role in anti-inflammatory processes, and the alteration of its metabolism is associated with the inflammatory processes of pancreatitis. This study was performed to evaluate the expression of the vitamin D receptor (VDR) and the two major enzymes that regulate vitamin D metabolism, 1α-hydroxylase (CYP27B1) and 24-hydroxylase (CYP24A1), in the canine pancreas and to compare their degrees of immunoreactivity between normal and inflamed pancreases. Five normal and inflamed pancreatic tissues each were obtained from six dogs. The expression of VDR, CYP24A1, and CYP27B1 were determined immunohistochemically, and the degree of immunostaining was assessed semiquantitatively. The VDR was expressed in the ducts, acini, and islets of Langerhans of normal pancreases and in the ducts and acini of inflamed ones. There was a significant difference in the immunoreactivity score for VDR in the islets of Langerhans between normal (median, 3 [interquartile range, 2-7.5] score) and inflamed pancreatic tissues (0 [0-0.5] score, p  = 0.03). CYP24A1 was expressed in the ducts and islets of Langerhans in both normal and inflamed pancreases, whereas CYP27B1 was expressed in the ducts and acini in only some normal and inflamed pancreatic tissues. This study showed that VDR expression decreased in inflamed pancreases and demonstrated CYP24A1 and CYP27B1 expression in the canine pancreas for the first time. These findings indicate that the pancreas could regulate the metabolism and biological activity of vitamin D and suggest that a decrease in these might be related to the pathophysiology of pancreatitis., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Lee, Kim, Koo, Chae, Wang, Kim, Yun, Yang, Kang and Kim.)

Background/aim: Fingolimod is a sphingosine-1-phosphate receptor modulator that prevents lymphocytes egress from lymphoid organs. It has been used as a disease-modifying drug for human multiple sclerosis and has shown better therapeutic effects than other conventional therapies. Therefore, this study was performed to obtain preclinical data of fingolimod in dogs., Materials and Methods: Nine laboratory Beagle dogs were used and randomized into three groups for pharmacokinetics (PK) and pharmacodynamics (PD). The dogs were administered once with a low-dose (0.01 mg/kg, n=3), medium-dose (0.05 mg/kg, n=3), and high-dose (0.1 mg/kg, n=3) of fingolimod, orally. Samples were collected serially at predetermined time points, and whole blood fingolimod concentrations were measured using high-performance liquid chromatography-mass spectrometry. Differential counts of leukocytes over time were determined to identify immune cells' response to fingolimod., Results: Regarding PK, the concentration of fingolimod in the blood increased in a dose-dependent manner, but it was not proportional. Regarding PD, the number of lymphocytes significantly decreased compared to baseline in all dose groups (low-dose, p=0.0002; medium-dose, p<0.0001; high-dose, p=0.0012). Eosinophils were significantly reduced in low- (p=0.0006) and medium- (p=0.0006) doses, and neutrophils were also significantly reduced in medium-(p=0.0345) and high- (p=0.0016) doses., Conclusion: This study provides the basis for future clinical applications of fingolimod in dogs with immune-mediated diseases, such as meningoencephalitis of unknown etiology., (Copyright © 2023, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Introduction: Cardiovascular and renal diseases are known to affect each other in the cardiovascular renal axis disorder (CvRD). Although CvRD, which includes myxomatous mitral valve disease (MMVD) and chronic kidney disease (CKD), has been described in dogs, there are only a few reports on the progression of CKD in accordance with the severity of MMVD. The aim of this study was to evaluate whether the presence of MMVD is associated with the rate of progression of CKD in dogs. The time from the initial diagnosis to the worsening of the International Renal Interest Society (IRIS) stage and the time for the occurrence of hyperphosphatemia and isosthenuria were evaluated., Materials and Methods: In this retrospective study, CKD progression was determined as an increase in the IRIS stage by at least one level and the development of hyperphosphatemia or isosthenuria. The CKD progression was compared in dogs with and without comorbid MMVD., Results: Dogs with CKD were divided into two groups: dogs with and without MMVD ( n = 63, concurrent group; n = 52, CKD group, respectively). The concurrent group was further divided into two subgroups based on the American College of Veterinary Internal Medicine guidelines (B1 group, n = 24; B2 group, n = 39). The time for progression of CKD from IRIS stage 1 to IRIS stage 2 was significantly shorter in the concurrent group than in the CKD group (log-rank test, p < 0.001). MMVD was associated with an increased risk of progression from stage 1 to stage 2 (hazard ratio, 6.442; 95% confidence interval (CI), 2.354 to 18.850; p < 0.001). The timing of the onset of hyperphosphatemia or isosthenuria in the concurrent group and the CKD group was not significantly different., Conclusion: The results of this study suggest that MMVD could be a risk factor for the progression of CKD. Our findings may help predict the prognosis of dogs with both CKD and MMVD compared to CKD only., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Yun, Koo, Yun, Chae, Lee, Cha, Kim, Kim, Yang and Kang.)

Background/aim: Tau is a microtubule-associated protein involved in the assembly and stabilization of microtubules. In human medicine, hyperphosphorylation of tau is associated with microtubule instability and is considered to play a role in the progression of multiple sclerosis (MS). MS is an autoimmune neurological disease that shares many characteristics, including pathological mechanisms, with canine meningoencephalitis of unknown etiology (MUE). With this background, this study investigated the presence of hyperphosphorylated tau in dogs with MUE and experimental autoimmune encephalomyelitis (EAE)., Materials and Methods: In total, eight brain samples were examined from two neurologically normal dogs, three dogs with MUE, and three canine EAE models. Anti-(phospho-S396) tau antibody was used for immunohisto-chemistry, which stained hyperphosphorylated tau., Results: In normal brain tissues, hyperphosphorylated tau was not found. In all the dogs with EAE and one of the dogs with MUE, immunoreactivity for S396 p-tau was observed in glial cell cytoplasm and the background in the periphery of the inflammatory lesion., Conclusion: These results suggest for the first time that tau pathology may be involved in the progression of neuroinflammation in dogs, similar to that in human MS., (Copyright © 2023, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)