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Abstract Background Neurofilament light chain (NfL) is released into the peripheral circulation by damaged axons. Objectives 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 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 3 times/month had significantly higher serum C3 (6.461 [4.695‐8.735] mg/mL; P

Abstract 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 Background To the best of our knowledge, this is the first report of female genital system infiltration of T-cell lymphoma in veterinary literature. Case presentation A 1.5-year-old, intact female Golden Retriever was referred due to melena and hyporexia that lasted for three weeks. Fever (40.5℃), tachycardia, tachypnoea, pale mucous membranes, and purulent vaginal discharge were identified on physical examination. Blood analyses revealed leucocytosis, anaemia, hypoalbuminemia, and increased lactate and C-reactive protein levels. On abdominal radiography, the small intestine was moderately deviated because of an oval-shaped mass (13 cm × 8.7 cm) located in the mid-abdomen. An enlarged tubular-shaped structure that had the opacity of soft tissue located in dorsal to the bladder to the middle of the abdomen, and an oval-shaped mass (5.28 cm × 3.26 cm), which was suspected to be a medial iliac lymph node located at the sixth to seventh lumbar level. Abdominal ultrasonography revealed gas and fluid in the lumen of the uterine horn with a severely thickened wall, round enlarged lymph nodes around the genitourinary system, and free fluid in the abdominal cavity. Based on these results, pyometra was suspected, and an exploratory laparotomy was performed for ovariohysterectomy. The resected ovary and uterus were macroscopically hypertrophied. Histopathological examination of the ovary and uterus revealed neoplastic proliferation of large round cells with strong immunoreactivity for CD3, indicating T-cell lymphoma. Therefore, the young dog was diagnosed with genital lymphoma. Conclusions The present report describes T-cell lymphoma infiltrating the uterus and ovaries in a young dog, which is rarely diagnosed and could aid in the differential diagnosis of genital diseases in young dogs.

Abstract 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 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 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 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.

Abstract 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 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.

Long-term use of proton-pump inhibitors can induce fundic gland polyps in the human stomach. However, this phenomenon has not been described in the veterinary literature. A 5-year-old intact female Maltese dog was referred to our hospital with chronic intermittent vomiting. The dog had been administered omeprazole (0.7–1.0 mg/kg PO q24 h) for the management of hydrocephalus for over 4 years; the omeprazole dose was increased to 10 mg/kg PO q24 h 8 months prior to presentation at referring hospital. Abdominal ultrasonography revealed marked thickening of the gastric wall with multi-lobulated, thickened folds. Subsequent endoscopy revealed marked polypoid lesions, and histological examination of the biopsy samples was consistent with the fundic gland polyps associated with proton-pump inhibitor use in humans. The lesions resolved after cessation of omeprazole, as assessed by ultrasonography. This report describes a case of fundic gland polyps following the long-term administration of omeprazole in a dog.

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

Multiple endocrine disorders are uncommon in veterinary medicine, and the disease combination is usually related to hypercortisolism or autoimmunity. Central-pituitary hypothyroidism, also refer to secondary hypothyroidism, can be caused by hypercortisolemic conditions and is well-recognized in human medicine. However, central hypothyroidism, including pituitary hypothyroidism, concurrent with hyperadrenocorticism, is rarely reported in veterinary medicine. A 7-year-old, intact female Miniature Schnauzer presented with generalized alopecia, scale, and pruritus and was diagnosed with superficial pyoderma and Malassezia dermatitis. Hormonal tests were performed, and the results indicated multiple endocrinopathies with a combination of non-adrenal dependent hyperadrenocorticism and central-pituitary hypothyroidism. Magnetic resonance imaging (7 T) and high-resolution research tomography positron emission tomography were performed to differentiate neuroendocrine tumors; however, no lesion was found in the hypothalamic to pituitary region. Hyperadrenocorticism was managed first to control endocrinopathy. After controlling hypercortisolism, a weak elevation of free thyroxine (T4) was revealed, whereas total T4 and thyroid-stimulating hormone (TSH) were still undetectable, and hypothyroidism management was added. About 9 months after the management, both endocrine diseases were well controlled, and clinical signs improved; however, serum TSH was unmeasured consistently. This case study describes a case of multiple endocrinopathies in a Miniature Schnauzer dog diagnosed with central-pituitary hypothyroidism concurrent with non-adrenal dependent hyperadrenocorticism without pituitary macroadenoma.

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.

A 12-year-old castrated male domestic shorthair cat weighing 6.7 kg presented with acute hindlimb paralysis and tachypnea. The femoral pulse was absent bilaterally. Thoracic radiography showed finding compatible with cardiogenic pulmonary edema. Echocardiography revealed hypertrophic cardiomyopathy phenotype and a spontaneous echocardiographic contrast in the left atrium, suggesting cardiogenic arterial thromboembolism. Oxygen supplementation, diuretics, and antithrombotic and thrombolytic agents were also administered. However, hindlimb motor function was not restored. Severely increased aspartate aminotransferase and creatinine phosphokinase, as well as neutropenia with a degenerative left shift were identified, and amputation was considered to prevent sepsis caused by necrosis of the ischemic tissues. 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET)/computed tomography was performed to evaluate the metabolic activity of the muscle tissues and determine the level of amputation. There was no 18F-FDG uptake in the extremities of either the hind limbs or the caudal parts of the bilateral femoral muscle mass, suggesting a loss of metabolic activity in the area. Considering the wide affected area, a decreased quality of life was predicted postoperatively, and the cat was euthanized at the owner’s request. Postmortem muscle biopsy confirmed weak atrophy of the left femoral muscle and prominent atrophy of the right calf. This case report describes the use of 18F-FDG PET in a cat with ischemia caused by cardiogenic arterial thromboembolism.

IntroductionCardiovascular 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 methodsIn 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.ResultsDogs 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.ConclusionThe 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.

Abstract 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 .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 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

Abstract 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 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.

A 5-year-old male Maltese dog was presented with generalized tonic seizures and hypermetria. Multiple nodular subcortical cerebellar enhancements and meningeal enhancement were observed on magnetic resonance imaging. Fluorodeoxyglucose-positron emission tomography/computed tomography was performed due to suspicion of neoplastic disease, and no fluorodeoxyglucose uptake was observed in the intracranial structures. In PET images of this dog, absent fluorodeoxyglucose uptake was identified in the brain indicating no cerebral metabolism, strongly suggested brain death. The dog had no spontaneous breathing and no brainstem reflexes for more than 24 h after the termination of anesthesia. Through these results, this dog was diagnosed with unexpected brain death, and it is presumed that the cause was anesthesia. We report herein a case of brain death in a dog diagnosed using fluorodeoxyglucose-positron emission tomography/computed tomography.

Abstract Background In human medicine, 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) has been used to differentiate between benign and malignant adrenal tumors and to identify metastases. However, canine adrenocortical carcinomas identified by 18F-FDG PET/computed tomography (CT) have not been reported. Case presentation A 13-year-old, castrated male, Cocker Spaniel dog with severe systolic hypertension exhibited an adrenal mass approximately 3.6 cm in diameter on ultrasonography. There was no evidence of pulmonary metastasis or vascular invasion on thoracic radiography and abdominal ultrasonography, respectively. 18F-FDG PET/CT was performed to identify the characteristics of the adrenal mass and the state of metastasis. One hour after injection of 5.46 MBq/kg 18F-FDG intravenously, the peripheral region of the adrenal mass visually revealed an increased 18F-FDG uptake, which was higher than that of the liver, and the central region of the mass exhibited necrosis. The maximal standardized uptake value (SUV) of the adrenal mass was 3.24; and relative SUV, calculated by dividing the maximal SUV of the adrenal tumor by the mean SUV of the normal liver, was 5.23. Adrenocortical carcinoma was tentatively diagnosed and surgical adrenalectomy was performed. Histopathologic examination of the resected adrenal mass revealed the characteristics of an adrenocortical carcinoma. After adrenalectomy, systolic blood pressure reduced to below 150 mmHg without any medication. Conclusion This is the first case report of 18F-FDG PET/CT findings in a dog with suspected adrenocortical carcinoma and may provide valuable diagnostic information for adrenocortical carcinoma in dogs.

An 8-year-old neutered male Yorkshire Terrier dog presented with head pressing, vestibular ataxia, neck tenderness, and no oculocephalic reflex. A demarcated lesion in the pons was identified on MRI. The patient was tentatively diagnosed with a glioma and was treated with hydroxyurea plus imatinib and prednisolone. After 30 days of therapeutic treatment, the patient showed a clear improvement in neurological signs, which lasted for 1117 days. On day 569 after the initiation of treatment, 18F-fluorodeoxyglucose (FDG)-positron emission tomography (PET) was performed with no significant findings on visual analysis. The average and maximal standardized uptake values (SUVs) were 1.92 and 2.29, respectively. The tumor-to-normal-tissue (T/N) ratio was 0.97. The first evidence of clinical deterioration was noticed on day 1147. On day 1155, 3,4-dihydroxy-6-[18F]-fluoro-l-phenylalanine (18F-FDOPA)-PET was performed. High uptake of 18F-FDOPA was observed in the intracranial lesion. The mean and maximal SUVs of the tumor were 1.59 and 2.29, respectively. The T/N ratio was 2.22. The patient was euthanized on day 1155 and histopathologic evaluations confirmed glioma (astrocytoma). This case shows that chemotherapy with hydroxyurea plus imatinib may be considered in the treatment of canine glioma. Furthermore, this is the first case describing the application of 18F-FDG and 18F-FDOPA in a dog with glioma.

Abstract 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

Abstract 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

A 12-year-old intact female Miniature Pinscher dog weighing 5.4 kg presented with a history of seizures. On neurological examination, postural reactions were decreased in the left-sided limbs, and menace responses were bilaterally absent. Magnetic resonance imaging (MRI) of the brain was performed, and a solitary amorphous mass (2.7 × 1.9 × 2.2 cm) was observed on the right side of the frontal lobe. Based on the signalment, clinical signs, and MRI findings, a brain tumor was tentatively diagnosed, and meningioma was suspected. The dog was treated with hydroxyurea, prednisolone, and other antiepileptic drugs. One week after the treatment began, postural reactions returned to normal, and the menace response improved. At 119 days after treatment, 18F-fluoro-L-phenylalanine (18F-FDOPA) positron emission tomography (PET) was performed. Marked 18F-FDOPA uptake was observed in the lesion. The mean and maximal standardized uptake values of the lesion were 2.61 and 3.72, respectively, and the tumor-to-normal tissue ratio was 1.95. At 355 days after the initial treatment, a second MRI scan was performed and the tumor size had increased to 3.5 × 2.8 × 2.9 cm. The dog died 443 days after the initial treatment and was definitively diagnosed with grade 1 meningioma by histopathological examination. Immunohistochemical staining for Ki67 and L-type amino acid transporter 1 was positive and negative for p53, respectively. The labeling index of Ki67 was 2.4%. This is the first case to demonstrate 18F-FDOPA PET findings in a clinical case of a dog histologically diagnosed with a meningioma.

There is only one previous report of canine goitrous hypothyroidism caused by iodine deficiency from 1986. The present case report describes the novel diagnostic methods and long-term outcomes of a dog diagnosed with goitrous hypothyroidism caused by iodine deficiency. A 4-year-old neutered, female Pomeranian dog presented with a cervical mass, lethargy, and inactivity. The dog had a history of eating home-cooked diets sold by a private seller for 1 year. The physical examination and ultrasonography showed two bilaterally symmetric masses in the mid-cervical area (left, 1.8 × 1.4 cm; right, 2.3 × 1.8 cm), and they were suspected to be the thyroid glands. To identify the function of the thyroid gland, the basal concentrations of thyroid hormones [total T4 (tT4) and thyroid-stimulating hormone (TSH)] were measured and a TSH stimulation test was performed: baseline tT4, 0.5 μg/dL (reference interval, 1–4 μg/dL), baseline TSH, 0.81 μg/dL (reference interval, 0.05–0.42 μg/dL), and post-tT4, 1 μg/dL (6 h after the injection of TSH). The values indicated primary hypothyroidism. The urinary iodine concentration was 302 μg/L, which was markedly lower than that of normal dogs (1,289 μg/L). Thyroid scintigraphy with technetium-99m pertechnetate was also performed to quantify the activity of the thyroid gland, and the thyroid-to-salivary ratio was 3.35. Based on the results of these examinations and patient history, the dog was diagnosed with diet-induced (iodine deficiency) goitrous hypothyroidism. The dog was treated with iodine (62.5 μg/day). At 31 days after treatment, clinical signs and thyroid hormones were normalized (tT4, 1.3 μg/dL; TSH, 0.24 μg/dL). One year after treatment, the dog was well with normal concentrations of thyroid hormones (tT4, 1.8 μg/dL; TSH, 0.27 μg/dL) and a partially reduced goiter (left, 1.6 × 1.1 cm; right, 1.2 × 0.9 cm). This is the first case to describe novel diagnostic methods and long-term outcomes of a dog diagnosed with goitrous hypothyroidism caused by iodine deficiency.

Abstract Background Positron emission tomography (PET) is increasingly being used as an imaging modality for clinical and research applications in veterinary medicine. Amyloid PET has become a useful tool for diagnosing Alzheimer’s disease (AD) in humans, by accurately identifying amyloid-beta (Aβ) plaques. Cognitive dysfunction syndrome in dogs shows cognitive and pathophysiologic characteristics similar to AD. Therefore, we assessed the physiologic characteristics of uptake of 18F-flutemetamol, an Aβ protein-binding PET tracer in clinical development, in normal dog brains, for distinguishing an abnormal state. Static and dynamic PET images of six adult healthy dogs were acquired after 18F-flutemetamol was administered intravenously at approximately 3.083 MBq/kg. For static images, PET data were acquired at 30, 60, and 90 min after injection. One week later, dynamic images were acquired for 120 min, from the time of tracer injection. PET data were reconstructed using an iterative technique, and corrections for attenuation and scatter were applied. Regions of interest were manually drawn over the frontal, parietal, temporal, occipital, anterior cingulate, posterior cingulate, and cerebellar cortices, cerebral white matter, midbrain, pons, and medulla oblongata. After calculating standardized uptake values with an established formula, standardized uptake value ratios (SUVRs) were obtained, using the cerebellar cortex as a reference region. Results Among the six cerebral cortical regions, the cingulate cortices and frontal lobe showed the highest SUVRs. The lowest SUVR was observed in the occipital lobe. The average values of the cortical SUVRs were 1.25, 1.26, and 1.27 at 30, 60, and 90 min post-injection, respectively. Tracer uptake on dynamic scans was rapid, peaking within 4 min post-injection. After reaching this early maximum, cerebral cortical regions showed a curve with a steep descent, whereas cerebral white matter demonstrated a curve with a slow decline, resulting in a large gap between cerebral cortical regions and white matter. Conclusion This study provides normal baseline data of 18F-flutemetamol PET that can facilitate an objective diagnosis of cognitive dysfunction syndrome in dogs in future.

This study aimed to identify the physiological 18F-fluoro-2-deoxy-D-glucose (FDG) uptake in cats using positron emission tomography/computed tomography (PET/CT) and determine its characteristics by comparing physiological differences with dogs. Seven healthy cats and six healthy beagle dogs were examined using FDG-PET/CT. Regions of interest (ROIs) were manually drawn over 41 detailed structures of 5 gross structures (brain, head and neck, musculoskeleton, thorax, and abdomen). The mean and maximum standard uptake values (SUVmean and SUVmax) were calculated for each ROI. Physiological variation was classified as having increased radiopharmaceutical activity with no evidence of abnormal clinical or radiological findings. The brain had the highest SUV, which was observed in the cerebellum of both cats (SUVmean: 4.90 ± 1.04, SUVmax: 6.04 ± 1.24) and dogs (SUVmean: 3.15 ± 0.57, SUVmax: 3.90 ± 0.74). Cats had a significantly higher intracranial uptake than dogs did (P < 0.01). In the digestive system, the SUVs of the duodenum and jejunum were significantly higher in dogs than in cats (P < 0.05). FDG uptake of the submandibular tip, tonsils, neck of the gallbladder, and caudal colliculus were physiologically increased in cats. This study demonstrates physiological FDG uptake in normal tissues, and the differences between cats and dogs were interpreted based on species-specificity. This information contributes to improving the accurate diagnosis of cancer in cats and will aid in understanding glucose metabolism in both cats and dogs.

A 15.5-year-old, neutered, male, domestic shorthair cat was presented with neurologic dysfunctions. At presentation, an obtunded mental status and vestibular ataxia were identified. On neurologic examination, postural reactions were decreased-to-absent in all four limbs, and pupillary light reflexes showed bilaterally delayed results. Magnetic resonance imaging was performed, and a demarcated lesion was identified in the third ventricle. The cat was tentatively diagnosed with a brain tumor, which was suspected to be a meningioma. The cat was treated with hydroxyurea and prednisolone. Mental status was considered more alert, and ataxia improved following treatment. On the 106th day after the commencement of treatment, a 18F-fluorodeoxyglucose (FDG)-positron emission tomography (PET) scan was performed. On the PET images, a hypermetabolic region was found in the lesion. The average standardized uptake value of FDG was 2.47, and the tumor-to-normal-tissue ratio was 1.25. The cat died 408 days following the commencement of treatment, and a grade 1 meningioma was confirmed by postmortem histopathology. Immunohistochemistry for Ki-67 and p53 was performed. The labeling indices of Ki-67 and p53 were 2.56 and 0%, respectively. This case shows that chemotherapy with hydroxyurea and prednisolone may be considered in the treatment of feline meningiomas. Furthermore, this is the first case describing the application of FDG-PET to visualize a naturally occurring meningioma in a cat.

A 9-year-old, intact male Shih Tzu dog presented with systemic weakness and peracute onset of tetraplegia. Tetraplegia with lower motor neuron signs was noted upon neurological examination. Diseases that cause acute flaccid tetraparesis, such as acute fulminating myasthenia gravis, polyradiculoneuritis, tick paralysis, and botulism, were ruled out based on the medical history, normal electrophysiological tests, and non-response to the neostigmine challenging test. Initial 0.3-Tesla (T) magnetic resonance imaging (MRI) findings included sharply demarcated intramedullary lesions at the C3-C6 level, mainly involving gray matter, which appeared hypo- to iso- intense on T1-weighted images (WIs), and hyperintense on T2-WIs and fluid-attenuated inversion recovery images. There was no enhancement on post-contrast T1-WIs. Neutrophilic pleocytosis was observed in the cerebrospinal fluid analysis. No clinical responses were observed for the treatment of non-infectious myelitis with an immunosuppressive dosage of prednisolone. A follow-up 3-T MRI 6 days later demonstrated hyperintensity on diffusion-WI (DWI) and a decreased apparent diffusion coefficient (ADC) value (0.54 × 10−3 mm2/s) of the spinal lesions. Through histological examination, a fibrocartilaginous embolism was definitively confirmed. This is the first report to describe an ischemic spinal injury visualized by DWI and ADC mapping with high-field MRI in a chondrodystrophic dog diagnosed with a fibrocartilaginous embolism.

An 8.5-year-old intact female lion (Panthera leo) with a history of vomiting, lethargy, and anorexia was referred to our institution. On physical examination, the lion weighed 180 kg and had a rectal temperature of 40 °C. Blood analysis showed mild neutrophilic leukocytosis, and abdominal ultrasonography revealed an enlarged uterus with echogenic fluid. Based on the clinical signs and hematologic and ultrasonographic findings, the lion was tentatively diagnosed with pyometra. Ovariohysterectomy was performed using the lateral flank approach to avoid complications that can occur with ventral celiotomy. Surgery was performed successfully despite unexpected rupture of the uterus which had occurred before the surgery. The lion recovered uneventfully and continued to do well at the 1 year follow up after surgery. To the best of our knowledge, this is the first reported case of ovariohysterectomy with the lateral flank approach in a lion with pyometra. Our report suggests that ovariohysterectomy with the lateral flank approach could be considered as an alternative method for pyometra in wild big cats with risk of complications at the surgical site.

Background: Canine atopic dermatitis (CAD) is a hereditary pruritic and inflammatory allergic skin disease associated with elevated IgE levels. Although, several treatments for CAD exist, allergen-specific immunotherapy (ASIT) is the only treatment that induces tolerance to pathogenic allergens. Sublingual immunotherapy (SLIT) is effective, convenient, and safe. This case report describes the successful treatment of a dog with atopic dermatitis using SLIT, emphasizing the efficacy and safety of SLIT as a long-term management strategy for CAD. Case: A 3-year-old spayed female Dachshund presented with non-seasonal chronic pruritus and generalized alopecia. The onset of pruritus occurred at 6 months of age, and its severity, measured by the pruritus visual analog scale, score was 5 out of 10. Dermatological examination revealed alopecia and scales on the dorsum and tail, and alopecia, lichenification, and crust on the medial side of the forelimbs. Diagnostic tests confirmed superficial pyoderma and Malassezia dermatitis. Initial treatment included amoxicillin/clavulanate, itraconazole, and a shampoo containing chlorhexidine gluconate and miconazole nitrate. An elimination diet trial was performed using a commercial diet to diagnose canine adverse food reaction (CAFR). However, 11 days after treatment initiation, the microbial and fungal skin infections and pruritus did not improve. Prednisolone was subsequently prescribed to alleviate pruritus and evaluate the response to glucocorticoids. At 24 days after the administration of prednisolone, pruritus reduction and lesion improvement were observed. Thereafter, prednisolone was tapered to 0.5 mg/kg EOD and discontinued 38 days after the initial administration. After prednisolone discontinuation, cytology did not reveal any cocci or Malassezia sp. Therefore, treatment with amoxicillin/clavulanate and itraconazole was discontinued. Two weeks after the discontinuation of prednisolone, pruritus relapsed, and cytology revealed no infection. The dog was initially treated with oclacitinib and planned to be managed with ASIT following an intradermal skin test at 2 weeks later. A provocative challenge was performed after the pruritus, and the lesions were well managed with oclacitinib. Because the clinical signs did not worsen, CAFR was excluded. The Favrot criteria was used to diagnose CAD by ruling out other skin conditions. An intradermal skin test was performed for 27 allergens, and oclacitinib was administered for SLIT, with allergens showing a positive reaction. After the administration of SLIT and oclacitinib, pruritus was well controlled and no recurrence was observed. At 763 days and 1638 days after the commencement of SLIT, oclacitinib and SLIT were discontinued, respectively. Notably, 9 months after discontinuing SLIT, complete remission of CAD was observed. Discussion: ASIT is used in veterinary medicine to treat CAD. A comprehensive clinical study found that SLIT has a success rate of 55%. The oral mucosa's low pro-inflammatory cell counts underscores SLIT's safety. Considering its efficacy and safety, ASIT was initiated with SLIT. ASIT can take > 12 months to improve CAD. Therefore, oclacitinib was prescribed to control pruritus. Complete remission of CAD was confirmed at the time of writing 9 months after SLIT discontinuation. This case indicates that SLIT could be an effective and safe therapeutic option for the long-term management of CAD. [ABSTRACT FROM AUTHOR]

Background/Aim: Fingolimod is a sphingosine1-phosphate receptor modulator that prevents lymphocytes egress from lymphoid organs. It has been used as a diseasemodifying 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; highdose, 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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]