ABSTRACT A 5‐year‐old castrated male Maltese dog presented with generalized tonic‐clonic cluster seizures. The seizures first occurred 10 days prior and progressed gradually. Upon presentation, the dog exhibited signs of obtundation, head turn and tetraparesis. Magnetic resonance imaging showed diffuse multifocal lesions of the cerebral white and grey matter extending from the left frontal lobe to the occipital lobe, along with ventriculomegaly. The dog was diagnosed with meningoencephalitis of unknown etiology (MUE) concurrent with hydrocephalus. Treatment was initiated with immunosuppressants and antiseizure medication. Blood tests during treatment indicated hyponatremia and hypochloremia. Additionally, plasma hypoosmolality, high urine osmolality and natriuresis were identified. Moreover, based on physical examination, the dog was considered euvolemic. The dog had normal adrenal, thyroid and renal functions. Water restriction led to a mild improvement of hyponatremia, and the dog was diagnosed with a syndrome of inappropriate secretion of the antidiuretic hormone (SIADH). Although the electrolyte imbalance partially improved with water restriction, the dog experienced severe thirst. Consequently, tolvaptan, a vasopressin receptor antagonist, was administered at 3 mg/kg PO daily, and water restriction was eased. Hyponatremia improved with these treatments. On day 130, the seizure recurred, leading the owner to discontinue treatment; subsequently, the dog was lost to follow‐up. In veterinary medicine, SIADH associated with brain diseases is often assumed to be attributed to hypothalamic–pituitary axis dysfunction, though inflammatory conditions can also cause hyponatremia. This report presents a case of SIADH accompanied by MUE, highlighting the role of inflammation as a cause of SIADH in dogs.

BACKGROUND:Hypercortisolism (HC) is a common endocrine disorder in dogs that is often associated with pancreatitis. However, the relationship between cortisol concentration, pancreatic injury (PI) markers, and serum specific canine pancreatic lipase immunoreactivity (Spec cPL) concentration elevation remains unclear. HYPOTHESIS/OBJECTIVES:To investigate the prevalence of PI, identify risk factors for elevated Spec cPL, and evaluate changes in Spec cPL concentrations after treatment. ANIMALS:Seventy-one client-owned dogs diagnosed with naturally occurring HC between 2015 and 2024. METHODS:Retrospective cross-sectional study with a nested cohort analysis. Dogs were classified as PI (Spec cPL ≥400 μg/L) or non-PI (Spec cPL <400 μg/L). Clinical and laboratory variables, including abdominal ultrasonography findings, were analyzed. Risk factors were identified using logistic regression analysis. A subset of dogs with follow-up data was analyzed to assess changes in Spec cPL concentration after treatment for HC. RESULTS:The PI comprised 16 dogs, with 7 (44%) showing ultrasonographic signs of pancreatitis. Univariate analysis showed significant intergroup differences in gamma-glutamyl transferase, blood urea nitrogen (BUN), symmetric dimethylarginine, cholesterol, C-reactive protein, urine protein-to-creatinine ratio (UPC), and post-low-dose dexamethasone suppression test (LDDST) cortisol concentrations. Multivariate analysis further identified BUN (odds ratio [OR], 1.05; 95% CI, 1.01-1.09; P =.02), UPC (OR, 1.84; 95% CI, 1.09-3.11; P =.02), and post-LDDST cortisol (OR, 1.55; 95% CI, 1.11-2.17; P =.01) as risk factors. Trilostane treatment significantly reduced the post-ACTH cortisol and Spec cPL concentrations. CONCLUSIONS AND CLINICAL IMPORTANCE:PI could occur in dogs with HC, especially those having elevated post-LDDST cortisol, BUN, and UPC.

Jujube (Ziziphus jujuba Mill.) is a widely consumed fruit in East Asia, yet its sharp-ended pits pose a high risk of gastrointestinal perforation in humans. While well-documented in human medicine, jujube pit ingestion in dogs has not previously been reported in the veterinary literature. This report describes a 15-year-old neutered male Maltese dog that presented with anorexia and lethargy five days after accidentally ingesting whole jujubes. Abdominal radiographs identified multiple intraluminal gastric foreign bodies demonstrating a distinctive, orientation-dependent sign: circular (transverse) or spindle-shaped (sagittal) opacities featuring a characteristic central longitudinal stripe. Although abdominal ultrasonography was limited in this specific case due to severe acoustic shadowing from localized gastric gas, the unique radiographic marker provided a reliable diagnostic clue before surgical confirmation. A gastrotomy was performed to successfully retrieve six intact, sharp-pointed pits, and the dog recovered uneventfully. To the authors’ knowledge, as the first report to describe the clinical progression and specific radiographic characteristics of jujube pits in a dog, this case highlights the central longitudinal stripe as a diagnostic clue. This marker facilitates the differentiation of jujube pits from other foreign bodies on plain radiographs, allowing for timely surgical intervention to prevent catastrophic complications.

A 6-year-old castrated male Bengal cat developed a subcutaneous mass at a previous vaccination site, which was initially diagnosed as cutaneous T-cell lymphoma following surgical excision at a local hospital. The cat was referred for metastatic evaluation and further treatment. Computed tomography revealed a residual tumor at the excision site, and an additional thoracic subcutaneous mass was identified. Both lesions were surgically excised and submitted for histopathologic and immunohistochemical examination. Despite the initial diagnosis of lymphoma, immunohistochemistry demonstrated that the neoplastic cells were negative for multiple lineage-specific markers, including CD3, Pax5, CD20, and cytokeratin, but showed strong MUM-1 positivity in mitotically active cells. These findings supported a diagnosis of plasmacytoma. This case emphasizes a diagnostic challenge in distinguishing round cell tumors in cats and the critical role of immunohistochemistry in achieving an accurate diagnosis. The tumor also showed aggressive clinical behavior, including suspected distant metastasis, and may have arisen in association with chronic inflammation at a prior injection site.

BACKGROUND:Hematologic indices are identified as biomarkers in various inflammatory diseases and in human epilepsy. HYPOTHESIS/OBJECTIVES:To identify the most accurate hematologic index and evaluate its diagnostic utility in dogs with idiopathic epilepsy (IE). ANIMALS:A total of 46 dogs with IE, 24 with hydrocephalus, 39 with meningoencephalitis of unknown etiology (MUE), 17 with brain tumors (BTs), and 55 healthy controls. Of these, 6 hydrocephalus, 24 MUE, and 11 BT dogs presented with seizures and were classified as structural epilepsy for comparison with IE. METHODS:This retrospective study analyzed hematologic indices and used receiver operating characteristic (ROC) curves to identify the most accurate marker, whose diagnostic utility was subsequently evaluated. RESULTS:The platelet-to-lymphocyte ratio (PLR) demonstrated the highest diagnostic performance among the evaluated indices. Median PLR was significantly higher in IE dogs (132.3 [102.0-160.0]) than in controls (94.9 [77.6-108.4], P < .0001), but lower than that in dogs with MUE (240.8 [164.6-357.5], P < .0001), BT (246.5 [178.8-360.8], P < .0001), and hydrocephalus (164.0 [110.1-194.5], P < .0001). The area under the ROC curve was 0.73 for differentiating IE vs controls, 0.78 for IE vs structural brain diseases, and 0.85 for IE vs structural epilepsy. Optimal PLR cutoffs were 111.0 (sensitivity 67.4%, specificity 78.2%) to distinguish IE vs controls, 161.9 (sensitivity 71.3%, specificity 76.1%) for IE vs structural brain diseases, and 178.3 (sensitivity 84.8%, specificity 78.1%) for IE vs structural epilepsy. CONCLUSIONS AND CLINICAL IMPORTANCE:Platelet-to-lymphocyte ratio shows promise as a biomarker for diagnosing IE in dogs and distinguishing it from structural brain diseases, including those with seizures.

Serum microRNAs (miRNAs) serve as diagnostic and prognostic biomarkers for various diseases. The serum concentration of miRNA-375 (miR-375), which is abundantly expressed in pancreatic islet cells, is increased in dogs with experimentally induced pancreatic injury and naturally occurring acute pancreatitis. However, this has not been reported in dogs with diabetes mellitus (DM). This study aimed to compare the expression of serum cfa-miR-375 between dogs with DM and healthy dogs and examine changes in serum cfa-miR-375 levels after insulin administration in dogs with DM. Twenty dogs with DM and 18 healthy dogs were included. The relative expression of serum cfa-miR-375 using reverse transcription and real-time PCR were evaluated. The primary endpoint was the comparison of serum cfa-miR-375 expression between dogs with DM and healthy dogs. The mean +/- standard deviation (SD) fold change (FC) of serum cfa-miR-375 was significantly higher (P = 0.048) in dogs with DM (2.30 +/- 2.018) than in healthy dogs (1.294 +/- 0.560). The FC of serum miR-375 was significantly increased (P = 0.01) after treatment (4.017 +/- 2.054) than before treatment (2.322 +/- 2.608) in dogs with DM. The percentage change in cfa-miR-375 levels was positively correlated with the concentration of serum fructosamine post-treatment (r = 0.62, P = 0.01). Increased serum miR-375 levels may be associated with direct leakage from the damaged pancreas and pathological glucose regulation in canine DM.

Ureterolithiasis is a common cause of ureteral obstruction in dogs, often leading to kidney injury. Medical expulsive therapy (MET) using α-adrenergic antagonists has been proposed as a nonsurgical treatment option in selected cases and is thought to facilitate ureteral stone passage by reducing ureteral smooth muscle tone. A 9-year-old castrated male Chihuahua weighing 1.78 kg was presented with anorexia. Physical examination revealed 7% dehydration and pale mucous membranes. Serum biochemistry demonstrated severe azotemia, with markedly elevated symmetric dimethylarginine (>100 μg/dL; reference interval [RI], 0–14 μg/dL), blood urea nitrogen (157.9 mg/dL; RI, 7–25 mg/dL), and creatinine (2.2 mg/dL; RI, 0.5–1.5 mg/dL). On day 4 of hospitalization, ultrasonography revealed dilation of the renal pelvis (16.1 mm), ureteral distention (3.74 mm), and multiple ureteroliths (maximum diameter, 3.31 mm) at the ureterovesical junction. Antegrade pyelography confirmed a right ureteral obstruction. As the owner declined surgical intervention, MET including tamsulosin, was initiated with close clinical monitoring. After 3 days, improvement in azotemia and resolution of ureteral obstruction were observed. Although concurrent medical treatments were administered, this case provides clinical insight into the potential role of tamsulosin as part of medical management of obstructive ureterolithiasis in a dog with small distal ureteral stones.

Chronic kidney disease (CKD) in dogs is a progressive disorder, often accompanied by metabolic and inflammatory alterations. Insulin resistance (IR) is well documented in humans with CKD; however, supporting evidence is lacking in dogs with CKD. The present study aimed to investigate the presence of IR in dogs with CKD, examine its association with renal function markers (creatinine and symmetric dimethylarginine [SDMA]) and pro-inflammatory cytokines, and assess differences according to CKD stage. This retrospective cross-sectional study included 66 client-owned dogs: 30 healthy controls and 36 dogs with CKD. Dogs with CKD were staged as 1-2 (n = 20) or 3-4 (n = 16) according to the International Renal Interest Society (IRIS) guidelines. Fasting blood samples were analyzed for serum glucose, insulin, creatinine, SDMA, interleukin (IL)-6, IL-8 (C-X-C motif chemokine ligand 8; CXCL8), IL-18, and tumor necrosis factor (TNF)-α levels. Indices of IR and β-cell function were calculated using the homeostasis model assessment (HOMA)-IR and HOMA-β. Dogs with CKD had significantly higher insulin and HOMA-IR values than healthy controls (P < 0.05), whereas no differences were observed for HOMA-β values. HOMA-IR values did not differ between CKD stages 1-2 and 3-4, and no correlation was found with creatinine or SDMA. In contrast, IL-6, IL-18, and TNF-α concentrations were significantly elevated (P < 0.05) and positively correlated with HOMA-IR in dogs with CKD. These findings suggest that IR in dogs with CKD might be associated with pro-inflammatory cytokines, although no association was observed between IR and CKD severity.

An 8 yr old spayed female domestic shorthair presented with a 1 wk history of anorexia and lethargy. Cytological examination of the liver using fine-needle aspiration revealed numerous adipocytes, confirming hepatic lipidosis. The cat was hospitalized for treatment; subsequently, the clinical signs and blood analysis results improved. On day 17, the nasoesophageal tube was removed because of recovery of appetite and vitality. However, owing to insufficient voluntary food intake, partial parenteral nutrition (PPN) was initiated using an amino acid solution with a low branched-chain amino acid (BCAA)/aromatic amino acid (AAA) ratio and arginine deficiency. Within 24 hr of PPN administration, neurological signs were observed, including vocalization, panting, hyperactivity, and a subsequent comatose state. Although hepatic encephalopathy was considered, there was limited evidence of hepatic failure. The clinical course was most consistent with acute hyperammonemia secondary to arginine deficiency, although a contributing role of the low BCAA/AAA ratio cannot be excluded. This case suggests that amino acid PPN with arginine deficiency and a low BCAA/AAA ratio may contribute to neurological signs in cats, underscoring the importance of careful amino acid selection in nutritional formulations.

Meningoencephalitis of unknown etiology (MUE) is a common inflammatory central nervous system disease in dogs and is associated with a poor prognosis. The first 3 months post-diagnosis represent a critical prognostic window, as most mortalities occur within this period. The hemoglobin, albumin, lymphocyte, and platelet (HALP) score has emerged as a novel prognostic tool for predicting short-term mortality in various human diseases. However, its utility has not yet been evaluated in dogs with MUE. This retrospective study aimed to evaluate the predictive value of the HALP score for three-month and one-year mortality in 36 dogs diagnosed with MUE. The HALP score was significantly higher in survivors than in non-survivors at both the three-month and one-year time points. Receiver operating characteristic curve analysis demonstrated good predictive accuracy, with an area under the curve of 0.79 for three-month and 0.80 for one-year mortality. An optimal cut-off of 12.25 yielded 50.0% sensitivity and 95.0% specificity for predicting three-month mortality. For one-year mortality, a cut-off of 34.33 yielded 95.2% sensitivity and 66.7% specificity. Dogs with a HALP score ≤ 12.25 had a significantly shorter median survival time (31 days) than those with a score > 12.25 (283 days). Similarly, a score ≤ 34.33 was associated with a shorter median survival time (67.5 days) compared to those with a score > 34.33 (971 days). These findings suggest that the HALP score is a valuable, non-invasive indicator for risk stratification and predicting short-term mortality in dogs with MUE.

A 1-year-old Maltese dog weighing 1.6 kg was referred for evaluation of a persistent comatose mentation that developed within one day following treatments for seizures and hypoglycaemia. At presentation, the dog exhibited signs of mild dehydration (approximately 5%), pinpoint pupils, and hypothermia. Initial differential diagnoses included portosystemic shunt, glycogen storage disease (GSD), and congenital hypothyroidism based on clinical presentation and history. The bile acid and ammonia concentrations were within the reference intervals, thereby ruling out a portosystemic shunt. A thyroid panel was conducted, with the results revealing low serum total thyroxine concentrations with elevated thyroid-stimulating hormone concentrations, and subsequent thyroid-stimulating hormone stimulation test confirmed hypothyroidism. Euthanasia was performed at the owner's request. Histopathologic examination revealed idiopathic thyroid gland atrophy, diffuse vacuolar degeneration with glycogen accumulation in the liver and kidneys. The diagnosis was GSD type Ia and concurrent juvenile primary acquired hypothyroidism. This case highlights the importance of a comprehensive evaluation for concurrent congenital and acquired endocrine disorders in young dogs presenting with neurological and metabolic abnormalities.

An 8‐year‐old castrated male Miniature Poodle was referred due to polyuria, polydipsia and urinary incontinence, following 12 days of prednisolone administration (0.25 mg/kg q12h) for otitis externa. Upon physical examination, an abnormal heart rhythm was detected on cardiac auscultation without any associated clinical signs. Owing to suspected conduction abnormalities, electrocardiography (ECG) was performed, which revealed a Mobitz Type II second‐degree atrioventricular (AV) block. Blood analysis revealed hyperglycaemia (> 500 mg/dL; reference interval [RI] = 65–118 mg/dL), elevated fructosamine (361 µmol/L; RI = 177–314 µmol/L) and β‐hydroxybutyric acid concentrations (5.4 mmol/L; RI ≤ 2.5 mmol/L), leading to a diagnosis of diabetic ketosis. To manage the diabetic ketosis, porcine lente insulin (Caninsulin, MSD) was administered at a dose of 0.33 U/kg q12h. Three days after initiating insulin therapy, the clinical signs improved, a stable blood glucose curve with a nadir of 150 mg/dL was observed, and the β‐hydroxybutyric acid concentration decreased to 1.4 mmol/L. Follow‐up ECG confirmed resolution of the AV block. Subsequently, the diabetes mellitus (DM) was well managed, and the AV block did not recur. A strong association between DM and AV block is reported in humans. However, studies investigating the relationship between DM and AV block in veterinary medicine are limited. This case report describes the potential for acute‐onset DM to induce cardiac conduction disturbances in dogs.

An 8-year-old neutered male Miniature Poodle, weighing 6.7 kg, was presented with lethargy, anorexia, and single seizure episode. Neurological examination revealed bilaterally absent menace reflexes and an obtunded mental status. Magnetic resonance imaging showed a papilliform shaped mass measuring 1.2 × 1.4 × 1.3 cm in size, with a volume of 1.17 cm3 in the third ventricle. 3,4-dihydroxy-6-[18F] fluoro-l-phenylalanine (18F-FDOPA) positron emission tomography/computed tomography (PET/CT) was performed 53 days after presentation, revealing a hypermetabolic region in the intraventricular mass with mean and maximal standardized uptake values (SUVmean and SUVmax) of 1.2 and 1.42, respectively, and a tumor to normal tissue (T/N) ratio of 1.33. The mass lesion measured 1.3 × 1.4 × 1.2 cm in size, with a volume of 1.09 cm3 on contrast-enhanced CT images. The metabolic tumor volume (MTV) was 1.184 cm.3 No evidence of brain parenchymal metastases was observed. Therefore, the dog was tentatively diagnosed with a brain tumor, which was suspected to be a choroid plexus papilloma (CPP) and chemotherapy with prednisolone and cyclophosphamide was initiated. As worsening clinical signs were observed, a second 18F-FDOPA PET/CT scan was performed on day 183. The SUVmean, SUVmax, and T/N ratio of the lesion were 1.49, 1.85, and 1.62, respectively. The mass lesion measured 1.0 × 1.0 × 1.3 cm in size, with a volume of 0.68 cm3 on contrast-enhanced CT images, whereas the MTV was increased to 2.217 cm3. The dog died 186 days after the presentation. To the best of our knowledge, this is the first report describing the 18F-FDOPA PET/CT findings in a dog with an intraventricular brain tumor suspected of having CPP. In the present case, although the lesion size decreased on CT contrast imaging, an increase in the MTV was observed on follow-up 18F-FDOPA PET/CT after chemotherapy. Thus, an increase in MTV post-chemotherapy combined with the worsening clinical signs and limited survival period in dogs correlates with poor prognosis, as previously reported in a human study. This case offers significant diagnostic insights into canine intraventricular tumors within the field of veterinary medicine.

Background: Meningoencephalitis of unknown etiology (MUE) is a representative sterile inflammatory disease of the central nervous system (CNS) in dogs. The treatment involves the use of immunosuppressive therapies. Despite intensive immunosuppressive therapy, the survival time of MUE remains short. Fingolimod is a novel immunomodulatory drug primarily used to treat human neuroinflammatory diseases such as multiple sclerosis. However, fingolimod has not yet been used in veterinary medicine. Therefore, this study aimed to identify the potential therapeutic effect of fingolimod as an alternative treatment agent for MUE in dogs, using a canine experimental autoimmune encephalomyelitis (EAE) model. Materials, Methods & Results: The canine EAE model was induced using brain tissues obtained from client-owned dog. Eight grams of forebrain tissue were homogenized in an ice bath for 5 min with phosphate-buffered saline. The resulting suspension was emulsified with an equal amount of Freund’s complete adjuvant. A laboratory Beagle dog was subcutaneously injected with the homogenate in the axillary and inguinal regions (a total of 4 sites) under sedation. The dog received a booster injection 7 days later using the same procedure as the 1st injection. After 25 days of the 1st injection, the dog showed decreased activity and hyporexia. When a magnetic resonance imaging (MRI) examination was performed to determine whether the inflammatory lesion was induced, a lesion in the left white matter of the frontal lobe was identified as hyperintense in T2-weighted and fluid-attenuated inversion recovery images and hypointense to isointense in T1-weighted images. Additionally, cerebrospinal fluid analyses revealed a slight increase in total protein concentration and severe mononuclear pleocytosis. The EAE dog was prescribed oral fingolimod [0.05 mg/kg once daily]. At 14 and 28 days post-fingolimod therapy, assessments of clinical signs and 2nd and 3rd MRIs were performed to evaluate therapeutic effectiveness. The clinical signs and most lesions were no longer observed. CSF analysis results were also normal at 14 and 28 days after the commencement of fingolimod therapy. Discussion: The canine EAE model and MUE share several key similarities, making the EAE model a valuable tool for studying MUE. Both conditions are characterized by immune-mediated inflammation of the CNS, leading to demyelination and neurological deficits. The treatment approaches for both conditions often involve the use of immunosuppressive therapies to control inflammation and prevent further neurological damage. These similarities in pathogenesis, clinical presentation, and therapeutic strategies emphasize the relevance of the EAE model in understanding the mechanisms underlying MUE and in developing effective treatments for MUE. Fingolimod was known to be well tolerated and effective, causing a swift decrease in peripheral lymphocytes without any adverse effects at oral doses ranging from 0.01 mg/kg to 0.1 mg/kg in dogs. Despite being a single case, this study evaluated fingolimod as a novel immunomodulatory agent for MUE. When applied for 4 weeks in a canine EAE model, fingolimod revealed a remarkable therapeutic effect by showing recovery of clinical signs, resolution of MRI lesions, and normalization of abnormal CSF findings. Therefore, fingolimod has shown potential as an alternative novel treatment agent for dogs with MUE. Keywords: dog, EAE, fingolimod, treatment, meningoencephalitis, MUE, S1PR.

A 12-year-old castrated male domestic shorthair cat was referred for respiratory distress. Physical examination revealed a systolic heart murmur at the left apex and crackles in all lung fields. Thoracic radiography showed Valentine-shaped cardiomegaly, pulmonary oedema, and pleural effusion. Echocardiography revealed focal thickening of the interventricular septum [11.01 mm; reference interval (RI) = 3.00-5.20 mm] and left ventricular posterior wall (7.41 mm; RI = 3.00-5.10 mm) during diastole. In the apex region, the free wall was focally thinned to approximately 1.6 mm with hypokinetic myocardial movement, indicating thin and hypokinetic myocardial segments. Additionally, decreased left atrial fractional shortening (12.5%; RI = 23.9-34.9%) and an increased left atrial-to-aortic ratio (2.87; RI = 0.88-1.43) were observed, along with spontaneous echocardiographic contrast in the left atrium, indicating increased thrombotic risk. The electrocardiogram showed a left axis deviation with small R waves and deep S waves in lead II, which is consistent with a left anterior fascicular block caused by delayed conduction in the left anterior fascicle. This case report describes the coexistence of a left anterior fascicular block and thin, hypokinetic myocardial segments in feline hypertrophic cardiomyopathy, suggesting a possible pathophysiological link.

An 8-year-old castrated male Pomeranian with a non-resectable functional thyroid carcinoma and concurrent myxomatous mitral valve disease was referred for radioactive-iodine therapy. Due to clinical thyrotoxicosis at referral and concurrent cardiac disease, the radioiodine dose was selected conservatively at the lower end of the reported therapeutic range. Despite a conservative radioactive iodine dose, the dog developed acute thyrotoxic decompensation consistent with thyroid storm (manifesting as anxiety, diarrhea, hyperthermia, hypersalivation, and marked tachycardia) within hours of treatment. Propranolol and butorphanol administration led to rapid clinical stabilization. Before the second radioactive iodine therapy, methimazole and propranolol were used for subsequent management, effectively controlling thyrotoxicosis risk and enabling a higher radioiodine dose. Serum thyroxine normalized within 1 month after the second treatment, and the dog maintained complete clinical remission thereafter. Radioactive iodine therapy served as definitive therapy to prevent recurrent life-threatening thyrotoxicosis, resulting in a euthyroid state and long-term survival. This case describes the first documented case of a dog with thyroid carcinoma developing probable thyroid storm associated with radioiodine treatment and subsequently achieving a favorable prognosis.

ObjectivesThis study aimed to evaluate changes in serum insulin-like growth factor type 1 (IGF-1) concentrations in cats with hyperthyroidism before and after radioactive iodine (RAI) treatment, as well as investigate the correlation between thyroid volume and serum IGF-1 concentrations.MethodsA total of 13 cats with hyperthyroidism and 14 healthy controls were included. Serum total thyroxine (TT4)/thyroid-stimulating hormone (TSH) and IGF-1/insulin-like growth factor binding protein-3 (IGFBP-3) concentrations were measured using chemiluminescence immunoassay and ELISA, respectively, at presentation and 6 months after RAI treatment. The results were compared with thyroid volume measured using scintigraphy. Data are presented as median (interquartile range [IQR]) and analysed using non-parametric tests.ResultsSerum TT4 concentrations significantly decreased from 9.30 µg/dl (IQR 6.49-12.7) to 2.23 µg/dl (IQR 1.34-2.94) after RAI treatment (P <0.001), while TSH levels increased from 0.021 ng/ml (IQR 0.021-0.021) to 0.125 ng/ml (IQR 0.050-0.257) (P = 0.002). IGF-1 levels significantly increased from 329 ng/ml (IQR 240-479) to 572 ng/ml (IQR 402-1038) after RAI treatment (P = 0.011), while IGFBP-3 levels did not differ. Serum creatinine concentrations significantly increased from 1.3 mg/dl (IQR 1.2-1.6) to 2.0 mg/dl (IQR 1.7-2.3) after RAI treatment (P = 0.006). No correlation was observed between IGF-1 and any variable, except IGFBP-3 (rs = 0.587; P = 0.039) in the pretreatment group. IGF-1 and body weight were significantly positively correlated after RAI treatment (rs = 0.696; P = 0.011) but not before. In healthy cats, IGF-1 was negatively correlated with serum TT4 (rs = -0.627; P = 0.019).Conclusions and relevanceThe increased serum IGF-1 concentrations after RAI treatment may reflect the restoration of anabolic status in cats with hyperthyroidism. In this study population, no correlation was found between thyroid volume and serum IGF-1 concentrations.

An 8-year-old neutered male Maltese dog was presented with 6 palpable cutaneous masses on the neck and thorax 1 y after the surgical excision of mast cell tumors (MCT) from the mid-thoracic and right axillary regions. Before chemotherapy, the sum of the masses' diameters was 19.0 cm. 18F-fluorodeoxyglucose (FDG)-positron emission tomography/computed tomography (PET/CT) revealed hypermetabolic lesions within the skin overlying the ventral thorax, bilateral prescapular lymph nodes, and right axillary lymph node. The dog was diagnosed with MCT recurrence and treated with combination chemotherapy comprising imatinib, vinblastine, and prednisolone. After completion of 2 16-week chemotherapy regimens, the sum of the masses' diameters decreased to 3.6 cm. For assessment of the chemotherapy response and guidance for subsequent therapeutic plans, follow-up FDG-PET/CT was undertaken 25 d after completion of the 2nd chemotherapy regimen. It demonstrated a reduction in FDG uptake in all areas compared with that on the initial scan, except for the middle thoracic mass. After follow-up FDG-PET/CT, a 3rd chemotherapy regimen was implemented, and the dog died 416 d after the initiation of chemotherapy. There are no reports of a combination chemotherapy with imatinib, vinblastine, and prednisolone for treating canine cutaneous MCT. This case highlighted the potential therapeutic use of this combination chemotherapy for recurrent canine MCTs. Furthermore, this report indicates that FDG-PET/CT may be useful for assessing malignancy, evaluating chemotherapy responses, and establishing treatment plans for canine cutaneous MCTs. Key clinical message: Combination chemotherapy of imatinib, vinblastine, and prednisolone is a potential therapeutic regimen for recurrent cutaneous MCTs in dogs. In addition, FDG-PET/CT may be a potentially useful tool for assessing malignancy, evaluating chemotherapy responses, and guiding further therapeutic decisions.

Cushing's syndrome (CS) is a common endocrine disorder in dogs that can significantly impair their quality of life. Diagnosis is often challenging because of its variable clinical presentation, making it difficult to identify suitable candidates for further diagnostic tests. This study employed machine learning algorithms to assist in CS diagnosis using routinely available screening diagnostics, including complete blood count, serum chemistry panel, and urinalysis parameters such as urine specific gravity and urine protein-to-creatinine ratio. Data were collected from 153 control dogs initially suspected of CS but later excluded and 152 dogs with confirmed CS. A boosted tree algorithm (gradient boosting) was trained on 80% of the collected data, with the remaining 20% reserved for testing. The developed model demonstrated an accuracy of 88.5% [95% confidence interval (CI): 80.5-96.5%], a sensitivity of 83.3% (95% CI: 70.7-96.7%), a specificity of 93.5% (95% CI: 84.9-100%), and an area under the receiver operating characteristic curve of 0.912 (95% CI: 0.835-0.988), indicating excellent discriminatory ability. A user-friendly graphical interface was also developed to facilitate clinical implementation, potentially improving diagnostic efficiency and owner satisfaction.

A 7-year-old neutered female Shih Tzu presented with bilateral skin lesions and a subcutaneous mass in the submandibular region. The initial lesion on the right appeared as a plaque, followed by the development of an ulcer on the opposite side 2-3 days later. Despite treatment with antibiotics, antifungal drugs and anti-inflammatory steroids, lesions persisted. There was an initial improvement with steroids; however, the lesions developed into scars, erythema and papules. A biopsy revealed eosinophilic and mixed-cell dermatitis requiring treatment with immunosuppressive steroids and cyclosporine, which resolved the plaque and ulcer but only partially reduced the subcutaneous mass. Surgical resection was considered, and subsequent skull radiography revealed alveolar bone loss. During surgery, a sinus tract was identified extending from teeth 309 to 409, indicating that the tissue changes were likely due to drainage from the periodontal disease. Based on clinical history and examination results, the case was definitively diagnosed as an odontogenic cutaneous sinus tract (OCST). Following surgery, no recurrence of the lesion or mass was observed. This is the first case report describing the histopathological features of a submandibular OCST in a dog, highlighting the importance of considering this condition when submandibular lesions do not fully respond to immunosuppressive therapy.