Use of 18-Fluorodeoxyglucose Positron Emission Tomography and Near-Infrared Fluorescence-Guided Imaging Surgery in the Treatment of a Gastric Tumor in a Dog.

A 13-year-old Maltese dog with an abdominal mass underwent 18F-FDG PET/computed tomography (CT) for tumor localization and metastatic evaluation. PET/CT scans revealed a gastric mass near the esophagogastric junction and demonstrated mean and maximum standardized uptake values (SUVs) of 4.596 and 6.234, respectively, for the abdominal mass. Subsequent surgery incorporated ICG for NIR fluorescence-guided imaging, aiding in precise tumor localization and margin assessment. The excised mass was identified as a low-grade leiomyosarcoma on histopathology. The dog underwent PET/CT imaging six months postoperatively following the excision of the mass, which confirmed the absence of recurrence or residual lesions during follow-up. NIR fluorescence imaging using ICG demonstrated efficacy in real-time tumor visualization and margin assessment, a technique not previously reported in veterinary literature. The PET/CT findings complemented the diagnosis and provided valuable insights into metastasis. The absence of recurrence or complications in postoperative follow-up underscores the potential of these imaging modalities in enhancing surgical precision and improving prognosis in canine gastric tumors.

Case report: Sclerosing encapsulating peritonitis in a cat with disseminated pancreatic adenocarcinoma of presumed ductal origin.

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.

Remission of diabetes mellitus induced by prednisolone in combination with cyclosporine toxicity in a cat.

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.

Can neutrophil-to-lymphocyte and platelet-to-lymphocyte ratios be used as markers for hypercortisolism in dogs?

Changes in neutrophil-to-lymphocite ratio (NLR) and platelet-to-lymphocyte ratio (PLR) have been identified in dogs with hypercortisolism (HC), but, no studies have investigated the changes in these inflammatory biomarkers as cost-effective and available parameters for the diagnosis and management of HC. This study was performed to evaluate whether NLR and PLR could be used as biomarkers for the diagnosis and treatment response in dogs with HC. This retrospective study included 67 dogs with HC, 58 dogs with non-adrenal illness (NAI), and 39 healthy dogs. NLR and PLR were compared among the three groups. Cut-off values of NLR and PLR for HC screening and percent change in biomarkers for assessing treatment response were evaluated. In addition, the NLR and PLR were compared before and after trilostane treatment. NLR and PLR were significantly higher in the HC group than in the NAI and healthy groups. The NLR cut-off value of 4.227 had a sensitivity of 67.16% and specificity of 65.52%, and the PLR cut-off value of 285.0 had a sensitivity of 56.72% and specificity of 70.69% for differentiating between dogs with HC and those with NAI, respectively. Furthermore, a significant decline in NLR was observed after treatment in the well-controlled HC group. The cutoff value of percent change in NLR to identify well-controlled HC was -7.570%; sensitivity and specificity were 100% and 63.64%, respectively. Therefore, NLR and PLR might be used cautiously as supportive biomarkers for HC diagnosis, and NLR could be a potential monitoring tool in assessing the treatment response of HC in dogs.

Use of neurofilament light chain to identify structural brain diseases in dogs.

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.

Myxomatous mitral valve disease and associated pulmonary hypertension might increase serum angiopoietin-2 in dogs.

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.

Oesophageal stricture in a cat with true pleuroperitoneal hernia.

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.

An evaluation of the physiological uptake range of 18F-fluoro-2-deoxy-D-glucose in normal ovaries of seven dogs using positron emission tomography/computed tomography.

Introduction: This study evaluated the physiological uptake range of 18F-fluoro-2-deoxy-D-glucose (18F-FDG) in the normal ovaries of seven dogs using positron emission tomography/computed tomography (PET/CT). Materials and methods: The dogs were subjected to general anesthesia and were positioned in ventral recumbency for PET/CT scans. The dosage of 18F-FDG ranged from 0.14 to 0.17 mCi/kg and was administered intravenously followed by 0.9% NaCl flushing; PET/CT images of each dog were obtained precisely 60 min after the injection of 18F-FDG. The regions of interest were drawn manually, and standardized uptake values (SUV) were calculated to evaluate the 18F-FDG uptake in each ovary. The maximum and mean SUVs (SUV max and SUV mean) for all the ovaries of the dogs were then computed. Results: The range of SUV max and SUV mean of the normal ovaries of the dogs were 1.28-1.62 and 1.07-1.31 (mean ± standard deviation), respectively. Conclusion: This is the first study to investigate the normal 18F-FDG uptake baseline data of normal canine ovaries using PET/CT scans. These data will help clinicians in identifying malignant tumors before anatomical changes in the ovary through PET/CT scans.

Serum concentrations of complement C3 and C4 in dogs with idiopathic epilepsy.

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.

Expression of sphingosine-1-phosphate receptor 1 in neuroinflammation of canine brains.

Sphingosine-1-phosphate (S1P) is a signaling lipid mediator that is involved in multiple biological processes. The S1P/S1P receptor (S1PR) signaling pathway has an important role in the central nervous system. It contributes to physiologic cellular homeostasis and is also associated with neuroinflammation. Therefore, this study was performed to evaluate the expression of S1PR in dogs with meningoencephalitis of unknown etiology (MUE) and experimental autoimmune encephalomyelitis (EAE). The analysis used 12 brain samples from three neurologically normal dogs, seven dogs with MUE, and two canine EAE models. Anti-S1PR1 antibody was used for immunohistochemistry. In normal brain tissues, S1PR1s were expressed on neurons, astrocytes, oligodendrocytes, and endothelial cells. In MUE and EAE lesions, there was positive staining of S1PR1 on leukocytes. Furthermore, the expression of S1PR1 on neurons, astrocytes, oligodendrocytes, and endothelial cells was upregulated compared to normal brains. This study shows that S1PR1s are expressed in normal brain tissues and leukocytes in inflammatory lesions, and demonstrates the upregulation of S1PR1 expression on nervous system cells in inflammatory lesions of MUE and EAE. These findings indicate that S1P/S1PR signaling pathway might involve physiologic homeostasis and neuroinflammation and represent potential targets for S1PR modulators to treat MUE.

A single-blind randomised study comparing the efficacy of fluconazole and itraconazole for the treatment of Malassezia dermatitis in client-owned dogs.

BACKGROUND: No reports have compared the clinical therapeutic efficacy of fluconazole and itraconazole in canine Malassezia dermatitis. OBJECTIVES: The study aimed to compare the clinical therapeutic efficacy of fluconazole and itraconazole and to evaluate the adverse effects of fluconazole in canine Malassezia dermatitis. ANIMALS: Sixty-one client-owned dogs with Malassezia dermatitis. MATERIALS AND METHODS: The enrolled animals were randomly divided into groups receiving 5 mg/kg fluconazole (5FZ), 10 mg/kg fluconazole (10FZ) or 5 mg/kg itraconazole (5IZ). The drugs were orally administered once daily for 28 days. Cytological examination, clinical index score (CIS), pruritus Visual Analog Scale (PVAS) evaluation and blood analysis (for 5FZ only) were performed on Day (D)0, D14 and D28. RESULTS: On D14, significant reductions in mean yeast count (MYC), CIS and PVAS were observed in the 5FZ (n = 20, p < 0.01), 10FZ (n = 17, p < 0.01) and 5IZ (n = 16, p < 0.05) groups. In all three groups, a significant reduction (p < 0.001) in MYC, CIS and PVAS expression was observed on D28. There was no significant difference in the percentage reduction of MYC, CIS and PVAS among the groups. Moreover, there was a significant difference (p < 0.05) in each group between D14 and D28, except for the percentage reduction in MYC in the 10FZ and 5IZ groups. No adverse effects of fluconazole were observed in the 5FZ or 10FZ groups. CONCLUSIONS AND CLINICAL RELEVANCE: This study indicates that 5FZ and 10FZ are as effective as itraconazole in canine Malassezia dermatitis.

Serratia marcescens-associated subcutaneous abscess in a dog.

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.

Case report: Fundic gland polyps caused by long-term omeprazole use in a Maltese dog.

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.

Case report: Central-pituitary hypothyroidism concurrent with hyperadrenocorticism without pituitary macroadenoma in a Miniature Schnauzer dog.

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.

Expression of vitamin D receptor, CYP24A1, and CYP27B1 in normal and inflamed canine pancreases.

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.

Preliminary study of neurofilament light chain as a biomarker for hypoxia-induced neuronal injury in dogs.

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.

Case report: Evaluation of hindlimb ischemia using 18F-fluorodeoxyglucose positron emission tomography in a cat with cardiogenic arterial thromboembolism.

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.

T-cell lymphoma infiltrating the uterus and ovaries of a Golden Retriever: a case report.

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.

Association between Hyperglycemia and Canine Serum Pancreatic Lipase Immunoreactivity Concentration in Diabetic Dogs.

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.

Heart failure in a cat due to hypertrophic cardiomyopathy phenotype caused by chronic uncontrolled hyperthyroidism.

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.