Omeprazole in a Dog With Gastrinoma

A 9-year-old male German Shepherd Dog was presented with the primary complaints of vomiting, profuse watery diarrhea, anorexia, and severe weight loss. The dog developed hematemesis and melena, which were unresponsive to treatment with an H₂-receptor antagonist and a gastrointestinal protectant. A marked neutrophilia, panhypoproteinemia, hypokalemia, and mildly increased activities of alkaline phosphatase and alanine aminotransferase were the only relevant abnormalities found on a CBC, serum biochemical profile, and urinalysis. An exploratory laparotomy revealed several small nonresectable masses at the root of the mesentery, which were identified histologically as a neuroendocrine neoplasm. Immunohistochemical staining of the neoplasm was positive for gastrin and negative for insulin, glucagon, pancreatic polypeptide, and vasoactive intestinal polypeptide. Fasting serum gastrin concentrations were high. Zollinger-Ellison syndrome was diagnosed, and the dog was treated with omeprazole, an H+, K+-ATPase inhibitor. All clinical signs resolved, and the dog remains asymptomatic 2 years later. Omeprazole may be the gastric acid antisecretory drug of choice for dogs with gastrinoma.     

Fanconi's Syndrome in a Dog With Primary Hypoparathyroidism

An 11 -year-old castrated male mixed breed dog was referred for evaluation of muscle twitching, polyuria, polydipsia, anorexia, and periocular alopecia. Primary hypoparathyroidism was diagnosed by documenting decreased serum concentrations of parathyroid hormone and ionized calcium. Neurological, gastrointestinal, and dermatological signs resolved after calcium repletion. Initially, 1,25-dihydroxycholecalcif erol PO was required to correct the hypocalcemia. Dihydrotachysterol, in combination with oral calcium supplementation, was used for long-term maintenance of normal serum calcium concentration. Aminoaciduria, glucosuria, and hyperchloremic metabolic acidosis were consistent with a diagnosis of Fanconi's syndrome. This diagnosis was further supported by the presence of hypokalemia and increased urinary fractional excretion of sodium, potassium, calcium, phosphorus, and magnesium. Renal tubular dysfunction resolved after oral supplementation with calcium and vitamin D₃. Fanconi's syndrome in this dog may have been caused by decreased serum concentration of 1,25-dihydroxycholecalciferol, which was secondary to decreased parathyroid hormone production.     

Tumor-Associated Erythrocytosis in a Dog With Nasal Fibrosarcoma

Erythrocytosis (hematocrit, 79%) was diagnosed in an 8-year-old, neutered female, mixed-breed dog with an intranasal fibrosarcoma. Both serum and tumor erythropoietin (Ep) activities were elevated, as determined by the polycythemic exhypoxic mouse model, and the Ep activity was neutralized in that model by rabbit anti-Ep antibodies. Tumor resection normalized the hematocrit.     

Monoclonal Gammopathy in a Dog With Visceral Leishmaniasis

One dog with visceral leishmaniasis associated with monoclonal gammopathy is described. Most dogs with visceral leishmaniasis present with hyperproteinemia due to a polyclonal gammopathy, but the possibility of monoclonal gammopathy must be considered. Because dogs accompany their owners when they travel, the diagnosis of leishmaniasis should be considered if an animal with monoclonal gammopathy has visited an area where the disease is endemic. The observation of Leishmania in the macrophages of a bone marrow, lymph node smear, or skin biopsy specimen is diagnostic.     

Monoclonal Gammopathy in a Dog With Chronic Pyoderma

A monoclonal gammopathy composed of immunoglobulin G, with concurrent light-chain proteinuria and generalized lymph node plasmacytosis, was associated with chronic pyoderma in a dog. A uniform population of plasma cells was observed cytologically and histologically in multiple lymph node specimens. A diagnosis of monoclonal gammopathy of unknown significance was eventually made by exclusion of other known causes of monoclonal gammopathy, resolution after antibiotic therapy, and no evidence of lymphoproliferative disease after 11 months of follow-up and subsequent necropsy. This report expands the diagnostic considerations for monoclonal gammopathies in the dog.     

Incessant Atrial Tachycardias in a Dog With Tricuspid Dysplasia

In a dog, tricuspid regurgitation due to congenital tricuspid dysplasia resulted in extreme right heart enlargement and right heart failure. Incessant supraventricular tachycardias were present, requiring the intravenous administration of verapamil to reduce the ventricular rate. Oral therapy using a combination of verapamil and quinidine was partially effective in controlling the ventricular rate during the following week. At that time, electrophysiologic studies were performed. They revealed that a succession of several atrial tachycardias with different cycle lengths, including one episode of atrial flutter, was present. Atrial activity was spanning the majority of the cycle length in all these arrhythmias. Epicardial mapping was performed during the atrial flutter. This enabled the detection of a depolarization wave-front traveling counterclockwise from the dorsolateral right atrium toward the right appendage, following the tricuspid valve annulus. No areas of abnormal conduction were detected. Because programmed electric stimulation maneuvers could not be performed, definitive conclusions about the mechanism of the arrhythmia could not be drawn. The two most likely possibilities were circus movement using part of the dilated tricuspid valve annulus as an anatomic barrier or a leading circle type of re-entry.     

Echocardiography and Surgery in a Dog With Left Atrial Rupture and Hemopericardium

Endocardial splitting and left atrial rupture were diagnosed in a dog with mitral regurgitation that experienced the sudden onset of collapsing episodes, weakness, depression, labored breathing, and weak pulses. Thoracic radiographs showed a rounded cardiac silhouette with prominent left atrium consistent with hemopericardium due to left atrial rupture. Two-dimensional echocardiography confirmed the presence of severe mitral valve disease, pericardial fluid, and a laminated blood clot caudal to the left ventricle. A sterile emergency thoracotomy was performed, the hemopericardium and blood clot were removed, and the rupture site in the left atrium was repaired with reinforced sutures. The dog recovered from surgery but died the next day, presumably from a ventricular arrhythmia.     

Thrombocytopathia and Light-Chain Proteinuria in a Dog Naturally Infected With Ehrlichia canis

A 6–year-old dog was presented for evaluation of recurrent epistaxis. Platelet counts, biochemical tests, and coagulation tests were within the normal range, but a mucosal bleeding time was prolonged; there was hyperproteinemia and a monoclonal gammopathy. Heterogeneity of light chains appeared in urine, however, thus suggesting that the gammopathy was polyclonal. Platelet aggregation tests showed decreased responsiveness to collagen. An Ehrlichia canis indirect fluorescent-antibody titer was positive (1:40). Treatment with tetracycline, melphalan, and prednisone resulted in a rapid clinical improvement that persisted for at least 3 years.     

“阿黑”和“阿黄”

"阿黑"和"阿黄"是母女俩,"阿黑"是妈妈,"阿黄"是女儿.它俩的名字都是我给起的,因为"阿黑"毛色全黑,"阿黄"被毛灰黄,所以就这么叫了.那"阿黄"不随它妈呢,可能是它爸被毛是灰黄的缘故吧!     

Hemolytic Transfusion Reactions in a Dog With an Alloantibody to a Common Antigen

Alloantibodies to high-frequency red cell antigens, defined as inherited traits occurring in 92% to 99% or more of the general population, are recognized as a cause of hemolytic transfusion reactions in humans. Here we describe a dog (dog erythrocyte antigen [DEA] 1.2-and DEA 4-positive) sensitized by prior blood transfusion, for which a compatible blood donor could not be found; transfusion of DEA 1.1-negative blood resulted in hemolytic transfusion reactions. Patient serum from days 1 (before first transfusion) and 16 was available for further testing; using 4 dogs with different blood types as potential donors, the major crossmatches were compatible using serum from day 1. However the crossmatches were all incompatible with serum from day 16, indicating that the patient was sensitized to an antigen after the first transfusion. The presence of an alloantibody against DEA 1.1 was not ruled out in this patient, but the incompatibility reactions of patient serum with red cells from donors negative for DEA 1.1 indicated that an alloantibody against a red cell antigen other than DEA 1.1 or any other known DEA for which typing reagents were available (DEA 3, 5, and 7) was present. Subsequently, red cells from 1 of the patient's siblings (DEA 1.2-, 4-, and 7-positive) were found not to agglutinate when incubated with patient's serum from day 16, ruling out the presence of an anti-DEA 7 antibody, and suggesting that an alloantibody against a common red cell antigen missing in the patient and sibling was responsible for the blood incompatibility reactions. Failure to obtain a compatible crossmatch with several universal donors in a dog previously transfused should raise a suspicion that an alloantibody to a common red cell antigen may exist and that a sibling may be a source of compatible blood.     

Pancreatic Polypeptide and Insulin-Secreting Tumor in a Dog With Duodenal Ulcers and Hypertrophic Gastritis

A 7-year-old spayed female Cocker Spaniel was hospitalized with a history of chronic vomiting, anorexia, and weight loss. Laboratory abnormalities included leukocytosis, metabolic alkalosis, hypoglycemia, hypoproteinemia, and hyperinsulinemia. Gastroscopy and ultrasonography revealed multiple gastric masses and a possible pancreatic mass, respectively. Examination of tissues obtained at necropsy showed a pancreatic adenocarcinoma with hepatic metastasis, gastric hypertrophy, and multiple duodenal ulcers. Immunocytochemical staining of the neoplasia was positive for pancreatic polypeptide (PP) and insulin and negative for gastrin, calcitonin, adrenocorticotropic hormone (ACTH), serotonin, L-enkephalin, chromagranin, glucagon, and somatostatin. Subsequent serum gastrin and PP assays showed a fasting hypergastrinemia with a normal response of gastrin to provocative testing and extremely increased PP values. The high PP values may have resulted in the vomiting and gastrointestinal ulceration. A PP-secreting tumor has not previously been reported in the dog.     

Orthodromic Reciprocating Tachycardia and Heart Failure in a Dog With a Concealed Posteroseptal Accessory Pathway

A 4-month-old male Labrador Retriever was presented for recurrent bouts of pulmonary edema associated with tachycardia. Initial physical examination and echocardiography were unremarkable, and the electrocardiogram revealed only an intraventricular conduction disturbance. Subsequent recordings showed paroxysmal supraventricular tachycardia (SVT) (340 beats/min), which consistently produced pulmonary edema. The supraventricular tachycardia was unresponsive to adenosine, esmolol, and propranolol; was variably and transiently responsive to various vagal maneuvers and precordial thumps; and was always responsive to IV diltiazem. Multiple life-threatening episodes of SVT occurred, however, despite the chronic administration of oral diltiazem, propranolol, and procainamide. Diastolic cardiac dysfunction was documented by Doppler echocardiography and was thought to contribute to the development of pulmonary edema. A subsequent electrophysiologic study confirmed the presence of an atrioventricular posteroseptal accessory pathway that participated in orthodromic reciprocating tachycardia. This pathway was determined to conduct only in the retrograde direction ("concealed accessory pathway"). Intraoperative IV procainamide titration terminated the arrhythmia, which could not be reinduced when procainamide blood concentration approximated 20 μg/dL. Increasing the oral procainamide dose to achieve such plasma concentrations was successful in eliminating orthodromic reciprocating tachycardia, preventing heart failure, and returning Doppler indices of diastolic function to normal.     

Postcaval Thrombosis and Delayed Shunt Migration After Pleuro-Peritoneal Venous Shunting for Concurrent Chylothorax and Chylous Ascites in a Dog

Simultaneous chylothorax and chylous ascites related to intestinal lymphangiectasia was diagnosed in a 4-year-old spayed female dog. Palliative pleural and peritoneal drainage was accomplished by placement of fenestrated silastic sheeting into surgically created diaphragmatic defects, and implantation of a pleuro-peritoneal venous shunt. The immediate postoperative period was complicated by acute renal failure secondary to postcaval thrombosis originating at the site of placement of the efferent pump catheter and extending to the level of the renal veins. Rapid resolution of this complication was accomplished with systemic anticoagulation. Clinical signs related to fluid accumulation resolved for 10 weeks after which acute decompensation occurred and the dog was euthanatized. Postmortem examination showed that reaccumulation of fluid was associated with migration of the efferent limb of the shunt from the caudal vena cava.     

Central Diabetes Insipidus in a Dog With a Pro-Opiomelanocortin-Producing Pituitary Tumor ot Causing Hyperadrenocorticism

Central diabetes insipidus was diagnosed by vasopressin measurements during hypertonic stimulation in a 9-year-old male giant Schnauzer with polyuria and polydipsia. The impaired release of vasopressin was believed to be caused by a large pituitary tumor, which was visualized by computed tomography. Studies of the function of the anterior lobe and the pars intermedia of the pituitary gland were conducted, and high concentrations of ACTH and α-melanotrophic hormone (α-MSH) were found without concomitant hyperadrenocorticism. Studies of the molecular size of the immunoreactive ACTH in plasma by gel filtration revealed that most of the circulating immunoreactivity was not ACTH but its precursor pro-opiomelanocortin (POMC) and low-molecular-weight POMC-derived peptides. The pituitary tumor of this dog probably originated from melanotrophic cells of the pars intermedia. The sensitivity of the pituitary-adrenocortical system for the suppressive effect of dexamethasone was unaffected.