Plasma 14C-cholic acid clearance in healthy dogs and dogs with cholestasis or a congenital portosystemic shunt.

The clearance profiles of intravenously injected tracer doses of radioactively labelled cholic acid were investigated in healthy dogs, dogs with a congenital portosystemic shunt and dogs with cholestasis. The rate constants and residual plasma activity were significantly different in the healthy and diseased dogs, but it was not possible to differentiate between the dogs with portosystemic shunting and cholestasis because the results were determined not only by factors involved in plasma bile acid clearance but also by the enterohepatic circulation.

Iatrogenic copper deficiency associated with long-term copper chelation for treatment of copper storage disease in a Bedlington Terrier.

A 9-year-old Bedlington Terrier was evaluated because of weight loss, inappetence, and hematemesis. Copper storage disease had been diagnosed previously on the basis of high hepatic copper concentration. Treatment had included dietary copper restriction and administration of trientine for chelation of copper. A CBC revealed microcytic hypochromic anemia. High serum activities of liver enzymes, high bile acid concentrations, and low BUN and albumin concentrations were detected. Vomiting resolved temporarily with treatment, but the clinicopathologic abnormalities persisted. Results of transcolonic portal scintigraphy suggested an abnormal shunt fraction. Results of liver biopsy and copper quantification revealed glycogen accumulation and extremely low hepatic copper concentration. Serum and hair copper concentrations were also low. Chelation and dietary copper restriction were tapered and discontinued. Clinical signs and all clinicopathologic abnormalities improved during a period of several months.

Idiopathic noncirrhotic portal hypertension in dogs: 33 cases (1982-1998).

OBJECTIVE: To describe clinical signs, diagnostic findings, and outcome in dogs with idiopathic intrahepatic portal hypertension. DESIGN: Retrospective study. ANIMALS: 33 dogs. PROCEDURE: Medical records of dogs with portal hypertension of intra-abdominal origin were reviewed. Dogs with intra-abdominal portal hypertension of vascular causes or with hepatic histopathologic changes consistent with severe diffuse hepatobiliary disease were excluded. History and results of physical examination, clinicopathologic tests, diagnostic imaging studies, histologic examination, and treatment were summarized. Outcome was determined in 26 dogs. RESULTS: Dogs were referred most often because of ascites, intermittent vomiting or diarrhea, and polydipsia of several months' duration. Microcytosis, high serum alkaline phosphatase and alanine transaminase activities, hepatic dysfunction, urine specific gravity < or = 1.021, and abdominal transudate were the predominant clinicopathologic features. Microhepatia, abdominal effusion, and multiple anomalous venous anastomoses were the major findings of diagnostic imaging. Hepatic histopathologic changes were consistent with idiopathic noncirrhotic portal hypertension and were indistinguishable from those of dogs with surgically created portocaval anastomosis. Outcome was determined for 19 dogs released from hospital; 13 dogs remained healthy with mostly palliative treatment for periods of 5 months to 9 years. CONCLUSIONS AND CLINICAL RELEVANCE: The clinical signs, clinicopathologic test results, portal pressure, and gross appearance of the liver of dogs with idiopathic noncirrhotic portal hypertension may be identical to those of dogs with cirrhosis; therefore liver biopsy is crucial. Because the prognosis for idiopathic noncirrhotic portal hypertension is generally favorable, owners of affected dogs should be discouraged from choosing euthanasia.

Clinical hypothyroidism associated with trimethoprim-sulfadiazine administration in a dog.

Treatment of a 9-year-old spayed female mixed-breed dog with trimethoprim-sulfadiazine for a prolonged period resulted in clinical signs of hypothyroidism, and results of thyroid gland function tests were indistinguishable from those associated with endogenous hypothyroidism. Drug-induced hypothyroidism was diagnosed on the basis of history, normal thyroid uptake of sodium pertechnetate, and complete recovery of thyroid gland function after administration of trimethoprim-sulfadiazine was discontinued.

Evaluation of microcytosis in 18 Shibas.

OBJECTIVE: To determine whether microcytosis is a typical finding in Shibas. DESIGN: Prospective study. ANIMALS: 18 Shibas. PROCEDURE: Blood and serum samples were obtained for automated hematologic analyses (18 dogs) and for determination of ferritin concentration, using ELISA (14 dogs). Blood samples from 30 clinically normal dogs of various other breeds was analyzed to establish a reference range for ferritin concentration. RESULTS: Erythrocyte mean corpuscular volume in Shibas ranged from 55.6 to 69.1 fl (mean+/-SD, 61.2+/-4.3 fl; median, 60.6 fl; reference range, 63 to 73 fl). Microcytosis was identified in 12 of 18 dogs. Males and females were affected equally. Mean corpuscular hemoglobin concentration was slightly low (range, 32.0 to 33.9%; reference range, 34 to 38%) in 6 dogs, 4 of which had microcytic RBC. Serum ferritin concentrations ranged from 61.2 to 277.0 ng/ml (mean+/-SD, 110.6+/-51.4 ng/ml; median, 106 ng/ml). Reference range for serum ferritin concentration was 50.7 to 440.0 ng/ml (mean+/-SD, 121.2+/-67.1 ng/ml; median, 111.5 ng/ml). Thrombocytopenia (range, 110,000 to 196,000 platelets; reference range, 200,000 to 450,000 platelets) was found in 7 dogs, 6 of which also had microcytic RBC. CLINICAL IMPLICATIONS: Microcytosis can be a typical finding in Shibas. Common origin of Shibas and Akitas, a breed predisposed to microcytosis, suggests a hereditary basis for this finding.

Factor X deficiency in a cat.

Severe congenital deficiency of factor X was diagnosed in a 3-year-old castrated male domestic shorthair cat with clinical signs of generalized seizures and prolonged bleeding after venipuncture. Heritability of factor X deficiency was suspected because of a prolonged Russell's viper venom time in the dam and reductions in factor X activity in the dam and 1 sibling. To our knowledge, factor X deficiency in cats has not been reported previously. Definitive diagnosis for animals with clinical signs of coagulopathy may require repetition of coagulation screening tests using different assay methods or specific coagulation factor analyses.

Characterization of iron status in young dogs with portosystemic shunt.

Microcytosis is a common laboratory finding in dogs with congenital portosystemic shunt (PSS), although its pathogenesis is not yet understood. Because the most common cause of microcytosis in dogs is absolute or relative iron deficiency, iron status was evaluated in 12 young dogs with PSS. Complete blood counting was done before surgical correction in all dogs, and in 5 dogs after surgery, by use of an automated hematology analyzer. Serum iron concentration and total iron-binding capacity (TIBC) were determined coulometrically, and percentage of transferrin saturation was calculated. Erythrocyte protoporphyrin content was quantified by use of front-face fluorometry. Serum ferritin concentration was measured by use of ELISA. Serum ceruloplasmin content was determined colorimetrically (with p-phenylenediamine dihydrochloride as substrate) as an indirect indicator of subclinical inflammation, which may result in impaired iron utilization. Special stains were applied to liver (10 dogs; Gomori's) and bone marrow aspiration biopsy (7 dogs; Prussian blue) specimens for qualitative assessment of tissue iron content. Nonpaired Student's t-tests were used to compare serum iron concentration, TIBC, percentage of transferrin saturation, and erythrocyte protoporphyrin, ferritin, and ceruloplasmin concentrations in dogs with PSS with those in clinically normal dogs. All dogs had microcytosis before surgery; microcytosis resolved in 3 dogs after surgical correction. Serum iron concentration and TIBC were significantly lower in PSS-affected dogs than in clinically normal dogs. Erythrocyte protoporphyrin, ferritin, and ceruloplasmin concentrations in PSS-affected dogs were not significantly different from those in health dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Management of portal hypertension and its consequences.

Increased pressure in the protal venous system results from impedance to blood flow at any point along it's course from the splanchnic circulation through the liver to the right heart. Typical manifestations of sustained increases in portal venous pressure commonly may include accumulation of abdominal fluid and development of acquired portosystemic shunts. Pathophysiology of altered portal vascular dynamics, diagnostic approach for animals suspected of having an intra-abdominal source of portal hypertension and treatment options are discussed.

Tethered spinal cord and an intradural lipoma associated with a meningocele in a Manx-type cat.

An 8-month-old neutered male Manx-type cat was evaluated because of clear fluid that had been draining from a skin mass dorsocaudal to the sacrum for 1 week. Neurologically, the cat had poor postural reactions and poor withdrawal reflexes in the hind limbs. Ultrasonography of the dorsal sacral area revealed a 3-cm-long hypoechoic tract extending from the skin mass cranioventrally to the area of the sacrum. The tract appeared to contain a circular mass. Results of myelography and computed tomography helped to confirm the diagnosis of a meningocutaneous tract containing a mass. Surgical exploration was performed and the tract was excised. Histologic changes were similar to those in human beings with tethered spinal cord syndrome and an intradural lumbosacral lipoma. Surgery was indicated in this cat to prevent progression of neurologic signs associated with tethered cord syndrome and to prevent problems associated with loss of CSF through a fistulated meningocele.

Risk factors associated with acute pancreatitis in dogs: 101 cases (1985-1990).

The medical records of 101 dogs with acute pancreatitis, diagnosed on the basis of medical histories of acute vomiting, with serum lipase or amylase activity greater than the reference range, or with gross signs of pancreatitis at surgery or histopathologic evidence at necropsy, were evaluated to identify potential risk factors for the development of acute pancreatitis. Age, sex, and breed of dogs with acute pancreatitis were compared with those from a reference population of 100 dogs admitted for other medical emergencies during the same period. Analysis of multiple regression models indicated that dogs > 7 years old were at increased risk for acute pancreatitis. Spayed dogs and castrated male dogs had an increased risk, compared with that of sexually intact males. Similarly, terrier and nonsporting breeds appeared to be at higher risk of developing acute pancreatitis than were other breed types. Most dogs in this study (63/101) had intercurrent diseases, including diabetes mellitus (n = 14), hyperadrenocorticism (n = 12), chronic renal failure (n = 8), neoplasia (n = 17), congestive heart failure (n = 6), and autoimmune disorders (n = 5). Fourteen dogs had undergone anesthesia or surgery in the week before admission; only 3 had undergone abdominal procedures. Recent medication use was listed in 52 of 101 cases. Antibiotics (n = 18) and corticosteroids (n = 18) were most frequently described. Anticancer chemotherapeutic agents (n = 5) and organophosphate insecticides (n = 5) also were listed.(ABSTRACT TRUNCATED AT 250 WORDS)

Hepatotoxicity associated with pharmacologic agents in dogs and cats.

Historical aspects, mechanisms, and treatment of hepatotoxicity associated with pharmacologic agents in dogs and cats are discussed. All agents that cause clinically relevant drug-induced hepatotoxicity have been reviewed within the last 5 years; therefore, only selected drugs that more recently have been observed to cause hepatic injury in companion animals are described in detail. These include diethylcarbamazine/oxibendazole, phenobarbital, and trimethoprim/sulfadiazine.

Intrahepatic postsinusoidal venous obstruction in a dog.

Intrahepatic postsinusoidal obstruction, similar to congenital Budd-Chiari syndrome in human patients, was diagnosed in a young Basenji dog. Sonographic, radiographic, and manometric studies were used in antemortem localization of this unusual functional lesion, that was believed to be congenital.

Hematologic values and plasma and tissue folate concentrations in dogs given phenytoin on a long-term basis.

During earlier investigations of the hepatic effects in dogs of long-term administration of phenytoin alone or in combination with primidone, erythrocytic macrocytosis, neutropenia, neutrophilic hypersegmentation, and thrombocytopenia were observed. Such abnormalities were observed most often in dogs given phenytoin and resembled those known to be attributable to folate deficiency in human beings with epilepsy treated with phenytoin. To pursue the theory that these hematologic aberrations were caused by drug-induced folate deficiency, 12 dogs were given a diet specifically formulated to contain a minimally adequate concentration of folate. After 2 weeks, phenytoin was administered daily (400 mg, PO, q 8 h) to 8 of the 12 dogs for 54 weeks. A CBC, bone marrow aspiration biopsy, and measurement of plasma and RBC folate concentrations were done every 3 weeks. Bone marrow aspirates were examined by transmission electron microscopy after 24 and 36 weeks, and at the end of the treatment period. Hepatic folate concentration was also determined in all dogs before and after treatment. Excretion of formiminoglutamic acid, as a marker of folate deficiency, was measured in all dogs at the end of the study. All dogs remained healthy throughout the treatment phase. Consistent abnormalities were not observed in the blood or bone marrow of treated dogs. Plasma and RBC folate concentrations decreased in control and treated dogs as a result of dietary restriction (P less than or equal to 0.02), and remained stable until the end of the study. The RBC folate content decreased further in treated dogs (P less than or equal to 0.02), although the hepatic folate content was similar in control and treated dogs. Treated dogs did not excrete formiminoglutamic acid more rapidly than did control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Medical management of recurrent seizures in dogs and cats.

The problem of recurrent seizures is a common and challenging one in veterinary medical practice. The pathophysiology and pharmacologic suppression of focal seizure activity have been studied extensively in basic research settings, yet little is known of the genesis, modulation, and termination of generalized seizures, the most common form of seizures noted to occur in companion animals. Knowledge concerning the pharmacokinetic fate of anticonvulsant drugs currently used in veterinary medicine is adequate, though prospective clinical studies of the efficacy of these drugs in the treatment of various types of seizures are lacking. This study will review the available literature regarding the pharmacology, use, and side effects of anticonvulsant drugs currently available for control of recurrent seizures in companion animals. Alternative anticonvulsant drugs will also be described.

Idiopathic pleural effusion and pulmonary thromboembolism in a dog with autoimmune hemolytic anemia.

Pleural effusion and pulmonary thromboembolism were diagnosed in a dog with autoimmune hemolytic anemia. Clinical signs of tachypnea, then dyspnea in association with pleural effusion, developed after 10 days of immunosuppressive corticosteroid therapy (greater than 2 mg/kg of body weight/d, PO). The diagnosis of pulmonary thromboembolism was made tentatively on the basis of results of a radionuclide lung perfusion scan and was confirmed by exploratory thoracotomy and lung biopsy. Tachypnea and pleural effusion gradually resolved without specific treatment, and additional episodes of anemia or dyspnea have not been observed. The pathogenesis of these findings was suspected to be related to corticosteroid-induced thrombotic tendencies, persistent thrombocytosis (greater than 800,000 cells/microliters), and vascular injury caused by repeated jugular venous catheterization. Pulmonary thromboembolism should be considered in dogs that develop clinical signs of tachypnea and/or pleural effusion during administration of immunosuppressive dosages of corticosteroids.