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Abstract

OBJECTIVE

To determine hepatic copper concentrations and zonal distribution in ferrets with and without hepatobiliary disease, validate rhodanine-based qualitative copper scoring and digital copper quantification in ferret hepatic samples, and ascertain whether clinical features predicted copper accumulation.

ANIMALS

34 ferrets, including 7 with necroinflammatory disease, 5 with hepatocellular carcinoma, 13 with non-necroinflammatory disease, and 9 with no hepatobiliary disease.

PROCEDURES

Rhodanine-based digital copper quantification was validated by use of liver dually measured by atomic absorption spectroscopy and digital scanning (R 2 = 0.98). Clinical features and hepatic copper scores and concentrations (dry weight liver) were compared between groups. Zonal copper distribution was determined.

RESULTS

Hepatic copper concentration was strongly correlated with copper scores (ρ = 0.88). Ferrets with hepatobiliary disease were significantly older and had significantly higher serum alkaline phosphatase and γ-glutamyltransferase activities and creatinine concentrations. Centrilobular copper accumulated in 23 of 34 (64%) ferrets with (n = 15) and without (8) hepatobiliary disease. Median copper concentrations were not significantly different between ferrets with and without hepatobiliary disease but were significantly higher within neoplastic hepatic tissue in ferrets with hepatocellular carcinoma. Hepatic copper concentrations exceeded feline (> 180 µg/g) and canine (> 400 µg/g) reference limits in 19 and 9 ferrets, respectively. Hepatic copper > 1,000 µg/g occurred in 5 ferrets with and 2 without hepatobiliary disease. Clinical features did not predict copper accumulation.

CLINICAL RELEVANCE

Rhodanine-based digital copper quantification and qualitative copper scoring discerned liver copper accumulation in ferrets. Ferrets with and without hepatobiliary disease displayed a propensity for centrilobular hepatic copper accumulation of uncertain clinical importance. Clinical and clinicopathologic features could not exclusively implicate pathologic copper accumulation.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate prognostic factors, survival, and treatment protocols for immune-mediated hemolytic anemia (IMHA) in dogs.

Design—Retrospective study.

Animals—151 dogs with IMHA not associated with underlying infectious or neoplastic disease.

Procedure—Information recorded from review of medical records included signalment at the time of initial evaluation; vaccination history; 30-, 60-, and 365-day follow-up outcomes; laboratory data; results of imaging studies; and necropsy findings. Dogs were grouped according to the presence of spherocytes, autoagglutination, a regenerative erythrocyte response, and treatments received (azathioprine, azathioprine plus ultralowdose aspirin, azathioprine plus mixed–molecular-weight heparin [mHEP], or azathioprine plus ultralow-dose aspirin plus mHEP) for comparisons. All dogs received glucocorticoids.

Results—Cocker Spaniels, Miniature Schnauzers, neutered dogs, and female dogs were overrepresented. Alterations in certain clinicopathologic variables were associated with increased mortality rate. Rates of survival following treatment with azathioprine, azathioprine plus ultralow-dose aspirin, azathioprine plus mHEP, and azathioprine plus ultralow-dose aspirin plus mHEP were 74%, 88%, 23%, and 70%, respectively, at hospital discharge; 57%, 82%, 17%, and 67%, respectively, at 30 days; and 45%, 69%, 17%, and 64%, respectively, at 1 year. In comparison, mean survival rates at discharge and at 30 days and 1 year after evaluation collated from 7 published reviews of canine IMHA were 57%, 58%, and 34%, respectively.

Conclusions and Clinical Relevance—Treatment with a combination of glucocorticoids, azathioprine, and ultralow-dose aspirin significantly improved short-and long-term survival in dogs with IMHA. (J Am Vet Med Assoc 2005;226:1869–1880)

Full access
in Journal of the American Veterinary Medical Association

Abstract

Objective

To determine whether the urine cortisol-to-creatinine ratio (UCCR) could replace the ACTH stimulation test in monitoring effectiveness of mitotane induction treatment in dogs with pituitary-dependent hyperadrenocorticism (PDH).

Animals

15 dogs with PDH.

Procedure

All 15 dogs were given an induction dose of mitotane (o, p'-DDD: 35 to 50 mg/kg of body weight/d) for 3 to 14 days. During the induction period, free-catch morning urine samples were collected for determination of UCCR, followed by ACTH stimulation testing, every other day. Treatment response was divided into 3 categories: well-controlled PDH (post-ACTH serum cortisol concentration ≥ 28 nmol/L but ≤ 138 nmol/L), deficient cortisol secretion (post-ACTH serum cortisol concentration < 28 nmol/L), and excess cortisol secretion (post-ACTH serum cortisol concentration > 138 nmol/L).

Results

The linear relation between UCCR and post-ACTH serum cortisol concentration was significant (P < 0.001); however, the prediction intervals surrounding the line were too broad to be clinically useful. The UCCR overlapped among the 3 categories of treatment response. Nevertheless, dogs with PDH receiving mitotane induction treatment and with UCCR > 79 × 10−6 were always classified as having excess cortisol secretion.

Conclusion and Clinical Relevance

The UCCR failed to predict post-ACTH cortisol concentration during mitotane induction treatment sufficiently close to be a clinically reliable indicator of treatment control. Seemingly, however, UCCR > 79 × 10−6 obtained from a dog with PDH during mitotane induction would indicate inadequate adrenal cortex destruction and the need for continued mitotane induction; UCCR ≤ 79 × 10−6 would be inconclusive. (Am J Vet Res 1998;59:258–261)

Free access
in American Journal of Veterinary Research

Abstract

Adrenocortical function was assessed in 27 Beagle pups at 2, 4, 6, 8, 10, and 12 weeks of age by determination of plasma sodium, potassium, and chloride concentrations; serum aldosterone and cortisol concentrations; and plasma ACTH concentrations. Serum cortisol concentration was measured before and 1 and 2 hours after IM administration of 2.2 IU of acth/kg of body weight. Serum progesterone concentration also was determined for all pups at 2, 4, and 6 weeks of age.

Mean baseline cortisol concentration was lower for pups 8 weeks old or younger than for mature dogs. Nevertheless, mean serum ACIH-stimulated cortisol concentration in dogs of all age groups increased into the adult reference range after administration of acth. For pups 4 weeks old or younger, increase in cortisol concentration was maximal at 2 hours after acth administration. However, in pups between 6 and 12 weeks of age, the increase in cortisol concentration was maximal 1 hour after acth administration in about a third of the pups, whereas the remaining pups had peak values at 2 hours.

Mean plasma sodium, potassium, and chloride concentrations for each age group were within the reference ranges established for mature dogs, with the exception of lower mean plasma sodium and chloride concentrations in pups 4 weeks old or younger. Mean serum aldosterone concentration in pups of each age group was substantially higher than the range of aldosterone concentrations for clinically normal mature dogs. Median progesterone concentration was uniformly less than 0.2 ng/ml for all pups 6 weeks old or younger.

The normal endogenous acth concentration and adequate cortisol responses to exogenous acth seen in our pups would support functional pituitary gland and adrenal cortex for cortisol production. The low baseline cortisol concentration observed in the pups of this study may be related to reduced binding of cortisol to plasma proteins, as exists in human infants. The hyponatremia and increased aldosterone concentration may be explained by reduced renal tubular response to aldosterone, as also evidenced in the human infant kidney.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To compare morphologic diagnoses determined from needle biopsy specimens obtained from the livers of dogs and cats with morphologic diagnoses determined from wedge biopsy specimens.

Design—Prospective study.

Animals—124 dogs and cats.

Procedure—2 needle biopsy specimens were obtained from each animal; wedge biopsy specimens were obtained from the same liver lobe during laparotomy or postmortem examination. Histologic features were scored independently by 3 individuals; a morphologic diagnosis was rendered after histologic features were scored. Cases were included only if at least 2 of the 3 examiners agreed on the morphologic diagnosis; the definitive diagnosis was considered to be the morphologic diagnosis rendered for the wedge biopsy specimen. Physical characteristics (length, width, surface area, degree of fragmentation, and number of portal triads for needle biopsy specimens and surface area for wedge biopsy specimens) were determined.

Results—Definitive diagnoses included hepatic necrosis (n = 10), cholangitis-cholangiohepatitis (13), chronic hepatitis-cirrhosis (12), canine vacuolar hepatopathy (11), portosystemic vascular anomaly-microvascular dysplasia (17), neoplasia (10), miscellaneous hepatic disorders (18), and no hepatic disease (33). For individual examiners, the morphologic diagnosis assigned to needle biopsy specimens agreed with the morphologic diagnosis assigned to wedge biopsy specimens for 56 and 67% of the specimens. All 3 examiners agreed on the morphologic diagnosis assigned to needle and wedge biopsy specimens for 44 and 65% of the specimens, respectively. Morphologic diagnoses assigned to needle biopsy specimens concurred with the definitive diagnosis for 59 of 124 (48%) animals.

Conclusions and Clinical Relevance—Results suggest that needle biopsy specimens of the liver from dogs and cats must be interpreted with caution. (J Am Vet Med Assoc 2002;220:1483–1490)

Full access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To evaluate 3 methods for measuring urine bile acids (UBA) and compare their diagnostic performance with that of the serum bile acids (SBA) test and other routine screening tests in dogs with hepatic disorders.

Design—Prospective study.

Animals—15 healthy dogs, 102 dogs with hepatic disorders, and 9 dogs with clinical signs of hepatic disorders that were found to have nonhepatic disorders.

Procedures—Blood and urine samples were collected from sick dogs and healthy dogs for serum biochemical analyses, and determination of concentrations of SBA and UBA. Urine samples were obtained from 15 healthy dogs to establish an upper cutoff value for UBA concentrations. The UBA were measured by use of a quantitative-linked enzymatic colorimetric method. Three analytical modifications were evaluated; 1 quantified only urine sulfated bile acids (USBA), 1 only urine nonsulfated bile acids (UNSBA), and 1 quantified both (USBA plus UNSBA). The UBA values were standardized with the urine creatinine concentration.

Results—The UNSBA-to-creatinine ratio and USBA plus UNSBA-to-creatinine ratio tests had the best diagnostic performance of the UBA tests; each had a substantially higher specificity, slightly higher positive predictive value, slightly lower negative predictive value, and lower sensitivity than the SBA test. These UBA-to-creatinine values were positively correlated with SBA values. The USBA-to-creatinine ratio had poor sensitivity, indicating a low rate of bile acid sulfation in dogs.

Conclusions and Clinical Relevance—The UBA can be measured in dogs with sufficient repeatability and accuracy for clinical application. The UNSBA-to-creatinine ratio and USBA plus UNSBA-to-creatinine ratio identified dogs with hepatic disorders nearly as well as the SBA test. (J Am Vet Med Assoc 2003;222: 1368–1375)

Full access
in Journal of the American Veterinary Medical Association

Abstract

OBJECTIVE

To characterize the association between peritoneopericardial diaphragmatic hernia (PPDH) or congenital central diaphragmatic hernia (CCDH) and ductal plate malformations (DPMs) in dogs and cats.

ANIMALS

18 dogs and 18 cats with PPDH or CCDH and 19 dogs and 18 cats without PPDH or CCDH.

PROCEDURES

Evaluation of clinical details verified PPDH or CCDH and survival times. Histologic features of nonherniated liver samples were used to categorize DPM. Immunohistochemical staining for cytokeratin-19 distinguished bile duct profiles per portal tract and for Ki-67–assessed cholangiocyte proliferation. Histologic features of herniated liver samples from PPDH or CCDH were compared with those of pathological controls (traumatic diaphragmatic hernia, n = 6; liver lobe torsion, 6; ischemic hepatopathy, 2).

RESULTS

DPM occurred in 13 of 18 dogs with the proliferative-like phenotype predominating and in 15 of 18 cats with evenly distributed proliferative-like and Caroli phenotypes. Congenital hepatic fibrosis DPM was noted in 3 dogs and 2 cats and renal DPM in 3 dogs and 3 cats. No signalment, clinical signs, or clinicopathologic features discriminated DPM. Kaplan Meier survival curves were similar in dogs and cats. Bile duct profiles per portal tract in dogs (median, 5.0; range, 1.4 to 100.8) and cats (6.6; 1.9 to 11.0) with congenital diaphragmatic hernias significantly exceeded those in healthy dogs (1.4; 1.2 to 1.6) and cats (2.3; 1.7 to 2.6). Animals with DPM lacked active cholangiocyte proliferation. Histologic features characterizing malformative bile duct profiles yet without biliary proliferation were preserved in herniated liver lobes in animals with DPM.

CONCLUSIONS AND CLINICAL RELEVANCE

DPM was strongly associated with PPDH and CCDH. Because DPM can impact health, awareness of its coexistence with PPDH or CCDH should prompt biopsy of nonherniated liver tissue during surgical correction of PPDH and CCDH.

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in Journal of the American Veterinary Medical Association

Abstract

Objective—To determine risk, clinical features, and treatment responses for gallbladder disorders in Shetland Sheepdogs.

Design—Retrospective case-control study.

Animals—38 Shetland Sheepdogs with gallbladder disease.

Procedures—Medical records were reviewed for signalment, history, physical findings, laboratory results, imaging features, coexistent illnesses, histologic findings, treatments, and survival rates.

Results—Mature dogs with gastrointestinal signs were predisposed (odds ratio, 7.2) to gallbladder disorders. Gallbladder mucocele was confirmed in 25 dogs. Concurrent problems included pancreatitis, hyperlipidemia, corticosteroid excess, hypothyroidism, protein-losing nephropathy, diabetes mellitus, cholelithiasis, and gallbladder dysmotility. Mortality rate was 68% with and 32% without bile peritonitis. Nonsurvivors had high WBC and neutrophil count and low potassium concentration. Although preprandial hypercholesterolemia, hypertriglyceridemia, and high serum liver enzyme activities were common, gallbladder disease was serendipitously discovered in 11 of 38 dogs. Histologic examination (n = 20 dogs) revealed gallbladder cystic mucosal hyperplasia in 20 dogs, cholecystitis in 16, periportal hepatitis in 9, and vacuolar hepatopathy in 7. Surgery included cholecystectomy (n = 17) and cholecystoenterostomy (4). In 1 hyperlipidemic dog without clinical signs, gallbladder mucocele resolved 6 months after beginning use of a fat-restricted diet and ursodeoxycholic acid.

Conclusions and Clinical Relevance—Shetland Sheepdogs are predisposed to gallbladder disorders, with mucoceles and concurrent dyslipidemia or dysmotility in many affected dogs. Most dogs were without clinical signs during mucocele development. Low survival rate after cholecystectomy in clinically affected dogs suggested that preemptive surgical interventions may be a more appropriate treatment strategy.

Full access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To evaluate the influence of treatment with ultralow-dose aspirin (ULDAsp) on platelet aggregation, P-selectin (CD62P) expression, and formation of platelet-leukocyte aggregates in clinically normal dogs.

Animals—18 clinically normal dogs.

Procedures—Studies were conducted before and 24 hours after ULDAsp administration (0.5 mg/kg, PO, q 24 h, for 2 days). Whole blood impedance aggregometry for the assessment of platelet function was performed with sodium citrate–anticoagulated blood and aggregation agonists (ADP at 20, 10, and 5 μmol/L; collagen at 10, 5, and 2 μg/mL). Onset, maximum response, and rate of platelet aggregation were recorded. Flow cytometric assays were configured to detect thrombin-induced CD62P expression and platelet-leukocyte aggregates in EDTA-anticoagulated whole blood. Externalized platelet CD62P and constitutive CD61 (GPIIIa) were labeled with antibodies conjugated to phycoerythrin (PE) and fluorescein isothiocyanate (FITC), respectively. Red blood cell–lysed paraformaldehyde-fixed EDTA-anticoagulated whole blood was dual labeled with CD61-FITC and a panleukocyte antibody (CD18-PE) to characterize platelet-leukocyte aggregates.

Results—ULDAsp significantly delayed platelet aggregation onset with ADP at 20 μmol/L by 54% to 104%, attenuated maximum aggregation with various concentrations of ADP and collagen by ≥ 41%, and slowed aggregation rate with the highest ADP and collagen concentrations by ≥ 39%. Depending on the parameter tested, up to 30% of dogs failed to have an ULDAsp effect. Thrombin stimulation significantly increased CD62P expression in platelets and platelet-leukocyte aggregates, but ULDAsp did not alter basal or thrombin-stimulated CD62P expression.

Conclusions and Clinical Relevance—ULDAsp treatment of clinically normal dogs impaired platelet aggregation in most dogs, but did not influence CD62P platelet membrane expression. (Am J Vet Res 2010;71:1294–1304)

Full access
in American Journal of Veterinary Research