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Abstract

CASE DESCRIPTION

A 6-month-old sexually intact male Clumber Spaniel was evaluated because of small stature, recurrent dermatitis of the head, and progressive pigmentary hepatopathy.

CLINICAL FINDINGS

Clinicopathologic findings included nonanemic hypochromic microcytosis, hypocholesterolemia, persistently high serum liver enzyme activities, and anicteric hyperbilirubinemia. Histologic examination of liver biopsy specimens collected when the dog was 6 months and 2 years of age revealed expansion and bridging of portal tracts, occasional centrilobular parenchymal collapse, scattered lymphoplasmacytic infiltrates, and dark red to brown pigment within large aggregates of macrophages, engorged bile canaliculi, and hepatocytes. The pigment failed to stain for the presence of iron, copper, bile, and glycoprotein and, when examined with polarized microscopy, emitted a yellow to green birefringence with occasional Maltese cross configurations. Further analyses confirmed marked porphyrin accumulation in blood, urine, feces, and liver tissue; protoporphyrin accumulation in RBCs and liver tissue; and a signature porphyrin profile and fluorescence peak consistent with erythropoietic protoporphyria. Advanced protoporphyric hepatopathy was diagnosed. The chronic dermatopathy was presumed to reflect protoporphyric photosensitivity.

TREATMENT AND OUTCOME

Management was focused on avoiding conditions known to induce heme synthesis and catabolism, administrating ursodeoxycholic acid and antioxidants S-adenosylmethionine and vitamin E, and avoiding sunlight exposure. At follow-up at 4 years of age, the dog was stable without evidence of jaundice but with probable persistent erythropoietic protoporphyria–related solar dermatopathy.

CLINICAL RELEVANCE

Clinical and histologic features of congenital erythropoietic protoporphyria and resultant protoporphyric hepatopathy, the diagnosis, and the successful management of a dog with these conditions over 4 years were described. Veterinarians should consider porphyric syndromes when unusual pigmentary hepatopathies are encountered.

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in Journal of the American Veterinary Medical Association

Abstract

Objective—To evaluate differences in hepatic copper concentrations in Labrador Retrievers with and without chronic hepatitis.

Design—Retrospective case-control study.

Sample—Liver tissue specimens from 36 Labrador Retrievers with chronic hepatitis and 36 age- and sex-matched Labrador Retrievers without chronic hepatitis (control dogs).

Procedures—Liver tissue specimens were obtained during 2 study periods (1980 to 1997 and 1998 to 2010). For each tissue specimen, a histologic score was assigned independently by each of 2 interpreters, and the hepatic copper concentration was qualitatively determined via rhodanine staining and quantitatively determined via atomic absorption spectroscopy.

Results—Mean hepatic copper concentration was significantly higher in dogs with chronic hepatitis (614 μg/g of dry weight [range, 104 to 4,234 μg/g of dry weight]), compared with that in control dogs (299 μg/g of dry weight [range, 93 to 3,810 μg/g of dry weight]), and increased significantly over time. A higher proportion of liver tissue specimens collected during the 1998–2010 study period had hepatic copper concentrations > 400 μg/g of dry weight (the upper limit of the reference range), compared with the proportion of liver tissue specimens collected during the 1980–1997 study period. The qualitative copper score did not accurately predict quantitative hepatic copper concentration in 33% of study dogs.

Conclusions and Clinical Relevance—Results suggested that the increase in hepatic copper concentrations in Labrador Retrievers with and without chronic hepatitis over time may be the result of increased exposure of dogs to environmental copper, most likely via the diet.

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in Journal of the American Veterinary Medical Association

Abstract

OBJECTIVE To establish reference limits for hepatic bile duct-to-arteriole ratio (BD:A) and bile duct-to-portal tract ratio (BD:PT) in healthy cats and assess whether these parameters could be used to support a diagnosis of biliary ductopenia in cats.

SAMPLE Hepatic biopsy samples from healthy cats (n = 20) and cats with ductopenia (2).

PROCEDURES Hepatic biopsy samples from healthy cats were used to count the number of bile ducts and hepatic arterioles in 20 portal tracts for each cat. Mean BD:A and mean BD:PT for each cat were calculated, and these values were used to determine reference limits for mean BD:A and mean BD:PT. Results of histologic evaluation, including immunohistochemical staining in some instances, were compared for healthy cats versus cats with ductopenia.

RESULTS Of the 400 portal tracts from healthy cats, 382 (95.5%) and 396 (99.0%) had BD:A and BD:PT, respectively, ≥ 1.0, with less variability in BD:A. Mean BD:A and BD:PT were markedly lower in both cats with ductopenia, compared with values for healthy cats. However, only mean BD:A for cats with ductopenia was below the reference limit of 0.59.

CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that systematic evaluation of BD:A, with a lower reference limit of 0.59 to define biliary ductopenia in cats, may be a discrete and easily applied morphometric tool to enhance detection of ductopenia in cats. However, application of this ratio required evaluation of ≥ 20 portal tracts with cross-sectioned portal elements to determine a mean BD:A value.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate the influence of a 1,4- butanedisulfonate stable salt of S-adenosylmethionine (SAMe) administered orally on clinicopathologic and hepatic effects induced by long-term administration of prednisolone in dogs.

Animals—12 healthy dogs.

Procedure—Following a pilot study (4 dogs), 2 groups of 4 dogs received prednisolone (2.2 mg/kg) orally once daily (84-day trial). One group received SAMe (20 mg/kg/d divided in 2 doses) for 42 days and then a placebo for 42 days; the other group received treatments in the reverse order. Before and during the trial, numerous variables were monitored, including serum total alkaline phosphatase (ALP) and glucocorticoid- induced ALP (G-ALP) activities, serum haptoglobin concentration, and total and oxidized glutathione (TGSH and GSSG) and thiobarbiturate-reacting substances (TBARS) concentrations in erythrocytes and liver tissue (days 0, 42, and 84). Hepatic specimens also were examined microscopically.

Results—The stable salt of SAMe was biologically available; plasma concentrations of SAMe or prednisolone were not affected by coadministration. Compared with baseline values, serum ALP and GALP activities and haptoglobin concentrations increased and erythrocyte GSSG and TBARS concentrations decreased with both treatments. Erythrocyte TGSH concentration decreased with the prednisolone- placebo treatment. Administration of SAMe appeared to conserve erythrocyte TGSH values and did not inhibit hepatocyte glycogen vacuolation but increased hepatic TGSH concentration and improved the hepatic tissue GSSG:TGSH ratio.

Conclusions and Clinical Relevance—In dogs, administration of 20 mg of SAMe/kg/d may mitigate the apparent pro-oxidant influences of prednisolone but did not block development of classic clinicopathologic or histologic features of vacuolar hepatopathy. (Am J Vet Res 2005;66:330–341)

Full access
in American Journal of Veterinary Research

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 assess the influence of meal ingestion and orally administered erythromycin on gallbladder volume in dogs.

Animals—22 healthy dogs.

Procedures—Ultrasonographically determined gallbladder dimensions in unsedated dogs were used to calculate volume. Measurements were recorded after food was withheld for 12 hours (time 0) and 15, 30, 45, 60, 90, and 120 minutes after a 100-g meal without (n = 22) or with erythromycin (1.0 mg/kg [7], 2.5 mg/kg [7], and both dosages [8]). Gallbladder ejection fraction represented the percentage of volume change from time 0. Intraday and interday coefficients of variation determined operator repeatability and physiologic variation.

Results—We did not detect significant differences in gallbladder volume per unit of body weight between treatments at time 0 or in ejection fraction percentage within or between treatments. Median time 0 gallbladder volume was 0.6 mL/kg (range, 0.4 to 1.9) but was > 1.0 mL/kg in 3 of 22 (14%) dogs and ≤ 1.0 mL/kg in 19 of 22 (86%) dogs. Twenty dogs achieved an ejection fraction ≥ 25% with at least 1 treatment, but 2 dogs with a gallbladder volume ≤ 1.0 mL/kg at time 0 did not. Intraday and interday coefficients of variation were 18% and 25%, respectively.

Conclusions and Clinical Relevance—Gallbladder volume ≤ 1.0 mL/kg at time 0 and ejection fraction ≥ 25% were typical. No treatment consistently induced greater gallbladder contraction. Dogs with a gallbladder volume > 1.0 mL/kg and ejection fraction < 25% may require a combined meal and erythromycin protocol.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine the diagnostic value of protein C (PC) for detecting hepatobiliary disease and portosystemic shunting (PSS) in dogs.

Design—Prospective study.

Animals—238 clinically ill dogs with (n = 207) and without (31) hepatobiliary disease, including 105 with and 102 without PSS.

Procedures—Enrollment required routine hematologic, serum biochemical, and urine tests; measurement of PC activity; and a definitive diagnosis. Total serum bile acids (TSBA) concentration and coagulation status, including antithrombin activity, were determined in most dogs. Dogs were grouped into hepatobiliary and PSS categories. Specificity and sensitivity were calculated by use of a PC cutoff value of 70% activity.

Results—Specificity for PC activity and TSBA concentrations was similar (76% and 78%, respectively). Best overall sensitivity was detected with TSBA, but PC activity had high sensitivity for detecting PSS and hepatic failure. Protein C activity in microvascular dysplasia (MVD; PC ≥ 70% in 95% of dogs) helped differentiate MVD from portosystemic vascular anomalies (PSVA; PC < 70% in 88% of dogs). A receiver operating characteristic curve (PSVA vs MVD) validated a useful cutoff value of < 70% activity for PC.

Conclusions and Clinical Relevance—Combining PC with routine tests improved recognition of PSS, hepatic failure, and severe hepatobiliary disease and signified a grave prognosis when coupled with hyperbilirubinemia and low antithrombin activity in hepatic failure. Protein C activity can help prioritize tests used to distinguish PSVA from MVD and sensitively reflects improved hepatic-portal perfusion after PSVA ligation.

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in Journal of the American Veterinary Medical Association

Abstract

Objective—To determine disorders associated with vacuolar hepatopathy (VH), morphologic hepatic and clinicopathologic abnormalities, and affiliation with steroidogenic hormone excess in dogs.

Design—Retrospective case series.

Animals—336 dogs with histologically confirmed moderate or severe VH.

Procedures—Information on signalment, results of diagnostic testing, definitive diagnoses, and exposure to glucocorticoids (ie, exogenous glucocorticoid administration or high endogenous concentrations of steroidogenic hormones) was obtained from medical records. Dogs were grouped by underlying disorder, glucocorticoid exposure, acinar zonal distribution of lesions, and histologic severity.

Results—12 disease groups (neoplastic, acquired hepatobiliary, neurologic, immune-mediated, gastrointestinal tract, renal, infectious, cardiac disease, diabetes mellitus, portosystemic vascular anomaly, adrenal gland dysfunction, and miscellaneous disorders) were identified. There were 186 (55%) dogs with and 150 (45%) dogs without evidence of glucocorticoid exposure. Acinar zonal distribution of hepatic vacuolation and clinicopathologic values did not differ between dogs with and without evidence of glucocorticoid exposure. However, a 3-fold increased likelihood of severe VH was associated with steroidogenic hormone exposure. Of 226 dogs with high serum alkaline phosphatase activity, 102 (45%) had no evidence of glucocorticoid exposure.

Conclusions and Clinical Relevance—Results suggest that neoplasia and congenital or acquired hepatobiliary disease are common in dogs with VH and provide support for the suggestion that VH, high alkaline phosphatase activity, and illness-invoked physiologic stress may be associated. Histologic confirmation of VH should initiate a diagnostic search for a primary disease if glucocorticoid treatment and hyperadrenocorticism are ruled out.

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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 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)

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in Journal of the American Veterinary Medical Association