Hepatic copper concentrations in Labrador Retrievers with and without chronic hepatitis: 72 cases (1980–2010)

Johnston, Andrea N.; McDonough, Sean P.; Wakshlag, Joseph J.; Warner, Karen L.

doi:10.2460/javma.242.3.372

Cited by 49 publications

(138 citation statements)

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“…Clarification of such terminology is important because excessive dietary copper intake in some dogs seems to cause PCH when copper accumulates and initiates tissue injury. 19 We suggest that the term hepatopathy rather than hepatitis be used to describe the PCH syndrome. Despite high hepatic copper concentrations in animals with PCH, some affected dogs and cats lack necroinflammatory liver lesions at the time of initial detection of the problem.…”

Section: Discussionmentioning

confidence: 99%

“…Hepatic copper accumulation has been increasingly identified for dogs, likely secondary to dietary copper supplementation since 1997, which has complicated selection of treatments. 19 Rather than using a hepatic copper concentration cutoff value for selection of treatments, we advocate collaboration between clinicians and pathologists for determination of the importance of hepatic copper concentrations in consideration of the location of lobular injury, other concurrent liver injury or inflammation, and values of clinicopathologic markers of liver disease (especially serum ALT activity). For determination of a diagnosis of PCH for cats, we recommend consideration of not only the hepatic copper concentration (> 700 µg/g of dry weight), but also identification of a centrilobular copper distribution and unique hepatocellular vacuolar change.…”

Section: Discussionmentioning

confidence: 99%

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Presumed primary and secondary hepatic copper accumulation in cats

Hurwitz

Randolph²,

McDonough³

et al. 2014

javma

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Presumed primary and secondary hepatic copper accumulation in cats

Hurwitz

Randolph²,

McDonough³

et al. 2014

javma

Self Cite

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“…Copper distribution was characterized for zone and number of hepatocytes demonstrating copper-protein cytosolic aggregates with severity designated by numerical scoring (0 ¼ no copper, 1 ¼ a few foci of hepatocytes [<2/10Â field] inconsistently distributed in zone 3, 2 ¼ consistent involvement of <25% of zone 3 hepatocytes [2-4/10Â field], 3 ¼ consistent involvement of >25% to 50% of zone 3 hepatocytes; 4 ¼ consistent involvement of !50% to 75% of zone 3 and zone 2 hepatocytes, and 5 ¼ panlobular involvement of most hepatocytes). 30 …”

Section: Histologic Assessmentsmentioning

confidence: 99%

Ductal Plate Malformation in the Liver of Boxer Dogs

et al. 2016

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Ductal plate malformations (DPMs) represent developmental biliary disorders with a wide phenotypic spectrum. This study characterizes DPM in 30 Boxer dogs. Median age was 1.5 (range, 0.3-10.0) years, with 12 dogs <1 year. Clinical features included increased serum levels of liver enzymes (28), gastrointestinal signs (16), poor body condition (14), abdominal effusion (9), and hepatic encephalopathy (2). Additional malformations included gallbladder atresia (8), atrophied left liver (2), absent quadrate lobe with leftdisplaced gallbladder (1), portal vasculature atresia (left liver, 1), intrahepatic portosystemic shunt (1), and complex intrahepatic arteriovenous malformation (1). All dogs had portal tracts dimensionally expanded by a moderate-to-severe multiple small bile duct phenotype embedded in abundant extracellular matrix; 80% displayed variable portal-to-portal bridging. Quantitative analysis confirmed significantly increased fibrillar collagen and a 3-fold increased portal tract area relative to 6 Boxer and 10 non-Boxer controls. Biliary phenotype was dominated by tightly formed CK19-positive ductules, typically 10 to 15 mm in diameter, with 3 to >30 profiles per portal tract, reduced luminal apertures, and negative Ki-67 immunoreactivity. CK19-positive biliary epithelium intersected directly with zone 1 hepatocytes as a signature feature when considered with other DPM characteristics. Phenotypic variation included a multiple small bile duct phenotype (all dogs), predominantly thin-walled sacculated ducts (4), well-formed saccular ducts (4), and sacculated segmental, interlobular, and intralobular ducts (Caroli malformation, 2 dogs, one with bridging portal fibrosis). Histologic evidence of portal venous hypoperfusion accompanied increased biliary profiles in every case. We propose that this spectrum of disorders be referred to as DPM with appropriate modifiers to characterize the unique phenotypes.

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“…AH can be induced by a variety of stimuli, including toxins, adverse drug reactions, infectious disease ( i.e, canine adenovirus‐1 infection, leptospirosis), or is considered idiopathic . In the last few decades, copper toxicosis is recognized with increased frequency as an etiologic factor in the development of both AH and CH in several dog breeds, including the Labrador retriever …”

mentioning

confidence: 99%

Sensitivity and Specificity of PlasmaALT,ALP, and Bile Acids for Hepatitis in Labrador Retrievers

Dirksen

Burgener

Rothuizen

et al. 2017

Veterinary Internal Medicne

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BackgroundBiochemical indicators for diagnosing liver disease are plasma alanine aminotransferase activity (ALT), alkaline phosphatase activity (ALP), and bile acid concentration (BA).ObjectivesTo determine the sensitivity and specificity of ALT, ALP, and BA for detecting primary hepatitis (PH) in clinically healthy Labrador retrievers and investigate whether ALT and ALP can discriminate between dogs with PH and nonspecific reactive hepatitis (RH).Animals191 clinically healthy and 51 clinically ill Labrador retrievers with hepatic histopathology.MethodsRetrospective study. Medical records were reviewed for ALT, ALP, preprandial BA, liver histopathology, and hepatic copper concentrations.ResultsIn 64% (122/191) of the clinically healthy Labrador retrievers, hepatic histology revealed inflammatory infiltrates. This frequency might be biased because part of them was included as first‐line relatives of dogs with copper‐associated hepatitis. Sensitivity of ALT, ALP, and BA in this population for detecting acute hepatitis was 45, 15, and 15%, respectively. For chronic hepatitis, sensitivity was 71, 35, and 13%, respectively. Specificity of ALT, ALP, and BA was >90% for AH, CH, and RH. When increased liver enzymes were present, median ALT was significantly higher in PH cases (312 U/L, range 38–1,369) compared to RH cases (91 U/L, range 39–139) (P < .001). There was no difference in ALP between dogs with a PH and a RH (P = .361).Conclusions and Clinical ImportanceHistopathologic abnormalities in the liver were present in the majority of apparent clinically healthy Labrador retrievers. The sensitivity of ALT, ALP, and BA for detecting acute and chronic hepatitis in this population was low. More sensitive biomarkers are needed for early detection of liver disease in apparent clinically healthy dogs.

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Hepatic copper concentrations in Labrador Retrievers with and without chronic hepatitis: 72 cases (1980–2010)

Abstract: 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.

Cited by 49 publications

References 40 publications

Presumed primary and secondary hepatic copper accumulation in cats

Presumed primary and secondary hepatic copper accumulation in cats

Ductal Plate Malformation in the Liver of Boxer Dogs

Sensitivity and Specificity of PlasmaALT,ALP, and Bile Acids for Hepatitis in Labrador Retrievers

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