Search Results

You are looking at 1 - 10 of 197 items for :

  • "hepatopathy" x
  • Refine by Access: All Content x
Clear All

progressive hepatopathy. Protoporphyric hepatopathy initiates in periportal regions with progressive development of fibrotic bridging septa that are marginated by porphyrin-engorged macrophages, mixed inflammatory infiltrates, and single necrotic hepatocytes

Full access
in Journal of the American Veterinary Medical Association

Vacuolar hepatopathy is a common hepatic disorder in dogs that typically is associated with glucocorticoid excess. In an unpublished review of 500 hepatic biopsy specimens obtained from client-owned dogs examined during the past 7 years at the

Full access
in Journal of the American Veterinary Medical Association

. Another subset of liver specimens (n = 35) was stained with rhodanine to inspect for possible copper-associated hepatopathy. In these dogs and in 1 additional dog, hepatic copper was quantified by atomic absorption spectroscopy (n = 13) or by digital

Full access
in Journal of the American Veterinary Medical Association

A minoaciduric canine hypoaminoacidemic hepatopathy syndrome (ACHES) is defined by severe hypoaminoacidemia, 1 – 3 hepatocutaneous-associated hepatopathy, 4 – 8 and aminoaciduria. 1 , 3 This is the most common cause of superficial necrolytic

Open access
in American Journal of Veterinary Research

Introduction Over the past 20 years, some internists have perceived an increase in copper-associated hepatopathy incidences in dogs. 1 Copper is an essential nutrient in canine diets and involved in numerous biological functions such as, but

Open access
in Journal of the American Veterinary Medical Association

copper-associated hepatitis or copper-associated hepatopathy (CAH), is the most common known cause of chronic hepatitis in dogs. 6 Clinical features are varied and can range from asymptomatic dogs with minimal increases in liver enzyme activities to dogs

Full access
in Journal of the American Veterinary Medical Association

SUMMARY

Dogs are particularly susceptible to development of glucocorticoid-induced hepatopathy, but the mechanisms are not well understood. We investigated the pathogenesis of glucocorticoid hepatopathy by examining sequential morphologic and biochemical changes in the liver of dogs during steroid administration.

Six adult Beagles were given prednisolone acetate (4 mg/kg of body weight, once daily for 24 days, im). Serum samples and percutaneous liver biopsy specimens were obtained before the start of the study (treatment day [td] 0) and at td 5, 10, 15, and 25. There were significant (P < 0.05) and progressive increases in serum activities of alkaline phosphatase, γ-glutamyltransferase, and alanine transaminase. Light microscopic changes in liver biopsy specimens included progressive hepatocellular swelling and vacuolation. Electron microscopy revealed glycogen accumulation, peripheral displacement of organelles, and prominent dilatation of bile canaliculi, compared with findings at td 0. Liver biopsy specimens taken at td 25 had significantly (P < 0.05) increased activities of the plasma membrane enzymes, alkaline phosphatase and γ-glutamyltransferase, and 5'-nucleotidase was significantly (P < 0.01) decreased. Subcellular fractionation on reorientating sucrose density gradients revealed high-density peaks of alkaline phosphatase and γ-glutamyltransferase, compatible with a specific increase in the biliary canalicular component of the enzyme activities. Neutral α-glucosidase activity was shifted to the denser fractions, indicative of an increase in the proportion of rough to smooth endoplasmic reticulum and consistent with enhanced synthesis of plasma membrane proteins. There also was evidence for progressive increase in fragility of intracellular organelles, particularly lysosomes.

These findings indicate that glucocorticoid hepatopathy in dogs is associated with progressive alterations not only to the plasma membrane, but also to other subcellular organelles.

Free access
in American Journal of Veterinary Research

A minoaciduric canine hypoaminoacidemic hepatopathy syndrome (ACHES) is a recently defined condition occurring in dogs with hepatocutaneous-associated hepatopathy, hypoaminoacidemia, and variable aminoacidurias. Urine amino acid losses were most

Open access
in American Journal of Veterinary Research

Abstract

Objective

To determine the usefulness of a new method of measuring acoustic backscatter and attenuation in the liver of dogs with experimental steroid-induced hepatopathy.

Animals

10 clinically normal dogs.

Procedure

Steroid hepatopathy was induced by daily injections of prednisone (2 mg/kg of body weight, IM). Dogs were evaluated histologically and were sonographically imaged on days 0, 3, 7, 10, and 14. Acoustic backscatter and attenuation were measured from in vivo images of dogs, using a video signal method, and compared with results obtained from analysis of the unprocessed radio frequency signal.

Results

Histologic evaluation revealed midzonal, predominantly water-filled vacuoles in hepatocytes by day 7, which persisted for the remainder of the study and significantly (P = 0.0001) increased liver weight on day 14. Attenuation and backscatter increased during the experimental period. Mean effective attenuation difference was higher (P = 0.015) in the liver imaged through a left paraxyphoid window in experimental dogs by day 3. Significantly (P < 0.05) greater attenuation persisted in the liver of experimental dogs throughout the experimental period. Mean backscatter ratio was significantly increased (P = 0.02) by day 10. Uncorrected pixel intensity of the liver in 2 experimental dogs was approximately equal to that of the spleen on day 10 and greater than that of the spleen on day 14.

Conclusion

Administration of prednisone to dogs results in increased acoustic backscatter and attenuation in the liver.

Clinical Relevance

The video signal method is a sensitive technique for detecting subtle acoustic changes in the liver of dogs. (Am J Vet Res 1996;57:1690–1694)

Free access
in American Journal of Veterinary Research

Abstract

OBJECTIVE

To retrospectively evaluate safety and tolerance of leflunomide for long-term treatment of canine idiopathic immune-mediated polyarthritis (IMPA).

ANIMALS

27 dogs with clinical signs and synovial fluid cytology supportive of IMPA with ≥ 6 months’ follow-up after starting leflunomide.

METHODS

Medical records were reviewed to identify dogs prescribed leflunomide for treatment of IMPA from February 2012 to May 2022. Initial leflunomide doses of 2 to 4 mg/kg once daily were prescribed and were titrated to the lowest effective dose with concurrent anti-inflammatory therapy. Complete blood count, serum chemistry, and clinical signs were monitored throughout the course of treatment.

RESULTS

Adverse effects potentially attributable to leflunomide noted in 9 of 27 dogs (33%) included vomiting, diarrhea, lethargy, decreased or absent appetite, polyuria and polydipsia, and secondary antibiotic responsive infection and were self-limiting or resolved with outpatient therapy. Alkaline phosphatase (ALP) and alanine aminotransferase (ALT) elevation were documented in all dogs prescribed leflunomide plus prednisone, with persistent liver enzyme elevation in 6 of 9 dogs (67%) and normalization after antibiotic therapy in 3 of 9 dogs (33%). The majority of dogs prescribed leflunomide plus NSAID (11/17 [65%] dogs) did not experience liver enzyme elevation; 2 of 17 (12%) dogs developed transient antibiotic-responsive liver enzyme elevations, and 4 of 17 (23%) dogs had persistent liver enzyme elevation.

CLINICAL RELEVANCE

Leflunomide was well tolerated for long-term management of IMPA. A significant difference in liver enzyme elevation was identified between dogs prescribed prednisone versus NSAID in combination with leflunomide. Leflunomide with NSAID therapy resulted in less hepatotoxicity compared with leflunomide with prednisone.

Open access
in Journal of the American Veterinary Medical Association