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Hepatic lipidosis is a common disease associated with inappetence in cats. Successful treatment requires nutritional supplementation, which is typically administered through a feeding tube (eg, gastrotomy tube or esophagostomy tube). Placement of

Full access
in Journal of the American Veterinary Medical Association

Summary

The effect of long-term voluntary fasting on hematologic variables, biochemical profiles, and liver histologic findings was assessed in 15 obese cats (> 40% overweight). Clinical signs and laboratory results consistent with hepatic lipidosis were observed in 12 of 15 cats after 5 to 7 weeks of fasting, and were associated with 30 to 35% reduction of initial body weight. Histologic examination of successive liver biopsy specimens revealed that obesity was not associated with liver parenchymal lipid accumulation, but that fasting resulted in lipidosis in all 15 cats. The long-term fast was associated with an early (after 2 to 4 weeks of fasting) and significant (P< 0.05) reduction in serum urea, glucose, and albumin concentrations, and RBC mass. Fasting for 5 to 7 weeks was associated with a significant (P< 0.05) increase in hepatic-associated enzyme activities and in total and direct serum bilirubin concentrations. Significant (P< 0.05) changes in serum alkaline phosphatase developed as early as 3 weeks before the onset of hyper-bilirubinemia. Except for development of hepatic lipidosis, cats appeared to tolerate the fast without other adverse effect. This study confirmed that longterm fasting may induce clinical hepatic lipidosis in obese cats. Fasting appears to induce a syndrome of hepatic lipidosis that is indistinguishable from feline idiopathic hepatic lipidosis and may be an appropriate model to study the pathophysiologic features and treatment of hepatic lipidosis.

Free access
in American Journal of Veterinary Research

Summary

In this study, we compared hepatic ultrastructure in healthy cats, in cats with severe hepatic lipidosis, and in cats with experimentally induced, chronic, extrahepatic bile duct occlusion. Ultrastructural features unique to the lipidosis syndrome included an apparent reduction in number of peroxisomes and alteration in their morphologic features. The quantity of endoplasmic reticulum, Golgi complexes, and lysosomes was subjectively reduced, and paucity of cytosolic glycogen was observed. Bile canaliculi appeared collapsed because of cytosolic distention with lipid. Mitochondria were reduced in number and were markedly pleomorphic. Cristae assumed a variety of shapes, lengths, and orientations. Ultrastructural features of bile duct occlusion were similar to those described in other species and differed from those in cats with hepatic lipidosis.

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in American Journal of Veterinary Research

Summary

The accuracy of ultrasonography in detection of feline hepatic lipidosis was studied retrospectively. The following ultrasonographic criteria were associated positively with severe hepatic lipidosis: the liver hyperechoic, compared with falciform fat; the liver isoechoic or hyperechoic, compared with omental fat; poor visualization of intrahepatic vessel borders; and increased attenuation of sound by the liver. In a group of 36 cats with clinically apparent hepatobiliary disease and in which liver biopsy was done, liver hyperechoic, compared with falciform fat, was the best criterion for diagnosis of severe hepatic lipidosis with 91% sensitivity, 100% specificity, and 100% positive predictive value.

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in American Journal of Veterinary Research

Objective

To identify factors associated with hepatic lipidosis (HL) in llamas and alpacas.

Design

Retrospective case series.

Animals

30 llamas and 1 alpaca.

Procedures

Medical records were searched to identify llamas or alpacas in which a histologic diagnosis of HL was made. Information was retrieved on signalment, history, clinical and laboratory findings, and results of necropsy or examination of biopsy specimens. Data were analyzed using descriptive statistics and χ2 analyses.

Results

Females were affected more often than males; however, the sex distribution was not different from that of the camelid population in the diagnostic laboratory's database. Fifty-four percent of the females were pregnant, and 46% were lactating. Most affected camelids were 6 to 10 years old. Anorexia and recent weight loss were common (51.6% of camelids). An infective agent was found in only one llama, and toxins and mineral deficiencies were not identified. The most common abnormalities on serum biochemical analysis were a high concentration of bile acids, high activities of γ-glutamyltrans-ferase (GGT) and aspartate aminotransferase (AST), and hypoproteinemia. Concentrations of nonesterified fatty acids (NEFA) and β-hydroxybutyrate (β-HB) were high in those camelids in which these compounds were assayed. Twenty-nine camelids did not survive.

Clinical Implications

Sick camelids should be considered at risk for developing HL, especially those with anorexia or the metabolic demands of pregnancy and lactation. Other stresses also appear to contribute. High concentrations of NEFA, γ-HB, and bile acids; high activities of GGT and AST; and hypoproteinemia may indicate that HL has developed. (J Am Vet Med Assoc 1999;214:1368–1372)

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in Journal of the American Veterinary Medical Association

SUMMARY

Concentrations of total, free, and esterified carnitine were determined in plasma, liver, and skeletal muscle from cats with idiopathic hepatic lipidosis and compared with values from healthy cats. The mean concentrations of plasma, liver, and skeletal muscle total carnitine; plasma and skeletal muscle free carnitine; and plasma and liver esterified carnitine were greater (P < 0.05) in cats with idiopathic hepatic lipidosis than in control cats. The mean for the ratio of free/total carnitine in plasma and liver was lower (P < 0.05) in cats with idiopathic hepatic lipidosis than in control cats. These data suggest that carnitine deficiency does not contribute to the pathogenesis of feline idiopathic hepatic lipidosis.

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in American Journal of Veterinary Research

Abstract

Objective

To determine urinary orotic acid (OA) conentration and evaluate the urinary OA-to-creatinine ratio (OACR) in cats with hepatic lipidosis (HL).

Animals

20 cats with HL and 20 clinically normal cats.

Procedure

Hepatic lipidosis was diagnosed on the basis of clinical signs, results of serum biochemical analyses, exclusion of other concurrent illness, and cytologic or histologic evaluation of liver biopsy specimens. Urine samples were collected from each cat and frozen at −20 C until assayed. Urine creatinine concentrations were determined, using an alkaline picrate method followed by spectrophotometric assay. Urine OA concentration was determined, using high-performance liquid chromatography. Minimum amount of detectable OA in feline urine was 1 µg/ml. Because of small interfering peaks near the base of the OA peak, the minimum quantifiable concentration of OA was determined to be 5 pg/ml. Urinary OACR was compared in both groups of cats.

Results

Differences in urinary OACR were not detected between clinically normal cats and cats with HL. Peaks were not detected for urinary OA in any of the 20 clinically normal cats. Of the 20 HL cats, 14 did not have detectable peaks for urinary OA. Of the 6 HL cats that had detectable urinary OA peaks, 3 had values of < 5 µg/ml.

Conclusions

Apparently, OACR does not increase significantly in cats with HL.

Clinical Relevance

Urinary OACR is not a useful diagnostic test for HL in cats. (Am J Vet Res 1999; 60:753–754)

Free access
in American Journal of Veterinary Research

Summary

The medical records of 23 American Miniature Horses with hyperlipidemia, hyperlipemia, or hepatic lipidosis were reviewed. The most common clinical signs were anorexia and lethargy. The mean duration of clinical signs was 2.4 days. A primary disease was identified in 19 cases. Enterocolitis was the most common primary disease (n = 10). Intentional feed restriction, as part of treatment for colic, resulted in hyperlipemia in 2 horses and hyperlipidemia in 1. Four horses had primary hyperlipemia, 3 of which had signs of hepatoencephalopathy secondary to hepatic lipidosis. Dextrose, heparin, and insulin were the most common treatments. The overall survival was 61% (14/23). All horses with peak serum triglyceride concentrations > 1,200 mg/dl died or were euthanatized, whereas all but 1 with peak serum triglyceride concentrations < 1,200 mg/dl survived. These findings suggest that when American Miniature Horses, like other ponies and donkeys, are in a negative energy balance, they can rapidly develop hyperlipidemia or hyperlipemia. Early detection and treatment may improve survival.

Free access
in Journal of the American Veterinary Medical Association

Abstract

Objectives—To determine whether feed restriction induces hepatic lipidosis (HL) in llamas and to evaluate the metabolic changes that develop during feed restriction.

Animals—8 healthy adult female llamas.

Procedure—Llamas were fed grass hay at a rate of 0.25% of their body weight per day for 13 to 28 days. Llamas were monitored by use of clinical observation, serum biochemical analyses, and ultrasound-guided liver biopsies.

Results—All 8 llamas lost weight and mobilized fat. Five llamas developed HL, including 4 that were nursing crias. During the period of feed restriction, mean serum concentration of bile acids and activities of aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH), and γ-glutamyl transferase (GGT) were significantly higher in llamas that developed HL, compared with llamas that did not. Mean insulin-to-cortisol concentration ratios were lower in llamas with HL before and up to 7 days of feed restriction, compared with those that did not develop HL.

Conclusions and Clinical Relevance—HL in llamas may be induced by severe feed restriction, particularly in the face of increased energy demand. Llamas with weight loss attributable to inadequate dietary intake may develop biochemical evidence of hepatopathy and HL. Increases in serum concentration of bile acids and activities of GGT, AST, and SDH may indicate the development of HL in llamas and identify affected animals for aggressive therapeutic intervention. (Am J Vet Res 2001;62:1081–1087)

Full access
in American Journal of Veterinary Research

Summary

A protein that has 2 subunits with molecular weight of 35,000 and 23,000 was detected in serum of cattle with hepatic lipidosis (fatty liver). The protein was purified from serum obtained from a cow with fatty liver, and was identified as haptoglobin, which is known to have hemoglobin-binding capacity and to be an acute-phase protein. To assess the relevance of haptoglobin in fatty liver, cattle were classified in 3 groups (healthy control, haptoglobin-positive, and haptoglobin-negative); liver triglyceride content and several serum biochemical variables were evaluated for the 3 groups. Compared with the control and haptoglobin-negative cattle, haptoglobin-positive cattle had significantly (P < 0.01) higher liver triglyceride content, serum bilirubin concentration, and aspartate transaminase activity. Serum haptoglobin concentration was high in slaughter cattle (27 of 40 cattle tested), particularly in cows (20/28).

Free access
in American Journal of Veterinary Research