Biomedical subjects

S A Center

Publications and source records attributed to S A Center.

At least 19 recordsLinked to original sources

PubMed1999

Chronic liver disease: current concepts of disease mechanisms.

Optimal management of chronic liver disease requires an understanding of aetiological factors or conditions initiating and sustaining tissue damage. Injury may derive initially from toxin or xenobiotic exposure (direct, biotransformation adducts, hypersensitivity responses or immune-mediated mechanisms), infectious organisms, inborn errors of metabolism, or pathological accumulations of transition metals (iron or copper), endotoxins or membranocytolytic bile acids. Secondarily, cells and mediators associated with inflammation, pathological expression of major histocompatibility foci on hepatocytes and biliary epithelia, aberrant initiation of apoptosis, modification of the extracellular matrix, and depletion of natural antioxidants can each play pivotal roles. Cholestatic liver injury derived from extrahepatic mechanical obstruction or intrahepatic cholestasis (many causes) can induce membrane damage subsequent to accumulation of membranocytolytic bile acids, copper retention, and membrane peroxidation. This paper reviews contemporary issues of chronic hepatocellular injury and hepatic fibrosis with the aim of broadening the clinical perspective of treatment strategies.

Animals↗

PubMed1998

Nutritional support for dogs and cats with hepatobiliary disease.

Nutritional intake in the patient with hepatobiliary disease provides the cornerstone of balanced medical care. Optimal recommendations require consideration of general nutritional principles, special species requirements and contemporary needs uniquely related to the patient's medical problem. Although general recommendations follow well-established guidelines developed to meet metabolic requirements for normal health, there is little information regarding altered requirements in animals that are ill. Consequently, recommendations for animals have been derived empirically from studies completed in humans, most work having been done in patients with end stage cirrhosis or liver failure complicated by hepatic encephalopathy. This is problematic because most veterinary patients with liver disease are not in hepatic failure and do not suffer from hepatic encephalopathy. Iatrogenic malnutrition can develop in patients when protein-restricted diets are inappropriately recommended. Insufficient energy intake and negative nitrogen balance can complicate a patient's condition, impairing tissue regeneration and recovery from disease. This paper reviews strategies that can be used to individualize nutritional management in small companion animals with hepatobiliary disease. Consideration is given to both the known and controversial issues regarding energy requirements, dietary energy distribution, vitamin and micronutrient supplementation, the special requirements of the cat with hepatic lipidosis, as well as strategies effective for palliation of hepatic encephalopathy.

Animals↗

PubMed1998

Naturally acquired leptospirosis in 36 dogs: serological and clinicopathological features.

Case records of 36 dogs with confirmed leptospirosis diagnosed at the New York State College of Veterinary Medicine from 1980 to 1995 were reviewed retrospectively, and clinical, serological and pathological findings were recorded to characterise the epidemiology of this disease in upstate New York. Titres were directed predominantly against serovars grippotyphosa and/or pomona in 31 of 34 dogs. Convalescent titres were measured for 53 per cent of dogs. The most common clinical presentation was acute renal failure. Increased liver enzyme activity was documented in 22 of 36 dogs. It is clear from this study that Leptospira pomona and grippotyphosa are important pathogens capable of causing severe renal and hepatic injury in dogs.

Animals↗

PubMed1998

Calcipotriol toxicity in a dog.

A six-month-old Labrador retriever was presented for investigation of acute polyuria, polydipsia and haematemesis six hours following ingestion of a tube of the topical antipsoriatic vitamin D analogue, calcipotriol. Transient hypercalcaemia, azotaemia, proteinuria, thrombocytopenia and ventricular arrhythmias ensued. Abdominal ultrasonography and echocardiography revealed evidence of diffuse soft tissue mineralisation. Despite 13 days of intensive supportive care, the dog was euthanased due to continued haematemesis and anorexia. Necropsy confirmed mineralisation and necrosis of multiple organ systems consistent with vitamin D toxicity.

Animals↗

PubMed1998

Use of the urine cortisol-to-creatinine ratio for monitoring dogs with pituitary-dependent hyperadrenocorticism during induction treatment with mitotane (o,p'-DDD).

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 > or = 28 nmol/L but < or = 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 x 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 x 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 < or = 79 x 10(-6) would be inconclusive.

Adrenocortical Hyperfunction↗

PubMed1997

Suspected microscopic hepatic arteriovenous fistulae in a young dog.

Portal hypertension can develop from any disorder that obstructs portal blood flow and may cause ascites in young dogs. Anomalous hepatic arteriovenous (AV) connections are rare but should be suspected in any young dog with portal hypertension or ascites. All previous reports of dogs with hepatic AV fistulae have documented macroscopic connections between the arterial and venous systems. Identical clinical signs and histopathologic findings can develop in dogs in which a macroscopic hepatic AV connection cannot be detected. Microscopic AV connections may be responsible for clinical signs in these dogs.

Animals↗

PubMed1996

Fulminant hepatic failure associated with oral administration of diazepam in 11 cats.

Acute fulminant hepatic necrosis was associated with repeated oral administration of diazepam (1.25 to 2 mg, PO, q 24 or 12 h), prescribed for behavioral modification or to facilitate urination. Five of 11 cats became lethargic, atactic, and anorectic within 96 hours of initial treatment. All cats became jaundiced during the first 11 days of illness. Serum biochemical analysis revealed profoundly high alanine transaminase and aspartate transaminase activities. Results of coagulation tests in 3 cats revealed marked abnormalities. Ten cats died or were euthanatized within 15 days of initial drug administration, and only 1 cat survived. Histologic evaluation of hepatic tissue specimens from each cat revealed florid centrilobular hepatic necrosis, profound biliary ductule proliferation and hyperplasia, and suppurative intraductal inflammation. Idiosyncratic hepatotoxicosis was suspected because of the rarity of this condition. Prior sensitization to diazepam was possible in only 1 cat, and consistent risk factors that could explain susceptibility to drug toxicosis were not identified. On the basis of the presumption that diazepam was hepatotoxic in these cats, an increase in serum transaminase activity within 5 days of treatment initiation indicates a need to suspend drug administration and to provide supportive care.

Animals↗

PubMed1996

High dietary chloride content associated with loss of therapeutic serum bromide concentrations in an epileptic dog.

Bromide treatment was successful in controlling seizures in an 11-year-old Dachshund with epilepsy and presumptive phenobarbital-associated hepatopathy. Because bromide does not induce liver enzyme activity and does not seem to be hepatotoxic, it can be used to control seizures in dogs with concurrent epilepsy and hepatic disease. In this dog, institution of a special calculolytic diet with high chloride content was associated with a decrease in serum bromide concentrations and the recurrence of seizures. High chloride intake increases the elimination of bromide in dogs, leading to higher dosage requirements for bromide in dogs fed high-chloride diets.

Animals↗

PubMed1996

Effects of oral ursodeoxycholic acid in healthy cats on clinicopathological parameters, serum bile acids and light microscopic and ultrastructural features of the liver.

A blind, placebo-controlled study evaluated the effects of ursodeoxycholic acid (UDCA) given orally, at a dose of 15 mg kg-1 per day for eight weeks, on the physical condition, haematological and serum biochemical profiles, urinalysis, total serum bile acids (TSBA) and hepatic histology of four healthy cats. There were no clinically important significant differences between the groups or within the treatment groups in clinicopathological parameters. TSBA concentrations or histology. A significant lower concentration/proportion of taurochenodeoxycholic acid was observed in the treated cats (P = 0.05). Only one treated cat accumulated measurable quantities of UDCA, and the compound appeared to be non-toxic. It did not increase the concentration of TSBA, and accumulated minimally in the serum. It should be investigated for therapeutic use in cats with hepatobiliary disease.

Administration, Oral↗

PubMed1995

Measurement of serum bile acids concentrations for diagnosis of hepatobiliary disease in cats.

Serum bile acid concentrations were measured after food had been withheld for 12 hours (fasting serum bile acid [FSBA] concentration) and 2 hours after a meal (post-prandial serum bile acid [PSBA] concentration) using a direct enzymatic procedure in 108 cats clinically suspected of having hepatobiliary disease. In all cats, liver tissue was examined histologically to confirm the diagnosis. Twenty-six cats did not have histologic evidence of hepatobiliary disease and served as controls. The remaining 82 cats had hepatobiliary disease including hepatic lipidosis (n = 20), portosystemic vascular anomaly (n = 24), hepatic necrosis (n =13), hepatic neoplasia (n = 8), or cholestatic hepatic disease(n = 17). Sensitivity and specificity of measuring FSBA and PSBA concentrations were calculated for each test alone and when results were interpreted in combination (ie, in series and in parallel), and were compared with sensitivity and specificity of routinely used serum biochemical tests, including measuring serum activities of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and gamma-glutamyltransferase, and measuring serum concentrations of cholesterol, BUN, and total bilirubin. When tests were considered individually, determination of FSBA and PSBA concentrations had higher specificity than did the other tests (using a cutoff of 15 mumol/L for FSBA concentration and of 20 mumol/L for PSBA concentration). Determination of PSBA concentration had the highest sensitivity of all single tests in cats with hepatic lipidosis, portosystemic vascular anomaly, or cholestasis; determination of alanine aminotransferase activity or PSBA concentration had the highest sensitivity for cats with hepatic necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Adrenocortical function in neonatal and weanling beagle pups.

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 ACTH-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.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗

PubMed1993

Serum bile acids in companion animal medicine.

Quantification of total serum bile acids is used as a method for appraising liver function and perfusion in contemporary small animal practice. This article provides a historical perspective and a comprehensive review of bile acid physiology, laboratory methodologies for bile acid quantification, and normal values published for total serum bile acids measured using the spectrophotometric enzymatic method and for serum bile acids measured using validated radioimmunoassay procedures. The variables influencing the enterohepatic circulation of bile acids and, consequently, the fasting and postprandial serum bile acid concentrations are discussed with the intent of clarifying the application of test results to clinical patients. A brief discussion of the therapeutic use of dehydrocholate and ursodeoxycholic acid in clinical patients is provided.

Animals↗

PubMed1993

3 alpha-Hydroxylated bile acid profiles in clinically normal cats, cats with severe hepatic lipidosis, and cats with complete extrahepatic bile duct occlusion.

Concentrations of 3 alpha-hydroxylated bile acids were measured in serum and urine of clinically normal (healthy) cats (n = 6), cats with severe hepatic lipidosis (n = 9), and cats with complete bile duct occlusion (n = 4). Bile acid concentrations were measured by use of a gradient flow high-performance liquid chromatography procedure with an acetonitrile and ammonium phosphate mobile phase and an in-line postanalytic column containing 3 alpha-hydroxy-steroid dehydrogenase and a fluorescence detector. Specific identification of all bile acid peaks was not completed; unidentified moieties were represented in terms of their elution time (in minutes). Significant differences in serum and urine bile acid concentrations, quantitative and proportional, were determined among groups of cats. Cats with hepatic lipidosis and bile duct occlusion had significantly (P > or = 0.05) greater total serum and urine bile acids concentrations than did healthy cats. The proportion of hydrophobic bile acids in serum, those eluting at > or = 400 minutes, was 1.9% for healthy cats, 3.3% for cats with lipidosis, and 5.4% for bile duct-obstructed cats. Both groups of ill cats had a broader spectrum of unidentified late-eluting serum bile acids than did healthy cats; the largest spectrum developed in bile duct-occluded cats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Ultrastructural hepatocellular features associated with severe hepatic lipidosis in cats.

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.

Animals↗

PubMed1992

Diagnostic efficacy of serum alkaline phosphatase and gamma-glutamyltransferase in dogs with histologically confirmed hepatobiliary disease: 270 cases (1980-1990).

The diagnostic efficacy of serum alkaline phosphatase (ALP) and gamma-glutamyltransferase (GGT) activities was examined, using the records of 270 dogs initially suspected of having hepatobiliary disease on the basis of history, findings on physical examination, results of baseline screening tests, or any combination of these data. Histologic examination of hepatic tissue was performed in each dog. Sixty-three dogs did not have histologic evidence of hepatobiliary disease and served as the control group. On the basis of diagnosis, dogs were assigned to 1 of 8 groups: dogs with cirrhosis (n = 34), steroid hepatopathy (n = 16), hepatic neoplasia (primary and secondary, n = 36), chronic hepatitis (n = 14), chronic passive congestion (n = 5), hepatic necrosis (n = 17), portosystemic vascular anomaly (n = 35), and cholestasis (extrahepatic bile-duct obstruction and intrahepatic cholestasis, n = 50). Of the 207 dogs with hepatobiliary disease, 29 (14%) had normal ALP and GGT activities, 31 (15%) had normal ALP activity, and 112 (54%) had normal GGT activity. Of the 63 control dogs, 29 (46%) had normal serum ALP and GGT activities, 32 had normal ALP activity (ALP specificity, 51%), and 55 had normal GGT activity (GGT specificity, 87%). The specificity of ALP and GGT in parallel (positive result = result of either test abnormal) was 46%, and in series (positive result = results of both tests abnormal) was 91%. The highest median activities of ALP developed in dogs with cholestasis, steroid hepatopathy, chronic hepatitis, and hepatic necrosis. The highest median activities of GGT developed in dogs with steroid hepatopathy, cholestasis, and hepatic necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗

PubMed1992

Presumptive trimethoprim-sulfadiazine-related hepatotoxicosis in a dog.

Administration of trimethoprim-sulfadiazine in a dog was associated with vomiting, inappetence, and icterus, and high values of alanine transaminase, aspartate transaminase, alkaline phosphatase, gamma-glutamyltransferase, and total bilirubin concentration. The clinical signs and biochemical abnormalities resolved after discontinuation of the treatment. Histologic examination of sections from a liver biopsy specimen revealed moderate, predominantly portal hepatitis with cholestasis.

Animals↗

PubMed1991

Evaluation of twelve-hour preprandial and two-hour postprandial serum bile acids concentrations for diagnosis of hepatobiliary disease in dogs.

In samples collected from 170 dogs suspected of having hepatobiliary disease, preprandial serum bile acids (PRSBA) and postprandial serum bile acids (POSBA) concentrations were measured, using a spectrophotometric enzymatic method. Dogs were assigned to 8 disease groups and 1 control group on the basis of hepatic histopathologic findings. Pre- and postprandial SBA concentrations and results of routine biochemical analyses (including total bilirubin, albumin, and BUN concentrations, and serum alkaline phosphatase (ALP), alanine transaminase (ALT), and aspartate transaminase (AST) activities) were expressed, using 4 indices: sensitivity, specificity, positive predictive value, and negative predictive value. Single tests and combinations of tests in series were evaluated. For diagnosis of hepatobiliary disease, the specificity of PRSBA was 100% at values greater than 20 mumol/L and of POSBA was 100% at values greater than 25 mumol/L. Test combinations with the best sensitivity for diagnosing the following diseases were: PRSBA-POSBA for cirrhosis, portosystemic vascular anomaly, and glucocorticoid hepatopathy; PRSBA-POSBA or PRSBA-ALP for cholestasis; PRSBA-POSBA or ALT-AST for chronic hepatitis; PRSBA-ALT for hepatic necrosis and passive congestion; and PRSBA-ALP for neoplasia. Test combinations with the overall highest sensitivity and positive predictive value for the fewest number of tests were PRSBA-POSBA, and either PRSBA or POSBA combined with an enzyme activity (ALT, AST, or ALP). The overall test efficacy for PRSBA vs POSBA was nearly identical: for PRSBA, it was 82.4%, and for POSBA, it was 82.3%. On the basis of the results of this study, PRSBA greater than 20 mumol/L or POSBA greater than 25 mumol/L (measured by use of an enzymatic procedure) indicates histopathologic abnormalities of the hepatobiliary system or portosystemic vascular anastomosis. Seemingly, determination of SBA concentrations can be used to indicate the propriety for hepatic biopsy. Pre- and postprandial serum bile acids concentrations should be evaluated in conjunction with routinely used hepatobiliary screening tests for best diagnostic advantage.

Alanine Transaminase↗

PubMed1991

Juvenile-onset polyarthritis syndrome in Akitas.

Two young Akitas were examined because of manifestation of a juvenile-onset form of polyarthritis. A search of medical records at the New York State College of Veterinary Medicine found 6 more similarly affected Akitas. The clinical manifestations were marked by cyclic febrile illness and signs of profound joint-related pain. Two dogs had concurrent aseptic meningitis. The syndrome resembles juvenile rheumatoid arthritis in human beings, although it shares features with systemic lupus erythematosus. Pedigree analysis of affected Akitas supported a heritable component to the syndrome. Treatment with immunosuppressive drugs was effective in 2 dogs that achieved complete remission, and in 2 dogs that achieved only partial remission. Classification of this syndrome is difficult and may represent an "overlap" syndrome commonly described in human beings.

Animals↗