Hypertrophic osteopathy associated with adenocarcinoma of the esophageal glands in a dog.
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Biomedical subjects
Publications and source records attributed to S A Center.
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Serum bile acid concentrations have been shown to be a predictive indicator of hepatobiliary disease in persons. However, there has been only limited use of bile acid values in the clinical diagnosis of hepatobiliary disease in the dog and cat because of technical difficulties associated with many bile acid assays. A rapid enzymatic method previously developed for the quantitation of 3-hydroxy bile acids in persons has been adapted for use in the dog and cat. Nonsulfated 3-hydroxy bile acids are converted to 3-oxo bile acids by 3 alpha-hydroxysteroid dehydrogenase and reduction of NAD+ to NADH. In a coupled diaphorase catalyzed reaction, H+ is transferred to nitrotetrazolium blue to produce a diformazan dye, which is measured spectrophotometrically at 540 nm. Nonspecific interfering dehydrogenase activities present in the dog and the cat serums were inhibited by heating the serum to 60 C for 30 minutes or by the addition of sodium pyruvate. Standard curves prepared from various serum sodium taurocholate concentrations in dogs and cats are linear to 250 mumol/L. The assay is sensitive for the detection of bile acid concentrations as low as 2.5 mumol/L in sera from dogs and cats. In validation studies quantitative recovery of known concentrations of 7 primary and secondary, conjugated and unconjugated, 3-hydroxy bile acids from pooled canine serum was 95.3 +/- 7.9% (mean +/- SEM) and that from pooled feline serum was 101.4 +/- 8.2%.(ABSTRACT TRUNCATED AT 250 WORDS)
A solid-phase radioimmunoassay for the measurement of total conjugated bile acids was validated for use in dogs and cats. The method used an 125I-labeled iodoglycocholate tracer and polypropylene assay tubes coated with rabbit antiserum against the major conjugated bile acids. Standard solutions of sodium taurocholate provided with the kit and serial dilutions of canine and feline sera containing low, medium, and high endogenous bile acid concentrations inhibited binding of the [125I]iodoglycocholate tracer to the antibody in a parallel manner; this inhibition indicated specificity of the assay for bile acids in the serum of dogs and cats. Increased serum bile acid concentrations in animals with liver disease confirmed the biologic specificity of the assay in dogs and cats. Accuracy was shown by quantitative recovery of purified sodium taurocholate from canine and feline sera. Intra-assay precision was 7.2% to 17.3% for dogs and 8.5% to 18.5% for cats. Interassay precision was 4.8% to 17.2% for dogs and 3.5% to 11.2% for cats. The sensitivity of the assay in dogs and cats was 0.4 mumol/L. Solid-phase radioimmunoassay is a valid method for the direct measurement of total conjugated bile acids in the dog and cat, and is of value in the diagnosis of hepatobiliary disease in these species.
The effect of propranolol on thyroid function was evaluated in 6 mature euthyroid Beagles. Propranolol was administered orally in doses of 20 mg given 3 times daily for 2 weeks and then increased to 40 mg given 3 times daily for an additional 2 weeks. Six age- and sex-matched, euthyroid Beagles served as controls. Serum base-line concentrations of tetraiodothyronine (T4), triiodothyronine (T3), and reverse triiodothyronine (rT3) were measured before propranolol administration and at weekly intervals thereafter. Thyroid response to 5 IU of aqueous thyroid stimulating hormone administered IV was monitored before propranolol administration and at the 2- and 4-week treatment intervals. The T4, T3, and rT3 concentrations were measured by radioimmunoassay. There were no significant differences in base-line or postthyroid stimulating hormone serum concentrations of T4, T3, or rT3 in any individual or between the treatment or control groups at any treatment interval (P greater than 0.05). Seemingly, the therapeutic use of propranolol in euthyroid dogs should not alter thyroid hormone metabolism.
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Bile duct obstruction was induced in 6 cats by surgical ligation and transection of the common bile duct. Clinical and laboratory changes were monitored weekly for 25 to 54 days. Clinical signs of obstruction were similar in all cats and included anorexia, pyrexia, lethargy, intermittent vomiting, weight loss, palpable gallbladder, hepatomegaly, and bleeding tendencies. Tissue jaundice and acholic feces were evident grossly as early as postsurgical day (PSD) 4 with a mean onset of jaundice at PSD 5.3 +/- 0.4. Hematologic changes were initially characterized by a mild neutrophilic leukocytosis that increased with the chronicity of bile duct obstruction. Regenerative anemia developed in 4 cats associated with gastrointestinal blood loss. Acute serum biochemical changes were characterized by a marked increase in the mean values of aspartate aminotransferase, alanine aminotransferase, total cholesterol, and copper. Comparatively, only moderate increases in mean serum alkaline phosphatase activity were observed. Mean total bilirubin values increased remarkably at postsurgical week (PSW) 1, reaching a maximal value of 23.1 +/- 4.4 mg/dl at PSW 3 with 71.6 +/- 2.7% direct bilirubin. With chronicity of bile duct obstruction ranging from PSW 3 to PSW 7, the mean serum values of aspartate aminotransferase, alanine aminotransferase, total cholesterol, serum alkaline phosphatase, and total and direct bilirubin stabilized and then declined, whereas the increased mean serum copper values persisted. At PSD 25 to 54, hepatic copper values and serum bile acids were markedly increased. Seemingly, clinicopathologic changes of induced cholestatic hepatic injury depended largely on the duration of biliary obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)
Sulfobromophthalein (BSP) and indocyanine green (ICG) were given in single-dose IV injections to dogs and plasma disappearances were measured. The BSP was given at a dose of 5 mg/kg of body weight, and ICG was given at doses of 1.0 and 1.5 mg/kg. The half-life for BSP was 4.2 +/- 0.8 minutes, and for ICG at the 1.0 mg/kg dose, 9.0 +/- 2.0 minutes, and at the 1.5 mg/kg dose, 8.4 +/- 1.9 minutes. The disappearance rate (percentage per minute) for BSP was 17.0 +/- 3.2, and for ICG at the small dose level, 8.1 +/- 1.7, and at the large dose level, 8.7 +/- 2.2. The clearances (ml/min/kg) for BSP were 15.4 +/- 6.2 and for ICG at the small dose level, 3.7 +/- 0.7, and at the large dose level, 3.9 +/- 0.7. The 30-minute percentage retentions for BSP were 1.9 +/- 1.1 and for ICG at the small dose level, 14.7 +/- 5.0, and for ICG at the large dose level, 11.4 +/- 3.0. All of the differences between BSP and ICG means for these values measured were statistically significant (P less than 0.01). There were no significant differences between sexes or between the ICG doses for any of the values (P greater than 0.05).
Plasma disappearances of sulfobromophthalein (BSP) and indocyanine green (ICG) given in single-dose IV injections to cats were measured. The BSP was given at a dose of 5 mg/kg of body weight; ICG was given at a dose of 1.5 mg/kg of body weight. The half-life, disappearance rate (percent per minute) and clearance (ml/min/kg) were determined during the initial phase of plasma dye elimination. The half-life for BSP was 2.2 +/- 0.7 minutes, and for ICG, 3.8 +/- 0.9 minutes. The disappearance rate for BSP was 34.7 +/- 10.1, and for ICG, 19.2 +/- 4.5. The clearance for BSP was 26.3 +/- 23.1 and for ICG, 8.6 +/- 4.1. The 30-minute percentage retention for BSP was 0.6 +/- 0.8% and for ICG, 7.3 +/- 2.9%. In the cat, ICG was cleared from the plasma less rapidly than BSP. There were no significant differences between males and females for these values. For both BSP and ICG, a significantly shorter half-life, faster disappearance rate, and lower 30-minute percentage retention were observed in the cat, compared with values observed in the dog given similar dye dosages. Clearance curves for BSP and ICG in the cat were similar to those in the dog, indicating that the 2 species may have similar volumes of dye distribution and excretory mechanisms. The results of the present study indicate that the 30-minute plasma level following a 5 mg/kg dose of BSP in normal cats is often too low for measurement, whereas the 30-minute plasma concentration of ICG following a 1.5 mg/kg dose is adequate. For the 30-minute dye retention test in the cat, ICG may be a preferred diagnostic agent.
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The effect of experimentally induced cystitis and iatrogenic blood contamination on the urine protein/creatinine ratio (U P/C) was evaluated in 17 dogs. Before they were included in the study, all dogs were judged to be healthy on the basis of physical examination, serum concentrations of urea nitrogen and creatinine, complete urinalysis, and a U P/C less than 0.4. A single urine sample was contaminated with increasing quantities of canine fresh whole blood (PCV = 42%; total protein = 6.2 g/dl). When added blood was equal to or greater than 25% of the total urine sample volume, the U P/C exceeded 3.5, a finding consistent with nephrotic range proteinuria. When added blood was 10% of the total urine sample volume, the U P/C was less than 1.8. Eleven Beagles underwent routine laparotomy during which a cystotomy was done. The median U P/Cs on postoperative days 1 and 2 were significantly increased compared with preoperative values (P less than 0.05); no U P/C exceeded 2.0. Renal biopsies performed on postoperative day 3 eliminated renal proteinuria as a source of urine protein. Five dogs had bacterial cystitis experimentally induced. At 72 and 96 hours after bacterial inoculation, the median U P/Cs were significantly increased (P less than 0.05); individual values ranged from 1.5 to 40.8. Renal biopsies performed between 5 and 6 days after inoculation eliminated renal proteinuria as a source of urine protein. Cytologic evaluation of urine sediment in each group did not correlate with the magnitude of the increase in the U P/C. The U P/C significantly increased in each model of lower urinary tract inflammation.(ABSTRACT TRUNCATED AT 250 WORDS)
Clinical, radiographic, electromyographic, and pathologic findings in a cat with fibrodysplasia ossificans progressiva are described. The features of five previously reported cases of this feline disorder are also presented. This disorder affects young adult to middle-aged cats of both sexes. Characteristic clinical features include progressive stiffness of gait, with enlargement of proximal limb musculature. Radiography reveals multiple mineralized densities within the affected musculature. The clinical course is rapid, with development of severe disability within 2 weeks to several months. Electromyographic and pathologic findings suggest that this is a disorder of connective tissue, affecting primarily the epimysium, tendons, and fasciae, and results in marked proliferation of fibrovascular connective tissue, with associated chondroid and osseous metaplasia.
The physical, clinicopathologic, and survival rates of 77 cats with severe spontaneous hepatic lipidosis are detailed in this report. Cats were subdivided into groups designated as idiopathic lipidosis if no other disease process was recognized, or secondary lipidosis if another disease process was diagnosed. Cats were also subdivided into groups designated as survivors or nonsurvivors on the basis of successful recuperation at 4 months after initial diagnosis. Differences between disease and survival groups were evaluated for significance. Overall, more female cats and middle-aged cats were affected. Presenting complaints of vomiting, anorexia, weakness, and weight loss were common. Physical assessment of most cats showed obvious hepatomegaly, jaundice, dehydration, and a weight loss > or = 25% of usual body weight. Neurobehavioral signs indicative of hepatic encephalopathy, other than ptyalism and depression, were rare. Clinicopathologic features are characterized by hyperbilirubinemia and increased activities of serum ALT, AST, and ALP, with only small if any increase in gamma GT activity. Clinical features distinguishing cats with hepatic lipidosis from those with other serious cholestatic disorders include absence of hyperglobulinemia and low gamma GT activity relative to ALP activity. Although coagulation tests were abnormal in 45% of cats tested (n = 44), few cats showed clinical bleeding tendencies. Most cats received prophylactic vitamin K1 therapy. Forty two cats received aggressive nutritional and supportive care and of these 55% survived. Cats with idiopathic disease were significantly younger, had significantly higher ALP activity and bilirubin concentration, and had a slightly better survival rate than cats with secondary lipidosis. Low PCV, hypokalemia, and an older age were significantly related to nonsurvival. Because of the variety of diets and food supplements used in case management, the influence of nutritional factors on survival could not be evaluated.
Hepatoportal microvascular dysplasia (MVD), a congenital disorder of the hepatic vasculature, is described in a kindred of Cairn Terrier dogs. Cairn Terrier dogs (n = 165) were evaluated using the serum bile acid test. Affected dogs, identified by abnormal fasting or postprandial serum bile acid concentrations, were divided into 2 groups. Group 1 dogs (n = 147) were used for pedigree analysis. Group 2 dogs (n = 18) were characterized on the basis of history, physical examination, clinicopathologic studies, diagnostic imaging of the liver and portal circulation, and hepatic histopathology. Group 2 contained control dogs (n = 2), dogs with hepatoportal MVD (n = 11), and dogs with macroscopic portosystemic vascular anomalies (PVSA) (n = 5). With the exception of high serum bile acid concentrations, dogs with hepatoportal MVD were indistinguishable from control dogs on the basis of history, physical examination, clinicopathologic findings, survey abdominal radiography, abdominal ultrasound, or transcolonic scintigraphy. Contrast portography in dogs with MVD revealed abnormalities of terminal twigs of the portal vasculature with out large intrahepatic or extrahepatic shunting vessels. Histopathologic abnormalities in dogs with hepatoportal MVD were similar to those reported for dogs with PSVA. Pedigree analysis suggested an autosomal inheritance for MVD. Dogs with MVD had high serum bile acid concentrations, abnormal indocyanine green clearance, and hepatic pathology suggestive of PSVA, but they lacked characteristic clinical findings of PSVA. The clinical significance of MVD is unclear. Dogs with MVD were clinically normal when evaluated but long-term follow-up is not yet available. Dogs with hepatoportal MVD should be identified at an early age to avoid confusion in future diagnostic evaluations.
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We describe 4 young male Doberman Pinschers (3 littermates and 1 unrelated dog) with a syndrome resembling idiopathic or noncirrhotic portal hypertension of humans. Each dog was evaluated for a hepatopathy resulting in portal hypertension, development of portosystemic collateral vessels, and hepatic encephalopathy. These dogs differ from previous reports of young dogs with hepatic insufficiency associated with portal hypertension and acquired portal systemic shunting by their lack of intrahepatic arteriovenous fistulae, portal vein atresia, or intrahepatic fibrosis. Clinicopathologic features included erythrocyte microcytosis, normal to mildly increased liver enzyme activities, increased concentrations of serum bile acids, reduced plasma indocyanine green clearance, and normal total bilirubin concentration. Abdominal ultrasonography disclosed a small liver and portosystemic collateral vessels. Radiographic imaging studies confirmed hepatofugal portal circulation and discounted hepatic arteriovenous fistulae. Histopathologic features in liver tissue from each dog were similar and consistent in all sections examined. Common findings included increased cross-sectional views of hepatic arterioles; hepatic lobular atrophy; scanty increase in connective tissue around some large portal triads; and absence of inflammation, disturbed lobular architecture, bile duct proliferation, or intrahepatic cholestasis.
The medical records of 11 cats with histopathologic findings consistent with central nervous system (CNS) Cuterebra larvae myiasis were retrospectively examined to determine if clinical features could identify this disorder antemortem. Young to middle-aged indoor-outdoor domestic shorthaired cats presenting with acute neurologic signs from July through September predominated. Many cats recently had clinical signs consistent with upper respiratory disease. Most cats presented for depression, lethargy, or seizures. Almost all cats had abnormal rectal temperatures, either hypethermia or hypothermia. Peripheral leukocytosis and eosinophilia were not characteristic of cats with CNS cuterebriasis. Cerebrospinal fluid analysis did not consistently disclose evidence of inflammation. Common neurologic deficits included blindness, abnormal mentation, and signs of unilateral prosencephalic disease. No specific clinical or clinicopathologic test was diagnostic for CNS cuterebriasis.
Urine bile acid (UBA) tests reflecting "average" serum bile acid (SBA) concentrations may have greater practical utility than paired SBA samples in cats. This study evaluated whether urine sulfated bile acids (USBAs), urine nousulfated bile acids (UNSBAs), or a combined approach had a clinical utility equivalent to SBAs. Routine serum biochemistry tests, SBA concentrations, and urine samples were collected from 54 cats with hepatobiliary disease, 17 cats with nonhepatic disorders, and 8 healthy cats. UBAs were measured by a quantitative enzymatic colorimetric method, and results were normalized with urine creatinine (UCr) concentrations. Significantly higher values occurred in cats with liver disease than in cats without liver disease for USBA : UCr, UNSBA:UCr, and (USBA and UNSBA) : UCr, P < .05 each. UBA tests with diagnostic performance (sensitivity [SS], specificity [SP], and positive and negative predictive values [PV+ and PV-]) equivalent to SBAs were the UNSBA : UCr and the combined test (SS: 87, 87 versus 85; SP: 88, 88 versus 88; PV+: 96, 96 versus 96; PV-: 68, 65 versus 68; UNSBA : UCr, [USBA, and UNSBA]: UCr versus SBA, respectively). Clinical applications of the UNSBA : UCr or the combined (USBA and UNSBA) : UCr test should be useful as convenient diagnostic tests for identifying cats with liver disease and high SEA concentrations.