Portosystemic Vascular Anomalies Research Articles

Results of clinical and hematological examination in dogs with congenital portosystemic shunts

The article presents the results of a clinical and hematological study of data obtained from dogs, mainly small ornamental breeds, with subsequently confirmed portosystemic shunts. As a result of the work, it was determined that all animals had a disorder of the nervous system, which was the reason for their owners to contact the veterinary clinic to examine the pets. Thus, according to the results of the analysis of the anamnesis and during the full-time clinical examination, tremor, ataxia, impaired consciousness, apathy, play movements, auto-aggression and causeless aggression or vocalization, mydriasis were observed in sick dogs. A laboratory blood test revealed a number of signs indicating the possible presence of portosystemic vascular anomalies in the examined dogs, namely, hypoproteinemia (48.4±3.094 g/l) with dysproteinemia, an increase in the activity of ALT, AST and alkaline phosphatase enzymes up to 188.2±85.573 IU/l, 121.5±20.061 IU/l and 514.6±110.851 IU/l, respectively. A pronounced increase in the concentration of bile acids in the blood before and after feeding was also noted, up to 82.5±16.57 µmol/l and 155.4±26.103 µmol/l, respectively. An analysis of the results of a morphological blood test showed the presence of such nonspecific changes as hypochromic anemia (hemoglobin concentration was 129.3 ± 5.631 g/l) and leukocytosis (the number of leukocytes in the blood of sick dogs was 17.7 ± 2.586*109 /l). Thus, we can conclude that the complex of clinical and laboratory studies carried out may be sufficient for the differential diagnosis of portosystemic vascular anomalies in dogs, but, nevertheless, the final diagnosis is possible only with the use of instrumental diagnostic methods.

Untargeted metabolomic profiling of serum from dogs with chronic hepatic disease

BackgroundChronic hepatopathies present a diagnostic challenge, with different diseases being associated with similar clinical and laboratory findings. Characterization of dogs with chronic hepatopathies can be difficult and require costly diagnostic procedures such as acquisition of a liver biopsy specimen. Noninvasive and inexpensive biomarkers that reliably characterize chronic hepatopathies such as chronic hepatitis or a congenital portosystemic vascular anomaly may decrease the need for costly or invasive diagnostic testing and guide novel therapeutic interventions.ObjectiveTo investigate differences in the serum metabolome among healthy dogs, dogs with congenital portosystemic shunts, and dogs with chronic hepatitis.AnimalsStored serum samples from 12 healthy dogs, 10 dogs with congenital portosystemic shunts, and 6 dogs with chronic hepatitis were analyzed.MethodsThe serum metabolome was analyzed with an untargeted metabolomics approach using gas chromatography–quadrupole time of flight mass spectrometry.ResultsPrincipal component analysis and heat dendrogram plots of the metabolomics data showed clustering among individuals in each group. Random forest analysis showed differences in the abundance of various metabolites including increased aromatic amino acids and xylitol in dogs with congenital portosystemic shunts. Based on the univariate statistics, 50 metabolites were significantly different among groups.Conclusions and Clinical ImportanceThe serum metabolome varies among healthy dogs, dogs with congenital portosystemic shunts, and dogs with chronic hepatitis. Statistical analysis identified several metabolites that differentiated healthy dogs from dogs with vascular or parenchymal liver disease. Further targeted assessment of these metabolites is needed to confirm their diagnostic reliability.

Avaliação ultrassonográfica da anomalia vascular portossistêmica em cão: relato de caso

Relata-se a avaliação ultrassonográfica, com auxílio do Doppler em cores, da anomalia vascular portossistêmica em um cão da raça Poodle Toy, que apresentou edema pulmonar e alterações gastrintestinais. Ao exame ultrassonográfico, foram observados vasos portais dilatados e tortuosos. Esses resultados associados aos achados clínicos e laboratoriais permitem identificar a anomalia vascular portossistêmica no paciente.

Effect of storage on microcytosis observed in dogs with portosystemic vascular anomalies

Microcytosis is a common laboratory finding in dogs with iron deficiency and congenital portosystemic vascular anomalies (PSVA), however artefactual changes due to blood storage may occur which could mask this feature. This study evaluated the effects of storage on microcytosis in dogs with congenital PSVA. Full haematological parameters were measured on the day of sampling and following 24 h storage at room temperature, in unaffected dogs ( n = 13) and in dogs affected with PSVA ( n = 24). Storage for 24 h resulted in significantly higher MCV values in both groups of dogs ( P < 0.01). The percentage increase in MCV was greater in the control dogs (median 8.07%, range 5.64–9.31%) compared to affected dogs (median 6.05%, range 3.12–15.21%) ( P < 0.02). Storage of 1 ml EDTA blood samples at ambient temperature for 24 h prior to analysis, as occurs when samples are posted to external laboratories, will have significant effects on MCV and may mask microcytosis in dogs with PSVA.

Evaluation of plasma protein C activity for detection of hepatobiliary disease and portosystemic shunting in dogs

To determine the diagnostic value of protein C (PC) for detecting hepatobiliary disease and portosystemic shunting (PSS) in dogs. Prospective study. 238 clinically ill dogs with (n = 207) and without (31) hepatobiliary disease, including 105 with and 102 without PSS. Enrollment required routine hematologic, serum biochemical, and urine tests; measurement of PC activity; and a definitive diagnosis. Total serum bile acids (TSBA) concentration and coagulation status, including antithrombin activity, were determined in most dogs. Dogs were grouped into hepatobiliary and PSS categories. Specificity and sensitivity were calculated by use of a PC cutoff value of 70% activity. Specificity for PC activity and TSBA concentrations was similar (76% and 78%, respectively). Best overall sensitivity was detected with TSBA, but PC activity had high sensitivity for detecting PSS and hepatic failure. Protein C activity in microvascular dysplasia (MVD; PC > or = 70% in 95% of dogs) helped differentiate MVD from portosystemic vascular anomalies (PSVA; PC < 70% in 88% of dogs). A receiver operating characteristic curve (PSVA vs MVD) validated a useful cutoff value of < 70% activity for PC. Combining PC with routine tests improved recognition of PSS, hepatic failure, and severe hepatobiliary disease and signified a grave prognosis when coupled with hyperbilirubinemia and low antithrombin activity in hepatic failure. Protein C activity can help prioritize tests used to distinguish PSVA from MVD and sensitively reflects improved hepatic-portal perfusion after PSVA ligation.

Vacuolar hepatopathy in dogs: 336 cases (1993–2005)

To determine disorders associated with vacuolar hepatopathy (VH), morphologic hepatic and clinicopathologic abnormalities, and affiliation with steroidogenic hormone excess in dogs. Retrospective case series. Animals-336 dogs with histologically confirmed moderate or severe VH. Information on signalment, results of diagnostic testing, definitive diagnoses, and exposure to glucocorticoids (ie, exogenous glucocorticoid administration or high endogenous concentrations of steroidogenic hormones) was obtained from medical records. Dogs were grouped by underlying disorder, glucocorticoid exposure, acinar zonal distribution of lesions, and histologic severity. 12 disease groups (neoplastic, acquired hepatobiliary, neurologic, immune-mediated, gastrointestinal tract, renal, infectious, cardiac disease, diabetes mellitus, portosystemic vascular anomaly, adrenal gland dysfunction, and miscellaneous disorders) were identified. There were 186 (55%) dogs with and 150 (45%) dogs without evidence of glucocorticoid exposure. Acinar zonal distribution of hepatic vacuolation and clinicopathologic values did not differ between dogs with and without evidence of glucocorticoid exposure. However, a 3-fold increased likelihood of severe VH was associated with steroidogenic hormone exposure. Of 226 dogs with high serum alkaline phosphatase activity, 102 (45%) had no evidence of glucocorticoid exposure. Results suggest that neoplasia and congenital or acquired hepatobiliary disease are common in dogs with VH and provide support for the suggestion that VH, high alkaline phosphatase activity, and illness-invoked physiologic stress may be associated. Histologic confirmation of VH should initiate a diagnostic search for a primary disease if glucocorticoid treatment and hyperadrenocorticism are ruled out.

Association ofHelicobacterwith Cholangiohepatitis in Cats

Infection withHelicobacterspp. is increasingly linked with hepatobiliary inflammation and neoplasia in people and in a variety of animals. We sought to determine ifHelicobacterspecies infection is associated with Cholangiohepatitis in cats. Deoxyribonucleic acid was extracted from tissue blocks from cats with Cholangiohepatitis (32), noninflammatory liver disease (13), and cats with normal liver histology (4). Deoxyribonucleic acid was polymerase chain reaction‐amplified with 2 sets ofHelicobactergenus‐specific primers, gel purified, and sequenced. Polymerase chain reaction‐positive hepatic tissue was further examined with Steiner's stain, immunocytochemistry forHelicobacterspecies, and eubacterial fluorescent in situ hybridization. Gastric tissues of cats with knownHelicobacterinfection status served as controls for deoxyribonucleic acid extraction and sequence comparison.Helicobacterspecies were detected in 2/32 cats with Cholangiohepatitis, and 1/17 controls. Sequences had 100% identity withHelicobacterspecies liver,Helicobacter pylori, andHelicobacter fenelliaelcinaediiin a cat with suppurative cholangitis,Helicobacterspecies liver,Helicobacter pylori, andHelicobacter nemistrineaein a cat with mild lymphocytic portal hepatitis, andHelicobacter billsin a cat with portosystemic vascular anomaly. In contrast, sequences from gastric biopsies showed highest homology (99–100%) to“Helicobacter heilmannii,” Helicobacter bizzozeronii, Helicobacter felis, andHelicobacter salomonis.Fluorescent in situ hybridization revealed a semicurved bacterium, withHelicobacter‐like morphology, in an intrahepatic bile duct of the cat with suppurative cholangitis. This study has identifiedHelicobacterdeoxyribonucleic acid in 2/32 cats with Cholangiohepatitis and 1/13 cats with noninflammatory liver disease. Deoxyribonucleic acid sequences of hepaticHelicobacterspecies were distinct from those found in the stomach and are broadly consistent with those identified in cat intestine and bile, and hepatobiliary disease in people and rodents.

Association of Helicobacter with Cholangiohepatitis in Cats

Infection with Helicobacter spp. is increasingly linked with hepatobiliary inflammation and neoplasia in people and in a variety of animals. We sought to determine if Helicobacter species infection is associated with cholangiohepatitis in cats. Deoxyribonucleic acid was extracted from tissue blocks from cats with cholangiohepatitis (32), noninflammatory liver disease (13), and cats with normal liver histology (4). Deoxyribonucleic acid was polymerase chain reaction-amplified with 2 sets of Helicobacter genus-specific primers, gel purified, and sequenced. Polymerase chain reaction-positive hepatic tissue was further examined with Steiner's stain, immunocytochemistry for Helicobacter species, and eubacterial fluorescent in situ hybridization. Gastric tissues of cats with known Helicobacter infection status served as controls for deoxyribonucleic acid extraction and sequence comparison. Helicobacter species were detected in 2/32 cats with cholangiohepatitis, and 1/17 controls. Sequences had 100% identity with Helicobacter species liver, Helicobacter pylori, and Helicobacter fenelliae/cinaedii in a cat with suppurative cholangitis, Helicobacter species liver, Helicobacter pylori, and Helicobacter nemistrineae in a cat with mild lymphocytic portal hepatitis, and Helicobacter bilis in a cat with portosystemic vascular anomaly. In contrast, sequences from gastric biopsies showed highest homology (99-100%) to "Helicobacter heilmannii," Helicobacter bizzozeronii, Helicobacter felis, and Helicobacter salomonis. Fluorescent in situ hybridization revealed a semicurved bacterium, with Helicobacter-like morphology, in an intrahepatic bile duct of the cat with suppurative cholangitis. This study has identified Helicobacter deoxyribonucleic acid in 2/32 cats with cholangiohepatitis and 1/13 cats with noninflammatory liver disease. Deoxyribonucleic acid sequences of hepatic Helicobacter species were distinct from those found in the stomach and are broadly consistent with those identified in cat intestine and bile, and hepatobiliary disease in people and rodents.

INTRAHEPATIC PORTOSYSTEMIC VENOUS SHUNT IN A NEONATAL ROAN ANTELOPE (HIPPOTRAGUS EQUINUS COTTONI)

A 6-day-old, female roan antelope (Hippotragus equinus cottoni) was diagnosed with a single intrahepatic portosystemic venous shunt at necropsy. Clinical signs had included weakness, lethargy, hypothermia, diarrhea, and a weak suckle response. Multiple seizure episodes were associated with hypoglycemia and characterized by vocalization, muscle fasciculations, and disorientation. Hematologic abnormalities included anemia with hypochromasia, anisocytosis, poikilocytosis, and leukopenia with neutropenia and lymphopenia. Serum biochemical abnormalities included elevations in blood urea nitrogen and total serum bile acid concentration. A portosystemic vascular anomaly should be a differential diagnosis for nonthriving, exotic ruminant calves with overt or subtle neurologic signs, persistent hypoglycemia, and/or elevated bile acids. In very young calves, total bile acid concentration may be more useful in establishing a diagnosis than blood ammonia concentration.

Metabolomics as a diagnostic tool for hepatology: validation in a naturally occurring canine model

Human hepatopathies are a diagnostic challenge, with many distinct diseases having similar clinical signs and laboratory findings. Naturally occurring canine hepatic disease provides an excellent model for human diseases and similar diagnostic dilemmas exist; differentiating canine congenital portosystemic vascular anomalies (PVA) from acquired hepatopathies is difficult and traditionally requires invasive diagnostic procedures. The emerging post-genomic science of metabolomics is concerned with detecting global changes of populations of endogenous low molecular weight metabolites in biological samples and offers the possibility of identifying surrogate profiles of disease. Metabolomics couples sensitive metabolite analysis with sophisticated pattern recognition techniques. In this study, a metabolomic strategy has been employed to assess metabolite changes in the plasma of dogs with congenital PVA and acquired hepatic disease. Plasma samples were collected from 25 dogs, comprising 9 dogs with congenital PVA, 6 with acquired hepatopathy and 10 with non-hepatic disorders. Low molecular weight metabolites were analyzed by liquid chromatography-mass spectrometry (LC-MS). Following identification of metabolites, multivariate data analysis was used to compare profiles amongst groups. The analysis demonstrated significant disturbances in the plasma bile acid and phospholipid profiles of dogs with portovascular anomalies. In contrast to traditional laboratory parameters, the metabolomic strategy was able to produce a clear segregation between all three study groups. In conclusion, this study demonstrates the potential of metabolomics as a diagnostic tool for naturally occurring hepatic disease. With further validation, this approach will improve diagnostic capabilities, provide an insight into pathogenetic mechanisms, and ultimately inform therapeutic decision making in clinical hepatology.

Effect of breed on anatomy of portosystemic shunts resulting from congenital diseases in dogs and cats: a review of 242 cases

To evaluate the effect of species and breed on the anatomy of portosystemic vascular anomalies in dogs and cats. Retrospective study of 233 dogs and nine cats presenting to the University Veterinary Centre, Sydney. Case records were evaluated for breed, sex, age, anatomical and histological diagnosis. Cases were included when a portosystemic vascular anomaly resulted from a congenital or developmental abnormality of the liver or portal venous system. Disease conditions included single congenital portosystemic shunt with patent portal vasculature (214 dogs, nine cats), portal vein aplasia (nine dogs), multiple acquired shunts resulting from portal vein hypoplasia (seven dogs), biliary atresia (one dog) and microvascular dysplasia (one dog). One Maltese had a single, congenital shunt and multiple acquired shunts resulting from hepatic cirrhosis. Breeds that were significantly over-represented included the Maltese, Silky Terrier, Australian Cattle Dog, Bichon Frise, Shih Tzu, Miniature Schnauzer, Border Collie, Jack Russell Terrier, Irish Wolfhound and Himalayan cat. Bichon Frise with shunts were significantly more likely to be female than male (12:2, P < 0.001). Two hundred and fourteen dogs (91.4%), and all cats, had shunts that were amenable to attenuation. Inoperable shunts occurred in 19 dogs (8.2%). Fifty six of 61 (92%) operable shunts in large breed dogs were intrahepatic, versus 10/153 (7%) in small breeds (P < 0.0001). Breeds that were not predisposed to portosystemic shunts were significantly more likely to have unusual or inoperable shunts than dogs from predisposed breeds (29% versus 7.6%, P < 0.0001). No significant relationship between breed and shunt type could be determined in cats. Breed has a significant influence on shunt anatomy in dogs. Animals presenting with signs of portosystemic shunting may suffer from a wide range of operable or inoperable conditions. Veterinarians should be aware that unusual or inoperable shunts are much more likely to occur in breeds that are not predisposed to congenital portosystemic shunts.

Liver glutathione concentrations in dogs and cats with naturally occurring liver disease.

To determine total glutathione (GSH) and glutathione disulfide (GSSG) concentrations in liver tissues from dogs and cats with spontaneous liver disease. Liver biopsy specimens from 63 dogs and 20 cats with liver disease and 12 healthy dogs and 15 healthy cats. GSH was measured by use of an enzymatic method; GSSG was measured after 2-vinylpyridine extraction of reduced GSH. Concentrations were expressed by use of wet liver weight and concentration of tissue protein and DNA. Disorders included necroinflammatory liver diseases (24 dogs, 10 cats), extrahepatic bile duct obstruction (8 dogs, 3 cats), vacuolar hepatopathy (16 dogs), hepatic lipidosis (4 cats), portosystemic vascular anomalies (15 dogs), and hepatic lymphosarcoma (3 cats). Significantly higher liver GSH and protein concentrations and a lower tissue DNA concentration and ratio of reduced GSH-to-GSSG were found in healthy cats, compared with healthy dogs. Of 63 dogs and 20 cats with liver disease, 22 and 14 had low liver concentrations of GSH (micromol) per gram of tissue; 10 and 10 had low liver concentrations of GSH (nmol) per milligram of tissue protein; and 26 and 18 had low liver concentrations of GSH (nmol) per microgram of tissue DNA, respectively. Low liver tissue concentrations of GSH were found in cats with necroinflammatory liver disease and hepatic lipidosis. Low liver concentrations of GSH per microgram of tissue DNA were found in dogs with necroinflammatory liver disease and cats with necroinflammatory liver disease, extrahepatic bile duct occlusion, and hepatic lipidosis. Low GSH values are common in necroinflammatory liver disorders, extrahepatic bile duct occlusion, and feline hepatic lipidosis. Cats may have higher risk than dogs for low liver GSH concentrations.

Postprandial Venous Ammonia Concentrations in the Diagnosis of Hepatobiliary Disease in Dogs

A postprandial ammonia tolerance test (PPATT) was performed on normal dogs and dogs with signs that suggested they may have liver disease. All dogs underwent transcolonic scintigraphy, liver biopsy, or both and were assigned to extrahepatic disease, primary hepatocellular, and congenital portosystemic vascular anomalies (PSVA) groups. Each dog was fed a chicken and rice diet providing 25% of its estimated daily metabolizable energy requirement (MER) as an ammonia challenge. This is practical in patients with liver disease because ammonium chloride administration often causes vomiting or ammonia toxicity. Venous ammonia concentrations were measured before feeding and every 2 hours after feeding for 8 hours. No difference in mean ammonia concentrations between dogs with extrahepatic disease and control dogs was found. Therefore, the specificity of the PPATT was 100%. Dogs with hepatocellular disease showed no change in mean ammonia concentration at any time point, before or after feeding, but sensitivity was greatest when venous ammonia was measured 6 hours after feeding (sensitivity before feeding, 28%, and after feeding, 36%). Among dogs with congenital PSVA, mean ammonia concentrations were higher than the reference range at all time points before and after feeding, and peak mean ammonia concentration occurred 6 hours after feeding. In this group, the sensitivity of the PPATT was 81% before feeding and 91% 6 hours after feeding. This study demonstrates that the measurement of venous ammonia concentration is a useful test to detect congenital PSVA, and the sensitivity of the test may be improved by sampling 6 hours after feeding. The PPATT has poor sensitivity in detecting primary hepatocellular disease.

Glomerular Filtration Rate and Renal Volume in Dogs with Congenital Portosystemic Vascular Anomalies before and after Surgical Ligation

Glomerular filtration rate (GFR) and renal volume were evaluated in dogs with confirmed portosystemic vascular anomalies (PSVA) before and after surgical ligation of their PSVA. Pre‐ and postligation CBC, serum biochemistry, urinalysis, abdominal ultraso‐nography with measurement of renal volume, and per rectal scintigraphy were performed to document resolution of abnormalities consistent with portosystemic shunting. GFR was estimated by plasma99mTc‐diethylenetriaminepentaacetic acid (99mTc‐DTPA) clearance before (n = 21) and after (n = 12) surgical correction of PSVA. Preligation99mTc‐DTPA GFR was increased (median, 5.64 mL/minute/kg; range, 3.53–8.49 mL/minute/kg; reference range, 2.83–4.47 mL/minute/kg) in 81% (17/21) of dogs. Postligation99mTc‐DTPA GFR decreased in all 12 evaluated dogs (median change =—42%;P&lt; .001). Preligation renal volume was above the reference range for the left and right kidneys in 71% (10/14) and 69% (11/16) of dogs evaluated, respectively. Right renal volume decreased significantly (n = 5; median change, —45%;P= .03) after surgical ligation of PSVA. These findings document increased GFR and renal volume in dogs with PSVA, which may explain in part the low blood urea nitrogen and serum creatinine concentrations encountered in these dogs. Knowledge of changes in GFR associated with PSVA ligation may prove helpful in the anesthetic, drug, and dietary management of affected dogs.

Glomerular filtration rate and renal volume in dogs with congenital portosystemic vascular anomalies before and after surgical ligation.

Glomerular filtration rate (GFR) and renal volume were evaluated in dogs with confirmed portosystemic vascular anomalies (PSVA) before and after surgical ligation of their PSVA. Pre- and postligation CBC, serum biochemistry, urinalysis, abdominal ultrasonography with measurement of renal volume, and per rectal scintigraphy were performed to document resolution of abnormalities consistent with portosystemic shunting. GFR was estimated by plasma 99mTc-diethylenetriaminepentaacetic acid (99mTc-DTPA) clearance before (n = 21) and after (n = 12) surgical correction of PSVA. Preligation 99mTc-DTPA GFR was increased (median, 5.64 mL/minute/kg; range, 3.53-8.49 mL/minute/kg; reference range, 2.83-4.47 mL/minute/kg) in 81% (17/21) of dogs. Postligation 99mTc-DTPA GFR decreased in all 12 evaluated dogs (median change = -42%; P < .001). Preligation renal volume was above the reference range for the left and right kidneys in 71% (10/14) and 69% (11/16) of dogs evaluated, respectively. Right renal volume decreased significantly (n = 5; median change, -45%; P = .03) after surgical ligation of PSVA. These findings document increased GFR and renal volume in dogs with PSVA, which may explain in part the low blood urea nitrogen and serum creatinine concentrations encountered in these dogs. Knowledge of changes in GFR associated with PSVA ligation may prove helpful in the anesthetic, drug, and dietary management of affected dogs.

Iron status and erythrocyte volume in dogs with congenital portosystemic vascular anomalies.

Microcytosis, hypochromasia, and low mean corpuscular hemoglobin are frequent hematologic abnormalities in dogs with portosystemic vascular anomalies (PSVA). The relationship of iron status to these abnormalities is unclear. We evaluated iron status and hematologic and biochemical parameters in dogs with congenital PSVA before (25 dogs) and after (11 dogs) partial ligation of the vascular anomaly. Serum iron concentration and total iron binding capacity were subnormal in 56% and 20% of dogs with PSVA, respectively. Transferrin saturation was normal in 68%, decreased in 20%, and increased in 12% of the dogs. Plasma ferritin concentration was either normal (56%) or high (44%), and was not associated with increases in ceruloplasmin concentration. Hepatic stainable iron was increased in 10 of 16 dogs. Mean corpuscular volume (MCV), mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration were decreased in more than 60% of dogs with PSVA. Serum biochemical abnormalities included high bile acid concentration and alanine transaminase (ALT) and alkaline phosphatase (ALP) activities; and low urea, creatinine, cholesterol, and total protein concentrations. Serum iron concentration and clinical status (normal or PSVA) significantly influenced MCV (P = .003 and P < .001, respectively), whereas age, ceruloplasmin, ferritin, cholesterol, bile acids, and total iron binding capacity did not. Partial ligation of PSVA was associated with resolution of clinical signs and the return to normal of iron status and all clinicopathologic abnormalities, except total fasting bile acid concentrations. These findings indicate that iron status is frequently abnormal in dogs with PSVA and that low serum iron concentration appears to be related to the development of microcytosis. The normalization of iron status and clinicopathologic abnormalities after treatment suggests that they are direct consequences of PSVA.

Characterization of hepatoportal microvascular dysplasia in a kindred of cairn terriers.

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.

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

Summary 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 (postprandial 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 γ- 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 μmol/L for fsba concentration and of 20 μmol/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 neoplasia; and determination of aspartate aminotransferase activity had the highest sensitivity for cats with hepatic necrosis. For all cats with hepatobiliary disease, determination of psba concentration had the highest sensitivity of any single test. Combination testing using results of measuring total serum bile acid concentrations in conjunction with results of measuring serum enzyme activity or total bilirubin concentration gave the best overall test performance. Results indicate that both the fsba and psba concentration should be determined, but that if paired samples cannot be collected, the psba concentration should be preferentially measured. In a small number of cats (6/108), the fsba concentration exceeded the psba concentration.

Hematologic changes associated with serum and hepatic iron alterations in dogs with congenital portosystemic vascular anomalies.

Serum and hepatic iron determinations and hematologic parameters were measured in 10 dogs with congenital portosystemic vascular anomalies. Anemia, hypoferremia, and microcytosis were present in 70%, 70%, and 60% of the dogs, respectively. An increase in hepatic iron content was observed in all dogs. These results suggest a relationship between altered hepatic blood flow and abnormal iron metabolism in dogs with congenital portosystemic vascular anomalies.

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

Summary The diagnostic efficacy of serum alkaline phosphatase (alp) and γ-glutamy I transferase (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. In most dogs with hepatobiliary disease, the magnitude of variation (measured value/highest normal value) for alp was greater than that for ggt. The sensitivity of alp exceeded that of ggt in all groups but the passive congestion group. The high sensitivity of alp increased the sensitivity of testing in parallel, compared with the sensitivity of testing in series. The positive predictive value (+ pv) was greater for ggt than for alp in all groups except dogs with portosytemic vascular anomaly. The + pv of testing in series was greater than the + pv associated with single tests or testing in parallel in all groups except dogs with passive congestion and with portosystemic vascular anomaly. Single tests or testing in parallel provided a greater negative predictive value (− pv) than did testing in series in most groups, although the differences were small in individual groups. The exception was the steroid hepatopathy group, in which testing in series provided the greatest − pv. The poor specificity of serum alp activity in the detection of hepatobiliary disease in dogs was confirmed by our data. Serum ggt activity was less influenced by nonhepatic disease processes or enzymeinducing drugs, compared with serum alp activity. The diagnostic value of alp and ggt was greater when tests were evaluated in series.