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Abstract

Objective—To describe clinical signs, diagnostic findings, and outcome in dogs with idiopathic intrahepatic portal hypertension.

Design—Retrospective study.

Animals—33 dogs.

Procedure—Medical records of dogs with portal hypertension of intra-abdominal origin were reviewed. Dogs with intra-abdominal portal hypertension of vascular causes or with hepatic histopathologic changes consistent with severe diffuse hepatobiliary disease were excluded. History and results of physical examination, clinicopathologic tests, diagnostic imaging studies, histologic examination, and treatment were summarized. Outcome was determined in 26 dogs.

Results—Dogs were referred most often because of ascites, intermittent vomiting or diarrhea, and polydipsia of several months' duration. Microcytosis, high serum alkaline phosphatase and alanine transaminase activities, hepatic dysfunction, urine specific gravity ≤ 1.021, and abdominal transudate were the predominant clinicopathologic features. Microhepatia, abdominal effusion, and multiple anomalous venous anastomoses were the major findings of diagnostic imaging. Hepatic histopathologic changes were consistent with idiopathic noncirrhotic portal hypertension and were indistinguishable from those of dogs with surgically created portocaval anastomosis. Outcome was determined for 19 dogs released from hospital; 13 dogs remained healthy with mostly palliative treatment for periods of 5 months to 9 years.

Conclusions and Clinical Relevance—The clinical signs, clinicopathologic test results, portal pressure, and gross appearance of the liver of dogs with idiopathic noncirrhotic portal hypertension may be identical to those of dogs with cirrhosis; therefore liver biopsy is crucial. Because the prognosis for idiopathic noncirrhotic portal hypertension is generally favorable, owners of affected dogs should be discouraged from choosing euthanasia. (J Am Vet Med Assoc 2000; 218:392–399)

Full access
in Journal of the American Veterinary Medical Association
in Journal of the American Veterinary Medical Association

Objective

To determine whether microcytosis is a typical finding in Shibas.

Design

Prospective study.

Animals

18 Shibas.

Procedure

Blood and serum samples were obtained for automated hematologic analyses (18 dogs) and for determination of ferritin concentration, using ELISA (14 dogs). Blood samples from 30 clinically normal dogs of various other breeds was analyzed to establish a reference range for ferritin concentration.

Results

Erythrocyte mean corpuscular volume in Shibas ranged from 55.6 to 69.1 fl (mean ± SD, 61.2 ± 4.3 fl; median, 60.6 fl; reference range, 63 to 73 fl). Microcytosis was identified in 12 of 18 dogs. Males and females were affected equally. Mean corpuscular hemoglobin concentration was slightly low (range, 32.0 to 33.9%; reference range, 34 to 38%) in 6 dogs, 4 of which had microcytic RBC. Serum ferritin concentrations ranged from 61.2 to 277.0 ng/ml (mean ± SD, 110.6 ± 51.4 ng/ml; median, 106 ng/ml). Reference range for serum ferritin concentration was 50.7 to 440.0 ng/ml (mean ± SD, 121.2 ± 67.1 ng/ml; median, 111.5 ng/ml). Thrombocytopenia (range, 110,000 to 196,000 platelets; reference range, 200,000 to 450,000 platelets) was found in 7 dogs, 6 of which also had microcytic RBC.

Clinical Implications

Microcytosis can be a typical finding in Shibas. Common origin of Shibas and Akitas, a breed predisposed to microcytosis, suggests a hereditary basis for this finding. (J Am Vet Med Assoc 1998;212: 1258–1259)

Free access
in Journal of the American Veterinary Medical Association
in Journal of the American Veterinary Medical Association

SUMMARY

During earlier investigations of the hepatic effects in dogs of long-term administration of phenytoin alone or in combination with primidone, erythrocytic macrocytosis, neutropenia, neutrophilic hypersegmentation, and thrombocytopenia were observed. Such abnormalities were observed most often in dogs given phenytoin and resembled those known to be attributable to folate deficiency in human beings with epilepsy treated with phenytoin. To pursue the theory that these hematologic aberrations were caused by drug-induced folate deficiency, 12 dogs were given a diet specifically formulated to contain a minimally adequate concentration of folate. After 2 weeks, phenytoin was administered daily (400 mg, po, q 8 h) to 8 of the 12 dogs for 54 weeks. A cbc, bone marrow aspiration biopsy, and measurement of plasma and rbc folate concentrations were done every 3 weeks. Bone marrow aspirates were examined by transmission electron microscopy after 24 and 36 weeks, and at the end of the treatment period. Hepatic folate concentration was also determined in all dogs before and after treatment. Excretion of formiminoglutamic acid, as a marker of folate deficiency, was measured in all dogs at the end of the study.

All dogs remained healthy throughout the treatment phase. Consistent abnormalities were not observed in the blood or bone marrow of treated dogs. Plasma and RBC folate concentrations decreased in control and treated dogs as a result of dietary restriction (P < 0.02), and remained stable until the end of the study. The rbc folate content decreased further in treated dogs (P < 0.02), although the hepatic folate content was similar in control and treated dogs. Treated dogs did not excrete formiminoglutamic acid more rapidly than did control dogs. Gross necropsy or histologic abnormalities were not identified in control or treated dogs. We concluded that long-term administration of phenytoin was not associated with clinical, hematologic, or biochemical evidence of folate deficiency in dogs.

Free access
in American Journal of Veterinary Research

SUMMARY

Microcytosis is a common laboratory finding in dogs with congenital portosystemic shunt (pss), although its pathogenesis is not yet understood. Because the most common cause of microcytosis in dogs is absolute or relative iron deficiency, iron status was evaluated in 12 young dogs with pss. Complete blood counting was done before surgical correction in all dogs, and in 5 dogs after surgery, by use of an automated hematology analyzer. Serum iron concentration and total iron-binding capacity (tibc) were determined coulometrically, and percentage of transferrin saturation was calculated. Erythrocyte protoporphyrin content was quantified by use of front-face fluorometry. Serum ferritin concentration was measured by use of elisa. Serum ceruloplasmin content was determined colorimetrically (with p-phenylene-diamine dihydrochloride as substrate) as an indirect indicator of subclinical inflammation, which may result in impaired iron utilization. Special stains were applied to liver (10 dogs; Gomori's) and bone marrow aspiration biopsy (7 dogs; Prussian blue) specimens for qualitative assessment of tissue iron content. Nonpaired Student's t-tests were used to compare serum iron concentration, tibc, percentage of transferrin saturation, and erythrocyte protoporphyrin, ferritin, and ceruloplasmin concentrations in dogs with pss with those in clinically normal dogs. All dogs had microcytosis before surgery; microcytosis resolved in 3 dogs after surgical correction. Serum iron concentration and tibc were significantly lower in pss-affected dogs than in clinically normal dogs. Erythrocyte protoporphyrin, ferritin, and ceruloplasmin concentrations in pss-affected dogs were not significantly different from those in healthy dogs. Excess iron was not detected consistently in liver or bone marrow samples. These results suggest that relative iron deficiency, perhaps associated with altered iron transport and not absolute iron deficiency, is related to microcytosis in dogs with pss.

Free access
in American Journal of Veterinary Research
in Journal of the American Veterinary Medical Association

Summary

The medical records of 101 dogs with acute pancreatitis, diagnosed on the basis of medical histories of acute vomiting, with serum lipase or amylase activity greater than the reference range, or with gross signs of pancreatitis at surgery or histopathologic evidence at necropsy, were evaluated to identify potential risk factors for the development of acute pancreatitis.

Age, sex, and breed of dogs with acute pancreatitis were compared with those from a reference population of 100 dogs admitted for other medical emergencies during the same period. Analysis of multiple regression models indicated that dogs > 7 years old were at increased risk for acute pancreatitis. Spayed dogs and castrated male dogs had an increased risk, compared with that of sexually intact males. Similarly, terrier and nonsporting breeds appeared to be at higher risk of developing acute pancreatitis than were other breed types.

Most dogs in this study (63/101) had intercurrent diseases, including diabetes mellitus (n = 14), hyperadrenocorticism (n = 12), chronic renal failure (n = 8), neoplasia (n = 17), congestive heart failure (n = 6), and autoimmune disorders (n = 5). Fourteen dogs had undergone anesthesia or surgery in the week before admission; only 3 had undergone abdominal procedures.

Recent medication use was listed in 52 of 101 cases. Antibiotics (n = 18) and corticosteroids (n = 18) were most frequently described. Anticancer chemotherapeutic agents (n = 5) and organophosphate insecticides (n = 5) also were listed.

We conclude that increasing age and particular breed types are risk factors for pancreatitis in dogs, and that spayed females and castrated males are at increased risk, compared with that for sexually intact male dogs. Intercurrent diseases, drug treatment, anesthesia, and surgery are potential risk factors that require additional verification.

Free access
in Journal of the American Veterinary Medical Association