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- Author or Editor: Gordon A. Andrews x
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Abstract
Objectives
To describe expression of the neuroendocrine marker chromogranin A (CgA) in canine and feline pancreatic islet cell tumors and their metastases, and to evaluate plasma CgA concentration in dogs and cats with insulinoma.
Sample Population
Paraffin-embedded tissues from 25 canine and 2 feline pancreatic islet cell tumors, 5 canine and 6 feline exocrine pancreatic tumors, and normal pancreatic tissue from 2 dogs and 2 cats. Heparinized plasma samples from 3 dogs and 2 cats diagnosed with insulinoma, and 10 control plasma samples from each species.
Procedure
Immunohistochemical analysis was performed on the 42 tissue specimens, using antisera against CgA, neuron-specific enolase, insulin, somatostatin, glucagon, and pancreatic polypeptide. The 25 plasma samples were evaluated, using a soluble-phase, double-antibody, equilibrium radioimmunoassay directed against the amino- and carboxy-terminal peptides of bovine CgA.
Results
Chromogranin A expression was found in 76% of canine and 2 of 2 feline pancreatic islet cell tumors. Of 7 animals with CgA immunoreactivity in primary tumors, 6 also had CgA immunostaining of metastatic lesions. Plasma CgA concentration in 2 dogs with insulinoma (0.9, 1.0 ng/ml) exceeded the reference range established for 10 clinically normal control dogs (0.50 ± 0.16 ng/ml). Feline plasma CgA samples had extensive nonspecific background immunoreactivity.
Conclusions
Chromogranin A is a useful immunohistochemical marker for pancreatic tumors of neuroendocrine origin and their metastases. Plasma CgA concentration determined by radioimmunoassay was high in 2 dogs with insulinoma.
Clinical Relevance
Immunohistochemical staining of tissues or cytologic specimens for CgA and/or neuron-specific enolase may help distinguish masses of unknown origin as neuroendocrine in nature. Increase in plasma CgA concentration may be useful diagnostically for animals with suspected neuroendocrine tumors. (Am J Vet Res1997;58:615–620)
Abstract
Objective—To determine signalment, history, clinical findings, results of autonomic function testing and other antemortem diagnostic tests, and pathologic findings in dogs with dysautonomia.
Design—Retrospective study.
Animals—65 dogs with dysautonomia.
Procedure—Case records of 68 dogs with a diagnosis of dysautonomia were reviewed; inclusion criteria included histologic confirmation of dysautonomia or clinical signs and results of pharmacologic testing consistent with dysautonomia.
Results—65 dogs fulfilled all criteria for dysautonomia. Dogs from rural environments were overrepresented, and cases of dysautonomia were reported for every month, although the highest number of cases was reported in February and March. Vomiting was the most common clinical sign, followed by diarrhea, signs of anorexia and depression, weight loss, and dysuria. The most common physical examination finding was decreased or absent anal tone, followed by absent pupillary light reflexes and elevated nictitating membrane. Results of pharmacologic te sting were consistent with dysautonomia, although no single test was 100% sensitive. Histologic lesions consistent with dysautonomia were found in the autonomic ganglia, brainstem nuclei, and ventral horns of the spinal cord.
Conclusions and Clinical Relevance—Dysautonomia is an endemic disease in Kansas, and a high index of suspicion of the disease can be made by combining clinical signs, physical examination findings, and results of pharmacologic testing. (J Am Vet Med Assoc 2002;220:633–639)
Summary
A murine IgM monoclonal antibody, which recognizes dog erythrocyte antigen (dea) 1.1, has been produced. The antibody correctly identified canine rbc possessing dea 1.1 in a panel of rbc typed by an independent laboratory. Reactivity of the monoclonal antibody was compared with canine anti-dea 1.1 antiserum with 163 rbc samples from 145 dogs. Results of agglutination tests with the 2 reagents were in agreement for all samples. A card agglutination test that uses the monoclonal antibody with blood is described. A monoclonal antibody-based test should facilitate blood typing for dea 1.1 in clinical practice.
Abstract
Case Description—An approximately 5-year-old sexually intact male alpaca was evaluated because of a right-sided maxillary mass that had recurred after previous surgical debulking.
Clinical Findings—Clinical, radiographic, and CT examination revealed an approximately 1.5-cm-diameter soft tissue mass associated with expansile osteolysis of the maxillary alveolar bone, beginning at the level of the right maxillary third premolar tooth extending caudally to the level of the rostral roots of the second molar tooth.
Treatment and Outcome—Right partial maxillectomy was performed, and histologic examination revealed an incompletely excised fibrosarcoma with osseous metaplasia. External beam radiation therapy to the tumor bed was initiated 1 month after surgery. Computerized planning was performed, and a total radiation dose of 48 Gy was prescribed in eleven 4.4-Gy fractions. Follow-up CT evaluations 6 and 58 weeks after radiation therapy was completed revealed no evidence of tumor recurrence. No clinical evidence of tumor recurrence was detected through 110 weeks after radiation therapy.
Clinical Relevance—The oral fibrosarcoma in the alpaca described here was successfully treated with surgical excision and adjuvant radiation therapy, resulting in excellent quality of life of the treated animal.
Abstract
Objective—To evaluate the use of serum biomarkers of cartilage and bone metabolism to predict the occurrence and severity of osteochondrosis (OC) lesions in the distal portion of the femur in growing swine.
Animals—71 gilts.
Procedures—At an abattoir, serum samples for analysis of 10 biomarkers indicative of cartilage and bone metabolism were obtained prior to processing of the pigs. The distal portion of each pig's left femur was directly examined and cut into longitudinal sections to evaluate the number and severity of abnormalities on the external surface, articular cartilage, and growth plate. Each specimen was categorized as with (n = 56) or without (15) OC, and an overall OC severity score was assigned to affected pigs. Logistic and linear regression analyses were performed to predict odds of OC on the basis of biomarker concentrations and predict the severity of OC values in affected pigs, respectively.
Results—Compared with values in unaffected pigs, serum concentrations of C-propeptide of type II collagen (CPII) and cartilage oligomeric matrix protein were significantly increased and concentrations of carboxy-terminal telopeptide of type II collagen 3/4-length fragment (C2C) and pyridinoline cross-links were significantly decreased in affected pigs. A 2-fold increase in CPII concentration increased the odds of pigs having OC by a factor of 97 (95% confidence interval, 6 to infinity). Changes in serum C2C concentration accounted for 49% of the variation in overall OC severity score.
Conclusions and Clinical Relevance—Assessment of serum biomarker concentrations may be useful in the diagnosis of OC and aid in reduction of lameness in swine herds.
Abstract
Objective—To determine hepatotoxicity of stanozolol in cats and to identify clinicopathologic and histopathologic abnormalities in cats with stanozololinduced hepatotoxicosis.
Design—Clinical trial and case series.
Animals—12 healthy cats, 6 cats with chronic renal failure, and 3 cats with gingivitis and stomatitis.
Procedures—Healthy cats and cats with renal failure were treated with stanozolol (25 mg, IM, on the first day, then 2 mg, PO, q 12 h) for 4 weeks. Cats with gingivitis were treated with stanozolol at a dosage of 1 mg, PO, every 24 hours.
Results—Most healthy cats and cats with renal failure developed marked inappetence, groomed less, and were less active within 7 to 10 days after initiation of stanozolol administration. Serum alanine transaminase (ALT) activity was significantly increased in 14 of 18 cats after stanozolol administration, but serum alkaline phosphatase activity was mildly increased in only 3. Four cats with serum ALT activity > 1,000 U/L after only 2 weeks of stanozolol administration had coagulopathies; administration of vitamin K resolved the coagulopathy in 3 of the 4 within 48 hours. All 18 cats survived, and hepatic enzyme activities were normal in all cats tested more than 4 weeks after stanozolol administration was discontinued. Two of the 3 cats with gingivitis developed evidence of severe hepatic failure 2 to 3 months after initiation of stanozolol treatment; both cats developed coagulopathies. Histologic evaluation of hepatic biopsy specimens from 5 cats revealed diffuse hepatic lipidosis and cholestasis without evidence of hepatocellular necrosis.
Conclusions and Clinical Relevance—Results suggest that stanozolol is hepatotoxic in cats. (J Am Vet Med Assoc 2000;217:681–684)
