A retrospective analysis of 85 dogs with hemangiosarcoma (HSA) that underwent complete necropsy, including gross examination of the brain, was conducted. Grossly identifiable intracranial lesions were present in 17 dogs. Twelve of 85 dogs (14.2%) had brain metastases. Four of 85 dogs (4.7%) had hemorrhagic lesions and/or ischemic necrosis without identifiable tumor. One dog had a primary central nervous system tumor. Signs of intracranial disease were present in six of 85 dogs (7.1%) with HSA; four had brain metastases and two had nonneoplastic lesions. Metastases had a propensity for cerebrum and gray matter. Dogs with brain metastases had more widely disseminated disease than dogs without brain metastases (P less than 0.001). Dogs with pulmonary metastases were at greater risk for developing brain metastases than dogs without pulmonary metastases (odds ratio = 8.31). Although thoracic radiography accurately identified ten of 12 dogs (83%) with pulmonary metastases, too few cases were available to assess the applicability/accuracy of thoracic radiography in predicting the presence or absence of brain metastases in dogs with malignancy and signs of intracranial disease.

Animals↗

PubMedDate not supplied

Intramedullary spinal cord metastasis in the dog.

Intramedullary spinal cord metastasis (ISCM) was diagnosed in three dogs with signs of myelopathy. The clinicopathologic features of ISCM in these and previously reported cases in the veterinary and human literature were compared. Myelopathic signs associated with ISCM may be the initial clinical manifestation of malignancy or may develop in the patient with known malignancy. Pain, a frequent manifestation of extradural compressive myelopathy, is not a consistent feature of ISCM. Survey spinal radiographs are usually unrewarding and cerebrospinal fluid (CSF) abnormalities nonspecific. Myelography is indicated to differentiate intramedullary lesions from more common extradural compressive lesions. Myelographic interpretation may be difficult, and intramedullary tumors must be differentiated from spinal cord edema or hemorrhage. Evidence of widely disseminated malignancy should increase suspicion for ISCM; hemangiosarcoma and lymphosarcoma should be considered the most likely histologic types. CSF cytology may be helpful in the diagnosis of patients with lymphosarcoma. Prognosis is poor due to the frequent presence of disseminated disease, although temporary response to corticosteroid therapy may be achieved. More aggressive therapeutic approaches, such as spinal irradiation and microsurgical resection of metastases, have been advocated in humans but have not been reported in the dog. Although it is an uncommon complication of systemic malignancy, ISCM should be considered in the differential diagnosis of myelopathy in the dog.

Animals↗

PubMedDate not supplied

Evaluation of serum and seminal plasma markers in the diagnosis of canine prostatic disorders.

Serum and seminal plasma concentrations or activities of acid phosphatase (AP), prostate specific antigen (PSA), and canine prostate specific esterase (CPSE) were measured in normal dogs, dogs with benign prostatic hyperplasia (BPH), dogs with bacterial prostatitis, and dogs with prostatic carcinoma to determine if these assays would be of value in differentiating dogs with prostatic carcinoma from normal dogs, and dogs with other prostatic disorders. In addition, tissue sections of prostatic adenocarcinomas were stained with antiprostatic AP, anti-CPSE, and anti-PSA antibodies to determine if these would be suitable immunohistochemical markers of prostatic carcinoma. Prostate-specific antigen was not detected in canine serum or seminal plasma. Serum and seminal AP activities did not differ significantly between normal dogs and those with prostatic diseases, or among dogs with different prostatic disorders. Serum CPSE activities were significantly higher in dogs with BPH than in normal dogs. Mean serum CPSE activities in dogs with BPH, bacterial prostatitis, and prostatic carcinoma were not significantly different from each other. Slight to moderate immunohistochemical staining of canine prostatic adenocarcinomas was noted for prostatic AP and PSA; most tumors did not stain for CPSE. These results show that proteins of prostatic origin appear in the serum of dogs as a result of prostatic pathology, especially BPH. Canine prostatic adenocarcinoma does not appear to be associated with significant increases in CPSE or AP activities, possibly because of down-regulation of these enzymes by prostatic carcinoma cells. It is also possible that failure to detect significant differences resulted from limited statistical power for some groups and pairwise analyses because of the small number of dogs evaluated.

Acid Phosphatase↗

PubMedDate not supplied

Idiopathic hypereosinophilic syndrome in 3 Rottweilers.

Three Rottweilers with marked peripheral eosinophilia and infiltration of the liver, spleen, lungs, and bone marrow with eosinophils were diagnosed with idiopathic hypereosinophilic syndrome (IHES). Mean serum immunoglobulin E concentrations were markedly high. On cytogenetic analysis, no evidence of karyotypic abnormalities was found in bone marrow aspirates. Despite an extensive search, no underlying cause for the eosinophilia could be identified. In this study, cytogenetic analysis and measurement of serum IgE concentrations were used to differentiate IHES and eosinophilic leukemia.

Animals↗

PubMedDate not supplied

The use of a synthetic prostaglandin E1 analog as a gastric protectant against aspirin-induced hemorrhage in the dog.

Misoprostol prevented gastric hemorrhage in dogs, each of which received aspirin (35 mg/kg body weight, orally q 8 hrs for 10 days). All dogs receiving aspirin alone had gastroscopic and histopathological lesions. No lesions were noted in four of five dogs given aspirin plus misoprostol (15 micrograms/kg body weight, q 8 hrs for five days; then 7.5 micrograms/kg body weight, q 8 hrs for five days). Four of 10 dogs receiving 15 micrograms/kg body weight of misoprostol developed diarrhea. The misoprostol dose was reduced to 7.5 micrograms/kg body weight, and the diarrhea subsided.

Alprostadil↗

PubMedDate not supplied

Carcinogenesis bioassay of acetamide, hexanamide, adipamide, urea and P-tolylurea in mice and rats.

As a part of the National Cancer Institute's effort to screen environmental and occupational chemicals for chronic toxicity and carcinogenicity, the amides acetamide, hexanamide, adipamide, urea, and p-tolylurea were fed to male and female C57B1/6 mice and Fischer 344 rats from 12 months. Rats received the following concentrations of compounds in their diets: acetamide, 2.36%; hexanamide, 1.5%; adipamide, 2.4% and 5.8%; urea, 0.45%, 0.9%, and 4.5%; and p-tolylurea, 0.2%. Mice received acetamide, 1.18% and 2.36%; hexanamide, 1.0% and 1.5%; adipamide, 1.6% and 2.4%; urea, 0.45%, 0.9%, and 4.5%; and p-tolylurea, 0.2%. In acetamide treated rats, there was a compound-related occurrence of neoplastic nodules (1/47 male, 3/48 female) and hepatocellular carcinomas (41/47 male, 33/48 female). The incidence, speed of onset and frequency of metastases, were greater in males than in females. In male mice treated with acetamide (low dose, 7/50; high dose, 7/46); hexanamide (low dose, 6/35; high dose, 6/39); and p-tolylurea (10/43), there was a compound-related increase in hematopoietic tumors, namely malignant lymphomas. Therefore, under the conditions of these studies, acetamide was an hepatocarcinogen in rats. In male mice, acetamide, hexanamide, and p-tolylurea caused malignant lymphomas. Urea and adipamide were considered to be non-carcinogenic.

Amides↗