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- Author or Editor: Mark D. Chalkley x
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CASE DESCRIPTION A 6-year-old castrated male Australian Shepherd was evaluated because of a recent onset of persistent hypoglycemia.
CLINICAL FINDINGS Physical examination results were generally unremarkable. No abnormalities were detected on thoracic radiographs, and abdominal ultrasonography revealed no obvious pancreatic lesion. Hematologic analysis revealed hypoglycemia with a high serum insulin-to-glucose concentration ratio.
TREATMENT AND OUTCOME Insulinoma was suspected; medical treatment with prednisone was initiated, and exploratory laparotomy was performed. No pancreatic lesions or masses were observed. Partial left pancreatectomy and hepatic and local lymph node biopsies were performed. Histologic examination revealed islet cell hypertrophy and hyperplasia, with no evidence of neoplasia. Results of a PCR assay of the pancreatic tissue for Bartonella infection were negative. Clinical, biochemical, and histopathologic findings were compatible with nesidioblastosis. The clinical signs, including hypoglycemia, resolved after surgery. On follow-up examination 8 months later, the dog was apparently healthy and results of a CBC and serum biochemical analysis, including blood glucose concentration, were within respective reference ranges.
CLINICAL RELEVANCE To our knowledge, this is the first report of nesidioblastosis in a dog for which clinical signs and clinicopathologic abnormalities resolved after partial pancreatectomy. Although extremely rare, nesidioblastosis should be considered a differential diagnosis in dogs with signs suggestive of insulinoma.
CASE DESCRIPTION A 2-year-old 5.2-kg (11.4-lb) neutered male domestic shorthair cat was referred because of a 6-week history of progressive paraparesis.
CLINICAL FINDINGS Neurologic examination revealed moderate ambulatory paraparesis with marked spinal hyperesthesia at the thoracolumbar junction. The lesion was localized to the T3-L3 spinal cord segment. Clinicopathologic testing, thoracic radiography, and abdominal ultrasonography revealed no abnormalities to explain the observed clinical signs. Advanced spinal imaging with MRI revealed an extradural right-lateralized mass originating from the L2 vertebral pedicle and causing severe spinal cord compression.
TREATMENT AND OUTCOME Surgical decompression was achieved by performance of a right-sided hemilaminectomy at L2. Histologic examination of biopsy samples obtained from the mass revealed an ill-defined zone of mature vascular proliferation extending through the preexisting vertebral bone, consistent with vertebral angiomatosis. After surgical recovery, adjuvant radiation therapy was initiated with a total dose of 48 Gy administered in 16 fractions of 3 Gy each over a 3-week period. Neurologic function rapidly improved to full ambulation with only minimal monoparesis of the right pelvic limb. Results of neurologic and MRI examination performed 26 months after surgery indicated no change in neurologic status or evidence of recurrence.
CLINICAL RELEVANCE To the authors' knowledge, this report was the first to describe the long-term outcome for vertebral angiomatosis in a cat. Surgical decompression and radiation therapy provided an excellent outcome in this case. Vertebral angiomatosis should be considered as a differential diagnosis for any young cat with thoracolumbar myelopathy secondary to a mass associated with the vertebral pedicle.