Case Description—A 4-year-old sexually intact male mixed-breed dog was evaluated because of clinical signs of acute-onset pelvic limb ataxia, rapidly progressing to paraplegia with severe spinal hyperesthesia.
Clinical Findings—General physical examination revealed pyrexia, tachycardia, and tachypnea. Neurologic examination demonstrated severe spinal hyperesthesia and paraplegia with decreased nociception. Magnetic resonance imaging revealed extradural spinal cord compression at T13-L1 and hyperintense lesions on T1- and T2-weighted images in the epaxial musculature and epidural space.
Treatment and Outcome—Decompressive surgery, consisting of a continuous dorsal laminectomy, with copious lavage of the vertebral canal was performed. Cultures of blood, urine, and surgical site samples were negative. Histologic examination results for samples obtained during surgery demonstrated suppurative myositis and steatitis. These findings confirmed a diagnosis of sterile idiopathic inflammation of the epidural fat and epaxial muscles with spinal cord compression. The dog's neurologic status started to improve 1 week after surgery. After surgery, the dog received supportive care including antimicrobials and NSAIDs. The dog was ambulatory 1 month after surgery and was fully ambulatory despite signs of mild bilateral pelvic limb ataxia 3 years after surgery.
Clinical Relevance—Although idiopathic sterile inflammation of adipose tissue, referred to as panniculitis, more commonly affects subcutaneous tissue, its presence in the vertebral canal is rare. Specific MRI findings described in this report may help in reaching a presumptive diagnosis of this neurologic disorder. A definitive diagnosis and successful long-term outcome in affected patients can be achieved by decompressive surgery and histologic examination of surgical biopsy samples.
Objective—To evaluate the impact of modulation of the membrane-bound efflux pump P-glycoprotein (P-gp) on plasma concentrations of orally administered prednisolone in dogs.
Animals—7 healthy adult Beagles.
Procedures—Each dog received 3 treatments (control [no treatment], rifampicin [100 mg/d, PO, for 21 days, as an inducer of P-gp], and ketoconazole [100 mg/d, PO, for 21 days, as an inhibitor of P-gp]). A single dose of prednisolone (1 mg/kg, PO) was administered on day 8 of each treatment period. There was a 7-day washout period between subsequent treatments. Plasma concentrations of prednisolone were determined by use of a validated liquid chromatography–tandem mass spectrometry method. Duodenum and colon biopsy specimens were obtained endoscopically from anesthetized dogs and assessed for P-gp protein labeling via immunohistochemical analysis and mRNA quantification via real-time PCR assay. Total fecal collection was performed for evaluation of effects of P-gp modulation on digestion of nutrients.
Results—Rifampicin treatment upregulated duodenal P-gp in dogs and significantly reduced the area under the plasma concentration-time curve of prednisolone. Ketoconazole typically downregulated expression of duodenal P-gp, with a subsequent increase in the area under the plasma concentration-time curve of prednisolone. There was a noticeable interindividual difference in response. Digestion of nutrients was not affected.
Conclusions and Clinical Relevance—Modulation of P-gp expression influenced plasma concentrations of prednisolone after oral administration in dogs. Thus, treatment response to prednisolone may be influenced by coadministration of P-gp–modulating medications or feed ingredients.