A new study shows that dogs presenting with intervertebral disk disease may be at higher risk for developing pancreatitis.
This was a prospective, case-controlled study. Of the 100 dogs that presented for spinal cord injury, 16 were excluded for lack of confirmed IVDH diagnosis. Eighty-four dogs were included in the study, with IVDH confirmed by myelography and/or magnetic resonance imaging, with further visual confirmation of herniated disk material during surgical decompression.
All study dogs exhibited at least grade III/V deficits (loss of voluntary motor function with or without voluntary micturition and nociception). Preadmission corticosteroid or nonsteroidal anti-inflammatory drug (NSAID) administration was recorded for each dog, as were signalment and physical and neurologic examination findings. The presence of GI signs (including hyporexia, diarrhea, vomiting, and abdominal pain) were recorded.
Eighteen healthy dogs from the same geographic region served as the control population. Each dog had a complete blood cell count, serum biochemical profile, and cPLI performed.
Results and Discussion
Of the 84 dogs with IVDH, neuroanatomic localization was cervical in 23 (27%) and thoracolumbar in 61 (73%). Forty-four of the dogs (52%) received no preadmission medications, 21 (25%) received corticosteroids, and 19 (23%) received NSAIDs. GI signs were present in 29 (35%) of the 84 dogs with IVDH. Serum cPLI concentrations were significantly higher in dogs with IVDH (median 153 ug/L, range 30-1000 ug/L) than in control dogs (median 44 ug/L, range 30-124 ug/L) (P < .01).
Proportionally, 45% of dogs (n = 38) in the IVDH group had cPLI concentrations of 200 ug/L or higher, whereas none of the dogs in the control group had cPLI concentrations of 200 ug/L or higher (P < .01). Of the 19 dogs with IVDH that had cPLI concentrations of more than 200 ug/L, 15 (79%) had cPLI concentrations within reference parameters along with resolution of neurologic and GI signs at retest 2 to 4 weeks later. There was no association with increased cPLI concentrations based on neuroanatomic localization, administration of preadmission medications, presence of GI signs, sex, or weight. There was, however, an association with cPLI concentrations and age: Dogs with cPLI concentrations over 200 ug/L were significantly older (P = .03).
These results are consistent with those of previous studies in humans, in which pancreatitis has been associated with spinal cord injury. This is believed to be due to the autonomic influences on pancreatic function and vascular tone. Autonomic dysregulation, which can occur during spinal cord injury, can incite inflammatory cytokines and reduce pancreatic perfusion, resulting in endothelial damage to pancreatic tissue and/or exacerbating the severity of pancreatitis.
One caveat to this study is that cPLI concentrations may be increased in dogs that do not have pancreatic disease; however, several studies have concluded that a cPLI concentration exceeding 400 ug/L is considered consistent with pancreatitis, while assays less than 200 ug/L were consistent with histologically normal pancreatic tissue. Concentrations between 200 and 400 ug/L were considered equivocal and should be evaluated further. Regardless, this study does show an association between dogs with IVDH and increased cPLI.
Dogs presenting with IVDH, particularly older dogs, are more likely to have increased cPLI concentrations and may be at risk for development of pancreatitis.
Dr. Packer is an associate professor of neurology/neurosurgery at Colorado State University College of Veterinary Medicine and Biomedical Sciences in Fort Collins, and is board certified in neurology by the American College of Veterinary Internal Medicine. She is active in clinical and didactic training of veterinary students and residents and has developed a comparative neuro-oncology research program at Colorado State University.
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