Abstract

It is clear that cutaneous lesions of metabolic epidermal necrosis in the dog can occur either with a demonstrable glucagon-secreting tumor or with hepatic disease without any detectable glucagonoma. Additional clinical case reports of the disease in cats are needed to better characterize the disease in this species. The lesions of NME-MEN may not represent a specific physiological mechanism of cutaneous disease but instead a pathophysiological process that can be triggered by several systemic metabolic abnormalities. The fact that NME is observed in association with a variety of conditions supports the theory that an overall metabolic derangement results in the rash. The prognosis for canine MEN is poor; however, some affected dogs have been maintained for many months with dietary management. High-quality protein diets such as Hill's Prescription Diet a/d (Hill's Pet Products) or other "recovery" diets may be helpful. Zinc and essential fatty acid supplementation may help some patients. Dietary supplementation with cooked egg yolks may be helpful. It is prudent to avoid corticosteroids in these cases, as development of diabetes mellitus worsens the prognosis. Histopathological examination of the pancreas coupled with determination of plasma glucagon may help define the characteristics of GS versus HS in dogs. It is possible that some dogs diagnosed with MEN-HS may have an undetected pancreatic tumor. Although the hepatic ultrasound findings in dogs with MEN-HS are becoming well characterized, it is possible for dogs with pancreatic neuroendocrine tumors to also have abnormal hepatic ultrasonography. As the presence of MEN and hepatic disease does not necessarily rule out the presence of a pancreatic tumor, prospective studies correlating plasma glucagon levels with pancreatic histopathology in cases of MEN-GS versus MEN-HS seem warranted.

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