Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3274110 | Médecine des Maladies Métaboliques | 2016 | 5 Pages |
Abstract
Identification of patients with increased risk of pancreatic cancer will improve their screening and prognosis by performing an early diagnosis. The link between diabetes and pancreatic cancer is well known, but the mechanisms at the basis of this relationship remain to be investigated. Several arguments show that diabetes in pancreatic cancer is paraneoplastic but not due to the destruction of pancreas. Indeed, diabetes occurs several months before the tumor is radiologically detectable, and its prevalence is the same regardless of the size of the tumor. Improvement of glycemia after tumoral surgery via decrease of insulin resistance also supports this concept. Moreover, experimental models show that glycemic dysregulation appears early during pancreatic carcinogenesis. It seems required to identify the specificities of a pancreatic cancer-induced diabetes that differ from the general features of a typical type 2 diabetes. The absence of metabolic syndrome and the absence of family history of diabetes are in favor of a paraneoplastic diabetes. Another specificity of this type of diabetes is weight loss that occurs before the diagnosis of diabetes, and which is different from cachexia. The pathophysiological mechanisms involve both a β-cell dysfunction secondary to secretion by cancer cells of paraneoplastic mediators as adrenomedullin, and an insulin resistance in peripheral tissues. Characterization of the mechanisms of paraneoplastic diabetes and identification of patients with increased cancer risk represent major challenges to select diabetic patients in whom pancreatic imaging monitoring could be helpful at diagnosis and during the follow-up.
Keywords
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Authors
A.-C. Paepegaey, B. Fève,