There are very few reports regarding the development of diabetes or worsening of preexisting diabetes in patients with renal cell carcinoma (Elias 2005; Palgon et al. 1986; Jobe et al. 1993; Callewaert et al. 1999). In one case, the patient was diagnosed with a preexisting insulin-dependent diabetes mellitus that became uncontrollable by insulin therapy. The patient underwent partial nephrectomy because of a histological papillary type and the control of his glycemia improved immediately and insulin need became identical to the premor-bid situation (Callewaert et al. 1999). The other three case reports did not have any history of diabetes melli-tus and the hyperglycemia resolved following nephrec-tomy. The mechanism for this syndrome is unclear and none of these patients had evidence of metastatic disease or family history of diabetes. No specific etiology was found, but the possibility of ectopic glucagon production was considered. Hypothetically, diabetes could develop in patients with renal cell carcinoma if the tumor was the source of hormones that antagonized the effect of insulin or promoted neoglucogenesis. Gluca-gon and growth hormones are able to produce such an effect. Other potential mechanisms include ectopic ACTH production, hyperprolactinemia causing insulin resistance, and the potential for the production of an insulin receptor antagonist (Plagon et al. 1986). There are several reports of the development of diabetes mel-litus in patients receiving cancer-related cytokine therapy with interleukin-2 or interferon and this maybe yet another mechanism (Shiba et al. 1998).

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