Metformin is a synthetic biguanide that improves insulin sensitivity and reduces hepatic gluconeogenesis. Aside being the first-line therapy for Type 2 Diabetes (T2D), many pleiotropic effects have been discovered in recent years, such as its capacity to reduce cancer risk and tumorigenesis. Although widely studied, the effect of metformin on thyroid cancer remains controversial. Potential mechanisms for its growth inhibitory effects have been elucidated in various preclinical studies that involved pathways related to adenosine mono-phosphate-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), mitochondrial glycerophosphate dehydrogenase (mGPDH), and the nuclear factor κB (NF-κB). Hyperinsulinemia increases cell glucose uptake and oxidative stress, and promotes thyroid cell growth, leading to hyperproliferation, carcinogenesis, and the development of malignant tumors. Furthermore, it has also been related to thyroid nodules size in nodular disease, as well as tumoral size in patients with thyroid cancer. Several clinical studies concluded that metformin might have an important role as an adjuvant therapy to reduce the growth of benign and malignant thyroid neoplasms. This suggests that metformin might be useful for patients with differentiated or poorly differentiated thyroid cancer and metabolic diseases such as insulin resistance or diabetes.
BackgroundCyclophosphamide may induce autoimmune diabetes through a decrease in suppressor T cells and increase of proinflammatory T helper type 1 response in animal models. In humans, this association is not as clear due to the presence of other risk factors for hyperglycemia, but it could be a precipitant for acute complications.Case presentationA 31-year-old Mestizo-Mexican woman with a history of systemic lupus erythematosus presented with severe diabetic ketoacidosis, shortly after initiating a multi-drug immunosuppressive therapy. She did not meet the diagnostic criteria for type 1 or type 2 diabetes and had no family history of hyperglycemic states. She persisted with hyperglycemia and high insulin requirements until the discontinuation of cyclophosphamide. After this episode, she recovered her endogenous insulin production and the antidiabetic agents were successfully withdrawn. After 1 year of follow up she is still normoglycemic.ConclusionCyclophosphamide may be an additional risk factor for acute hyperglycemic crisis. Glucose monitoring could be recommended during and after this treatment.
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