1. Introduction
Karl Doege and Roy Potter in 1930 described the presence of a non-beta-pancreatic cell tumor associated with hypoglycemia in a patient with a fibrous tumor in the mediastinum. Since then, the eponymous of these authors has been used to refer to the presence of an intrathoracic tumor associated with symptomatic, severe, and sustained hypoglycemia. The pathophysiological mechanisms that explain the hypoglycemic syndrome are glucose consumption by the tumor and excess secretion of insulin-like growth factor II (IGF-II), a protein that inhibits the release of glucose by the liver, and substances that inhibit its action or the secretion of counterinsular hormones, which leads to the failure of one of the mechanisms to prevent hypoglycemia.1
The solitary fibrous tumor (SFT) is a slow-growing, large tumor of mesenchymal origin that can cause Doege-Potter syndrome in about 2-4% of cases.2 The solitary fibrous tumor (SFT) is a slow-growing, large tumor of mesenchymal origin that can cause Doege-Potter syndrome in about 2-4% of cases. SFT is difficult to distinguish from other tumors, but on chest tomography, it generally appears as a round and well-defined homogeneous mass, large tumors can reach more than 20 cm in diameter, and 90% of them have benign features.3
For its diagnosis, immunohistochemical markers such as CD34 + are used, which is strongly expressed by this tumor, to differentiate it from other cancerous tumors. Complete surgical resection to negative margins, even for tumors classified as high risk, given the low global metastatic potential and the lack of efficacious adjuvant therapy, is the mainstay of localized SFT therapy.3,4
Here, we describe for the first time an interesting case of a Peruvian patient who accidentally discovered an intrathoracic tumor of mesenchymal origin, accompanied by severe and persistent hypoglycemia.