Solitary fibrous tumor of the pleura as a rare cause of severe hypoglycemia: Doege-Potter syndrome.

INTRODUCTION: Doege-Potter syndrome is a rare syndrome characterized by hypo-insulinemic hypoglycemia. It is caused by excessive ectopic secretion of insulin-like growth factor II from a solitary fibrous tumors of intrapleural or extrapleural origin. Laboratory tests reveal low levels of C-peptide and insulin, on the contrary insulin-like growth factor II level is elevated, which is characteristic for Doege-Potter syndrome. Majority of solitary fibrous tumors present no symptomatology, recurrent hypoglycemia is relatively rare, but it may be the only clinical manifestation. The therapy is surgical, consisting of radical en-bloc tumor resection. CASE REPORT: Authors present a case report of a patient with recurrent hypoglycemia caused solely by solitary fibrous tumor. Hypoglycemia resolved immediately after surgical resection and there were no recurrences. CONCLUSION: Doege-Potter syndrome should be considered as the differential diagnosis in a patient with suspicion on thoracic malignancy if accompanied by features suggestive of hypoglycemia. Prolonged follow up is strongly advised because of the risk of disease recurrence, even in patients with benign solitary fibrous tumors of the pleura (SFTP).

Fibronectin is not a serum spreading factor for HeLa cells.

The spreading of HeLa cells on plastic substratum is mediated by fibronectin-depleted foetal calf serum but not by fibronectin isolated by gelatin-Sepharose affinity chromatography. The same is true for freshly explanted chick embryonic chondrocytes. In contrast, BHK cell spreading exceeds 67% after 120 min at 37 degrees C in fibronectin-supplemented (10 micrograms ml-1) serum-free medium. Long-term cultivation of HeLa cells in Eagle's MEM supplemented with fibronectin-free serum is associated with the accumulation of cells in mitosis or before cytokinesis; many cells die and the remaining living cells, characterized by marked changes in morphology, multiply very slowly. It can be concluded therefore that fibronectin does not produce spreading in HeLa cells but forces them into mitosis.

Changes in serum and tissue fibronectin during ontogeny.

It has been proved that both in bovine and rat serum fibronectin concentration increases with age. While in foetal bovine the serum fibronectin concentration was 77 +/- 5 micrograms/ml, in adult cows the concentration of this protein reached 150.0 +/- 5.5 micrograms/ml. In newborn rats, the corresponding fibronectin concentration in the serum was 227 +/- 25 micrograms/ml as compared to 455 +/- 47 micrograms/ml in adult individuals. On the contrary, a drop in fibronectin concentration was found in the bovine glomerular basement membrane: fibronectin represents 3.8 +/- 0.6% of total protein in the newborn, while in animals older than two months this protein was not detectable. Accordingly, in newborn rats fibronectin represents 5.1 +/- 0.6% of total protein in the glomerular basement membrane and drops dramatically to 0.4 +/- 0.1% after one year of life with no detectable changes thereafter. In the alveolar basement membrane the changes are similar as in the glomerular basement membrane. While in newborn rats this protein represents 13.2 +/- 0.5% of total basement membrane protein, it drops to 3.2 +/- 0.3% after two years of life.