RESUMEN
Mesenchymal tumors including hemangiopericytomas, hepatocellular tumors, adrenal carcinomas, and a variety of other large tumors have been reported to produce excessive amounts of insulin-like growth factor (IGF) type II precursor, which binds weakly to insulin receptors and strongly to IGF-I receptors, leading to insulin like actions. In addition to increased IGF-II production, IGF-II bioavailability is increased due to complex alterations in circulating binding proteins. The authors of this article diagnosed non-islet cell tumor hypoglycemia from an 81-year-old male patient suffering from repetitive fasting hypoglycemia while he has not received any treatment for pulmonary hemangiopericytoma diagnosed in the past. Moreover, this topic is getting reported as the authors have experienced a significant improvement of catamnesis by a treatment with glucocorticoid.
Asunto(s)
Anciano de 80 o más Años , Humanos , Masculino , Disponibilidad Biológica , Proteínas Portadoras , Hemangiopericitoma , Hipoglucemia , Insulina , Factor I del Crecimiento Similar a la Insulina , Factor II del Crecimiento Similar a la Insulina , Receptor IGF Tipo 1 , Receptor de InsulinaRESUMEN
No abstract available.
RESUMEN
The thrombotic microangiopathy associated with cyclosporine A after kidney transplantation is a detrimental complication that could lead to the loss of transplanted kidney. Although the pathogenesis is still unclear, the decrease in the activity of von Willebrand Factor (VWF)-cleaving metalloprotease that cleaves unusually large von-Willebrand factor (UL-VWF), such as disintegrin-like metalloprotease with thrombospondin type 1 repeats (ADAMTS) 13, and the inhibitory factors of ADAMTS 13 are reported. Therefore, we measured the activity of ADAMTS 13 and the inhibitory factors in a patient with thrombotic microangiopathy after kidney transplantation. A 28 year-old female patient with hemolytic anemia, thrombocytopenia and impaired renal function after the kidney transplantation was diagnosed as thrombotic microangiopathy after renal biopsy. The activity of ADAMTS 13 during the acute stage of thrombotic microangiopathy was reduced to 12%, but when the renal function returned to normal, ADAMTS 13 level returned to 100%. However, the autoantibody of ADAMTS 13 was not detected. The results from this study suggest that the pathogenesis of thrombotic microangiopathy associated with cyclosporine A after the kidney transplantation could be associated with the decrease in the activity of ADAMTS 13.