Mikkel Andreassen1,2, Emma Ilett1,2, Dominik Wiese3,4, Emily P Slater3,4, Marianne Klose1,2, Carsten Palnæs Hansen2,5, Norman Gercke3,4, Seppo W Langer2,6, Andreas Kjaer2,7, Elisabeth Maurer3,4, Birgitte Federspiel2,8, Peter H Kann3,9, Detlef K Bartsch3,4, Ulrich Knigge1,2,5. 1. Department of Endocrinology Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. 2. European Neuroendocrine Tumor Society Center of Excellence, Rigshospitalet, Copenhagen, Denmark. 3. European Neuroendocrine Tumor Society, Philipps University, Marburg, Germany. 4. Department of Visceral, Thoracic and Vascular Surgery, Philipps University, Marburg, Germany. 5. Department of Surgery, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. 6. Department of Oncology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. 7. Department of Clinical Physiology, Nuclear Medicine, & PET and Cluster for Molecular Imaging, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. 8. Department of Pathology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. 9. Department of Gastroenterology and Division of Endocrinology, Philipps University, Marburg, Germany.
Abstract
INTRODUCTION: Diagnosis and pathological classification of insulinomas are challenging. AIM: To characterize localization of tumors, surgery outcomes, and histopathology in patients with insulinoma. METHODS: Patients with surgically resected sporadic insulinoma were included. RESULTS: Eighty patients were included. Seven had a malignant tumor. A total of 312 diagnostic examinations were performed: endoscopic ultrasonography (EUS; n = 59; sensitivity, 70%), MRI (n = 33; sensitivity, 58%), CT (n = 55; sensitivity, 47%), transabdominal ultrasonography (US; n = 45; sensitivity, 40%), somatostatin receptor imaging (n = 17; sensitivity, 29%), 18F-fluorodeoxyglucose positron emission tomography/CT (n = 1; negative), percutaneous transhepatic venous sampling (n = 10; sensitivity, 90%), arterial stimulation venous sampling (n = 20; sensitivity, 65%), and intraoperative US (n = 72; sensitivity, 89%). Fourteen tumors could not be visualized. Invasive methods were used in 7 of these 14 patients and localized the tumor in all cases. Median tumor size was 15 mm (range, 7 to 80 mm). Tumors with malignant vs benign behavior showed less staining for insulin (3 of 7 vs 66 of 73; P = 0.015) and for proinsulin (3 of 6 vs 58 of 59; P < 0.001). Staining for glucagon was seen in 2 of 6 malignant tumors and in no benign tumors (P < 0.001). Forty-three insulinomas stained negative for somatostatin receptor subtype 2a. CONCLUSION: Localization of insulinomas requires many different diagnostic procedures. Most tumors can be localized by conventional imaging, including EUS. For nonvisible tumors, invasive methods may be a useful diagnostic tool. Malignant tumors showed reduced staining for insulin and proinsulin and increased staining for glucagon.
INTRODUCTION: Diagnosis and pathological classification of insulinomas are challenging. AIM: To characterize localization of tumors, surgery outcomes, and histopathology in patients with insulinoma. METHODS:Patients with surgically resected sporadic insulinoma were included. RESULTS: Eighty patients were included. Seven had a malignant tumor. A total of 312 diagnostic examinations were performed: endoscopic ultrasonography (EUS; n = 59; sensitivity, 70%), MRI (n = 33; sensitivity, 58%), CT (n = 55; sensitivity, 47%), transabdominal ultrasonography (US; n = 45; sensitivity, 40%), somatostatin receptor imaging (n = 17; sensitivity, 29%), 18F-fluorodeoxyglucose positron emission tomography/CT (n = 1; negative), percutaneous transhepatic venous sampling (n = 10; sensitivity, 90%), arterial stimulation venous sampling (n = 20; sensitivity, 65%), and intraoperative US (n = 72; sensitivity, 89%). Fourteen tumors could not be visualized. Invasive methods were used in 7 of these 14 patients and localized the tumor in all cases. Median tumor size was 15 mm (range, 7 to 80 mm). Tumors with malignant vs benign behavior showed less staining for insulin (3 of 7 vs 66 of 73; P = 0.015) and for proinsulin (3 of 6 vs 58 of 59; P < 0.001). Staining for glucagon was seen in 2 of 6 malignant tumors and in no benign tumors (P < 0.001). Forty-three insulinomas stained negative for somatostatin receptor subtype 2a. CONCLUSION: Localization of insulinomas requires many different diagnostic procedures. Most tumors can be localized by conventional imaging, including EUS. For nonvisible tumors, invasive methods may be a useful diagnostic tool. Malignant tumors showed reduced staining for insulin and proinsulin and increased staining for glucagon.
Authors: Dirk-Jan van Beek; Sjoerd Nell; Helena M Verkooijen; Inne H M Borel Rinkes; Gerlof D Valk; Menno R Vriens Journal: Surgery Date: 2020-11-19 Impact factor: 4.348
Authors: Jess C Hercus; Pouneh Pasha; Sadiq Al Lawati; Peter Kim; Andre Mattman; Douglas Webber; David M Thompson Journal: Case Rep Endocrinol Date: 2022-10-07