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Ricardo V Lloyd - One of the best experts on this subject based on the ideXlab platform.

  • hyperinsulinemic hypoglycemia with Nesidioblastosis histologic features and growth factor expression
    Modern Pathology, 2009
    Co-Authors: Kandelaria M Rumilla, Geoffrey B Thompson, Lori A Erickson, Adrian Vella, Clive S Grant, Ricardo V Lloyd
    Abstract:

    Hypoglycemia secondary to Nesidioblastosis is rare in adults, and the pathogenesis of this condition is unknown. To determine factors leading to Nesidioblastosis in adults, we analyzed 36 cases of Nesidioblastosis including 27 cases of postgastric bypass Nesidioblastosis and 9 cases of idiopathic Nesidioblastosis in adults by immunohistochemistry using antibodies to insulin-like growth factor 1, insulin-like growth factor 2 (IGF2), insulin-like growth factor one receptor-alpha epidermal growth factor receptor, transforming growth factor-beta1 and 2, and transforming growth factor-beta receptor type 3. Fifty-two surgically excised pancreatic specimens from patients with benign exocrine tumors and no evidence of hypoglycemia were used as controls. There was increased IGF2, insulin-like growth factor receptor 1 receptor-alpha and transforming growth factor-beta receptor 3 expression in islets from Nesidioblastosis patients compared to controls. Peliosis-type vascular ectasia was more common in Nesidioblastosis patients compared to controls. These findings suggest that increased production of growth factors and growth factor receptors may contribute to the development of Nesidioblastosis in adults.

  • hyperinsulinemic hypoglycemia with Nesidioblastosis after gastric bypass surgery
    The New England Journal of Medicine, 2005
    Co-Authors: Geoffrey B Thompson, James C Andrews, Maria L Collazoclavell, Ricardo V Lloyd
    Abstract:

    We describe six patients (five women and one man; median age, 47 years; range, 39 to 54) with postprandial symptoms of neuroglycopenia owing to endogenous hyperinsulinemic hypoglycemia after Roux-en-Y gastric bypass surgery. Except for equivocal evidence in one patient, there was no radiologic evidence of insulinoma. Selective arterial calcium-stimulation tests, positive in each patient, were used to guide partial pancreatectomy. Nesidioblastosis was identified in resected specimens from each patient, and multiple insulinomas were identified in one. Hypoglycemic symptoms diminished postoperatively. We speculate that hyperfunction of pancreatic islets did not lead to obesity but that beta-cell trophic factors may have increased as a result of gastric bypass.

  • noninsulinoma pancreatogenous hypoglycemia a novel syndrome of hyperinsulinemic hypoglycemia in adults independent of mutations in kir6 2 and sur1 genes
    The Journal of Clinical Endocrinology and Metabolism, 1999
    Co-Authors: Neena Natt, Geoffrey B Thompson, James C Andrews, Clive S Grant, Jonathan A Van Heerden, Eva Lorenz, Andre Terzic, Ricardo V Lloyd
    Abstract:

    In adults, endogenous hyperinsulinemic hypoglycemia is almost invariably due to insulinoma. In these patients with insulinoma, neuroglycopenic episodes exclusively after meal ingestion and negative 72-h fasts are extraordinarily rare. We describe five adults with neuroglycopenic episodes from hyperinsulinemic hypoglycemia within 4 h of meal ingestion and negative 72-h fasts. Each had negative transabdominal ultrasonography, spiral computed tomographic scanning, and celiac axis angiography of the pancreas. However, all showed positive selective arterial calcium stimulation tests indicative of pancreatic β-cell hyperfunction. At pancreatic exploration, no insulinoma was detected by intraoperative ultrasonography and complete mobilization and palpation of the pancreas. Moreover, the resected pancreata showed islet hypertrophy and Nesidioblastosis, but no insulinoma. No definite disease-causing mutation was detected in Kir6.2 and SUR1 genes, which encode the subunits of the pancreatic ATP-sensitive potassium ...

Geoffrey B Thompson - One of the best experts on this subject based on the ideXlab platform.

  • selective arterial calcium stimulation with hepatic venous sampling differentiates insulinoma from Nesidioblastosis
    The Journal of Clinical Endocrinology and Metabolism, 2015
    Co-Authors: Scott M Thompson, Geoffrey B Thompson, Kandelaria M Rumilla, Adrian Vella, Clive S Grant, James C Andrews
    Abstract:

    Context: In adult patients with endogenous hyperinsulinemic hypoglycemia and negative or inconclusive noninvasive imaging, insulinoma and non-insulinoma pancreatogenous hypoglycemic syndrome (NIPHS) resulting from diffuse Nesidioblastosis must be considered in the differential diagnosis. It is not known whether the biochemical results of selective arterial calcium stimulation (SACST) with hepatic venous sampling can differentiate insulinoma from diffuse Nesidioblastosis. Objective: To determine the specificity of SACST with hepatic venous sampling in differentiating insulinoma from diffuse Nesidioblastosis. Design: Retrospective review (January 1996 to March 2014). Setting: Tertiary referral center. Patients or Other Participants: A total of 116 patients with biochemical evidence of endogenous hyperinsulinemic hypoglycemia and negative or inconclusive noninvasive imaging who were subsequently shown at surgery to have insulinoma (n = 42) or Nesidioblastosis (n = 74) after undergoing SACST with hepatic veno...

  • hyperinsulinemic hypoglycemia with Nesidioblastosis histologic features and growth factor expression
    Modern Pathology, 2009
    Co-Authors: Kandelaria M Rumilla, Geoffrey B Thompson, Lori A Erickson, Adrian Vella, Clive S Grant, Ricardo V Lloyd
    Abstract:

    Hypoglycemia secondary to Nesidioblastosis is rare in adults, and the pathogenesis of this condition is unknown. To determine factors leading to Nesidioblastosis in adults, we analyzed 36 cases of Nesidioblastosis including 27 cases of postgastric bypass Nesidioblastosis and 9 cases of idiopathic Nesidioblastosis in adults by immunohistochemistry using antibodies to insulin-like growth factor 1, insulin-like growth factor 2 (IGF2), insulin-like growth factor one receptor-alpha epidermal growth factor receptor, transforming growth factor-beta1 and 2, and transforming growth factor-beta receptor type 3. Fifty-two surgically excised pancreatic specimens from patients with benign exocrine tumors and no evidence of hypoglycemia were used as controls. There was increased IGF2, insulin-like growth factor receptor 1 receptor-alpha and transforming growth factor-beta receptor 3 expression in islets from Nesidioblastosis patients compared to controls. Peliosis-type vascular ectasia was more common in Nesidioblastosis patients compared to controls. These findings suggest that increased production of growth factors and growth factor receptors may contribute to the development of Nesidioblastosis in adults.

  • hyperinsulinemic hypoglycemia with Nesidioblastosis after gastric bypass surgery
    The New England Journal of Medicine, 2005
    Co-Authors: Geoffrey B Thompson, James C Andrews, Maria L Collazoclavell, Ricardo V Lloyd
    Abstract:

    We describe six patients (five women and one man; median age, 47 years; range, 39 to 54) with postprandial symptoms of neuroglycopenia owing to endogenous hyperinsulinemic hypoglycemia after Roux-en-Y gastric bypass surgery. Except for equivocal evidence in one patient, there was no radiologic evidence of insulinoma. Selective arterial calcium-stimulation tests, positive in each patient, were used to guide partial pancreatectomy. Nesidioblastosis was identified in resected specimens from each patient, and multiple insulinomas were identified in one. Hypoglycemic symptoms diminished postoperatively. We speculate that hyperfunction of pancreatic islets did not lead to obesity but that beta-cell trophic factors may have increased as a result of gastric bypass.

  • noninsulinoma pancreatogenous hypoglycemia a novel syndrome of hyperinsulinemic hypoglycemia in adults independent of mutations in kir6 2 and sur1 genes
    The Journal of Clinical Endocrinology and Metabolism, 1999
    Co-Authors: Neena Natt, Geoffrey B Thompson, James C Andrews, Clive S Grant, Jonathan A Van Heerden, Eva Lorenz, Andre Terzic, Ricardo V Lloyd
    Abstract:

    In adults, endogenous hyperinsulinemic hypoglycemia is almost invariably due to insulinoma. In these patients with insulinoma, neuroglycopenic episodes exclusively after meal ingestion and negative 72-h fasts are extraordinarily rare. We describe five adults with neuroglycopenic episodes from hyperinsulinemic hypoglycemia within 4 h of meal ingestion and negative 72-h fasts. Each had negative transabdominal ultrasonography, spiral computed tomographic scanning, and celiac axis angiography of the pancreas. However, all showed positive selective arterial calcium stimulation tests indicative of pancreatic β-cell hyperfunction. At pancreatic exploration, no insulinoma was detected by intraoperative ultrasonography and complete mobilization and palpation of the pancreas. Moreover, the resected pancreata showed islet hypertrophy and Nesidioblastosis, but no insulinoma. No definite disease-causing mutation was detected in Kir6.2 and SUR1 genes, which encode the subunits of the pancreatic ATP-sensitive potassium ...

James C Andrews - One of the best experts on this subject based on the ideXlab platform.

  • selective arterial calcium stimulation with hepatic venous sampling differentiates insulinoma from Nesidioblastosis
    The Journal of Clinical Endocrinology and Metabolism, 2015
    Co-Authors: Scott M Thompson, Geoffrey B Thompson, Kandelaria M Rumilla, Adrian Vella, Clive S Grant, James C Andrews
    Abstract:

    Context: In adult patients with endogenous hyperinsulinemic hypoglycemia and negative or inconclusive noninvasive imaging, insulinoma and non-insulinoma pancreatogenous hypoglycemic syndrome (NIPHS) resulting from diffuse Nesidioblastosis must be considered in the differential diagnosis. It is not known whether the biochemical results of selective arterial calcium stimulation (SACST) with hepatic venous sampling can differentiate insulinoma from diffuse Nesidioblastosis. Objective: To determine the specificity of SACST with hepatic venous sampling in differentiating insulinoma from diffuse Nesidioblastosis. Design: Retrospective review (January 1996 to March 2014). Setting: Tertiary referral center. Patients or Other Participants: A total of 116 patients with biochemical evidence of endogenous hyperinsulinemic hypoglycemia and negative or inconclusive noninvasive imaging who were subsequently shown at surgery to have insulinoma (n = 42) or Nesidioblastosis (n = 74) after undergoing SACST with hepatic veno...

  • hyperinsulinemic hypoglycemia with Nesidioblastosis after gastric bypass surgery
    The New England Journal of Medicine, 2005
    Co-Authors: Geoffrey B Thompson, James C Andrews, Maria L Collazoclavell, Ricardo V Lloyd
    Abstract:

    We describe six patients (five women and one man; median age, 47 years; range, 39 to 54) with postprandial symptoms of neuroglycopenia owing to endogenous hyperinsulinemic hypoglycemia after Roux-en-Y gastric bypass surgery. Except for equivocal evidence in one patient, there was no radiologic evidence of insulinoma. Selective arterial calcium-stimulation tests, positive in each patient, were used to guide partial pancreatectomy. Nesidioblastosis was identified in resected specimens from each patient, and multiple insulinomas were identified in one. Hypoglycemic symptoms diminished postoperatively. We speculate that hyperfunction of pancreatic islets did not lead to obesity but that beta-cell trophic factors may have increased as a result of gastric bypass.

  • noninsulinoma pancreatogenous hypoglycemia a novel syndrome of hyperinsulinemic hypoglycemia in adults independent of mutations in kir6 2 and sur1 genes
    The Journal of Clinical Endocrinology and Metabolism, 1999
    Co-Authors: Neena Natt, Geoffrey B Thompson, James C Andrews, Clive S Grant, Jonathan A Van Heerden, Eva Lorenz, Andre Terzic, Ricardo V Lloyd
    Abstract:

    In adults, endogenous hyperinsulinemic hypoglycemia is almost invariably due to insulinoma. In these patients with insulinoma, neuroglycopenic episodes exclusively after meal ingestion and negative 72-h fasts are extraordinarily rare. We describe five adults with neuroglycopenic episodes from hyperinsulinemic hypoglycemia within 4 h of meal ingestion and negative 72-h fasts. Each had negative transabdominal ultrasonography, spiral computed tomographic scanning, and celiac axis angiography of the pancreas. However, all showed positive selective arterial calcium stimulation tests indicative of pancreatic β-cell hyperfunction. At pancreatic exploration, no insulinoma was detected by intraoperative ultrasonography and complete mobilization and palpation of the pancreas. Moreover, the resected pancreata showed islet hypertrophy and Nesidioblastosis, but no insulinoma. No definite disease-causing mutation was detected in Kir6.2 and SUR1 genes, which encode the subunits of the pancreatic ATP-sensitive potassium ...

Michael J Zinner - One of the best experts on this subject based on the ideXlab platform.

  • post gastric bypass hyperinsulinism with Nesidioblastosis subtotal or total pancreatectomy may be needed to prevent recurrent hypoglycemia
    Journal of Gastrointestinal Surgery, 2006
    Co-Authors: Thomas E Clancy, Francis D Moore, Michael J Zinner
    Abstract:

    Symptomatic hyperinsulinemic hypoglycemia and pancreatic Nesidioblastosis have recently been described in a small series of patients after gastric bypass surgery for morbid obesity. In the limited published reports of patients with this condition, hyperinsulinism and Nesidioblastosis have been managed with distal or subtotal pancreatectomy, with the extent of resection guided by calcium angiography. However, Nesidioblastosis may involve the pancreas diffusely, and limited pancreatic resections may predispose patients to further hypoglycemic episodes. We have treated two patients with refractory hyperinsulinism and symptomatic hypoglycemia after successful gastric bypass surgery. One patient underwent an approximately 80% pancreatectomy with good results but subsequently experienced recurrent drop attacks and fainting from hyperinsulinism; a completion pancreatectomy via a pancreaticoduodenectomy was then required. A second patient had profound hyperinsulinemic hypoglycemia and was treated successfully with a subtotal (95%) pancreatectomy. Our experience, the third published report of post-gastric bypass Nesidioblastosis, suggests that the risk of recurrent symptomatic hyperinsulinism after limited pancreatectomy is significant and relative euglycemia may be achieved with subtotal or total pancreatectomy.

Thomas M. Stulnig - One of the best experts on this subject based on the ideXlab platform.

  • Insulin-Like Growth Factor 1 Predicts Post-Load Hypoglycemia following Bariatric Surgery: A Prospective Cohort Study
    2015
    Co-Authors: Bianca K. Itariu, Maximilian Zeyda, Gerhard Prager, Thomas M. Stulnig
    Abstract:

    Postprandial hypoglycemia is a complication following gastric bypass surgery, which frequently remains undetected. Severe hypoglycemic episodes, however, put patients at risk, e.g., for syncope. A major cause of hypoglycemia following gastric bypass is hyperinsulinemic Nesidioblastosis. Since pancreatic islets in Nesidioblastosis overexpress insulin-like growth factor 1 (IGF-1) receptor a and administration of recombinant IGF-1 provokes hypoglycemia, our main objective was to investigate the occurrence of post-load hypoglycemia one year after bariatric surgery and its relation to pre- and post-operative IGF-1 serum concentrations. We evaluated metabolic parameters including 2 h 75 g oral glucose tolerance test (OGTT) and measured IGF-1 serum concentration in thirty-six non-diabetic patients (29 f/7 m), aged 41.362.0 y with a median (IQR) BMI of 30.9 kg/m2 (27.5–34.3 kg/m2), who underwent elective bariatric surgery (predominantly gastric bypass, 83%) at our hospital. Post-load hypoglycemia as defined by a 2 h glucose concentration,60 mg/dl was detected in 50 % of patients. Serum insulin and C-peptide concentration during the OGTT and HOMA-IR (homeostatic model assessment–insulin resistance) were similar in hypoglycemic and euglycemic patients. Strikingly, pre- and post-operative serum IGF-1 concentrations were significantly higher in hypoglycemic patients (p = 0.012 and p = 0.007 respectively). IGF-1 serum concentration before surgery negatively correlated with 2 h glucose concentration during the OGTT (rho=20.58, p = 0.0003). Finally, IGF-1 serum concentrations before and after surgery significantly predicted post-load hypoglycemi

  • insulin like growth factor 1 predicts post load hypoglycemia following bariatric surgery a prospective cohort study
    PLOS ONE, 2014
    Co-Authors: Bianca K. Itariu, Maximilian Zeyda, Gerhard Prager, Thomas M. Stulnig
    Abstract:

    Postprandial hypoglycemia is a complication following gastric bypass surgery, which frequently remains undetected. Severe hypoglycemic episodes, however, put patients at risk, e.g., for syncope. A major cause of hypoglycemia following gastric bypass is hyperinsulinemic Nesidioblastosis. Since pancreatic islets in Nesidioblastosis overexpress insulin-like growth factor 1 (IGF-1) receptor α and administration of recombinant IGF-1 provokes hypoglycemia, our main objective was to investigate the occurrence of post-load hypoglycemia one year after bariatric surgery and its relation to pre- and post-operative IGF-1 serum concentrations. We evaluated metabolic parameters including 2 h 75 g oral glucose tolerance test (OGTT) and measured IGF-1 serum concentration in thirty-six non-diabetic patients (29 f/7 m), aged 41.3±2.0 y with a median (IQR) BMI of 30.9 kg/m2 (27.5–34.3 kg/m2), who underwent elective bariatric surgery (predominantly gastric bypass, 83%) at our hospital. Post-load hypoglycemia as defined by a 2 h glucose concentration <60 mg/dl was detected in 50% of patients. Serum insulin and C-peptide concentration during the OGTT and HOMA-IR (homeostatic model assessment–insulin resistance) were similar in hypoglycemic and euglycemic patients. Strikingly, pre- and post-operative serum IGF-1 concentrations were significantly higher in hypoglycemic patients (p = 0.012 and p = 0.007 respectively). IGF-1 serum concentration before surgery negatively correlated with 2 h glucose concentration during the OGTT (rho = −0.58, p = 0.0003). Finally, IGF-1 serum concentrations before and after surgery significantly predicted post-load hypoglycemia with odds ratios of 1.28 (95%CI:1.03–1.55, p = 0.029) and 1.18 (95%CI:1.03–1.33, p = 0.015), respectively, for each 10 ng/ml increment. IGF-1 serum concentration could be a valuable biomarker to identify patients at risk for hypoglycemia following bariatric surgery independently of a diagnostic OGTT. Thus, IGF-1 testing could help to prevent a significant complication of gastric bypass surgery.

  • Insulin-Like Growth Factor 1 Predicts Post-Load Hypoglycemia following Bariatric Surgery: A Prospective Cohort Study
    2014
    Co-Authors: Bianca K. Itariu, Maximilian Zeyda, Gerhard Prager, Thomas M. Stulnig
    Abstract:

    Postprandial hypoglycemia is a complication following gastric bypass surgery, which frequently remains undetected. Severe hypoglycemic episodes, however, put patients at risk, e.g., for syncope. A major cause of hypoglycemia following gastric bypass is hyperinsulinemic Nesidioblastosis. Since pancreatic islets in Nesidioblastosis overexpress insulin-like growth factor 1 (IGF-1) receptor α and administration of recombinant IGF-1 provokes hypoglycemia, our main objective was to investigate the occurrence of post-load hypoglycemia one year after bariatric surgery and its relation to pre- and post-operative IGF-1 serum concentrations. We evaluated metabolic parameters including 2 h 75 g oral glucose tolerance test (OGTT) and measured IGF-1 serum concentration in thirty-six non-diabetic patients (29 f/7 m), aged 41.3±2.0 y with a median (IQR) BMI of 30.9 kg/m2 (27.5–34.3 kg/m2), who underwent elective bariatric surgery (predominantly gastric bypass, 83%) at our hospital. Post-load hypoglycemia as defined by a 2 h glucose concentration