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At least 19 recordsLinked to original sources
PubMed1990

Unresponsiveness of insulinoma cells to secretin: significance of the secretin test in patients with insulinoma.

It is well known that B cells in the pancreas release insulin when stimulated by secretin, but there have been few reports on the response of insulinoma cells to secretin. In five patients with insulinoma, changes in serum immunoreactive insulin (IRI) concentration were measured after the intravenous injection of secretin into the peripheral vein before and after extirpation of the insulinoma. The extirpated insulinomas were cultured and tested for their response to secretin. The rise in serum IRI in response to secretin in patients with insulinoma was significantly slower and smaller than in normal volunteers. After removal of the insulinoma, the response to secretin became prompt and increased with time. Cultured insulinoma cells did not release insulin when stimulated by secretin. Therefore, it is concluded that the response of insulinoma cells to secretin is quite different from that of normal beta cells, and that the function of beta cells in the insulinoma-bearing pancreas is suppressed by the autonomous hypersecretion of insulin by the insulinoma. The extent of the decrease in function of the beta cells in patients with insulinoma can be estimated by the intravenous secretin test. Thus, the secretin test is sometimes useful in the differentiation of hypoglycemia due to insulinoma from that due to beta cell hyperplasia or alimentary hyperinsulinemia.

Adenoma, Islet Cell↗
PubMed1987

Effects of cytotoxic drugs and inhibitors of insulin secretion on a serially transplantable rat insulinoma and cultured rat insulinoma cells.

The effects of cytotoxic drugs and inhibitors of insulin secretion were examined in vivo in rats with a radiation-induced transplantable insulinoma, and in vitro using cultured rat insulinoma cells and the derived RINm5F insulin-secreting cell line. Administration of diazoxide to insulinoma-bearing rats resulted in a transient decrease of plasma insulin with a temporary rise of glucose concentrations. Mannoheptulose and somatostatin failed to affect the marked hyperinsulinaemia and hypoglycaemia. Streptozotocin produced a rapid and sustained decrease of insulin concentrations in insulinoma-bearing rats, accompanied by a progressive elevation of plasma glucose. Administration of alloxan failed to affect circulating insulin or glucose concentrations. In vitro, streptozotocin and alloxan exerted approximately equipotent time-dependent and concentration-dependent cytotoxic effects on insulinoma cells and RINm5F cells as established by cell staining with trypan blue. The cytotoxic actions of both drugs were decreased by agents believed to scavenge free radicals or to act as inhibitors of poly(ADP-ribose) synthetase. The results suggest that the cytotoxic actions of streptozotocin and alloxan on rat insulinoma cells and RINm5F cells are mediated by the generation of hydroxyl free radicals and DNA strand breaks. The ineffectiveness of alloxan in insulinoma-bearing rats probably reflects the high rate of decomposition of the drug in vivo.

Adenoma, Islet Cell↗
PubMed1990

Insulinomas in MEN-I patients: early detection and treatment of insulinomas in patients with the multiple endocrine neoplasia syndrome type-I.

In the multiple endocrine neoplasia syndrome type I (MEN-I syndrome), periodic screening of patients and their close relatives may improve prognosis and life expectancy. Although there is diffuse involvement of the pancreas with microadenomatosis, insulinomas in the MEN-I syndrome usually occur as single tumours. This is illustrated here by two patients with insulinomas and the MEN-I syndrome. Preoperative localization of the tumours was achieved accurately by digital subtraction angiography combined with dynamic computerized tomography after a bolus injection of contrast medium. At present, two and three years after elective surgery both patients are asymptomatic. The early detection and treatment of insulinomas is extremely important because of the high risk of cerebral damage associated with late diagnosis. Periodic investigation of MEN-I family members can promote the early diagnosis and treatment of insulinomas, especially in young patients, whose life expectancy and quality of life may be improved.

Adolescent↗
PubMed2001

Role of intraoperative insulin monitoring in surgical management of insulinoma.

BACKGROUND AND PURPOSE: Precise localization and surgical excision is the therapeutic strategy for insulinomas. However, it is often difficult to localize the insulinomas, because of their small size. Surgeons may not localize and remove all of them together, particularly in patients with multiple insulinomas. We reviewed our experience to confirm the efficacy of blood glucose and intraoperative immunoreactive insulin (IRI) monitoring for surgical management of insulinomas. PATIENTS AND METHODS: Thirty-nine patients with insulinoma were surgically treated in our department. Perioperative blood glucose monitoring was performed in 14 patients, intraoperative quick IRI assay of the peripheral blood in 10 patients, and assay of a portal sample in 4 patients by an IMX analyzer. RESULTS: Rebound response of blood glucose to insulinoma removal was not always noted (8/14; 57%). Seven of ten patients showed a decrease of peripheral serum IRI levels within 15 minutes after removal of the insulinoma. The other two patients showed a rebound response of peripheral blood glucose or portal IRI. All the patients who had intraoperative monitoring of peripheral blood and peripheral and portal IRI had no recurrent insulinoma syndrome after surgical removal of their insulinomas. CONCLUSION: Combined monitoring of peripheral blood glucose and peripheral and portal IRI are helpful in the surgical management of insulinomas, as they can indicate that no insulinoma remains.

Adolescent↗
PubMed1986

Benign pancreatic insulinoma: preoperative and intraoperative sonographic localization.

Twenty-nine patients with surgically proved benign pancreatic insulinoma were studied by preoperative or intraoperative sonography. Twenty-five patients had solitary pancreatic tumors; four had multiple tumors. Six of the patients with solitary insulinomas and one of the patients with multiple insulinomas had undergone previous unsuccessful exploration. Preoperative sonography was performed in 24 patients with solitary insulinomas, and 15 (63%) were localized. Intraoperative sonography was performed in 22 patients with solitary insulinomas, and 19 (86%) were visualized without having been previously located by palpation. Four of these visible solitary tumors (18%) were not detected by palpation at surgery. All the solitary insulinomas were detected with the combination of palpation and intraoperative sonography. In each of the six patients with solitary insulinoma who had undergone previous surgery, the tumor was visible with intraoperative sonography, which also demonstrated nonpalpable insulinomas in two of the four patients with multiple tumors. Preoperative real-time sonography is a sensitive, noninvasive, inexpensive method for localization of insulinoma. Intraoperative high-frequency sonography is a highly sensitive method for the detection of insulinoma. Intraoperative sonography is also valuable to determine the relationship of the insulinoma to pancreatic and bile ducts and thereby facilitate safe enucleation.

Adenoma, Islet Cell↗
PubMedDate not supplied

The surgical management of insulinoma.

Insulinoma is the most common endocrine tumor of the pancreas. Over 90% of the insulinomas are benign and single, and can be cured by simple excision. Depending on the location, insulinomas can be enucleated, might require partial or distal pancreatectomy or pancreaticoduodenectomy. Five cases with insulinoma successfully treated by surgical intervention, two by enuclation, two by distal pancreatectomy and splenectomy, and preservation of the spleen have been summarized. The management of insulinoma involves the diagnosis, localization of the tumor and treatment. Insulinomas are rare tumors of the pancreas. Nevertheless, it is the most common endocrine tumor of the pancreas. Specifically arising from the beta cells, of the islets of Langerham, that produce insulin (fig.1). Its incidence is one in 250,000 inhabitants. It can be seen at any age, but is more frequent in females between 4 and 82 years of age, with a mean of 45.5 years. Insulinomas are evenly distributed between the head, body and tail of the pancreas. Over 90% are benign and single and can be cured by simple excision. Depending on the location insulinomas can be enucleated, might require partial or distal pancreatectomy or a pancreaticoduodenectomy. Ten percent could be malignant when metastasis to peripancreatic lymph nodes or to the liver is detected. The course of the patient with malignant insulinoma is an indolent one. The release of insulin leads to fasting hypoglycemia producing confusion, loss of consciousness, coma or convulsions. The hypoglycemia in turn can induce the release of cathecolamines producing tachycardia, tremulousness and diaphoresis. The Whipple's triad must be present for the diagnosis of insulinoma; symptoms of hypoglycemia, glucose level below 50 mgs/dl and relief of symptoms by the administration of glucose. In large series the interval between the onset of symptoms and a definitive diagnosis of insulinoma was 37 months, with a range of 0 to 14 years.

Adenoma, Islet Cell↗
PubMed1998

[Videolaparoscopic excision of insulinoma. A study of 5 cases].

STUDY AIM: Evaluation of the feasibility of the videolaparoscopic resection in pancreatic insulinomas, and reporting of five cases. PATIENTS AND METHOD: From 1996 to 1998, a videolaparoscopic resection was attempted in five patients with sporadic, unique and benign insulinoma. The insulinoma was recognised and localised by preoperative ultrasonography in the pancreatic head (n = 1), body (n = 3) or tail (n = 1). For the videolaparoscopic procedure, three to five trocars were necessary. Cephalic and corporeal insulinomas were approached through an opening of the gastrocolic ligament and caudal insulinoma required mobilisation of the splenic flexure of the colon and dissection of the splenic pedicle. Peroperative ultrasonography was not used. RESULTS: Four resections were exclusively performed with videolaparoscopy: three enucelations and one distal pancreatectomy with splenic preservation. The cephalic insulinoma could not be found by laparoscopic exploration and required a laparotomy to be recognised and enucleated; it was located further down than expected. There were no postoperative complications in four patients. One enucleation was complicated by a pancreatic fistula that required reoperation. All the patients were cured with a 6- to 16-month follow-up. CONCLUSION: Selected insulinomas may be operated on with videolaparoscopy. Preoperative endoscopic ultrasonography is necessary for this selection. Videolaparoscopic approach is contraindicated in multiple insulinomas, in insulinomas located on the posterior wall or deeply located in the head of the pancreas, and in malignant tumors. Videolaparoscopic resection is mainly indicated in unique and benign insulinomas, superficially located on the anterior wall of the pancreas, to be resected by enucleation or distal pancreatectomy. Disadvantage of laparoscopic approach compared to conventional approach is the absence of palpation and difficulty to explore the whole pancreas; advantage is the lack of parietal incision and the good postoperative comfort.

Adult↗
PubMed2002

Minimally invasive endocrine surgery: laparoscopic resection of insulinomas.

Pancreatic insulinomas are mostly benign and solitary tumors. Successful management of patients with insulinoma relies on accurate localization of the tumors and the use of appropriate surgical techniques. However, preoperative radiological imaging studies often fail to localize the insulinomas because of the small tumor sizes. Conventional intraoperative ultrasonography combined with palpation has been widely used as the best localization tool. Since contact ultrasonography, a new technique for localizing pancreatic lesions, became available as a laparoscopic study, several surgeons have utilized laparoscopy for not only localization but also resection of insulinomas. Previous reports of laparoscopic ultrasonography for intraoperative identification of insulinomas showed a 100% success rate in cases with insulinoma localized by preoperative imaging studies, but a less satisfactory rate in cases with occult insulinoma. Laparoscopic resection of insulinomas located in the head of the pancreas is often difficult because of its anatomical relationship with important adjacent structures such as pancreatic duct and mesenteric vessels. In contrast, insulinomas located in the body or tail of the pancreas are laparoscopically resectable even when they are in close proximity to the major pancreatic duct. Laparoscopic procedure is a feasible technique with low morbidity for surgical management of insulinomas. Accurate preoperative localization is essential for safe performance of this minimally invasive procedure.

Endocrine Surgical Procedures↗
PubMed1997

A hyperinsulinaemic, sequentially eu- and hypoglycaemic clamp test to characterize autonomous insulin secretion in patients with insulinoma.

To better characterize autonomous insulin secretory behaviour in insulinoma patients and to establish diagnostic criteria with high accuracy, hyper-insulinaemic, sequentially eu- and hypoglycaemic clamp tests were performed in insulinoma patients and control subjects. Ten patients with insulinoma (benign in nine, histologically proven in nine) and 10 patients with suspected episodes of hypoglycaemia, in whom thorough clinical evaluation excluded an insulinoma, were examined. Five insulinoma patients were restudied after successful extirpation of the tumour. Suppression of C-peptide during low-dose [2 pmol kg-1 min-1 (20 mU kg-1 h-1) for 90 min, plasma insulin approximately 120 pmol L-1 (20 mUL-1)] and high-dose [8 pmol kg-1 h-1 (80 mU kg-1 h-1) for 90 min, plasma insulin approximately 450 pmol L-1 (75 mU L-1)] insulin infusion under euglycaemic conditions [plasma glucose 4.4-5.0 mmol L-1 (80-90 mg dL-1)] and during high-dose insulin infusion under hypoglycaemic conditions [glucose 2-2.2 mmol L-1 (40-45 mg dL-1)] was evaluated by radioimmunoassay (RIA). Euglycaemic hyper-insulinaemia suppressed C-peptide in control subjects (P < 0.0001), whereas in insulinoma patients apparently irregular changes in C-peptide concentrations (with spontaneous or paradoxical increments, P = 0.0006 vs. controls) were observed. The combination of hyper-insulinaemia and controlled hypoglycaemia led to a nearly complete suppression of C-peptide in normal subjects (from basal, 0.76 +/- 0.08-0.06 +/- 0.01 nmol L-1; maximum observed value 0.10 nmol L-1), which was more pronounced than at the point of discontinuation of prolonged fasting (> 48 h; 0.26 +/- 0.16 nmol L-1; P = 0.005). In insulinoma patients, C-peptide remained elevated under all conditions (P = 0.51 vs. prolonged fasting). All these findings were reversible after successful surgical removal of the insulinoma. Insulinoma patients could be identified as abnormal by (a) non-suppression of C-peptide even under hyperinsulinaemic/hypoglycaemic conditions (10 out of 10 patients) and (b) irregular increments in C-peptide under conditions that led to at least partial suppression in all normal subjects (9 out of 10 patients) and/or by an apparent shift to the left of insulin secretion relative to glucose concentrations (7 out of 10 patients). Controlled exposure to hyperinsulinaemic/hypoglycaemic conditions can help to characterize autonomous secretion in insulinoma patients and may be used as a diagnostic procedure when conventional methods yield equivocal results.

Adult↗
PubMed2001

Insulinoma-induced hypoglycemic death in mice is prevented with beta cell-specific gene therapy.

OBJECTIVE AND SUMMARY BACKGROUND DATA: Tumor-specific gene therapy can be achieved if a tumor-specific promoter can be identified. In this study the authors investigated the use of the rat insulin promoter (RIP) for insulinoma-specific expression of a reporter gene. Insulinoma-specific cytotoxicity using the suicide gene thymidine kinase (tk) was studied both in vitro and in vivo. RIPtk gene therapy, delivered by a nontoxic, noninflammatory liposomal delivery system, was used in an insulinoma ICR/SCID mouse model to prevent hypoglycemic death. METHODS: Rat insulin promoter (0.502 kb) was ligated to the reporter gene lacZ and ligated to the tk gene. These two genes were transfected into a mouse insulinoma (NIT) cell line to ascertain insulinoma-specific expression and insulinoma-specific cytotoxicity in vitro. Reverse transcriptase-polymerase chain reaction and electrophoretic mobility-shift assays were performed on NIT-1 cell RNA and nuclear extract, respectively, to determine the transcription factors present and responsible for RIP activation in NIT-1 cells. A mouse insulinoma model was created with NIT-1 cells. These mice were treated with the RIPtk gene, and both blood sugars and animal viability were monitored. RESULTS: Only NIT-1 cells stained blue after X-gal staining or had detectable levels of beta-galactosidase protein. A significant decrease in cell survival was observed in NIT-1 cells transfected with RIPtk in vitro. Messenger RNA for both BETA2 and PDX-1 was found in NIT-1 cells, and a supershift was observed for both BETA2 and PDX-1. Experimental mice treated with the RIPtk gene, delivered by a liposomal gene delivery system, maintained their blood glucose levels, and the animals did not die of hypoglycemia. CONCLUSIONS: The data suggest that the RIP is an insulinoma-specific promoter. An ICR/SCID mouse insulinoma model was used to show that insulinoma-specific cytotoxicity can be accomplished by RIP coupled to a suicide gene in vivo, preventing hypoglycemic death.

Animals↗
PubMed2006

Long-term in vitro growth of human insulin-secreting insulinoma cells.

OBJECTIVE: Long-term in vitro maintenance of human insulin-secreting insulinoma cells. METHODS: (1) Cell culture of ex vivo-derived insulinoma cell suspensions from 8 individual human donors, using various cell culture medium supplementations; (2) determination of insulin synthesis and secretion using immunocytochemistry and insulin and pro-insulin radioimmunoassays; (3) nestin-immunostaining of long-term in vitro grown insulinoma cell suspensions, and (4) phase-contrast light microscopy for analyzing the in vitro growth characteristics of the insulinoma cells. RESULTS: (1) Parallel persistence of in vitro insulinoma cell proliferation as well as insulin-synthesizing and -secreting capacity depended on both the co-culture of insulinoma cells with human fibroblasts and the supplementation of the cell culture medium with tissue culture supernatant derived from the rodent pituitary adenoma cell line GH-3; (2) immunostaining for insulin and secretagogin confirmed the neuroendocrine origin of the insulinoma cells grown in vitro; (3) insulin secretion capability persisted up to an observation period of 25 weeks; (4) insulin secretion rates after 6 weeks of in vitro growth ranged from 3.5 to 83.3 muU/ml/h/60,000 cells plated, and (5) after long-term in vitro growth of insulinoma-derived cell suspensions with persistent insulin-secreting capacity, nestin staining was observed predominantly in co-cultured fibroblasts. CONCLUSION: Our data describe for the first time the long-term in vitro culture of insulin-secreting human insulinomas and highlight the importance of beta-cell trophic factors for insulinoma cell growth.

Adult↗
PubMed1998

Culture of human insulinoma cells: development of a neuroendocrine tumor cell- and human pancreatic islet cell-specific monoclonal antibody.

We report on the culture of human insulinoma cells derived from a 32-year-old male patient with hyperinsulinism due to an insulinoma of the pancreas. A single-cell suspension was made by passing insulinoma fragments through a fine-gauge stainless-steel mesh. Cluster-forming insulinoma cells resembling pancreatic islets grew in the presence of fibroblasts. The insulinoma cell clusters could be differentiated from fibroblasts by using in situ pan optic staining and specific immunocytochemical staining (anti-human insulin and anti-human insulinoma monoclonal antibody (mAb) D24). mAb D24 was generated using insulinoma cells as antigen for immunization of a Balb/C mouse and cell fusion by the hybridoma cell technique. The anti-insulinoma cell mAb recognized a 32 kDa protein on immunoblot analysis of neuroendocrine tumor cells. D24 mAb also reacted immunohistochemically with normal pancreatic beta-cells and tumors such as vipoma, gastrinoma and carcinoid. Insulinoma cell clusters separated from fibroblasts by micromanipulation and plated into multiwell culture dishes exhibited an insulin-secretion rate of approximately 30 U/100 cells per 24 h with no insulin-secretory response to elevated glucose concentration. Purified insulinoma cells incubated with 1 ng/ml human nerve growth factor expressed neurofilament and neurite extension. These findings together with earlier observations in animal models suggest that human pancreatic beta-cells share some properties with neurons and are related to other neuroendocrine cells in the gastrointestinal tract.

Adult↗
PubMed1993

Gs alpha--identification of a gene highly expressed by insulinoma and other endocrine tumors.

BACKGROUND: The isolation of mRNA molecules that are either uniquely or more highly expressed by tumor and not normal tissue is a powerful tool in the study of cell regulation and growth. To this end we constructed a complementary DNA (cDNA) library from messenger RNA (mRNA) isolated from a human insulinoma and, by differential hybridization with cDNA from both normal pancreas and insulinoma, isolated clones more highly expressed by insulinoma. METHODS: Total RNA was isolated from human insulinoma and normal pancreas and purified to mRNA by oligo (dT) column. An insulinoma cDNA library was constructed and screened with 32P-labeled cDNA from pancreas and insulinoma. Northern blots from insulinoma, pancreas, carcinomas, normal endocrine tissues, and endocrine tumors were then probed with the 32P-labeled inserts. RESULTS: Two clones that consistently hybridized with 32P cDNA from insulinoma and not pancreas proved to represent mRNAs for insulin and the alpha subunit of the Gs protein. There was a markedly higher expression (30-fold) of the gene for Gs alpha in mRNA from insulinoma compared with normal pancreas by Northern blot analysis. We found Gs alpha to be more highly expressed by a pheochromocytoma, a corticotropin-producing islet cell tumor of the pancreas, and a corticotropin-producing thymic carcinoid (up to 35-fold) compared with normal pancreas, whereas normal endocrine tissues, a parathyroid adenoma, thyroid follicular adenoma, gastrinoma, and several carcinomas showed no expression. CONCLUSIONS: This study showed that Gs alpha is highly expressed in insulinoma and certain endocrine tumors. It is not expressed in several cancers or normal endocrine tissues. Others have implicated mutated Gs proteins in the tumorigenesis of pituitary and thyroid tumors. G proteins are also known to mediate hormonal transmembrane signaling. Its overexpression in four of seven endocrine tumors tested suggests that it may have a role in the unregulated hormone secretion and/or a role in the tumorigenesis of differentiated endocrine tumors.

DNA↗
PubMed2005

Chromosome 1q loss of heterozygosity frequently occurs in sporadic insulinomas and is associated with tumor malignancy.

The pathogenesis of sporadic insulinomas is not clear, and there are no reliable genetic determinants that are useful to distinguish malignant and benign forms of this tumor. It was reported that 1q LOH might contribute to pathogenesis in gastrinomas and was correlated with tumor progression. However, little data are available on 1q LOH in sporadic insulinomas. In our study, we determine whether 1q LOH occurs in sporadic insulinomas and is associated with tumor malignancy by performing 1q allelotyping with 17 markers in 40 tumors and pair normal DNA. Thirty-five (88%) insulinomas had 1q LOH. Of the 35 insulinomas with 1q LOH, 14 (40%) had 1q21.3-23.2 LOH over a 7.5 cM region (SRO-1), whereas LOH in 21 tumors (60%) occurred at 1q31.3 over an 11.4 cM area (SRO-2). Of 24 tumors without MEN1 LOH, 20 had either SRO-1 or SRO-2 LOH (83%), whereas in 16 tumors with MEN1 LOH, 9 were shown to have LOH at either SRO-1 or SRO-2 (56%) (p = 0.065). This result suggests that LOH at 2 SRO might be MEN1 gene independent and may contribute to the pathogenesis in a subset of insulinomas without MEN1 gene LOH. The presence of 1q21.3-23.2 LOH is significantly associated with malignancy of insulinomas (p = 0.014). The high frequency of LOH at 1q 21.3-23.2 and 1q31.3 suggests these 2 areas may harbor putative tumor suppressor genes that may play an important role in the tumorigenesis of a subset of insulinomas. LOH at 1q21.3-23.2, which was associated with tumor malignancy, could be one of the genetic markers for identifying malignancy in sporadic insulinomas.

Adolescent↗
PubMed1996

Peripheral nerve pathology in rats with streptozotocin-induced insulinoma.

Peripheral nerve structure was systematically examined in rats with insulinoma induced by streptozotocin (STZ). Normal Wistar rats, aged 3 months (n = 10), were treated with intravenous injections of STZ (20 mg/kg) and housed in plastic cages with free access to water and chow until 24 months of age. Three rats with insulinoma survived and were examined pathologically. Age-matched normal Wistar rats (n = 6) were used for comparison. The insulinoma-bearing rats showed a marked increase in body weight and decrease in blood glucose. In a teased nerve fiber study of the sciatic nerve, the percentage of abnormal fibers undergoing axonal degeneration and de- and remyelination in age-matched normal control rats was 3.9 +/- 2.5% (means +/- SD), whereas in the three insulinoma-bearing rats 49%, 50%, and 24%, respectively, of the fibers showed such changes. Regenerating fibers were also numerous in each insulinoma-bearing rat (36%, 42% and 27%, respectively). Morphometric analysis revealed smaller mean myelinated fiber and axonal areas in all the nerves examined (sciatic, tibial and sural) in insulinoma-bearing rats as compared to those in age-matched normal rats. Fiber area frequency histograms showed a decrease in large myelinated fibers and an increase in small regenerated fibers in insulinoma-bearing rats. Ultrastructurally, endoneurial microvessels exhibited a narrowed vascular lumen with swollen endothelial cells and vacuolar degeneration of pericytes, suggesting an involvement of vascular changes in the neuropathic development. The present study demonstrated marked structural changes in both motor and sensory peripheral nerves of rats bearing experimentally induced insulinoma. We consider that axonal degeneration, regeneration and demyelination constitute the main pathology in the peripheral nerves of insulinoma-bearing rats, although no particular difference in severity of the lesions between sensory and motor and between proximal and distal nerves was apparent.

Animals↗
PubMed2002

Blind distal pancreatectomy for occult insulinoma, an inadvisable procedure.

BACKGROUND: Fasting hypoglycemia with neuroglycopenic symptoms corrected by administration of glucose are the hallmarks for the diagnosis of insulinoma. Surgical resection is the treatment of choice for insulinomas, but localization of these lesions can be challenging. Blind distal pancreatectomy has been advocated for occult insulinomas not detected on imaging studies or during abdominal exploration. With the advent of newer localization techniques, we challenge the wisdom of this approach. STUDY DESIGN: The records of patients (multiple endocrine neoplasia excluded) with pathologically proved insulinoma who were screened at our institution or referred to us after a failed blind distal pancreatectomy were reviewed. All records included patient history and results of physical examination and routine blood and urine tests. The diagnosis of insulinoma was confirmed during a supervised fast. Patients with biochemically proved insulinoma underwent localization studies and operation. Studies included CT scans, MRI, transabdominal ultrasound, intraoperative ultrasonography, angiography (more recently, Ca++-stimulated arteriography), and venous sampling. RESULTS: From 1970 to 2000, 99 patients (34 men, 65 women; mean age 43 years) underwent operation. All patients with benign tumors (92) were cured after operation. Seventeen patients were referred to the NIH after a failed blind distal pancreatectomy. Of these, 5 were diagnosed as having factitious hypoglycemia. In the other 12 patients a tumor was localized in the pancreatic head. Two patients incorrectly diagnosed with nesidioblastosis after initial surgery were subsequently cured by resection of an insulinoma. CONCLUSIONS: The use of preoperative imaging studies, most notably Ca++-stimulated arteriography, and intraoperative ultrasonography permits detection of virtually all insulinomas, including reopcrated cases. When a tumor is not detected, the procedure should be terminated and the patient referred to a center capable of performing advanced preoperative and intraoperative localization techniques. With the preoperative and intraoperative imaging strategies currently available, the use of blind distal pancreatectomy for occult insulinoma should be abolished.

Adolescent↗