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Journal articles on the topic 'Nesidioblastose'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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1

Klaus, Daniele Gehlen, Diélly Cunha de Carvalho, and Jaime César Gelosa Souza. "Hipoglicemia por nesidioblastose: uma complicação rara da cirurgia bariátrica?" ABCD. Arquivos Brasileiros de Cirurgia Digestiva (São Paulo) 20, no. 4 (2007): 280–82. http://dx.doi.org/10.1590/s0102-67202007000400013.

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INTRODUÇÃO: A cirurgia bariátrica tem-se mostrado o método mais eficaz na resolução do diabetes mellitus tipo II, chegando a resultados superiores a 80% de cura da doença. Contudo, alguns estudos têm mostrado estado de hiperinsulinemia com hipoglicemia em certos pacientes obesos mórbidos após a realização da cirurgia bariátrica, ao que se denominou nesidioblastose, que corresponde ao hipercrescimento patológico das células beta pancreáticas. O objetivo desse estudo é realizar revisão bibliográfica sobre nesidioblastose pós-cirurgia bariátrica, através da pesquisa por artigos científicos publicados a partir de 2000. MÉTODOS: Realizou-se revisão bibliográfica de artigos científicos publicados a partir de 2000. A base de dados pesquisada foi o PubMed, através do site www.pubmed.gov. cruzando-se os descritores Nesidioblastose. Hiperinsulinismo. Hipoglicemia. Cirurgia bariátrica, complicações. REVISÃO DE LITERATURA: Revisou-se 14 publicações encontradas com o tema. Dentre elas, Cummings defende que após a realização da cirurgia bariátrica, ocorrem alterações no trânsito intestinal gerando estimulação e crescimento excessivo das células beta-pancreáticas e maior atividade dos hormônios pancreáticos, sugerindo possível causa para a nesidioblastose. Corroborando para desvendar a causa dessa doença, autores sugerem que o rápido trânsito alimentar duodenal após o bypass gástrico, eleva os níveis da peptídeo glucagonóide 1 e estimula, assim, a hiperinsulinemia hipoglicêmica nesses pacientes. De forma semelhante, outros defendem que a perda de peso após a cirurgia bariátrica, reduz muito a resistência à insulina devido à hipertrofia e hiperfunção das células beta-pancreáticas, o que é muito comum na obesidade, gerando a nesidioblastose. CONCLUSÃO: A nesidioblastose após cirurgia bariátrica pode representar o extremo patológico de um fenômeno benéfico para a maioria dos pacientes obesos mórbidos com diabetes do tipo II, porém em alguns casos raros esse fenômeno benéfico gera malefícios, ou seja, a nesidioblastose, que deve ser corrigida pela ressecção parcial do pâncreas, sob pena de ameaçar a vida desses pacientes.

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2

Hümmer, H., H. Böhles, J. Giedl, and R. Schück. "7/8 Pankreasresektion bei Nesidioblastose?" European Journal of Pediatric Surgery 43, no. 04 (1988): 281–83. http://dx.doi.org/10.1055/s-2008-1043470.

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3

Costa, Raquel R., Frederico F. R. Maia, and Levimar R. Araújo. "Hipoglicemia hiperinsulinêmica persistente endógena no adulto: relato de caso." Arquivos Brasileiros de Endocrinologia & Metabologia 51, no. 1 (2007): 125–30. http://dx.doi.org/10.1590/s0004-27302007000100020.

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A hipoglicemia hiperinsulinêmica persistente endógena em adultos é, na maioria dos casos, causada por insulinoma. A Nesidioblastose, uma hiperinsulinemia funcional rara por hiperplasia das células beta do pâncreas, tem sido descrita principalmente em neonatos. Apresentamos o caso de uma paciente de 34 anos com quadro clínico-laboratorial compatível com hipoglicemia hiperinsulinêmica endógena (Glicemia jejum: 54 mg/dl / Valor de referência (VR): 6099 mg/dl; Insulina sérica: 70,9 mcU/ml / VR: < 29,1 mcU/ml; e Peptídeo C: 7,1 ng/ml / VR: 1,15,0 ng/ml - simultâneos à glicemia). Foi aventada a hipótese de insulinoma. Em função da ausência de imagem característica aos exames radiológicos (ultra-som e tomografia de abdome), optou-se pela laparotomia exploradora, onde também não foi evidenciado tumor pancreático macroscopicamente. Os exames histopatológico e imuno-histoquímico evidenciaram hiperplasia de células beta, de segmento distal do pâncreas, compatível com nesidioblastose. A paciente evoluiu com estabilidade clínica por cerca de dois meses, quando se verificou recidiva das crises hipoglicêmicas, refratárias ao uso de Octreotide. Optou-se pela realização de "octreosan", que indicou nesidioblastose difusa, sendo procedida pancreatectomia parcial extensa. Seguiu-se o uso contínuo de Octreotide, com controle eficaz das crises hipoglicêmicas. Uma vez que esse é um diagnóstico raro no adulto, objetiva-se, nesse artigo, divulgar o manejo diagnóstico-terapêutico em casos de hipoglicemia hiperinsulinêmica endógena.

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4

Schatz, M., A. Wolf, K. H. Deeg, R. Meister, and G. Seitz. "Beidseitige Nebennierenblutung und Nesidioblastose eines makrosomen Neugeborenen." Monatsschrift Kinderheilkunde 147, no. 6 (1999): 557–61. http://dx.doi.org/10.1007/s001120050459.

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5

Kunz, Von Jochen, Holger Haberland, Andrea Schmidt, and Peter Amendt. "Immunhistochemischer Chromogranin A-Nachweis und morphometrische Befunde bei frühkindlicher Nesidioblastose." Acta Histochemica 89, no. 2 (1990): 131–40. http://dx.doi.org/10.1016/s0065-1281(11)80349-1.

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6

Henzen. "Hypoglykämien bei der Frau eines Diabetikers." Therapeutische Umschau 69, no. 12 (2012): 667–71. http://dx.doi.org/10.1024/0040-5930/a000346.

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Insulinome sind mit einer Inzidenz von 4 pro 100'000 eine seltene Erkrankung, vermeintliche Hypoglykämie-Symptome werden dagegen häufig auch von Menschen ohne Diabetes mellitus beschrieben. Die Liste der möglichen Ursachen ist sehr umfangreich, weshalb mittels Anamnese, Klinik und laborchemischen Untersuchungen der Verdacht auf ein Insulinom erhärtet werden bzw. ausgeschlossen werden muss. Wie bereits vor über 70 Jahren der New Yorker Chirurge Allen Whipple gefordert hat, ist eine strikte Beachtung der Trias: dokumentierte Hypoglykämie und Neuroglykopenie und Besserung auf Glukosezufuhr Voraussetzung für weitere diagnostische und therapeutische Schritte. Die hyperinsulinämische Hypoglykämie wird im Fastentest bewiesen, Ziel der bildgebenden Methoden ist die Lokalisation des Insulinoms für die chirurgische Resektion bzw. die Abgrenzung zur nicht-Insulinom bedingten pankreatogenen Hypoglykämie (Nesidioblastose). Als neue und hochsensitive Methode hat sich die GLP-1 Rezeptor Szintigraphie erwiesen, womit auch im vorliegenden Fallbeispiel eine zielgerichtete chirurgische Intervention möglich war.

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7

McElroy, Michele K., Andrew M. Lowy, and Noel Weidner. "Case report: focal nesidioblastosis (“nesidioblastoma”) in an adult." Human Pathology 41, no. 3 (2010): 447–51. http://dx.doi.org/10.1016/j.humpath.2009.09.002.

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8

Treiber, Gerlies. "Nicht-Diabetes-assoziierte Hypoglykämien." Journal für Klinische Endokrinologie und Stoffwechsel 13, no. 4 (2020): 177–81. http://dx.doi.org/10.1007/s41969-020-00124-7.

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ZusammenfassungDie Symptome einer Hypoglykämie sind häufig und unspezifisch. Echte Hypoglykämien sind selten und kommen meistens im Rahmen einer Insulintherapie vor. Die Diagnose einer Hypoglykämie bei Patienten ohne Diabetes erfordert das Vorliegen der Whipple-Trias mit dokumentierter Blutglukose ≤ 55 mg/dl, hypoglykämischen Symptomen und deren Verschwinden durch Zufuhr von Kohlenhydraten. Eine weitere Abklärung erfolgt mittels standardisiertem 72‑h Fastentest oder bei Patienten mit vorwiegend postprandialen Hypoglykämien einem 5‑h-Mahlzeitentoleranztest. Die parallele Messung von Plasmaglukose, Insulin, C‑Peptid, Proinsulin und Ketonen hilft in der Differenzierung zwischen Insulinom, faktitieller Gabe von Insulin und Sulfonylharnstoffen sowie Nesidioblastose (NIPHS) und Hypoglykämien nach bariatrischen Operationen. Die Messung von Insulin-Autoantikörpern ist hinweisend auf ein autoimmunes Insulinsyndrom und der Nachweis von „big“ IFG‑2 auf eine paraneoplastische Sekretion dieses Proteins bei Tumorerkrankungen. Erst wenn der Nachweis einer autonomen endogenen Hyperinsulinämie vorliegt, erfolgt die Lokalisationsdiagnostik. Dabei sind szintigrafische Untersuchungen mittels radioaktivem 68Gallium und Exendin‑4 und ein selektiver Kalzium-Stimulationstest in der Lokalisation von Insulinomen hilfreich. Therapeutisch ist eine Hypoglykämie akut durch Glukosegabe zu behandeln. Die langfristige Therapie besteht wenn möglich in der Beseitigung der auslösenden Ursache, Ernährungsmaßnahmen sowie medikamentöser Hemmung der Insulinsekretion.

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9

Caboclo, Edmundo Di Giaimo, and Moacyr Vergara de Godoy Moreira. "Mudança de função para atividade compatível de uma funcionária com restrição: relato de um caso de nesidioblastose após realização de cirurgia bariátrica." Revista Brasileira de Medicina do Trabalho 16, s1 (2018): 62–63. http://dx.doi.org/10.5327/z16794435201816s1p41.

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10

R., Madhumathi, Mohan C. N., and Prabhu S. "Islets of hypoglycaemia: a rare case of adult onset nesidioblastosis." International Journal of Advances in Medicine 7, no. 1 (2019): 185. http://dx.doi.org/10.18203/2349-3933.ijam20195669.

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A case of diffuse nesidioblastosis in an adult patient is reported in this study. A 24-year-old female with no known comorbidities presented with multiple episodes of documented recurrent hypoglycaemia and Hypoglycaemia induced seizures both in fasting and postprandial state. Her blood investigations revealed low plasma glucose levels, high insulin and C-peptide levels with positive 72-hour fast test. Her transabdominal USG and CECT abdomen did not reveal any abnormality, 68Ga DOTANOC PET CT done showed ill-defined diffuse somatostatin receptor expression in the pancreatic head and tail suggestive of nesidioblastosis. As patient was not willing for surgical treatment, hence started on medical treatment with oral nifedipine. Nesidioblastosis is very rare in adults. It is an important differential diagnosis in adults with hyperinsulinemic hypoglycemia although the incidence is very rare in adults. PET SCAN was used to non-invasively diagnose nesidioblastosis in this case. Surgery being the preferred choice of treatment in nesidioblastosis, there is limited data on medical line of management in nesidioblastosis.

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11

Orujov, Mushfig, Keith K. Lai та Catherine L. Forse. "Concurrent Adult-Onset Diffuse β-Cell Nesidioblastosis and Pancreatic Neuroendocrine Tumor: A Case Report and Review of the Literature". International Journal of Surgical Pathology 27, № 8 (2019): 912–18. http://dx.doi.org/10.1177/1066896919858129.

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Nesidioblastosis is an uncommon cause of organic persistent hyperinsulinemic hypoglycemia in adults. We report a case of adult-onset diffuse β-cell nesidioblastosis in a 49-year-old woman who was status-post Roux-en-Y gastric bypass and distal pancreatectomy for a well-differentiated pancreatic neuroendocrine tumor. While the neuroendocrine tumor was suspected to be an insulinoma, persistent hypoglycemia postoperatively suggested either incomplete resection or a second pancreatic neoplasm. Completion pancreatectomy revealed islet β-cell hyperplasia and nuclear pleomorphism consistent with β-cell nesidioblastosis. The patient’s blood glucose levels normalized after completion pancreatectomy. While β-cell nesidioblastosis and insulinomas can coexist in the same patient, pathologists should be aware of β-cell nesidioblastosis as a potential cause for hyperinsulinemic hypoglycemia and should exclude it in patients who have not shown definitive clinical response after surgical excision of a pancreatic neuroendocrine tumor.

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12

Garcia, J. Palla, Teresa França, Consiglieri Pedroso, Carlos Cardoso, and M'Olímpia Cid. "Nesidioblastosis in the Adult Surgical Management." HPB Surgery 10, no. 4 (1997): 201–9. http://dx.doi.org/10.1155/1997/81239.

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Nesidioblastosis is an exceedingly rare occurrence in the adult and, when it appears, it is usually part of a MEA1 syndrome.We present a case of nesidioblastosis in a young woman, with no concurrent endocrine pathology, while we discuss in detail the diagnostic and therapeutic problems posed by this condition.The selected treatment was sub-total pancreatectomy (70–80%) and the histopathologic and immunohistochemical tests of the surgical specimen showed: “Diffuse Nesidioblastosis”.The histopathologic and immuno-histochemical features of the resected pancreas are analysed in detail.

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13

Yurekli, Banu Sarer, Nilufer Ozdemir Kutbay, Ilker Altun, et al. "Adult Nesidioblastosis With Hypoglycemia Mimicking an Insulinoma: A Challenging Case." International Surgery 102, no. 7-8 (2017): 324–27. http://dx.doi.org/10.9738/intsurg-d-17-00020.1.

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Introduction: Nesidioblastosis is the primary cause of persistent hyperinsulinemic hypoglycemia in infants but it is a rare entity for the adults. Nesidioblastosis is defined as an increase of pancreatic beta cells in number and in size. Case Presentation: We describe a rare case of nesidioblastosis with positive endoscopic ultrasonography result mimicking an insulinoma. A 35-year-old female patient had hypoglycemic episodes with high insulin level. Her investigation revealed low venous plasma glucose, high insulin and C-peptide level with positive 72-hour fasting test suggestive of hyperinsulinemic hypoglycemia. Abdominal computed tomography did not show any mass lesion. Endoscopic ultrasonography revealed a mass lesion sized as 1 cm in diameter in the pancreas. But, insulinoma like lesion couldn't be found intra-operatively. It was decided to perform distal pancreatectomy. After distal pancreatectomy, nesidioblastosis was diagnosed histopathologically. The patient was free from her symptoms after surgery. Conclusion: This case illustrates difficulties and limitations of imaging modalities and false positive result of EUS in a case of nesidioblastosis. When there is no insulinoma like lesion during operation, operation should be performed as gradient guided pancreatectomy by the way of selective arterial calcium injection test.

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14

Zhao, Xiaohui, Bruce E. Stabile, Junqin Mo, Jun Wang, and Samuel W. French. "Nesidioblastosis Coexisting With Islet Cell Tumor and Intraductal Papillary Mucinous Hyperplasia." Archives of Pathology & Laboratory Medicine 125, no. 10 (2001): 1344–47. http://dx.doi.org/10.5858/2001-125-1344-ncwict.

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Abstract A coexisting of intraductal papillary mucinous hyperplasia (IPMH) and islet cell tumor with nesidioblastosis of the pancreas in a 51-year-old man is reported. All of the clinical data indicated an insulinoma. A distal pancreatectomy was performed. A discrete mass measuring 1.9 × 2.0 cm was grossly identified in the tail of the pancreas. There were no other gross lesions. An islet cell tumor with nesidioblastosis was confirmed by immunostains and ultrastructural study. In addition, an IPMH was found that involved mainly branches of the pancreatic duct. The islet cell tumor and IPMH were topographically separated; however, there was a histologically intimate relationship between the nesidioblastosis and the IPMH. These findings indicate that the IPMH may have derived from autocrine and paracrine influences on the existing duct epithelial cells. To the best of our knowledge, this is the first report of nesidioblastosis coexisting with islet cell tumor and IPMH.

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15

Wong, Mimi, Luke Conway, Caroline Cooper, Ashim Sinha, and Nirjhar Nandi. "NESIDIOBLASTOSIS IN AN ADULT WITH SHORT GUT SYNDROME AND TYPE 2 DIABETES." AACE Clinical Case Reports 5, no. 6 (2019): e375-e379. http://dx.doi.org/10.4158/accr-2019-0243.

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Objective: Adult nesidioblastosis is characterized by endogenous hyperinsulinemia typically causing post-prandial hypoglycemia, and most commonly occurs post-Roux-en-Y gastric bypass. Methods: We report a unique case of nesidioblastosis occurring in a 67-year-old female. Results: A 5-year history of symptomatic hypoglycemia occurred in a patient with short bowel syndrome and type 2 diabetes mellitus (T2DM) managed previously with a glucagon-like peptide 1 (GLP-1) agonist, which achieved significant weight loss. Continuous glucose monitoring captured 42 hypoglycemia episodes in a 2-week period, and following an oral glucose tolerance test there was the suggestion of a hyperinsulinemia state. She was managed with an open distal pancreatectomy, and subsequently required medical therapy to maintain euglycemia. Conclusion: We present the first case of nesidioblastosis occurring in a patient with short bowel syndrome, pre-existing T2DM managed with a GLP-1 agonist which achieved significant weight loss, all of which we speculate could have predisposed to hypoglycemia and development of nesidioblastosis.

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16

Toyomasu, Yoshitaka, Minoru Fukuchi, Takatomo Yoshida, et al. "Treatment of Hyperinsulinemic Hypoglycemia Due to Diffuse Nesidioblastosis in Adults: A Case Report." American Surgeon 75, no. 4 (2009): 331–34. http://dx.doi.org/10.1177/000313480907500413.

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An 82-year-old man was admitted to our hospital with a complaint of hypoglycemic syncope in the early morning. Insulinoma was suspected, but an abdominal CT showed no mass. Abdominal angiography showed a slight stain fed from the splenic artery. Arterial stimulation and venous sampling (ASVS) showed an abnormal insulin response only from the splenic artery. Under a provisional diagnosis of insulinoma, surgical treatment was undertaken. Although no pancreatic masses were palpable, we performed a distal pancreatectomy. Subsequently, a pathological examination revealed diffuse nesidioblastosis. Reported cases of diffuse nesidioblastosis have had common clinical features: postprandial hyperinsulinemic hypoglycemia, no abnormal findings in radiological examinations, and the presence of the ductulo-insular complex on histological examination. Surgical resection is recommended, but the extent of surgery is controversial. Our case had some clinical features of insulinoma but was diagnosed as diffuse nesidioblastosis according to histopathologic criteria. Because ASVS showed that the pancreatic body and tail had a lesion producing insulin abnormally, we performed a distal pancreatectomy to cure the hypoglycemia. Clinically, it is very difficult to distinguish diffuse nesidioblastosis from insulinoma. When we treat hyperinsulinemic hypoglycemia, ASVS can be an essential examination to decide the extent of pancreatectomy.

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17

Seki, Syuichiro, Tsuyomu Ikenoue, Naoki Murakami, et al. "Ectopic Nesidioblastosis." Pediatrics International 32, no. 3 (1990): 308–10. http://dx.doi.org/10.1111/j.1442-200x.1990.tb00829.x.

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18

Milner, R. D. "Nesidioblastosis unravelled." Archives of Disease in Childhood 74, no. 5 (1996): 369–72. http://dx.doi.org/10.1136/adc.74.5.369.

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19

Lozano-Melendez, Eduardo, Mercedes Aguilar-Soto, Luis Eugenio Graniel-Palafox, Laura Elena Ceceña-Martínez, Rafael Valdez-Ortiz, and Fabio Solis-Jimenez. "Adult Nesidioblastosis in Chronic Kidney Disease." Case Reports in Endocrinology 2019 (February 14, 2019): 1–6. http://dx.doi.org/10.1155/2019/7640384.

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Context. Nesidioblastosis is a rare cause of hyperinsulinemic hypoglycemia in adults. The diagnosis is further complicated in patients with kidney failure, since impaired renal function can cause hypoglycemia by itself and diagnostic criteria for this clinical scenario have not been developed yet. Case Description. We present the case report of a 36-year-old patient with end stage chronic kidney disease who presented to the emergency department because of hypoglycemia. However, the patient’s hypoglycemia did not respond well to medical treatment; the diagnosis of hyperinsulinemic hypoglycemia was made due to the presence of inappropriately high levels of insulin, proinsulin, and C-peptide during an episode of hypoglycemia. Imaging studies were performed without any conclusive findings; so selective intra-arterial pancreatic stimulation with hepatic venous sampling (SACTS) was done. Based on the results of this study the patient was referred for subtotal pancreatectomy. Classic criteria for the diagnosis of insulinoma with SACTS required a 2-fold increase in insulin levels but newer criteria suggest thresholds that are useful in the differential diagnosis of insulinoma and nesidioblastosis. In our patient, the former criteria were positive; however, the new criteria were not compatible with insulinoma but with nesidioblastosis, which was the final histopathological diagnosis. Conclusion. This seems to be the first case report of a patient with end stage chronic kidney disease and nesidioblastosis, as well as the first case of hyperinsulinemic hypoglycemia in the context of kidney failure diagnosed by SACTS. We consider this method to be very useful in patients with renal impairment because peripancreatic insulin levels do not depend on the renal function.

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20

Bozner, Peter, and Cynthia A. Donnell. "NESIDIOBLASTOSIS IN ADULTS." Southern Medical Journal 89, Supplement (1996): S100. http://dx.doi.org/10.1097/00007611-199610001-00203.

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21

Farley, David R. "Adult Pancreatic Nesidioblastosis." Archives of Surgery 129, no. 3 (1994): 329. http://dx.doi.org/10.1001/archsurg.1994.01420270107022.

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22

Andrews, R., M. Balsitis, K. Shurrock, and W. J. Jeffcoate. "Nesidioblastosis in adults." Postgraduate Medical Journal 68, no. 799 (1992): 389–90. http://dx.doi.org/10.1136/pgmj.68.799.389-a.

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23

DRAVECKA, I., and I. LAZUROVA. "Nesidioblastosis in adults." Neoplasma 61, no. 03 (2014): 252–56. http://dx.doi.org/10.4149/neo_2014_047.

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24

Kovács, Erzsébet, Hajnalka Németh, Éva Pásztor, and György Pfliegler. "Hyperinsulinemic hypoglycemia in adults. Case reports and a short review." Orvosi Hetilap 149, no. 35 (2008): 1659–64. http://dx.doi.org/10.1556/oh.2008.28399.

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A nem insulinoma eredetű tartós (perzisztáló) hyperinsulinaemiával járó hypoglykaemia oka a felnőttek körében ritkán előforduló nesidioblastosis. A nesidioblastosis hátterében álló inzulinszekréciós zavar molekuláris eltéréseken alapul. Morfológiailag különböző pancreassziget-, illetve béta-sejt-eltérések jellemzik, az inzulinhiperszekréció hátterében azonban körülhatárolható térfoglalás nem mutatható ki. A diagnózis alappillére az alacsony vércukorszint, a normoglykaemia intravénásan alkalmazott glükóz adásával történő fenntarthatósága, illetve az emelkedett inzulin- és C-peptid-szint. A hormontermelő tumor kizárásához mind invazív, mind nem invazív képalkotó módszerek szükségesek. A tartós, illetve ismétlődő hypoglykaemia káros hatásai gyógyszeres és/vagy sebészi kezeléssel előzhetők meg. Esetismertetés: A szerzők két betegük esetét ismertetik, akiknél felnőttkorban jelentkeztek a súlyos tünetekkel járó hypoglykaemiás epizódok. Nőbetegük „klasszikus” hypoglykaemiás tünetei 34 éves korban léptek fel: izzadás, szédülés, remegés, idegesség, illetve életveszélyes neuroglycopeniás jelek. Második, férfi betegük 22 éves, akinek fő panasza a hypoglykaemia ritka és szokatlan tünete, a nagyfokú éhségérzet mellett jelentkező puffadás volt. Az éhezési próbák mindkét esetben pozitívak voltak, vagyis hypoglykaemiás tünetek miatt fel kellett azokat függeszteni. Az inzulin- és a C-peptid-szintek magasak voltak, vénás inzulinszint-meghatározás az a. lienalis több pontjából és a képalkotó eljárások (komputertomográfia, mágneses rezonancia, pozitronemissziós tomográfia, angiográfia) nem tudtak igazolni térfoglalást. Az adatok alapján – szövettan hiányában is – a legvalószínűbb a felnőttkori nesidioblastosis diagnózisa. Diazoxid adásával mindkét esetben majdnem teljes tünetmentességet értek el, és neuroglycopeniás esemény a kezelés kezdete óta nem fordult elő. Következtetések: Ismeretlen eredetű hypoglykaemia esetén, ha a képalkotó eljárásokkal nincs körülírt képlet, a laboratóriumi adatok viszont egyértelműen emelkedett inzulinszekrécióra utalnak, gondolni kell nesidioblastosis lehetőségére. A sebészi beavatkozás veszélye pancreaselégtelenség éppúgy lehet, mint a betegség fennmaradása a hasnyálmirigy reszekciója miatt. Diazoxid adásával viszont tartós tünetmentesség érhető el ezen ritka kórképben, ezért érdemes elsőként ezt megkísérelni.

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Zarghamravanbakhsh, Paria, Swetha Murthi, and Emilia Pauline Liao. "A Rare Case of Adult Nesidioblastosis Causing Persistent Hypoglycemia in Patient With Atrial Fibrillation and Chronic Kidney Disease." Journal of the Endocrine Society 5, Supplement_1 (2021): A987—A988. http://dx.doi.org/10.1210/jendso/bvab048.2020.

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Abstract Nesidioblastosis is a very rare adult disorder in the absence of gastrointestinal surgery. Nesidioblastosis is a disorder of the endocrine pancreas causing hyperinsulinemic hypoglycemia. We describe a case of 83 year-old Caucasian male, with a 3-year history of severe refractory hypoglycemia with glucose level below 2.1 mmol/L. Confusion and sleepiness were reported as his neuroglycopenic symptoms. According to his family, his symptoms improved within 30 minutes of drinking orange juice. Hypoglycemia episodes mostly occurred while fasting and post exercise (after playing golf). His work up included low venous plasma glucose levels, high insulin and C-peptide levels that were consistent with an insulinoma. His history is remarkable for chronic kidney disease stage 3, penicillin allergy and atrial fibrillation with loop recorder for cardiac rhythm monitoring, which precluded him from undergoing CT with IV contrast or MRI studies. Abdominal computed tomography with oral contrast did not reveal any lesion. In an attempt to localize the suspected Insulinoma, he had celiac angiogram and portal vein sampling, which were inconclusive. He had a PET scan with dotatate that showed increased amount activity in the uncinate process of the pancreas. He was diagnosed with insulinoma and placed on monthly lanreotide injections, however continued to have severe hypoglycemia episodes. Due to persistent refractory hypoglycemia, patient underwent distal pancreatectomy and splenectomy and the histological findings were consistent with nesidioblastosis. Patient developed hyperglycemia in the post-operative course which was controlled with a carb consistent diet. This case demonstrates that differentiation between insulinoma and nesidioblastosis is very challenging, and in most cases, the diagnosis is made post operatively based on histologic findings.

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26

Saul, W., B. Willberg, and H. Bremer. "Die chirurgische Therapie der Nesidioblastose1." European Journal of Pediatric Surgery 39, no. 02 (2008): 96–98. http://dx.doi.org/10.1055/s-2008-1044183.

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Allué, Marta, Susana Ros, and Félix Lamata. "Pancreatic nesidioblastosis: Case report." Medicina Clínica (English Edition) 152, no. 6 (2019): 245–46. http://dx.doi.org/10.1016/j.medcle.2018.06.011.

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Casas Vara, Antonio, Ainhoa Fernández Bereciartúa, Miguel Ángel Rodríguez Muñoz, and Guadalupe González González. "Nesidioblastosis focal y difusa." Medicina Clínica 119, no. 5 (2002): 199. http://dx.doi.org/10.1016/s0025-7753(02)73361-7.

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Kistler, Caroline Hoell, and Kathleen Spiering. "Nesidioblastosis: A Case Study." Journal of Perinatal & Neonatal Nursing 11, no. 4 (1998): 65–74. http://dx.doi.org/10.1097/00005237-199803000-00009.

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30

Limongelli, P., A. Belli, L. Cioffi, et al. "Hepatobiliary and Pancreatic: Nesidioblastosis." Journal of Gastroenterology and Hepatology 27, no. 9 (2012): 1538. http://dx.doi.org/10.1111/j.1440-1746.2012.07183.x.

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31

Goossens, A., W. Gepts, J. M. Saudubray, et al. "Diffuse and Focal Nesidioblastosis." American Journal of Surgical Pathology 13, no. 9 (1989): 766–75. http://dx.doi.org/10.1097/00000478-198909000-00006.

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32

Angerpointner, Thomas A. "Surgical treatment of nesidioblastosis." Journal of Pediatric Surgery 20, no. 1 (1985): 101–2. http://dx.doi.org/10.1016/s0022-3468(85)80438-3.

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33

Puri, Prem. "Surgical treatment of nesidioblastosis." Journal of Pediatric Surgery 21, no. 11 (1986): 1011. http://dx.doi.org/10.1016/s0022-3468(86)80159-2.

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34

Kumar, Dinesh, Nancy E. Warner, and Tse-Ling Fong. "Nesidioblastosis of the Pancreas." American Journal of Clinical Pathology 93, no. 1 (1990): 161–62. http://dx.doi.org/10.1093/ajcp/93.1.161a.

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35

Kriger, A. G., A. V. Smirnov, D. V. Kalinin, et al. "Nesidioblastosis (diagnosis, surgical treatment)." Khirurgiya. Zhurnal im. N.I. Pirogova, no. 10 (2015): 16. http://dx.doi.org/10.17116/hirurgia20151016-29.

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Fong, T. L., N. E. Warner, and D. Kumar. "Pancreatic Nesidioblastosis in Adults." Diabetes Care 12, no. 2 (1989): 108–14. http://dx.doi.org/10.2337/diacare.12.2.108.

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Culberson, Donald, Elizabeth Manci, Arvind Shah, et al. "Nesidioblastosis in Sickle Cell Disease." Fetal and Pediatric Pathology 20, no. 2 (2001): 155–65. http://dx.doi.org/10.3109/15513810109168608.

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38

Kim, Albert, Jennifer R. Snaith, Hema Mahajan, and Deborah Jane Holmes‐Walker. "Nesidioblastosis following laparoscopic sleeve gastrectomy." Clinical Endocrinology 91, no. 6 (2019): 906–8. http://dx.doi.org/10.1111/cen.14083.

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Margulies, P., and E. Kahn. "Nesidioblastosis Versus Islet Cell Hyperplasia." Diabetes Care 12, no. 10 (1989): 751–52. http://dx.doi.org/10.2337/diacare.12.10.751.

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40

Walmsley, D., N. A. Matheson, S. Ewen, R. L. Himsworth, and J. S. Bevan. "Nesidioblastosis in an Elderly Patient." Diabetic Medicine 12, no. 6 (1995): 542–45. http://dx.doi.org/10.1111/j.1464-5491.1995.tb00538.x.

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Witteles, Ronald M. "Adult-Onset Nesidioblastosis Causing Hypoglycemia." Archives of Surgery 136, no. 6 (2001): 656. http://dx.doi.org/10.1001/archsurg.136.6.656.

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E. Culberson, Elizabeth A. Manci, A, Donald. "NESIDIOBLASTOSIS IN SICKLE CELL DISEASE." Pediatric Pathology & Molecular Medicine 20, no. 2 (2001): 155–65. http://dx.doi.org/10.1080/15227950151073192.

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43

Culberson, Donald E., Elizabeth A. Manci, Arvind K. Shah, et al. "Nesidioblastosis in Sickle Cell Disease." Pediatric Pathology & Molecular Medicine 20, no. 2 (2001): 155–65. http://dx.doi.org/10.1080/15513810109168608.

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44

Bergada, I., E. Aebert, and J. C. Cresto. "USE OF SOMATOSTATIN IN NESIDIOBLASTOSIS." Pediatric Research 28, no. 4 (1990): 423. http://dx.doi.org/10.1203/00006450-199010000-00050.

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Yagi, Minoru, Kunitoshi Shiraiwa, Masami Abiko, Hideo Sakuma, and Shigeru Hirai. "Familial nesidioblastosis in two sisters." Surgery Today 25, no. 2 (1995): 172–76. http://dx.doi.org/10.1007/bf00311094.

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Gacar, A., D. Pekmezci, M. O. Karayigit, Y. B. Kabak, and M. Y. Gulbahar. "Nesidioblastosis in a Simmental Calf." Journal of Comparative Pathology 147, no. 4 (2012): 491–94. http://dx.doi.org/10.1016/j.jcpa.2012.04.002.

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López, Vanessa, Carlos Alfonso Builes-Barrera, Germán Osorio, Carlos Hernando Morales, Juan Pablo Toro, and Alejandro Román-González. "Nesidioblastosis del adulto tras derivación gástrica." Revista Colombiana de Cirugía 32, no. 4 (2017): 319–29. http://dx.doi.org/10.30944/20117582.40.

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Milan, Stacey A., Ernest L. Rosato, Francis E. Rosato, Karen A. Chojnacki, Bernadette Profeta, and Serge A. Jabbour. "QS268. Pancreatic Nesidioblastosis Following Gastric Bypass." Journal of Surgical Research 144, no. 2 (2008): 373–74. http://dx.doi.org/10.1016/j.jss.2007.12.518.

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Restrepo, Katherine, Gloria Garavito, Leonardo Rojas, et al. "Nesidioblastosis del adulto coexistente con insulinoma." Revista Colombiana de Cancerología 13, no. 1 (2009): 49–60. http://dx.doi.org/10.1016/s0123-9015(09)70152-0.

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TANAKA, YOSHIAKI, TAKAHIRO ASAKAWA, KIMIO ASAGIRI, KENJIRO AKIYOSHI, SHIGEKI HIKIDA, and HIROYOSHI MIZOTE. "Nesidioblastosis Treated Successfully by 85% Pancreatectomy." Kurume Medical Journal 51, no. 1 (2004): 99–103. http://dx.doi.org/10.2739/kurumemedj.51.99.

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