An Uncommon Cause of Recurrent Presyncope, Dizziness, and Tachycardia: A Case Report of Diffuse, Adult-Onset Nesidioblastosis/Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS)
Open accessAbstract
Neurovegetative and autonomic symptoms are common presentations of various diseases, ranging from psychosomatic to severe organic disorders. A 23-year-old man presented with a history of recurrent presyncope, dizziness, and tachycardia. Repeated diagnostic work-up in various clinical settings could not identify any definite cause for approximately eight years. However, the incidental detection of postprandial and exercise-induced hypoglycemia was suggestive of an insulin-related disorder. A 72 h plasma glucose fasting test revealed endogenous hyperinsulinism. Upon imaging studies, no tumor mass potentially indicating insulinoma could be detected. 68Ga-DOTA-Exendin-4 PET/CT showed diffuse tracer enrichment throughout the whole pancreas. A subtotal pancreatectomy was performed, and the diagnosis of diffuse, adult-onset nesidioblastosis was established histopathologically. This corresponds to the clinical findings of a functional β-cell disorder, also known as non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS). After nine months, the symptoms recurred, making complete pancreatectomy necessary. Postoperative laboratory evaluation exhibited no residual endogenous C-peptide production. This case illustrates the diagnostic challenges in patients presenting with unspecific, neurovegetative and autonomic symptoms with a severe and rare underlying cause.
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TL;DR
A 23-year-old man with an eight-year history of recurrent presyncope, dizziness, and supraventricular tachycardia was ultimately diagnosed with diffuse, adult-onset nesidioblastosis/NIPHS after incidental self-measured postprandial and exercise-induced hypoglycemia prompted endocrine work-up. Subtotal pancreatectomy provided only temporary relief, and complete pancreatectomy was required nine months later.
Key findings
- The patient's symptoms began eight years before diagnosis with severe supraventricular tachycardia several times daily, accompanied by presyncope, dizziness, blurred vision, nausea, and other symptoms; repeated work-up across multiple specialties was inconspicuous except for inappropriate sinus tachycardia and other minor findings.
- Self-measured postprandial glucose was reproducibly 40–70 mg/dL (HbA1c 5.1%, 32.2 mmol/mol); a 4 h OGTT showed symptomatic declines at 60 min (78 mg/dL) and 210 min (50 mg/dL), and a 72 h fasting test showed persistent C-peptide >0.2 nmol/L and insulin >21 pmol/L with glucose 48–57 mg/dL.
- 68Ga-DOTA-Exendin-4 PET/CT showed diffuse tracer enrichment throughout the whole pancreas with no focal lesion; after subtotal pancreatectomy, recurrence at nine months showed residual pancreatic head uptake with SUVmax 10.26.
- Histopathology after both surgeries confirmed diffuse adult-onset nesidioblastosis (enlarged islets, hyperchromatic nuclei, physiological distribution of insulin/glucagon/somatostatin cells, Ki-67 <1%); two years postoperatively C-peptide was <0.1 ng/mL, confirming complete removal of endocrine pancreatic tissue.
Methods
Single case report of one 23-year-old male patient, with clinical history, laboratory testing (4 h OGTT, 72 h fasting plasma glucose test, autoantibody and hormonal screening), imaging (contrast-enhanced MRI, 68Ga-DOTA-Exendin-4 PET/CT), surgical intervention (subtotal left-sided spleen-preserving pancreatectomy, then complete pancreatectomy via classical Whipple procedure), and histopathological/immunohistochemical examination of surgical specimens. The paper also proposes a diagnostic algorithm for spontaneous hypoglycemia in adults and reviews treatment options; a companion literature review is described as submitted separately.
Limitations
The paper states no formal limitations section; it notes that mechanistic data on adult-onset NIPHS is scarce, that there is no established hypothesis to explain morphological differences between patients or to correlate morphology with clinical presentation, and that the extent of pancreatic resection in NIPHS remains controversial. Evident from the text: this is a single case (n=1), so findings are not generalizable; some OGTT values were not determined, and the significance of the patient's childhood glucose of 36 mg/dL was unclear because the preanalytical process could not be reconstructed; SACS was not performed.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
46 of 88 cited sources checked · 15 supported · 0 flagged · accuracy not yet measured
- Interpretationreasoning§ 1. Introduction · p. 2
This symptom finally led to the correct diagnosis of a functional β-cell disorder, also known as diffuse adult-onset nesidioblastosis or NIPHS.
“This symptom finally led to the correct diagnosis of a functional β -cell disorder, also known as diffuse adult-onset nesidioblastosis or non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS) [4-6].”
Quote in the paperSubstantial claim1 of 3 sources checked- cites [4] Geraghty, 2008, Hypoglycaemia in an Adult Male: A Surprising Finding in Pursuit of Insulinoma, Surgeon source
- cites [5] Qintar, 2012, Hypoglycemia Due to an Adult-Onset Nesidioblastosis, a Diagnostic and Management Dilemma, Avicenna J. Med. source
- cites [6] Jabri, 2004, Nesidioblastosis Associated with Hyperinsulinemic Hypoglycemia in Adults: Review of the Literature, Eur. J. Intern. Med. source
- Premisecitation§ 1. Introduction · p. 2
If clinical findings are suggestive of insulinoma but no tumor can be localized upon conventional imaging, rarer causes of recurrent spontaneous hypoglycemia in the adult patient must be considered: insulin autoimmune syndrome, also known as Hirata's disease, as well as functional β-cell disorders.
“If clinical findings are suggestive of insulinoma but no tumor can be localized upon conventional imaging, rarer causes of recurrent spontaneous hypoglycemia in the adult patient must be considered: insulin autoimmune syndrome, also known as Hirata's disease, as well as functional β -cell disorders [14,15].”
Quote in the paperSubstantial claim2 of 2 sources checked- cites [14] Cappellani, 2020, Insulin Autoimmune Syndrome (Hirata Disease): A Comprehensive Review Fifty Years after Its First Description, Diabetes, Metab. Syndr. Obes. Targets Ther. source
- cites [15] Tsujino, 2005, Noninsulinoma Pancreatogenous Hypoglycemia Syndrome: A Rare Case of Adult-Onset Nesidioblastosis, Intern. Med. source
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measured
- Interpretationcitation§ 2. The Case · p. 4
These findings are compatible with NIPHS/nesidioblastosis according to the diagnostic criteria described above.
“In conclusion, these findings are compatible with NIPHS/nesidioblastosis according to the diagnostic criteria described above (Figure 1) [14,15].”
Quote in the paperSubstantial claim2 of 2 sources checked- cites [14] Cappellani, 2020, Insulin Autoimmune Syndrome (Hirata Disease): A Comprehensive Review Fifty Years after Its First Description, Diabetes, Metab. Syndr. Obes. Targets Ther. source
- cites [15] Tsujino, 2005, Noninsulinoma Pancreatogenous Hypoglycemia Syndrome: A Rare Case of Adult-Onset Nesidioblastosis, Intern. Med. source
- Premisecitation§ Diagnostic Algorithm in Hypoglycemia · p. 10
Surgical procedures on the pancreas, especially total pancreatectomy, are associated with a considerable risk of morbidity and mortality.
“Of note, surgical procedures on the pancreas, especially total pancreatectomy, are associated with a considerable risk of morbidity and mortality [33,66-68].”
- Also stated in: § References · p. 11 · plain
“This is, however, accompanied by a considerable risk of morbidity and mortality, as illustrated by the presented case.”
Quote in the paperSubstantial claim4 of 4 sources checked- cites [33] Barbier, 2013, Impact of Total Pancreatectomy: Short- and Long-Term Assessment, Hpb source
The Post-operative course section reports 45% morbidity and 3.6% postoperative mortality among 56 patients who underwent total pancreatectomy, supporting the claim for that procedure. The study does not establish the risk for pancreatic surgical procedures more broadly. (LLM, conf=0.84)
Experimental — accuracy not yet measured - cites [66] Suzuki, 2017, The Clinical Outcomes after Total Pancreatectomy, Dig. Surg. source
- cites [67] Karagianni, 2012, Nutritional Status and Nutritional Support Before and After Pancreatectomy for Pancreatic Cancer and Chronic Pancreatitis, Indian J. Surg. Oncol. source
The Surgical Treatment of Chronic Pancreatitis section describes postoperative complications and operative morbidity, while the Enteral Nutrition section reports morbidity and mortality outcomes in patients undergoing upper gastrointestinal cancer surgery. The paper also describes serious consequences of total pancreatectomy, but the passages do not establish that its surgical morbidity or mortality risk is especially high relative to other pancreatic procedures. Page numbers were not available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measured - cites [68] Furbetta, N., Comandatore, A., Gianardi, D., Palmeri, M., Di Franco, G., Guadagni, S., Caprili, G., Bianchini, M., Fatucchi, L.M., and Picchi, M. (2021). Perioperative Nutritional Aspects in Total Pancreatectomy: A Comprehensive Review of the Literature. Nutrients, 13. source
The Introduction describes total pancreatectomy as highly invasive, and Section 4.3 explicitly associates it with postoperative morbidity. The passages found do not establish a considerable risk of mortality from the procedure; the broader claim about pancreatic surgery is also less directly addressed. (LLM, conf=0.84)
Experimental — accuracy not yet measured
- Also stated in: § References · p. 11 · plain
- Premisecitation§ 3. Discussion 3. Discussion · p. 8
Because somatostatin analogues also inhibit glucagon secretion, symptoms of hypoglycemia may occur even more frequently in a subset of NIPHS patients.
“Since these substances also inhibit the secretion of glucagon, symptoms of hypoglycemia may occur even more frequently in a subset of patients [52,61,62].”
Quote in the paperNot a substantial claim3 of 3 sources checked- cites [52] Koneshamoorthy, 2022, Case Report: Hypoglycemia Due to a Novel Activating Glucokinase Variant in an Adult—A Molecular Approach, Front. Endocrinol. source
The Clinical Case section reports that octreotide did not improve one patient’s hypoglycemia, while pasireotide improved it. Searches for glucagon inhibition and worsening hypoglycemia found no passage linking somatostatin analogues to more frequent hypoglycemia in a subset of patients. The copy also does not identify the patient as having NIPHS. (LLM, conf=0.76)
Experimental — accuracy not yet measured - cites [61] Dauriz, 2018, A Case Report of Insulinoma Relapse on Background Nesidioblastosis: A Rare Cause of Adult Hypoglycemia, J. Clin. Endocrinol. Metab. source
The Discussion says octreotide and lanreotide inhibit glucagon secretion, potentially impairing the response to hypoglycemia. It also says they may worsen the frequency of hypoglycemic episodes in insulinomas lacking SSTR2. That finding concerns a subset of insulinoma patients, not specifically a subset of patients with NIPHS. (LLM, conf=0.86)
Experimental — accuracy not yet measured - cites [62] Schwetz, 2016, Successful Medical Treatment of Adult Nesidioblastosis with Pasireotide over 3 Years, Medicine source
The Discussion (page unavailable) states that glucagon inhibition is mediated mainly by somatostatin receptor 2, supporting the claim that somatostatin analogues can inhibit glucagon secretion. It does not report more frequent hypoglycemic symptoms in a subset of NIPHS patients; instead, it describes avoidance of severe hypoglycemia with pasireotide. (LLM, conf=0.86)
Experimental — accuracy not yet measured
- Premisecitation§ 3. Discussion 3. Discussion · p. 8
A low-carbohydrate diet or α-glucosidase inhibitors are not effective in most patients with NIPHS.
“While a low carbohydrate diet or α -glucosidase inhibitors are not effective in most patients, the potassium channel activator diazoxide has been shown to alleviate symptoms in some cases [58,59].”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites [58] Leibowitz, 1995, Hyperinsulinemic Hypoglycemia of Infancy (Nesidioblastosis) in Clinical Remission: High Incidence of Diabetes Mellitus and Persistent Beta-Cell Dysfunction at Long-Term Follow-Up, J. Clin. Endocrinol. Metab. source
- cites [59] Dardano, 2020, Nesidioblastosis and Insulinoma: A Rare Coexistence and a Therapeutic Challenge, Front. Endocrinol. source
The Discussion lists a low-carbohydrate diet as a treatment option for nesidioblastosis but does not assess its effectiveness in most patients. It says common medical therapy was ineffective or caused side effects in one patient; the passages found do not address α-glucosidase inhibitors or establish the claimed outcome across patients (searched: low-carbohydrate diet, α-glucosidase inhibitors, acarbose). (LLM, conf=0.76)
Experimental — accuracy not yet measured
- Findingown data§ An Uncommon Cause of Recurrent Presyncope, Dizziness, and Tachycardia: A Case Report of Diffuse, Adult-Onset Nesidioblastosis/Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS) · p. 1
A 72 h plasma glucose fasting test revealed endogenous hyperinsulinism.
“A 72 h plasma glucose fasting test revealed endogenous hyperinsulinism.”
Quote in the paperSubstantial claim - Findingnone given§ An Uncommon Cause of Recurrent Presyncope, Dizziness, and Tachycardia: A Case Report of Diffuse, Adult-Onset Nesidioblastosis/Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS) · p. 1
Repeated diagnostic work-up in various clinical settings could not identify any definite cause for approximately eight years.
“Repeated diagnostic work-up in various clinical settings could not identify any definite cause for approximately eight years.”
Quote in the paperSubstantial claim - Findingown data§ An Uncommon Cause of Recurrent Presyncope, Dizziness, and Tachycardia: A Case Report of Diffuse, Adult-Onset Nesidioblastosis/Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS) · p. 1
68GaDOTA-Exendin-4 PET/CT showed diffuse tracer enrichment throughout the whole pancreas.
“68 GaDOTA-Exendin-4 PET/CT showed diffuse tracer enrichment throughout the whole pancreas.”
Quote in the paperSubstantial claim - Findingnone given§ 1. Introduction · p. 2
The repeated clinical evaluation of the patient by experts from various medical specialties did not reveal any significant abnormal findings.
“The repeated clinical evaluation of the patient by experts from various medical specialties did not reveal any significant abnormal findings.”
Quote in the paperSubstantial claim - Findingnone given§ An Uncommon Cause of Recurrent Presyncope, Dizziness, and Tachycardia: A Case Report of Diffuse, Adult-Onset Nesidioblastosis/Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS) · p. 1
A 23-year-old man presented with a history of recurrent presyncope, dizziness, and tachycardia.
“A 23-year-old man presented with a history of recurrent presyncope, dizziness, and tachycardia.”
Quote in the paperSubstantial claim - Findingnone given§ An Uncommon Cause of Recurrent Presyncope, Dizziness, and Tachycardia: A Case Report of Diffuse, Adult-Onset Nesidioblastosis/Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS) · p. 1
Postoperative laboratory evaluation exhibited no residual endogenous C-peptide production.
“Postoperative laboratory evaluation exhibited no residual endogenous C-peptide production.”
Quote in the paperNot a substantial claim - Findingown data§ An Uncommon Cause of Recurrent Presyncope, Dizziness, and Tachycardia: A Case Report of Diffuse, Adult-Onset Nesidioblastosis/Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS) · p. 1
Upon imaging studies, no tumor mass potentially indicating insulinoma could be detected.
“Upon imaging studies, no tumor mass potentially indicating insulinoma could be detected.”
Quote in the paperSubstantial claim - Findingown data§ 1. Introduction · p. 2
Incidental blood glucose measurements by the patient himself uncovered recurrent postprandial and exercise-induced hypoglycemia.
“However, incidental blood glucose measurements by the patient himself uncovered recurrent postprandial and exercise-induced hypoglycemia.”
Quote in the paperSubstantial claim- Rests on an assumption: The patient's self-reported symptoms and self-measured blood glucose values are reliable.
- Findingnone given§ 2. The Case · p. 4
Nutrition counseling and a subsequent low carbohydrate diet did not lead to a release from the symptoms.
“Nutrition counseling and a subsequent low carbohydrate diet, however, did not lead to a release from the symptoms.”
Quote in the paperNot a substantial claim - Findingnone given§ 2. The Case · p. 4
Hypoglycemic events became more frequent upon treatment with somatostatin analogues (up to fifteen hypoglycemic events/day).
“However, hypoglycemic events became more frequent upon treatment with the somatostatin analogues (up to fifteen hypoglycemic events/day).”
Quote in the paperSubstantial claim - Findingcitation§ 2. The Case · p. 4
Persistent C-peptide levels above 0.2 nmol/L and persistent insulin levels above 21 pmol/L after 72 h of fasting, alongside corresponding low venous blood glucose values, were interpreted as pathologic according to the classical literature on hyperinsulinemic hypoglycemia.
“Persistent C-peptide levels above 0.2 nmol/L and persistent insulin levels above 21 pmol/L after 72 h of fasting, alongside corresponding low venous blood glucose values, were interpreted as pathologic according to the classical literature on hyperinuslinemic hypoglycemia [30].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [30] Service, 1995, Hypoglycemic Disorders, N. Engl. J. Med. source
- Findingown data§ 2. The Case · p. 3
A 4 h oral glucose tolerance test (OGTT) showed conspicuous results with two symptomatic declines in blood glucose 60 min and 210 min after oral glucose (75 g) intake.
“A 4 h oral glucose tolerance test (OGTT) was performed and showed conspicuous results (Table 1). Two symptomatic declines in blood glucose were monitored 60 min and 210 min after oral glucose (75 g) intake.”
Quote in the paperSubstantial claim - Findingown data§ 2. The Case · p. 3
Fasting hypoglycemia was not reported.
“Fasting hypoglycemia was, however, not reported.”
Quote in the paperNot a substantial claim - Findingown data§ 2. The Case · p. 4
The patient could not walk more than 100 m anymore without suffering from hypoglycemia.
“The patient could not walk more than 100 m anymore without suffering from hypoglycemia, which led to his presentation at the Heidelberg University Hospital.”
Quote in the paperNot a substantial claim - Findingnone given§ 2. The Case · p. 4
The exocrine pancreas showed a regular histoarchitecture.
“The exocrine pancreas showed a regular histoarchitecture.”
Quote in the paperSubstantial claim - Findingnone given§ 2. The Case · p. 3
Symptomatic treatment attempts with bisoprolol, ivabradine, or a combination of ivabradine and metoprolol were unable to mitigate the symptoms.
“Symptomatic treatment attempts with bisoprolol, ivabradine, or a combination of ivabradine and metoprolol were unable to mitigate the symptoms.”
Quote in the paperNot a substantial claim - Findingown data§ 2. The Case · p. 3
The patient reported that the episodes occurred more frequently after food intake, physical exercise, or a combination of both.
“Of interest, the patient reported that the above-described episodes occurred more frequently after food intake, physical exercise, or a combination of both.”
Quote in the paperNot a substantial claim- Rests on an assumption: The patient's self-reported symptoms and self-measured blood glucose values are reliable.
- Findingown data§ 2. The Case · p. 4
A neuroendocrine tumor was not detected.
“A neuroendocrine tumor was not detected.”
Quote in the paperSubstantial claim - Findingown data§ 2. The Case · p. 4
Abdominal contrast-enhanced MRI did not reveal any lesion indicating insulinoma or another neuroendocrine tumor.
“Abdominal contrast-enhanced MRI did not reveal any lesion indicating insulinoma or another neuroendocrine tumor.”
Quote in the paperSubstantial claim - Findingnone given§ 2. The Case · p. 4
Screening for congenital metabolic disorders presenting with hypoglycemia was negative.
“Screening for congenital metabolic disorders presenting with hypoglycemia was negative.”
Quote in the paperNot a substantial claim - Findingown data§ 2. The Case · p. 3
Blood glucose measurements performed by the patient shortly (approximately 30 min) after meals reproducibly yielded unexpectedly low values in the range of 40-70 mg/dL.
“Blood glucose measurements performed by the patient shortly (approximately 30 min) after meals reproducibly yielded unexpectedly low values in the range of 40-70 mg/dL.”
Quote in the paperSubstantial claim- Rests on an assumption: The patient's self-reported symptoms and self-measured blood glucose values are reliable.
- Findingown data§ 2. The Case · p. 4
Histopathological examination revealed diffuse involvement of the pancreas by variably sized and shaped pancreatic islets containing enlarged neuroendocrine cells with round to oval hyperchromatic nuclei with dense nuclear chromatin and inconspicuous nucleoli.
“Histopathological examination revealed the diffuse involvement of the pancreas by variably sized and shaped pancreatic islets containing enlarged neuroendocrine cells with round to oval hyperchromatic nuclei with dense nuclear chromatin and inconspicuous nucleoli.”
Quote in the paperSubstantial claim - Findingnone given§ 2. The Case · p. 3
Attempts at stamina training resulted in multiple episodes of presyncope, usually after 15 min of exercise.
“Thus, attempts at stamina training resulted in multiple episodes of presyncope, usually after 15 min of exercise.”
Quote in the paperNot a substantial claim - Interpretationreasoning§ An Uncommon Cause of Recurrent Presyncope, Dizziness, and Tachycardia: A Case Report of Diffuse, Adult-Onset Nesidioblastosis/Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS) · p. 1
The histopathological diagnosis corresponds to the clinical findings of a functional β-cell disorder, also known as NIPHS.
“This corresponds to the clinical findings of a functional β -cell disorder, also known as non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS).”
Quote in the paperSubstantial claim - Interpretationnone given§ An Uncommon Cause of Recurrent Presyncope, Dizziness, and Tachycardia: A Case Report of Diffuse, Adult-Onset Nesidioblastosis/Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS) · p. 1
Incidental detection of postprandial and exercise-induced hypoglycemia was suggestive of an insulin-related disorder.
“However, the incidental detection of postprandial and exercise-induced hypoglycemia was suggestive of an insulin-related disorder.”
Quote in the paperSubstantial claim - Interpretationown data§ 3. Discussion 3. Discussion · p. 7
The presented case shows that the careful interpretation of symptoms and their correlation with daily activities can finally lead to the correct diagnosis.
“The presented case shows that the careful interpretation of symptoms and their correlation with daily activities can finally lead to the correct diagnosis.”
Quote in the paperSubstantial claim - Interpretationreasoning§ 2. The Case · p. 4
Therefore, the diagnosis of (occult) insulinoma seemed unlikely.
“Therefore, the diagnosis of (occult) insulinoma seemed unlikely.”
Quote in the paperSubstantial claim - Interpretationown data§ 3. Discussion 3. Discussion · p. 7
The slight hypokalemia detected during a symptomatic episode was the only initial laboratory finding that could have indicated hyperinsulinism, before actual hypoglycemia was recognized.
“Of interest, the slight hypokalemia detected during a symptomatic episode was the only initial laboratory finding that could have indicated hyperinsulinism, before actual hypoglycemia was recognized.”
Quote in the paperNot a substantial claim - Interpretationreasoning§ 1. Introduction · p. 2
NIPHS/nesidioblastosis rather represents a spectrum of related disorders with common and repeated, but not exclusive, clinical and histopathological findings.
“Therefore, NIPHS/nesidioblastosis rather represents a spectrum of related disorders with common and repeated, but not exclusive, clinical and histopathological findings.”
Quote in the paperNot a substantial claim - Interpretationreasoning§ 2. The Case · p. 4
As factitious or iatrogenic hypoglycemia could be ruled out, endogenous hyperinsulinemic hypoglycemia was diagnosed.
“As factitious or iatrogenic hypoglycemia could be ruled out, endogenous hyperinsulinemic hypoglycemia was diagnosed.”
Quote in the paperSubstantial claim- Rests on an assumption: Factitious or iatrogenic hypoglycemia could be ruled out.
- Interpretationreasoning§ 2. The Case · p. 4
These results pointed in the direction of an adult form of a functional β-cell disorder, also called non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS).
“Instead, these results pointed in the direction of an adult form of a functional β -cell disorder, also called non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS).”
Quote in the paperSubstantial claim - Interpretationreasoning§ 2. The Case · p. 4
Since the patient had no history of gastric bypass surgery and exhibited no signs of gastroparesis or dumping-like symptoms, post-gastric bypass hypoglycemic syndrome could be ruled out.
“Since the patient had no history of gastric bypass surgery and exhibited no signs of gastroparesis or dumping-like symptoms, post-gastric bypass hypoglycemic syndrome could be ruled out.”
Quote in the paperSubstantial claim - Interpretationreasoning§ 3. Discussion 3. Discussion · p. 8
The presence of fasting hypoglycemia during the 72 h fasting test together with concomitant postprandial and exercise-induced hypoglycemia made it necessary to definitely exclude an insulin-producing neoplasia in the presented patient.
“The presence of fasting hypoglycemia during the 72 h fasting test (although recognized very late during the test) and concomitant postprandial and exercise-induced hypoglycemia made it necessary to definitely exclude an insulin-producing neoplasia.”
Quote in the paperSubstantial claim - Premisereasoning§ References · p. 11
Surgical resection of parts or even the entire pancreas is often the only chance to effectively reduce or abolish hypoglycemic events in NIPHS.
“The surgical resection of parts or even the entire pancreas is often the only chance to effectively reduce or abolish hypoglycemic events.”
Quote in the paperSubstantial claim - Interpretationown data§ Diagnostic Algorithm in Hypoglycemia · p. 10
The rapid onset of new hypoglycemic events after partial pancreatectomy in the presented case is indicative of too much residual insulin-secreting pancreatic tissue.
“As the presented case shows, the rapid onset of new hypoglycemic events after partial pancreatectomy is indicative of too much residual insulin-secreting pancreatic tissue.”
Quote in the paperSubstantial claim - Premisecitation§ 3. Discussion 3. Discussion · p. 8
The histologic and clinical changes exhibited in patients with NIPHS differ considerably between patients.
“Of note, the histologic and clinical changes in exhibited in patients with NIPHS differ considerably.”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [22] Anlauf, 2005, Persistent Hyperinsulinemic Hypoglycemia in 15 Adults with Diffuse Nesidioblastosis: Diagnostic Criteria, Incidence, and Characterization of β-Cell Changes, Am. J. Surg. Pathol. source
- cites [24] Anlauf, 2008, Adult Diffuse Nesidioblastosis: Genetically or Environmentally Induced?, Hum. Pathol. source
- Interpretationreasoning§ 3. Discussion 3. Discussion · p. 8
Because PET/CT imaging rendered occult insulinoma very unlikely, the clinical diagnosis of NIPHS in the presented patient was justified even without SACS testing.
“Since PET/CT imaging rendered occult insulinoma very unlikely, the clinical diagnosis of NIPHS was justified even without SACS testing.”
Quote in the paperSubstantial claim - Premisenone given§ References · p. 11
Medical treatment of NIPHS, including low-carbohydrate diet, alpha-glucosidase inhibitors, diazoxide, calcium channel inhibitors, and somatostatin analogues, is only effective in a small subset of patients.
“Medical treatment includes a low-carbohydrate diet, alpha-glucosidase inhibitors, diazoxide, calcium channel inhibitors, and somatostatin analogues, but is only effective in a small subset of patients.”
Quote in the paperNot a substantial claim
- Classified as probably not a substantial claim. 47
- May combine two claims. 41
Classified as probably not a substantial claim.
Premisecitation§ 1. Introduction · p. 2Functional β-cell disorders are also known as adult-onset nesidioblastosis or non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS).
“The latter are a group of diseases also known as adult-onset nesidioblastosis or non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS) [5,16-20].”
Quote in the paperSubstantial claim3 of 6 sources checked- cites [5] Qintar, 2012, Hypoglycemia Due to an Adult-Onset Nesidioblastosis, a Diagnostic and Management Dilemma, Avicenna J. Med. source
- cites [16] Pathak, 2014, An Unusual Cause of Hypoglycemia in a Middle-Aged Female after Bariatric Surgery, J. Community Hosp. Intern. Med. Perspect. source
The Discussion describes NIPHS as hypoglycemia caused by pancreatic beta-cell hyperplasia, and the Abstract says the patient diagnosed with NIPHS had histology suggestive of nesidioblastosis. These passages connect the terms, but the paper does not say that functional β-cell disorders as a group are also known as adult-onset nesidioblastosis or NIPHS. (LLM, conf=0.81)
Experimental — accuracy not yet measured - cites [17] Pia, 2017, The Treatment of Hyperinsulinemic Hypoglycaemia in Adults: An Update, J. Endocrinol. Investig. source
- cites [18] Hannon, 2015, Amlodipine for the Medical Treatment of Adult-Onset Diffuse Nesidioblastosis, Pancreas source
- cites [19] Martignoni, 2003, Nesidioblastosis with Glucagon-Reactive Islet Cell Hyperplasia: A Case Report, Pancreas source
- cites [20] Gussinyer, 2002, Pancreatectomy Extension in Persistent Hyperinsulinaemic Hypoglycaemia: A New Strategy, Eur. J. Pediatr. Surg. source
Probably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing).
Premisecitation§ 1. Introduction · p. 2Genuine endocrine diseases, like pituitary or adrenal insufficiency, should also be considered especially if patients present with other symptoms suggestive of these diseases.
“Genuine endocrine diseases, like pituitary or adrenal insufficiency, should also be considered especially if patients present with other symptoms suggestive of these diseases [11,12].”
Quote in the paperNot a substantial claim2 of 2 sources checked- cites [11] Rizwan, 2023, Hypopituitarism Presenting as Recurrent Episodes of Hypoglycemia : Houssay Phenomenon, Cureus source
- cites [12] Sakurai, 2023, Hypoglycemic Hemiplegia Associated with Reversible Narrowing of the Contralateral Middle Cerebral Artery in a Patient with Adrenal Insufficiency, Intern. Med. source
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ 1. Introduction · p. 2Apart from severe diseases like liver, kidney or heart failure, the intake of alcohol, insulin, or insulin secretagogues needs to be ruled out.
“Apart from severe diseases like liver, kidney or heart failure, the intake of alcohol, insulin, or insulin secretagogues needs to be ruled out [7,9,10].”
Quote in the paperNot a substantial claim2 of 3 sources checked- cites [7] Cryer, 2009, Evaluation and Management of Adult Hypoglycemic Disorders: An Endocrine Society Clinical Practice Guideline, J. Clin. Endocrinol. Metab. source
- cites [9] Kittah, 2017, Pathogenesis and Management of Hypoglycemia, Eur. J. Endocrinol. source
- cites [10] Oueslati, 2022, Prevalence and Characteristics of Factitious Hypoglycaemia in Non-Diabetic Patients in a Department of Endocrinology, Endocrinol. Diabetes Metab. source
The Introduction (page unavailable) identifies intentional insulin use and oral hypoglycaemic agents as causes of factitious hypoglycaemia; the Discussion describes testing to distinguish insulin use from sulfonylurea ingestion. The Results also list alcohol intoxication as a cause of hypoglycaemia. The paper does not specify liver, kidney or heart failure, or state the full rule-out recommendation as written. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing).
Premisecitation§ 1. Introduction · p. 2The differential diagnosis of hypoglycemia in adult patients can be challenging.
“The differential diagnosis of hypoglycemia in adult patients can be challenging [7,8].”
Quote in the paperNot a substantial claim2 of 2 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ 1. Introduction · p. 2The differential diagnosis of patients presenting with unspecific, neurovegetative and autonomic symptoms is complex and involves a variety of diseases, including psychosomatic, neurologic, cardiologic, and endocrine disorders.
“The differential diagnosis of patients presenting with unspecific, neurovegetative and autonomic symptoms is complex and involves a variety of diseases, including psychosomatic, neurologic, cardiologic, and endocrine disorders [1,2].”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites [1] 2020, Syncope and Palpitations: A Review, Pediatr. Clin. N. Am. source
- cites [2] Spiegel, 2017, Dizziness in the Emergency Department: An Update on Diagnosis, Swiss Med. Wkly. source
The Aetiology section describes a diverse differential diagnosis for dizziness, including psychosomatic, central vascular, circulatory and hypoglycaemic causes. The paper addresses patients presenting with dizziness, however, not patients presenting with unspecific neurovegetative or autonomic symptoms generally; it also does not identify endocrine disorders as a broad diagnostic category. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisecitation§ 2. The Case · p. 5Diabetes type 3c is mainly characterized by an extraordinary insulin sensitivity, which can be explained in terms of the missing counterregulatory glucagon.
“Diabetes type 3c is mainly characterized by an extraordinary insulin sensitivity, which can be explained in terms of the missing counterregulatory glucagon [32-36].”
Quote in the paperNot a substantial claim2 of 5 sources checked- cites [32] Woodcock, 2019, Diabetes Care after Pancreatic Surgery, J. Diabetes Nurs.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [33] Barbier, 2013, Impact of Total Pancreatectomy: Short- and Long-Term Assessment, Hpb source
The Discussion (page not available) says pancreatic diabetes involves a complete lack of endogenous insulin and glucagon, leading to frequent, severe hypoglycaemia. The Endocrine function section reports frequent hypoglycaemic episodes after total pancreatectomy. Neither passage describes extraordinary insulin sensitivity or establishes that missing counterregulatory glucagon explains such sensitivity. (LLM, conf=0.84)
Experimental — accuracy not yet measured - cites [34] Cavallo, 2019, Management of Total Pancreatectomy-Induced Diabetes Mellitus : A Mini-Review, Austin Pancreat Disord
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [35] Zhao, 2023, Diabetes Management in Patients Undergoing Total Pancreatectomy: A Single Center Cohort Study, Front. Endocrinol. source
The Discussion (page not available) reports lower insulin needs after total pancreatectomy than in comparable patients with type 1 diabetes and says these may reflect increased peripheral insulin sensitivity and deficient pancreatic-glucagon counterregulation. It also names malabsorption as a possible contributor. The source therefore supports the proposed link, but not the claim that extraordinary insulin sensitivity chiefly characterizes all type 3c diabetes or that missing glucagon alone explains it. (LLM, conf=0.88)
Experimental — accuracy not yet measured - cites [36] Suto, 2021, Diabetic Control and Nutritional Status up to 1 Year after Total Pancreatectomy: A Nationwide Multicentre Prospective Study, Br. J. Surg. source
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisecitation§ 3. Discussion 3. Discussion · p. 8SACS was the gold standard in the past to detect an insulin gradient in the vessels supplying the pancreas, and this invasive method might be almost completely replaced by PET imaging in the future, e.g., with 68Ga DOTA-Exendin-4 PET/CT.
“While SACS was the gold standard in the past to detect an insulin gradient in the vessels supplying the pancreas, this invasive method might be almost completely replaced by PET imaging in the future, e.g., with 68 Ga DOTA-Exendin-4 PET/CT [38-41].”
Quote in the paperNot a substantial claim2 of 4 sources checked- cites [38] Thompson, 2015, Selective Arterial Calcium Stimulation with Hepatic Venous Sampling Differentiates Insulinoma from Nesidioblastosis, J. Clin. Endocrinol. Metab. source
The Discussion describes SACST as an invasive technique that measures an insulin rise after stimulation of pancreatic arterial distributions and reports high sensitivity for localizing occult insulinoma. It does not call SACST a past gold standard or predict its near-complete replacement by PET. Instead, the Discussion says emerging imaging techniques show promising early results but cannot yet distinguish occult insulinoma from diffuse nesidioblastosis. (LLM, conf=0.85)
Experimental — accuracy not yet measured - cites [39] Rao, 2014, Successful Management of Refractory Noninsulinoma Pancreatogenous Hypoglycemia Syndrome With Gastric Bypass Reversal: A Case Report, Am. J. Gastroenterol. source
- cites [40] Christ, 2020, Innovative Imaging of Insulinoma: The End of Sampling? A Review, Endocr. Relat. Cancer source
The Introduction (page unavailable) describes SACST as an invasive test recommended when conventional imaging cannot localize an insulinoma; it samples hepatic venous blood for insulin to identify an arterial territory. The Conclusion (page unavailable) predicts that GLP-1R imaging could end the need for SACST. The review does not call SACST a past gold standard, and its recommendation is limited to cases not localized by conventional imaging. (LLM, conf=0.82)
Experimental — accuracy not yet measured - cites [41] Antwi, 2018, Comparison of Glucagon-like Peptide-1 Receptor (GLP-1R) PET/CT, SPECT/CT and 3T MRI for the Localisation of Occult Insulinomas: Evaluation of Diagnostic Accuracy in a Prospective Crossover Imaging Study, Eur. J. Nucl. Med. Mol. Imaging source
May combine two claims.
Premisecitation§ 1. Introduction · p. 2Not all cases with histologically proven nesidioblastosis exhibit the same clinical pattern; some patients have a positive fasting test and also suffer from fasting or exercise-induced hypoglycemia.
“However, not all cases with histologically proven nesidioblastosis exhibit the same clinical pattern. Some patients, e.g., have a positive fasting test and also suffer from fasting or exercise-induced hypoglycemia [18,28,29].”
Quote in the paperSubstantial claim1 of 3 sources checked- cites [18] Hannon, 2015, Amlodipine for the Medical Treatment of Adult-Onset Diffuse Nesidioblastosis, Pancreas source
- cites [28] Kaczirek, 2003, Nesidioblastosis in Adults: A Challenging Cause of Organic Hyperinsulinism, Eur. J. Clin. Investig. source
- cites [29] Kim, 2016, Difficult Diagnosis and Localization of Focal Nesidioblastosis: Clinical Implications of 68Gallium-DOTAD-Phe1-Tyr3-Octreotide PET Scanning, Ann. Surg. Treat. Res. source
May combine two claims.
Premisecitation§ 3. Discussion 3. Discussion · p. 8Insulin secretion is reduced by somatostatin receptor type 2 and 5 signaling, while glucagon secretion is mainly inhibited by receptor type 2 signaling.
“Insulin secretion is reduced by somatostatin receptor type 2 and 5 signaling, while glucagon secretion is mainly inhibited by receptor type 2 signaling.”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [62] Schwetz, 2016, Successful Medical Treatment of Adult Nesidioblastosis with Pasireotide over 3 Years, Medicine source
May combine two claims.
Premisecitation§ 3. Discussion 3. Discussion · p. 8Exercise-induced or postprandial hyperinsulinemic hypoglycemia is not a defining feature of NIPHS, since some insulinoma patients also suffer from these symptoms.
“Above all, exercise-induced or postprandial hyperinsulinemic hypoglycemia is not a defining feature of NIPHS, since some insulinoma patients also suffer from these symptoms”
Quote in the paperNot a substantial claim1 of 3 sources checked- cites [55] Maher, 2022, Metastatic Insulinoma Presenting With Postprandial Hypoglycemia, AACE Clin. Case Rep. source
The Discussion (page unavailable) reports that insulinoma can present with postprandial hypoglycemia, supporting the point that this symptom is not exclusive to NIPHS. It does not address exercise-induced hypoglycemia or directly discuss which features define NIPHS. (LLM, conf=0.85)
Experimental — accuracy not yet measured - cites [56] Samos, 2020, Insulinoma Presenting with Postprandial Hypoglycemia and a Low Body Mass Index: A Case Report, World J. Surg.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [57] Kalman, 2007, Diffuse Nesidioblastosis as a Cause of Hyperinsulinemic Hypoglycemia in Adults: A Diagnostic and Therapeutic Challenge, Surgery source
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisecitation§ 3. Discussion 3. Discussion · p. 8Experimental evidence suggests that higher basal insulin secretion and changes in the resting membrane potential of β-cells might contribute to the biochemical and clinical findings of adult NIPHS.
“Some experimental evidence suggests that a higher basal insulin secretion, as well as changes in the resting membrane potential of β -cells, might contribute to the biochemical and clinical findings of the disease [50-52].”
Quote in the paperNot a substantial claim1 of 3 sources checked- cites [50] Conget, 1997, β-Cell Function Abnormalities in Islets from an Adult Subject with Nesidioblastosis and Autoantibodies against the Islet Cells, Pancreas source
- cites [51] Berglund, 2010, Electrical Short-Circuit in β-Cells from a Patient with Non-Insulinoma Pancreatogenous Hypoglycemic Syndrome (NIPHS): A Case Report, J. Med. Case Rep.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [52] Koneshamoorthy, 2022, Case Report: Hypoglycemia Due to a Novel Activating Glucokinase Variant in an Adult—A Molecular Approach, Front. Endocrinol. source
The Results (Pancreatic Islet Analysis; page unavailable) report higher glucose-stimulated insulin secretion in the patient’s islets, and the Discussion links altered β-cell function to a lower threshold for insulin release. The copy does not establish higher basal insulin secretion or report changes in resting membrane potential; its basal calcium measurement showed no significant difference. The evidence comes from one adult with an activating glucokinase variant, not adult NIPHS generally. (LLM, conf=0.83)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ 3. Discussion 3. Discussion · p. 8The most frequent underlying cause of hyperinsulinemic hypoglycemia in the adult patient is (benign) insulinoma.
“The most frequent underlying cause of hyperinsulinemic hypoglycemia in the adult patient is (benign) insulinoma [44].”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [44] Chadli, 2019, Hypoglycemia Controlled by Prednisone in an Occult Insulinoma or a Nesidioblastosis, Open J. Endocr. Metab. Dis. source
The Introduction identifies insulinoma as a tumor that causes hypoglycemia, and the Discussion says nesidioblastosis accounts for less than 5% of adult endogenous hyperinsulinism cases. Neither passage establishes that insulinoma is the most frequent cause of adult hyperinsulinemic hypoglycemia or that the insulinomas in question are benign. The indexed passages provide no page number for these sections. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ 3. Discussion 3. Discussion · p. 8It is estimated that about 1 in 10,000,000 people are diagnosed with idiopathic/sporadic adult-onset nesidioblastosis annually.
“It is estimated that about 1 in 10,000,000 people are diagnosed with this disease annually [45-48].”
Quote in the paperNot a substantial claim3 of 4 sources checked- cites [45] Yamada, 2020, Nationwide Survey of Endogenous Hyperinsulinemic Hypoglycemia in Japan (2017–2018): Congenital Hyperinsulinism, Insulinoma, Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome and Insulin Autoimmune Syndrome (Hirata’s Disease), J. Diabetes Investig. source
The Results (Non-insulinoma pancreatogenous hypoglycemia syndrome; page unavailable) report 10 patients with adult-onset nesidioblastosis, and the Discussion describes NIPHS as rare. Neither passage estimates one diagnosis per 10,000,000 people annually; the reported prevalence of 0.09 per 100,000 is for the broader NIPHS category, not annual diagnoses of nesidioblastosis. (LLM, conf=0.84)
Experimental — accuracy not yet measured - cites [46] Walmsley, 1995, Nesidioblastosis in an Elderly Patient, Diabet. Med. source
- cites [47] Mathur, 2009, Insulinoma, Surg. Clin. N. Am. source
The opening Insulinoma section gives an annual incidence of 4 per million for insulinoma, not idiopathic or sporadic adult-onset nesidioblastosis. Searches for nesidioblastosis and the claimed 1-in-10-million annual figure found no passage addressing that disease’s incidence in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measured - cites [48] Woo, 2015, Clinical Features and Causes of Endogenous Hyperinsulinemic Hypoglycemia in Korea, Diabetes Metab. J. source
The Discussion (page not available) says adult nesidioblastosis is very rare, accounting for approximately 0.5% of endogenous hyperinsulinemic hypoglycemia cases. It does not give an annual population diagnosis rate of 1 in 10,000,000 or an estimate specific to idiopathic or sporadic adult-onset disease. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ 3. Discussion 3. Discussion · p. 8The potassium channel activator diazoxide has been shown to alleviate symptoms in some cases of NIPHS.
“While a low carbohydrate diet or α -glucosidase inhibitors are not effective in most patients, the potassium channel activator diazoxide has been shown to alleviate symptoms in some cases [58,59].”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites [58] Leibowitz, 1995, Hyperinsulinemic Hypoglycemia of Infancy (Nesidioblastosis) in Clinical Remission: High Incidence of Diabetes Mellitus and Persistent Beta-Cell Dysfunction at Long-Term Follow-Up, J. Clin. Endocrinol. Metab. source
- cites [59] Dardano, 2020, Nesidioblastosis and Insulinoma: A Rare Coexistence and a Therapeutic Challenge, Front. Endocrinol. source
The Discussion (page unavailable) lists diazoxide among treatments reported in isolated nesidioblastosis case reports, supporting its use in some cases. It does not say that diazoxide alleviated symptoms in those cases; in the paper’s own Case Report, it was withdrawn because of adverse effects. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ 3. Discussion 3. Discussion · p. 8Stimulation of somatostatin receptors by octreotide, lanreotide, or pasireotide has repeatedly been described in the literature in the context of NIPHS.
“The stimulation of somatostatin receptors by octreotide, lanreotide, or pasireotide has also repeatedly been described in the literature in the context of NIPHS.”
Quote in the paperNot a substantial claim3 of 3 sources checked- cites [52] Koneshamoorthy, 2022, Case Report: Hypoglycemia Due to a Novel Activating Glucokinase Variant in an Adult—A Molecular Approach, Front. Endocrinol. source
The Introduction’s Clinical Case section (page unavailable) describes octreotide and pasireotide as somatostatin analogues that activate specified somatostatin receptors. It reports their use in one patient with hypoglycemia due to a glucokinase variant, but does not mention lanreotide or establish that receptor stimulation by these drugs has repeatedly been described in NIPHS. (LLM, conf=0.87)
Experimental — accuracy not yet measured - cites [61] Dauriz, 2018, A Case Report of Insulinoma Relapse on Background Nesidioblastosis: A Rare Cause of Adult Hypoglycemia, J. Clin. Endocrinol. Metab. source
The paper describes octreotide and lanreotide as somatostatin-receptor ligands used for refractory nesidioblastosis (Abstract), and discusses pasireotide as a multi-receptor ligand used in this case (Discussion; Conclusions). But it identifies only at least one earlier case of pasireotide use in adult nesidioblastosis (Abstract), so it does not establish that use of all three drugs in this context has repeatedly been described in the literature. (LLM, conf=0.82)
Experimental — accuracy not yet measured - cites [62] Schwetz, 2016, Successful Medical Treatment of Adult Nesidioblastosis with Pasireotide over 3 Years, Medicine source
The Introduction and Clinical Case (page not available) report pasireotide treatment for adult nesidioblastosis and an unsuccessful trial of octreotide. The Discussion also compares pasireotide with octreotide in a reported post-bypass hypoglycemia case. Our copy does not mention lanreotide or establish that all three drugs have repeatedly been described in the NIPHS literature. (LLM, conf=0.87)
Experimental — accuracy not yet measured
May combine two claims.
Premisecitation§ 3. Discussion 3. Discussion · p. 8Mechanistic data on adult-onset NIPHS is scarce, whereas the pathophysiology of persistent hyperinsulinemic hypoglycemia in childhood and infancy is well understood genetically and functionally.
“While the pathophysiology of persistent hyperinsulinemic hypoglycemia in childhood and infancy, which is morphologically similar to NIPHS, is well understood from a genetic and functional point of view, mechanistic data on adult-onset NIPHS is scarce [49].”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [49] Stanley, 2016, Perspective on the Genetics and Diagnosis of Congenital Hyperinsulinism Disorders, J. Clin. Endocrinol. Metab. source
The Abstract (page unavailable) describes genetic causes of congenital hyperinsulinism and advances in understanding pancreatic β-cell insulin secretion, supporting the childhood and infancy portion of the claim. The copy does not address whether mechanistic data on adult-onset NIPHS are scarce or establish the asserted morphological similarity; searches for NIPHS and adult nesidioblastosis found no such discussion. (LLM, conf=0.84)
Experimental — accuracy not yet measured
May combine two claims.
Premisecitation§ 3. Discussion 3. Discussion · p. 868Ga DOTA-Exendin-4 PET/CT is especially helpful in distinguishing occult or ectopic insulinoma from NIPHS and to separate focal and diffuse nesidioblastosis.
“The latter is especially helpful in distinguishing occult or ectopic insulinoma from NIPHS and to separate focal and diffuse nesidioblastosis [29].”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [29] Kim, 2016, Difficult Diagnosis and Localization of Focal Nesidioblastosis: Clinical Implications of 68Gallium-DOTAD-Phe1-Tyr3-Octreotide PET Scanning, Ann. Surg. Treat. Res. source
The Case Report and Discussion describe 68Ga-DOTATOC PET localizing a lesion in one patient with focal nesidioblastosis, not 68Ga DOTA-Exendin-4 PET/CT. The Discussion mentions NIPHS and the focal and diffuse forms of nesidioblastosis, but does not report that the claimed scan distinguishes insulinoma from NIPHS or separates the two forms (pages unavailable in our copy). (LLM, conf=0.76)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ Diagnostic Algorithm in Hypoglycemia · p. 10Boss and colleagues presented cell culture and mouse in vivo data on selective destruction of GLP-1-expressing cells via targeted photodynamic therapy.
“Boss and colleagues presented cell culture and mouse in vivo data on selective destruction of GLP-1-expressing cells via targeted photodynamic therapy.”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [70] Boss, 2020, Receptor-Targeted Photodynamic Therapy of Glucagon-like Peptide 1 Receptor-Positive Lesions, J. Nucl. Med. source
The Results sections report selective cell death in GLP-1R–positive cell cultures and cellular damage in GLP-1R–positive tumors in mice. The claim calls the targets “GLP-1-expressing cells,” but the paper identifies them as cells expressing the GLP-1 receptor (GLP-1R), not GLP-1 itself. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ Diagnostic Algorithm in Hypoglycemia · p. 10In the pre-CGM era, total loss of glycemic control was associated with severe complications in patients undergoing total pancreatectomy.
“In the pre-CGM era, the total loss of glycemic control was associated with severe complications in patients undergoing total pancreatectomy [35,66,69].”
Quote in the paperNot a substantial claim3 of 3 sources checked- cites [35] Zhao, 2023, Diabetes Management in Patients Undergoing Total Pancreatectomy: A Single Center Cohort Study, Front. Endocrinol. source
The Introduction (page unavailable) reports that early postoperative fasting glucose was an independent risk factor for complications after total pancreatectomy. It does not place that association in a pre-CGM era, describe a total loss of glycemic control, or specify that the complications were severe. (LLM, conf=0.83)
Experimental — accuracy not yet measured - cites [66] Suzuki, 2017, The Clinical Outcomes after Total Pancreatectomy, Dig. Surg. source
The Endocrine and Exocrine Replacement after TP section says patients were considered at high risk of hypoglycemia in the past, and the Long-Term Survival Rates after TP section reports deaths from post-TP hypoglycemia. The paper does not describe a total loss of glycemic control or specifically establish these complications as occurring in a pre-CGM era. (LLM, conf=0.86)
Experimental — accuracy not yet measured - cites [69] Zakaria, 2016, Total Pancreatectomy: Short- and Long-Term Outcomes at a High-Volume Pancreas Center, World J. Gastrointest. Surg. source
The Discussion (page not provided) says diabetes after total pancreatectomy can be difficult to control and cites reported deaths from hypoglycemia, though none occurred in this study. The Methods define major glycemic events as complications or readmissions related to severe hyperglycemia or hypoglycemia. The paper does not characterize these outcomes as a total loss of glycemic control or specifically place them in a pre-CGM era. (LLM, conf=0.83)
Experimental — accuracy not yet measured
May combine two claims.
Interpretationcitation§ 3. Discussion 3. Discussion · p. 8A positive fasting test neither confirms insulinoma nor excludes NIPHS.
“As can be seen from our case and other reports in the literature, a positive fasting test neither confirms insulinoma nor excludes NIPHS [53,54].”
Quote in the paperSubstantial claim1 of 2 sources checked- cites [53] Kaczirek, 2004, Nesidioblastosis: An Old Term and a New Understanding, World J. Surg. source
- cites [54] Maguire, 2015, Lesson of the Month 2: An Unusual Presentation of Hyperinsulinaemic Hypoglycaemia with Possible Underlying Diagnosis of Glucose-Sensitive Insulinoma or Islet Cell Hyperplasia, Clin. Med. source
- Rests on an assumption: In some cases, fasting hypoglycemia has been reported in patients with NIPHS.
May combine two claims.
Findingown data§ An Uncommon Cause of Recurrent Presyncope, Dizziness, and Tachycardia: A Case Report of Diffuse, Adult-Onset Nesidioblastosis/Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS) · p. 1A subtotal pancreatectomy was performed, and the diagnosis of diffuse, adult-onset nesidioblastosis was established histopathologically.
“A subtotal pancreatectomy was performed, and the diagnosis of diffuse, adult-onset nesidioblastosis was established histopathologically.”
Quote in the paperSubstantial claimMay combine two claims.
Findingnone given§ An Uncommon Cause of Recurrent Presyncope, Dizziness, and Tachycardia: A Case Report of Diffuse, Adult-Onset Nesidioblastosis/Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS) · p. 1After nine months, the symptoms recurred, making complete pancreatectomy necessary.
“After nine months, the symptoms recurred, making complete pancreatectomy necessary.”
Quote in the paperSubstantial claimMay combine two claims.
Findingnone given§ 2. The Case · p. 3These episodes occurred several times a day and were accompanied by presyncope, dizziness, blurred vision, nausea, urgent urination, shortness of breath, joint pain, muscle pain, and muscle weakness.
“These episodes occurred several times a day and were accompanied by presyncope, dizziness, blurred vision, nausea, urgent urination, shortness of breath, joint pain, muscle pain, and muscle weakness.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Findingnone given§ 2. The Case · p. 5Diabetic control was further complicated by early dumping syndrome and severe nausea.
“Diabetic control was further complicated by early dumping syndrome and severe nausea.”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown data§ 2. The Case · p. 5A complete pancreatectomy (classical Whipple procedure) was performed, and histopathological examination again confirmed a pattern typical of diffuse, adult nesidioblastosis.
“A complete pancreatectomy (classical Whipple procedure) was performed, and histopathological examination again confirmed a pattern typical of diffuse, adult nesidioblastosis.”
Quote in the paperSubstantial claimClassified as probably not a substantial claim.
Findingreasoning§ 2. The Case · p. 4Since conservative treatment was unsuccessful, the patient underwent a subtotal, left-sided, spleen-preserving pancreatectomy.
“Since conservative treatment was unsuccessful, the patient underwent a subtotal, left-sided, spleen-preserving pancreatectomy.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown data§ 2. The Case · p. 4Immunohistochemistry demonstrated a physiological distribution of insulin-, glucagon-, and somatostatin-producing cells within the islets, with a proliferation rate <1% (Ki-67).
“Immunohistochemistry demonstrated a physiological distribution of insulin-, glucagon-, and somatostatin-producing cells within the islets, with a proliferation rate < 1% (Ki-67).”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown data§ 2. The Case · p. 3The 23-year-old patient presented with a history of unspecific, neurovegetative symptoms in the Department of Endocrinology at the Heidelberg University Hospital.
“The 23-year-old patient presented with a history of unspecific, neurovegetative symptoms in the Department of Endocrinology at the Heidelberg University Hospital.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown data§ 2. The Case · p. 5In the case of total pancreatectomy, 1 IU of insulin can lead to a decrease in blood glucose of 50-70 mg/dL depending on the time of day, compared to 30-40 mg/dL in type 1 diabetes.
“In the case of total pancreatectomy, which leads to a total loss of glycemic control, 1 IU of insulin can lead to a decrease in blood glucose of 50-70 mg/dL (personal experience; insulin correction factor [see above]; this is compared to 30-40 mg/dL in type 1 diabetes) depending on the time of day, which makes the management of type 3c diabetes challenging.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingnone given§ 2. The Case · p. 3The symptom onset could be traced back to episodes of severe supraventricular tachycardia starting eight years prior.
“The symptom onset could be traced back to episodes of severe supraventricular tachycardia starting eight years prior.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Findingown data§ 2. The Case · p. 3The HbA1c at that time was 5.1% (32.2 mmol/mol), corresponding to an average blood glucose of 84 mg/dL.
“The HbA1c at that time was 5.1% (32.2 mmol/mol), corresponding to an average blood glucose of 84 mg/dL.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingnone given§ 2. The Case · p. 5On the 11th postoperative day, the patient developed a severe hemorrhagic shock due to the Forrest Ib bleeding of an ulcer in the gastroenterostomy.
“On the 11th postoperative day, the patient developed a severe hemorrhagic shock due to the Forrest Ib bleeding of an ulcer in the gastroenterostomy.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown data§ 2. The Case · p. 3During one acute episode, slight hypokalemia (3.37 mmol/L) was documented.
“When presenting at the emergency department of a local hospital during one acute episode, slight hypokalemia (3.37 mmol/L) was documented.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingreasoning§ 2. The Case · p. 5Due to cachexia, partial parenteral nutrition is still needed (950 kcal/day).
“Due to cachexia, partial parenteral nutrition is still needed (950 kcal/day).”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown data§ 2. The Case · p. 3Values in the same range were reported when the patient went for a walk within the first 2-3 h after food intake.
“Values in the same range were reported when the patient went for a walk within the first 2-3 h after food intake.”
Quote in the paperNot a substantial claim- Rests on an assumption: The patient's self-reported symptoms and self-measured blood glucose values are reliable.
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Findingnone given§ 2. The Case · p. 4The postoperative course was complicated by pancreatic fistula, which was treated conservatively, and delayed gastric emptying due to postoperative pyloric stenosis.
“The postoperative course was complicated by pancreatic fistula, which was treated conservatively, and delayed gastric emptying due to postoperative pyloric stenosis.”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown data§ 2. The Case · p. 468Ga-DOTA-Exendin-4 PET/CT did not reveal a focal enrichment, but a diffuse tracer enrichment throughout the whole pancreas.
“68 Ga-DOTA-Exendin-4 PET/CT, which targets glucagon-like peptide 1 (GLP-1)-expressing cells, did also not reveal a focal enrichment, but a diffuse tracer enrichment throughout the whole pancreas.”
Quote in the paperSubstantial claimMay combine two claims.
Findingnone given§ 2. The Case · p. 5After nine months, symptomatic hypoglycemia reappeared, which also became apparent since the patient used a continuous glucose monitoring (CGM) system.
“After nine months, symptomatic hypoglycemia reappeared, which also became apparent since the patient used a continuous glucose monitoring (CGM) system.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingnone given§ 2. The Case · p. 5The type 3c diabetes is well controlled with a combination of regular and NPH insulin.
“The type 3c diabetes is well controlled with a combination of regular (insulin correction factor: 50 mg/dL, insulin-to-carb ratio: 1:10) and NPH insulin (three times daily; 4 IU [6 a.m.], 3-4 IU [2 p.m.], 3-4 IU [10 p.m.]).”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown data§ 2. The Case · p. 5Extra-pancreatic insulin production was ruled out with 68Ga-DOTA-Exendin-4 PET/CT, which only revealed diffuse tracer enrichment in the residual pancreatic head with a maximum standardized uptake value (SUVmax) of 10.26.
“Extra-pancreatic insulin production was ruled out with 68 Ga-DOTA-Exendin-4 PET/CT, which only revealed diffuse tracer enrichment in the residual pancreatic head with a maximum standardized uptake value (SUVmax) of 10.26 (Figure 2).”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingnone given§ 2. The Case · p. 5Since hospital discharge, no severe hypoglycemic events have been reported.
“Since hospital discharge, no severe hypoglycemic events have been reported.”
Quote in the paperNot a substantial claimMay combine two claims.
Findingnone given§ 2. The Case · p. 3Screening for hepatic, renal, adrenal, and pituitary insufficiency, severe inflammation, insulin-like growth factor overproduction, or insulin/insulin receptor autoantibodies was negative.
“Screening for hepatic, renal, adrenal, and pituitary insufficiency, severe inflammation, insulin-like growth factor overproduction, or insulin/insulin receptor autoantibodies was negative.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Findingown data§ 2. The Case · p. 5Currently, the HbA1c of the patient is 6.6% [59.6 mmol/mol], corresponding to an average blood glucose of 143 mg/dL with a time in range (70-180 mg/dL) of approximately 70%, as documented by the CGM device.
“Currently, the HbA1c of our patient is 6.6% [59.6 mmol/mol], corresponding to an average blood glucose of 143 mg/dL with a time in range (70-180 mg/dL) of approximately 70%, as documented by the CGM device.”
Quote in the paperNot a substantial claimMay combine two claims.
Findingnone given§ 2. The Case · p. 4Upon diazoxide treatment, the patient became hypotonic, tachycardic, and developed angina pectoris, resulting in a non-ST-segment elevation myocardial infarction (NSTEMI).
“Upon diazoxide treatment, the patient became hypotonic, tachycardic, and developed angina pectoris, resulting in a non-ST-segment elevation myocardial infarction (NSTEMI).”
Quote in the paperNot a substantial claimMay combine two claims.
Findingreasoning§ 3. Discussion 3. Discussion · p. 8The clinical and laboratory findings in the presented patient were neither exclusively suggestive of insulinoma nor of a functional β-cell disorder.
“Taken together, the clinical and laboratory findings in our patient were neither exclusively suggestive of insulinoma nor of a functional β -cell disorder.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ 1. Introduction · p. 2Clinically, adult-onset nesidioblastosis presents with neuroglycopenic as well as adrenergic symptoms related to hypoglycemia, including impaired consciousness, visual, sensorimotor and speech abnormalities, headaches, seizures, anxiety, tremors, tachycardia, sweating, and many more.
“Clinically, adult-onset nesidioblastosis presents with neuroglycopenic as well as adrenergic symptoms related to hypoglycemia. These include impaired consciousness, visual, sensorimotor and speechabnormalities, headaches, seizures, anxiety, tremors, tachycardia, sweating, and many more [25].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [25] Luca, 2018, Clinical Presentation of 54 Patients with Endogenous Hyperinsulinaemic Hypoglycaemia: A Neurological Chameleon (Observational Study), Swiss Med. Wkly.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ 1. Introduction · p. 2Historically, nesidioblastosis represents a histopathological finding, which describes the budding or neoformation of endocrine islets cells from the exocrine ducts of the pancreas.
“Historically, nesidioblastosis represents a histopathological finding, which describes the budding or neoformation of endocrine islets cells from the exocrine ducts of the pancreas [21].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [21] Laidlaw, 1938, Nesidioblastoma, the Islet Tumor of the Pancreas, Am. J. Pathol.
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ 1. Introduction · p. 2Minor criteria for adult-onset nesidioblastosis comprise islet hypertrophy, islet hyperplasia, lobulated islets, and macronucleoli within the β-cells.
“Apart from that, minor criteria comprise islet hypertrophy, islet hyperplasia, lobulated islets, and macronucleoli within the β -cells [22-24].”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites [22] Anlauf, 2005, Persistent Hyperinsulinemic Hypoglycemia in 15 Adults with Diffuse Nesidioblastosis: Diagnostic Criteria, Incidence, and Characterization of β-Cell Changes, Am. J. Surg. Pathol. source
- cites [23] Anlauf, 2006, Microadenomatosis of the Endocrine Pancreas in Patients with and without the Multiple Endocrine Neoplasia Type 1 Syndrome, Am. J. Surg. Pathol. source
- cites [24] Anlauf, 2008, Adult Diffuse Nesidioblastosis: Genetically or Environmentally Induced?, Hum. Pathol. source
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ 1. Introduction · p. 2The gold standard for diagnosing insulinomas is the proof of hyperinsulinemic hypoglycemia in a prolonged 72 h fasting test.
“The gold standard for diagnosing insulinomas is the proof of hyperinsulinemic hypoglycemia in a prolonged 72 h fasting test [13].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [13] Stamatakos, 2009, Insulinoma: A Rare Neuroendocrine Pancreatic Tumor, Chirurgia
Probably not a substantial claim: may not pass S2 (checkable).
Interpretationreasoning§ An Uncommon Cause of Recurrent Presyncope, Dizziness, and Tachycardia: A Case Report of Diffuse, Adult-Onset Nesidioblastosis/Non-Insulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS) · p. 1This case illustrates the diagnostic challenges in patients presenting with unspecific, neurovegetative and autonomic symptoms with a severe and rare underlying cause.
“This case illustrates the diagnostic challenges in patients presenting with unspecific, neurovegetative and autonomic symptoms with a severe and rare underlying cause.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing), S4 (based).
Premisenone given§ 3. Discussion 3. Discussion · p. 7Rare diseases should be considered in patients if they present with progressive and/or additional symptoms.
“Rare diseases should be considered in patients if they present with progressive and/or additional symptoms.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based).
Premisenone given§ 3. Discussion 3. Discussion · p. 7If hyperinsulinemic hypoglycemia is suspected, a prolonged (4-6 h) oral glucose tolerance test (OGTT) and a 72 h fasting test should be performed.
“If hyperinsulinemic hypoglycemia is suspected, a prolonged (4-6 h) oral glucose tolerance test (OGTT) and a 72 h fasting test should be performed.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisereasoning§ 2. The Case · p. 5Patients suffering from type 3c diabetes have a high susceptibility to hypoglycemia since the autonomic symptoms of hypoglycemia can be missing.
“Patients suffering from this type of diabetes have a high susceptibility to hypoglycemia since the autonomic symptoms of hypoglycemia can be missing.”
Quote in the paperNot a substantial claimMay combine two claims.
Interpretationown data§ 2. The Case · p. 3Some values in the OGTT were not determined and therefore reactive postprandial hypoglycemia was suspected.
“Unfortunately, some values were not determined and therefore reactive postprandial hypoglycemia was suspected.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing). May combine two claims.
Premisenone given§ 3. Discussion 3. Discussion · p. 7The diagnostic work-up of patients presenting with unspecific, autonomic symptoms is very complex, and distinguishing harmless functional disorders from severe organic dysfunctions can be challenging.
“The diagnostic work-up of patients presenting with unspecific, autonomic symptoms is very complex, and distinguishing harmless functional disorders from severe organic dysfunctions can be challenging.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisecitation§ 1. Introduction · p. 2NIPHS comprises postprandial neuroglycopenic symptoms with documented hyperinsulinemic hypoglycemia, a negative 72 h fasting test, negative conventional imaging studies (MRI, CT), as well as a positive selective arterial calcium stimulation test with hepatic venous sampling (SACS).
“It comprises postprandial neuroglycopenic symptoms with documented hyperinsulinemic hypoglycemia, a negative 72 h fasting test, negative conventional imaging studies (MRI, CT), as well as a positive selective arterial calcium stimulation test with hepatic venous sampling (SACS) [26,27].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [26] Service, 1999, Noninsulinoma Pancreatogenous Hypoglycemia: A Novel Syndrome of Hyperinsulinemic Hypoglycemia in Adults Independent of Mutations in Kir6.2 and SUR1 Genes, J. Clin. Endocrinol. Metab.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [27] Mathavan, 2010, Management of Postgastric Bypass Noninsulinoma Pancreatogenous Hypoglycemia, Surg. Endosc. source
May combine two claims.
Interpretationown data§ 2. The Case · p. 5Two years postoperatively, no endogenous insulin production could be detected, as revealed by C-peptide levels below 0.1 ng/mL, which confirms the complete removal of all endocrine pancreatic tissue.
“Two years postoperatively, no endogenous insulin production could be detected, as revealed by C-peptide levels below 0.1 ng/mL, which confirms the complete removal of all endocrine pancreatic tissue.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Premisereasoning§ 2. The Case · p. 5Due to the reduction in or loss of functional endocrine pancreatic tissue, type 3c diabetes is pathophysiologically and clinically different from type 1 diabetes.
“Due to the reduction in or loss of functional endocrine pancreatic tissue, i.e., mainly insulin, glucagon, somatostatin, and pancreatic polypeptide-secreting cells, it is pathophysiologically and clinically different from type 1 diabetes.”
Quote in the paperNot a substantial claimMay combine two claims.
Interpretationreasoning§ 2. The Case · p. 4The slight increase in blood glucose between 48 h and 70 h was attributed to a residual hepatic and/or renal gluconeogenesis, meaning that the amount of insulin in the blood was not sufficient to fully suppress gluconeogenesis.
“The slight increase in blood glucose between 48 h and 70 h was attributed to a residual hepatic and/or renal gluconeogenesis, meaning that the amount of insulin in the blood was not sufficient to fully suppress gluconeogenesis.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based).
Premisenone given§ 3. Discussion 3. Discussion · p. 8Conventional sectional imaging of the abdomen helps to differentiate insulinoma from functional β-cell disorders.
“The conventional sectional imaging of the abdomen helps to differentiate insulinoma from functional β -cell disorders.”
Quote in the paperNot a substantial claimMay combine two claims.
Interpretationown data§ 2. The Case · p. 4The concomitant increase in insulin and C-peptide levels indicated a persistent and inadequately high secretion of insulin, supporting the finding of hyperinsulinemic hypoglycemia.
“The concomitant increase in insulin and C-peptide levels, however, indicated a persistent and inadequately high secretion of insulin, supporting the finding of hyperinsulinemic hypoglycemia.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisecitation§ 1. Introduction · p. 2Service et al. described the common findings associated with nesidioblastosis in 1999 and defined the term NIPHS for the clinical syndrome.
“Service et al. described the common findings associated with nesidioblastosis in 1999, and defined the term NIPHS for the clinical syndrome [26].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [26] Service, 1999, Noninsulinoma Pancreatogenous Hypoglycemia: A Novel Syndrome of Hyperinsulinemic Hypoglycemia in Adults Independent of Mutations in Kir6.2 and SUR1 Genes, J. Clin. Endocrinol. Metab.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing).
Premisecitation§ 3. Discussion 3. Discussion · p. 7Hypoglycemia in the non-diabetic adult patient needs a thorough clinical and laboratory work-up.
“Hypoglycemia in the non-diabetic adult patient needs a thorough clinical and laboratory work-up [4].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [4] Geraghty, 2008, Hypoglycaemia in an Adult Male: A Surprising Finding in Pursuit of Insulinoma, Surgeon source
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ 2. The Case · p. 5According to the American Diabetes Association (ADA), type 3c diabetes, also known as pancreoprivic diabetes, is defined as a special form of diabetes caused by a global dysfunction of the entire pancreas, as seen in acute or chronic pancreatitis, cystic fibrosis, pancreatic neoplasia, pancreatic trauma, or the partial/total surgical removal of the pancreas.
“According to the American Diabetes Association (ADA), type 3c diabetes, also known as pancreoprivic diabetes, is defined as a special form of diabetes caused by a global dysfunction of the entire pancreas, as seen in acute or chronic pancreatitis, cystic fibrosis, pancreatic neoplasia, pancreatic trauma, or the partial/total surgical removal of the pancreas (as in this case) [31].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [31] Association, 2021, Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-2021, Diabetes Care source
May combine two claims.
Premisecitation§ 3. Discussion 3. Discussion · p. 8There is currently no established hypothesis to explain the morphological differences between NIPHS patients or to correlate morphological findings with clinical presentations.
“There is, however, currently no established hypothesis to explain the morphological differences between patients or to correlate the morphological findings with clinical presentations [22,24].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [22] Anlauf, 2005, Persistent Hyperinsulinemic Hypoglycemia in 15 Adults with Diffuse Nesidioblastosis: Diagnostic Criteria, Incidence, and Characterization of β-Cell Changes, Am. J. Surg. Pathol. source
- cites [24] Anlauf, 2008, Adult Diffuse Nesidioblastosis: Genetically or Environmentally Induced?, Hum. Pathol. source
May combine two claims.
Premisenone given§ Diagnostic Algorithm in Hypoglycemia · p. 10In most cases, surgical intervention is the only definitive approach to reduce the frequency and intensity of hypoglycemic events and simultaneously allows for a definitive histological diagnosis.
“In most cases, surgical intervention is the only definitive approach to reduce the frequency and intensity of hypoglycemic events and simultaneously allows for a definitive histological diagnosis.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisecitation§ 3. Discussion 3. Discussion · p. 8Idiopathic/sporadic adult-onset nesidioblastosis with hyperinsulinemic hypoglycemia is an extremely rare disease that occurs much less frequently.
“Idiopathic/sporadic adult-onset nesidioblastosis with hyperinsulinemic hypoglycemia is an extremely rare disease that occurs much less frequently.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S4 (based). May combine two claims.
Premisenone given§ 4. Conclusions · p. 10Diffuse adult-onset nesidioblastosis is a rare disorder presenting with hyperinsulinemic hypoglycemia and various clinical symptoms that can easily be misinterpreted as, for example, an anxiety disorder.
“Diffuse adult-onset nesidioblastosis is a rare disorder presenting with hyperinsulinemic hypoglycemia and various clinical symptoms, which can easily be misinterpreted as, e.g., anxiety disorder.”
Quote in the paperNot a substantial claimMay combine two claims.
Premiseown data§ 3. Discussion 3. Discussion · p. 8Severe adverse effects of diazoxide treatment have been reported in NIPHS, as also illustrated by the presented case.
“However, severe adverse effects have been reported in this context, which is also illustrated by the presented case.”
Quote in the paperNot a substantial claimMay combine two claims.
Interpretationreasoning§ References · p. 11Novel imaging modalities such as 68Ga-DOTA-Exendin-4 PET/CT are helpful in distinguishing occult insulinomas from nesidioblastosis/NIPHS and help to avoid surgical intervention that is unnecessary or too extensive.
“Novel imaging modalities like 68 Ga-DOTA-Exendin-4 PET/CT are helpful in distinguishing occult insulinomas from nesidioblastosis/NIPHS and help to avoid surgical intervention that is unnecessary or too expansive.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationreasoning§ 3. Discussion 3. Discussion · p. 8Because octreotide and lanreotide mainly bind somatostatin receptor subtype 2, they inhibit both insulin and glucagon secretion, which might precipitate hypoglycemia.
“Since octreotide and lanreotide mainly bind somatostatin receptor subtype 2, the substances both inhibit insulin and glucagon secretion, which might precipitate hypoglycemia.”
Quote in the paperNot a substantial claimMay combine two claims.
Premisecitation§ 3. Discussion 3. Discussion · p. 8Many patients with NIPHS report postprandial hypoglycemia, while others present with exercise-induced hypoglycemia or a combination of both.
“While many patients with NIPHS report postprandial hypoglycemia, others present with exercise-induced hypoglycemia or a combination of both [28].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [28] Kaczirek, 2003, Nesidioblastosis in Adults: A Challenging Cause of Organic Hyperinsulinism, Eur. J. Clin. Investig. source
May combine two claims.
Premisecitation§ Diagnostic Algorithm in Hypoglycemia · p. 10Some NIPHS patients are relieved from all symptoms upon left-sided partial/subtotal pancreatectomy, while others need total pancreatectomy for symptom control.
“While some patients are relieved from all symptoms upon left-sided partial/subtotal pancreatectomy, others need to undergo total pancreatectomy for symptom control [63-65].”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites [63] Cristiano, 2014, Endogenous Hyperinsulinemic Hypoglycemia Syndrome: Surgical Treatment, Cir. Esp.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [64] Haghighi, 2016, Synchronous Nesidioblastosis, Endocrine Microadenoma, and Intraductal Papillary Mucinous Neoplasia in a Man Presenting with Hyperinsulinemic Hypoglycemia, Pancreas source
- cites [65] Clancy, 2006, Post−Gastric Bypass Hyperinsulinism With Nesidioblastosis: Subtotal or Total Pancreatectomy May Be Needed to Prevent Recurrent Hypoglycemia, J. Gastrointest. Surg. source
Classified as probably not a substantial claim.
Interpretationnone given§ 3. Discussion 3. Discussion · p. 8Histopathological confirmation of the diagnosis remains the gold standard in NIPHS/diffuse adult-onset nesidioblastosis.
“However, the histopathological confirmation of the diagnosis, as beautifully illustrated by Figure 1, still is the gold standard in NIPHS/diffuse adult-onset nesidioblastosis.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Interpretationreasoning§ Diagnostic Algorithm in Hypoglycemia · p. 10The rapid onset of new hypoglycemic events after partial pancreatectomy could be correlated with significant tracer uptake on 68Ga-DOTA-Exendin-4 PET/CT imaging.
“Of note, this could be correlated with significant tracer uptake upon imaging using 68 Ga-DOTA-Exendin-4 PET/CT.”
Quote in the paperNot a substantial claim
The paper relies on this without support.
The patient's self-reported symptoms and self-measured blood glucose values are reliable.
“Blood glucose measurements performed by the patient shortly (approximately 30 min) after meals reproducibly yielded unexpectedly low values in the range of 40-70 mg/dL.”
“Of interest, the patient reported that the above-described episodes occurred more frequently after food intake, physical exercise, or a combination of both.”
The paper relies on this without support.
Factitious or iatrogenic hypoglycemia could be ruled out.
“As factitious or iatrogenic hypoglycemia could be ruled out, endogenous hyperinsulinemic hypoglycemia was diagnosed.”
The paper relies on this without support.
In some cases, fasting hypoglycemia has been reported in patients with NIPHS.
“In some cases, fasting hypoglycemia was also reported in NIPHS.”
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BackgroundTotal pancreatectomy: Short- and long-term outcomes at a high-volume pancreas center
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Woo, C.-Y., Jeong, J. Y., Jang, J. E., Leem, J., Jung, C. H., Koh, E. H., Lee, W. J., Kim, M.-S., Park, J.-Y., Lee, J. B., et al. (2015) · Diabetes & Metabolism Journal · doi:10.4093/dmj.2015.39.2.126 · Cited by 32 · see citing works
The Clinical Outcomes after Total Pancreatectomy
Suzuki, S., Kajiyama, H., Takemura, A., Shimazaki, J., Nishida, K., & Shimoda, M. (2017) · Digestive Surgery · doi:10.1159/000449234 · Cited by 30 · cited 1× · see citing works
“In the pre-CGM era, the total loss of glycemic control was associated with severe complications in patients undergoing total pancreatectomy [35,66,69].”
BackgroundNesidioblastosis in an Elderly Patient
Walmsley, D., Matheson, N. A., Ewen, S., Himsworth, R. L., & Bevan, J. S. (1995) · Diabetic Medicine · doi:10.1111/j.1464-5491.1995.tb00538.x · Cited by 27 · see citing works
Valente, L. G., Antwi, K., Nicolas, G. P., Wild, D., & Christ, E. (2018) · Swiss Medical Weekly · doi:10.4414/smw.2018.14682 · Cited by 27 · cited 1× · see citing works
“These include impaired consciousness, visual, sensorimotor and speechabnormalities, headaches, seizures, anxiety, tremors, tachycardia, sweating, and many more [25].”
BackgroundSuccessful Medical Treatment of Adult Nesidioblastosis With Pasireotide over 3 Years: A Case Report
Schwetz, V., Horvath, K., Kump, P., Lackner, C., Perren, A., Forrer, F., Pieber, T. R., Treiber, G., Sourij, H., & Mader, J. K. (2016) · Medicine · doi:10.1097/md.0000000000003272 · Cited by 25 · cited 3× · see citing works
“subtype 5 and was effective in at least one NIPHS patient with hypoglycemia resistant to octreotide treatment [62].”
BackgroundSelf-citationNoninsulinoma Pancreatogenous Hypoglycemia Syndrome: A Rare Case of Adult-onset Nesidioblastosis
TSUJINO, M., SUGIYAMA, T., NISHIDA, K., TAKADA, Y., TAKANISHI, K., ISHIZAWA, M., & HIRATA, Y. (2005) · Internal Medicine · doi:10.2169/internalmedicine.44.843 · Cited by 24 · cited 2× · see citing works
“If clinical findings are suggestive of insulinoma but no tumor can be localized upon conventional imaging, rarer causes of recurrent spontaneous hypoglycemia in the adult patient must be considered: insulin autoimmune syndrome, also known as Hirata’s disease, as well as functional β-cell disorders [14,15].”
BackgroundResultRao, B. B., Click, B., Eid, G., & Codario, R. A. (2015) · Case Reports in Endocrinology · doi:10.1155/2015/384526 · Cited by 19 · see citing works
Perioperative Nutritional Aspects in Total Pancreatectomy: A Comprehensive Review of the Literature
Furbetta, N., Comandatore, A., Gianardi, D., Palmeri, M., Di Franco, G., Guadagni, S., Caprili, G., Bianchini, M., Fatucchi, L. M., Picchi, M., et al. (2021) · Nutrients · doi:10.3390/nu13061765 · Cited by 18 · see citing works
Diabetes management in patients undergoing total pancreatectomy: A single center cohort study
Zhao, T., Fu, Y., Zhang, T., Guo, J., Liao, Q., Song, S., Duo, Y., Gao, Y., Yuan, T., & Zhao, W. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1097139 · Cited by 18 · cited 2× · see citing works
“A current review article by Zhao and colleagues provides an in-depth discussion of this topic [35].”
BackgroundHypoglycemia due to an adult-onset nesidioblastosis, a diagnostic and management dilemma
Qintar, M., Sibai, F., & Taha, M. (2012) · Avicenna Journal of Medicine · doi:10.4103/2231-0770.99164 · Cited by 17 · see citing works
Nesidioblastosis with Glucagon-Reactive Islet Cell Hyperplasia: A Case Report
Martignoni, M. E., Kated, H., Stiegler, M., Büchler, M. W., Friess, H., Zimmermann, A., Schirp, U., & Nitzsche, E. U. (2003) · Pancreas · doi:10.1097/00006676-200305000-00016 · Cited by 17 · see citing works
Clinicophysiological outcomes after total pancreatectomy
Suzuki, S., Miura, J., Shimizu, K., Tokushige, K., Uchigata, Y., & Yamamoto, M. (2016) · Scandinavian Journal of Gastroenterology · doi:10.1080/00365521.2016.1211173 · Cited by 17 · see citing works
Receptor-Targeted Photodynamic Therapy of Glucagon-Like Peptide 1 Receptor–Positive Lesions
Boss, M., Bos, D., Frielink, C., Sandker, G., Bronkhorst, P., van Lith, S. A. M., Brom, M., Buitinga, M., & Gotthardt, M. (2020) · Journal of Nuclear Medicine · doi:10.2967/jnumed.119.238998 · Cited by 15 · cited 1× · see citing works
“A major challenge remains the adequate dosage, which guarantees relief from hypoglycemia while simultaneously preserving the other endocrine and exocrine functions of the pancreas [70].”
BackgroundPancreatectomy Extension in Persistent Hyperinsulinaemic Hypoglycaemia: A New Strategy
Martinez-Ibanez, V., Gussinyer, M., Toran, N., Lloret, J., Abad, P., Carrascosa, A., & Boix-Ochoa, J. (2002) · European Journal of Pediatric Surgery · doi:10.1055/s-2002-34476 · Cited by 14 · see citing works
Nesidioblastosis and Insulinoma: A Rare Coexistence and a Therapeutic Challenge
Dardano, A., Daniele, G., Lupi, R., Napoli, N., Campani, D., Boggi, U., Del Prato, S., & Miccoli, R. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00010 · Cited by 14 · cited 1× · see citing works
“While a low carbohydrate diet or α-glucosidase inhibitors are not effective in most patients, the potassium channel activator diazoxide has been shown to alleviate symptoms in some cases [58,59].”
Backgroundvon Alvensleben, J. C. (2020) · Pediatric Clinics of North America · doi:10.1016/j.pcl.2020.05.004 · Cited by 14 · see citing works
De Sousa, S. M. C., Haghighi, K. S., Qiu, M. R., Greenfield, J. R., & Chen, D. L. T. (2016) · Pancreas · doi:10.1097/mpa.0000000000000430 · Cited by 13 · see citing works
Suto, H., Kamei, K., Kato, H., Misawa, T., Unno, M., Nitta, H., Satoi, S., Kawabata, Y., Ohtsuka, M., Rikiyama, T., et al. (2021) · British Journal of Surgery · doi:10.1093/bjs/znab097 · Cited by 11 · see citing works
Koneshamoorthy, A., Seniveratne-Epa, D., Calder, G., Sawyer, M., Kay, T. W. H., Farrell, S., Loudovaris, T., Mariana, L., McCarthy, D., Lyu, R., et al. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.842937 · Cited by 11 · see citing works
An unusual cause of hypoglycemia in a middle-aged female after bariatric surgery
Pathak, R., Karmacharya, P., Salman, A., & Alweis, R. (2014) · Journal of Community Hospital Internal Medicine Perspectives · doi:10.3402/jchimp.v4.23118 · Cited by 10 · see citing works
Conget, I., Sam, Y., Somoza, N., Vives, M., Novials, A., Ariza, A., Fernández-Alvarez, J., Pujol-Borrell, R., & Gomis, R. (1997) · Pancreas · doi:10.1097/00006676-199701000-00011 · Cited by 9 · see citing works
Kim, J. R., Jang, J.-Y., Shin, Y. C., Cho, Y. M., Kim, H., Kwon, W., Han, Y. M., & Kim, S.-W. (2016) · Annals of Surgical Treatment and Research · doi:10.4174/astr.2016.91.1.51 · Cited by 9 · cited 2× · see citing works
“The latter is especially helpful in distinguishing occult or ectopic insulinoma from NIPHS and to separate focal and diffuse nesidioblastosis [29].”
BackgroundAmlodipine for the Medical Treatment of Adult-Onset Diffuse Nesidioblastosis
Martin-Grace, J., O’Tuathail, M., Hannon, M. J., Swan, N., O’Shea, D., & Tamagno, G. (2015) · Pancreas · doi:10.1097/mpa.0000000000000407 · Cited by 8 · see citing works
Dauriz, M., Maneschi, C., Castelli, C., Tomezzoli, A., Fuini, A., Landoni, L., Malleo, G., Ferdeghini, M., Bonora, E., & Moghetti, P. (2019) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2018-02007 · Cited by 8 · cited 1× · see citing works
“Since these substances also inhibit the secretion of glucagon, symptoms of hypoglycemia may occur even more frequently in a subset of patients [52,61,62].”
BackgroundSíndrome de hipoglucemia por hiperinsulinismo endógeno: tratamiento quirúrgico
de Santibañes, M., Cristiano, A., Mazza, O., Grossenbacher, L., de Santibáñes, E., Clariá, R. S., Sivori, E., Mónaco, R. G., & Pekolj, J. (2014) · Cirugía Española · doi:10.1016/j.ciresp.2013.04.025 · Cited by 7 · see citing works
Organic hyperinsulinism: radiological diagnostics and surgical treatment
Krieger, A. G., Smirnov, A. V., Берелавичус, С. В., et al. (2016) · Pirogov Russian Journal of Surgery · doi:10.17116/hirurgia2016614-22 · Cited by 7 · cited 1× · see citing works
“Biomedicines) and the following references [7,42,43].”
Hypoglycaemia in an adult male: A surprising finding in pursuit of insulinoma
Geraghty, M., Draman, M., Moran, D., Muldoon, C., Reynolds, J. V., & Cullen, M. J. (2008) · The Surgeon · doi:10.1016/s1479-666x(08)80097-2 · Cited by 6 · cited 1× · see citing works
“Hypoglycemia in the non-diabetic adult patient needs a thorough clinical and laboratory work-up [4].”
BackgroundBränström, R., Berglund, E., Curman, P., Forsberg, L. E., Höög, A., Grimelius, L., Berggren, P., Mattsson, P., Hellman, P., & Juntti‐Berggren, L. (2010) · Journal of Medical Case Reports · doi:10.1186/1752-1947-4-315 · Cited by 6 · see citing works
Insulinoma presenting with postprandial hypoglycemia and a low body mass index: A case report
Prídavková, D., Samoš, M., Kyčina, R., Adamicová, K., Kalman, M., Belicová, M., & Mokáň, M. (2020) · World Journal of Clinical Cases · doi:10.12998/wjcc.v8.i18.4169 · Cited by 6 · see citing works
Metastatic Insulinoma Presenting With Postprandial Hypoglycemia
Maher, M. D., Desai, D. N., & Bajaj, M. (2022) · AACE Clinical Case Reports · doi:10.1016/j.aace.2022.03.002 · Cited by 5 · see citing works
Oueslati, I., Terzi, A., Yazidi, M., Kamoun, E., & Chihaoui, M. (2022) · Endocrinology, Diabetes & Metabolism · doi:10.1002/edm2.375 · Cited by 5 · see citing works
Insulinoma: a rare neuroendocrine pancreatic tumor.
(2009) · PubMed · Cited by 4 · see citing works
Maguire, D. (2015) · Clinical Medicine · doi:10.7861/clinmedicine.15-5-495 · Cited by 4 · cited 1× · see citing works
“As can be seen from our case and other reports in the literature, a positive fasting test neither confirms insulinoma nor excludes NIPHS [53,54].”
ResultRao, B. B., Click, B., & Codario, R. (2014) · American Journal of Gastroenterology · doi:10.14309/00000434-201410002-01037 · Cited by 4 · see citing works
Sakurai, Y., Ohara, N., Fukai, Y., Seki, Y., Akiyama, K., Yoneoka, Y., Takada, T., Tani, T., Terajima, K., Ozawa, T., et al. (2023) · Internal Medicine · doi:10.2169/internalmedicine.0038-22 · Cited by 3 · cited 1× · see citing works
“Genuine endocrine diseases, like pituitary or adrenal insufficiency, should also be considered especially if patients present with other symptoms suggestive of these diseases [11,12].”
BackgroundHypopituitarism Presenting as Recurrent Episodes of Hypoglycemia: Houssay Phenomenon
Rizwan, T., Arora, G., Alchalabi, M., & Qureshi, F. (2023) · Cureus · doi:10.7759/cureus.37530 · Cited by 3 · cited 1× · see citing works
“Genuine endocrine diseases, like pituitary or adrenal insufficiency, should also be considered especially if patients present with other symptoms suggestive of these diseases [11,12].”
BackgroundHypoglycemia Controlled by Prednisone in an Occult Insulinoma or a Nesidioblastosis
Kérékou, A., El Aziz, S., Dédjan, A., Chadli, A., & Farouqi, A. (2019) · Open Journal of Endocrine and Metabolic Diseases · doi:10.4236/ojemd.2019.96007 · Cited by 2 · see citing works
Pancreatectomy extension in persistent hyperinsulinaemic hypoglycaemia: a new strategy
Martínez-Ibáñez, V., Gussinyer, M., & Torán, N. (2003) · Journal of Pediatric Surgery · doi:10.1016/s0022-3468(03)00150-7
Flagged first, then by citations
2 of the 76 references couldn’t be matched to a known paper.
Research works printed but not linked: 3
- Woodcock, 2019, Diabetes Care after Pancreatic Surgery, J. Diabetes Nurs., 23, 1
- Cavallo, 2019, Management of Total Pancreatectomy-Induced Diabetes Mellitus : A Mini-Review, Austin Pancreat Disord, 3, 1012
- Cristiano, 2014, Endogenous Hyperinsulinemic Hypoglycemia Syndrome: Surgical Treatment, Cir. Esp., 92, 547
Cited by
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Thapa, S., Kaur, K., Yadav, G., Kumari, D., & Phulware, R. (2023) · Autopsy and Case Reports · doi:10.4322/acr.2023.451 · Cited by 5 · see citing works
Sidana, S., Kapatia, G., Thakur, P., et al. (2024) · IJEM Case Reports · doi:10.4103/ijemcr.ijemcr_23_24
Lisboa, F. F., Junior, F., Ferreira, L., Dantas, G. D. C., & Cruz, G. (2025) · Journal of Surgery · doi:10.11648/j.js.20251303.11
Diagnosi differenziale della sindrome ipoglicemica
Belcastro, S., Giannone, B., & Bombonato, M. (2025) · L Endocrinologo · doi:10.1007/s40619-025-01718-6
Bavaria, S., Chana, A., Nurani, K., & Kimang’a, J. (2026) · World Journal of Diabetes · doi:10.4239/wjd.v17.i3.116660
- Authors
- Dieterle, M. P., Husari, A., Prozmann, S. N., Wiethoff, H., Stenzinger, A., Röhrich, M., Pfeiffer, U., Kießling, W. R., Engel, H., Sourij, H., Steinberg, T., Tomakidi, P., Kopf, S., & Szendroedi, J.
- Affiliations
- University of Freiburg (DE)
- University Hospital Heidelberg (DE)
- Pfalzklinikum for Psychiatry and Neurology AdÖR, Weinstr. 100, 76889 Klingenmünster, Germany
- Independent Researcher, 72250 Freudenstadt, Germany
- German Cancer Research Center (DE)
- Medical University of Graz (AT)
- Heidelberg University (DE)
- Corresponding author
- Dieterle, Martin Philipp
- ORCID
- Venue
- Biomedicines
- Publisher
- MDPI AG
- Published
- 2023-06-17
- Volume
- 11
- Issue
- 6
- Pages
- 1741
- ISSN
- 2227-9059 (ISSN-L)
- PMC
- PMC10296627
- OpenAlex
- W4381251859
- Semantic Scholar
- 99d549f745179aeb7dc94b8744624f223e0e7694
- Cited by
- 5
- References
- 76
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 1
- FWCI
- 0.85
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Biomedicines (publishedVersion, cc-by)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Epidemiology › Neuroendocrine Tumor Research Advances
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- endogenous hyperinsulinism, postprandial hypoglycemia, exercise-induced hypoglycemia, presyncope, dizziness, tachycardia, subtotal pancreatectomy, C-peptide
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-14.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-14.
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