A 67-Year-Old Woman with Recurrent Hypoglycemia: Non-Islet Cell Tumour Hypoglycemia
Open accessAbstract
THE CASE: A 67-year-old woman was brought to hospital by her husband, who had found her sweaty and unresponsive in the morning. She was hypoglycemic, with a plasma glucose level of 1.2 mmol/L (normal range 3.8–6.1 mmol/L). After receiving dextrose intravenously, she regained consciousness and her
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In NICTH, there is excess production of a modified IGF-II known as big IGF-II.
“However, in NICTH, there is excess production of a modified IGF-II known as big IGF-II.”
From Non-Diabetic Hypoglycemia: Evaluation and Management in Adults (2025) · cites this paper as [44]
The pathophysiology discussion (passage 1; page not provided) describes tumour production of incompletely processed pro-IGF-II, resulting in “big” IGF-II. It qualifies this mechanism as occurring in *some* tumours, whereas the claim states it without that qualification for NICTH generally. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThese smaller binary complexes and the higher amount of free big IGF-II contribute to greater bioavailability, leading to fasting hypoglycemia by suppressing hepatic gluconeogenesis and glycogenolysis, increasing skeletal muscle and adipose tissue glucose uptake, and decreasing lipolysis.
“These smaller, binary complexes and the higher amount of free big IGF-II contribute to greater bioavailability, leading to fasting hypoglycemia by suppressing hepatic gluconeogenesis and glycogenolysis, increasing skeletal muscle and adipose tissue glucose uptake, and decreasing lipolysis [42,44].”
From Non-Diabetic Hypoglycemia: Evaluation and Management in Adults (2025) · cites this paper as [44]
Split into 2 atoms — 1 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable, 1 not checked. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredThere is a much larger pool of unbound big IGF-II compared to unbound IGF-II, and if bound, big IGF-II preferentially binds to IGFBP-2.
“There is a much larger pool of unbound big IGF-II as compared to unbound IGF-II and if bound, big IGF-II preferentially binds to IGFBP-2.”
From Non-Diabetic Hypoglycemia: Evaluation and Management in Adults (2025) · cites this paper as [44]
The discussion of IGF biochemistry (page not provided) says that big IGF-II binds poorly to IGFBP-3 and forms smaller complexes, leaving more IGF-II available. It does not compare the sizes of the unbound big IGF-II and unbound IGF-II pools, or say that big IGF-II preferentially binds IGFBP-2. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe majority of IGF-II is bound to IGFBP-3, a large tertiary complex that typically does not interact with the insulin receptor.
“The majority of IGF-II is bound to IGF binding protein 3 (IGFBP-3), a large, tertiary complex that typically does not interact with the insulin receptor.”
From Non-Diabetic Hypoglycemia: Evaluation and Management in Adults (2025) · cites this paper as [44]
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Research works printed but not linked: 4
- Zapf J, Futo E, Peter M, Froesch ER. Can "big" insulin-like growth factor II in serum of tumor patients account for the development of extrapancre- atic tumor hypoglycemia? J Clin In- vest 1992;90:2574-84.
- Teale JD, Marks V. Inappropriately elevated plasma insulin-like growth factor II in relation to suppressed in- sulin-like growth factor I in the diag- nosis of non-islet cell tumour hypo- glycaemia. Clin Endocrinol (Oxf) 1990; 33:87-98.
- Baxter RC, Holman SR, Corbould A, Stranks S, Ho PJ, Braund W. Regula- tion of the insulin-like growth factors and their binding proteins by gluco- corticoid and growth hormone in nonislet cell tumor hypoglycemia. J Clin Endocrinol Metab 1995;80:2700-8.
- Perros P, Simpson J, Innes JA, Teale JD, McKnight JA. Non-islet cell tu- mour-associated hypoglycaemia: 111 In-octreotide imaging and efficacy of octreotide, growth hormone and glu- cocorticosteroids. Clin Endocrinol (Oxf) 1996;44:727-31.
Cited by
Sorted by citations
MANAGEMENT OF ENDOCRINE DISEASE: Pathogenesis and management of hypoglycemia
Kittah, N. E., & Vella, A. (2017) · European Journal of Endocrinology · doi:10.1530/eje-16-1062 · Cited by 107 · see citing works
Non-Diabetic Hypoglycemia: Evaluation and Management in Adults
Looi, E., & Lawler, H. M. (2025) · Journal of Clinical Medicine · doi:10.3390/jcm14134393 · Cited by 10 · see citing works
“These smaller, binary complexes and the higher amount of free big IGF-II contribute to greater bioavailability, leading to fasting hypoglycemia by suppressing hepatic gluconeogenesis and glycogenolysis, increasing skeletal muscle and adipose tissue glucose uptake, and decreasing lipolysis [42,44].”
- Authors
- Ma, R. C. W.
- Venue
- Canadian Medical Association Journal
- Publisher
- CMA Joule Inc.
- Published
- 2005-08-16
- Volume
- 173
- Issue
- 4
- Pages
- 359-361
- ISSN
- 0820-3946 (ISSN-L)
- 1488-2329
- PMC
- PMC1188218
- OpenAlex
- W2028381747
- Cited by
- 14
- References
- 0
- Citations by year
- 2025: 3 · 2024: 2 · 2020: 2 · 2018: 1 · 2017: 1 · 2013: 1
- FWCI
- 0.48
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Canadian Medical Association Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Neuroendocrine Tumor Research Advances
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pituitary Gland Disorders and Treatments
- Keywords
- recurrent hypoglycemia, non-islet cell tumor hypoglycemia, paraneoplastic hypoglycemia, plasma glucose, older women
- MeSH terms
- Aged, Female, Fibroma, Humans, Hypoglycemia, Pleural Neoplasms, Recurrence
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