Synthesis and secretion of insulin-like growth factor II by a leiomyosarcoma with associated hypoglycemia

W. H. Daughaday, M. A. Emanuelle, M. H. Brooks, A. L. Barbato, M. Kapadia, P. Rotwein

Research output: Contribution to journalArticle

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Abstract

We describe a case of recurrent hypoglycemia apparently caused by secretion of insulin-like growth factor II (IGF-II) by a leiomyosarcoma. A 67-year-old woman presented with recurrent severe hypoglycemia and a large mass in the thorax. During hypoglycemia, plasma cortisol was elevated, but insulin and growth hormone levels were low. After resection of a large leiomyosarcoma, the hypoglycemia resolved. After an eight-year remission, both the tumor and symptomatic hypoglycemia recurred. During a second operation a second large tumor was removed, with relief of the patient's hypoglycemia. The tumor contained high concentrations of IGF-II mRNA and 2100 ng of IGF-II immunoreactive peptide per gram. Filtration through a BioGel P-60 gel column established that 77 percent of the IGF-II was present as a larger molecule, demonstrating incomplete processing of the pro-IGF-II peptides. A similar fraction of high-molecular-weight IGF-II was present in the serum, indicating that the tumor was the chief source of IGF-II. The high-molecular-weight IGF-II found in both the tumor and serum was fully reactive with the IGF-II receptor. Radioimmunoassay showed that the concentrations of insulin-like growth factor I (IGF-I) in tumor and serum were low, suggesting feedback inhibition of growth hormone secretion by IGF-II. Eight months after reoperation, plasma concentrations of IGF-I and IGF-II were normal, and high-molecular-weight IGF-II was virtually undetectable. We conclude that the most likely cause of this patient's recurrent hypoglycemia was IGF-II produced by the leiomyosarcoma.

Original languageEnglish (US)
Pages (from-to)1434-1440
Number of pages7
JournalNew England Journal of Medicine
Volume319
Issue number22
StatePublished - 1988
Externally publishedYes

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Insulin-Like Growth Factor II
Leiomyosarcoma
Hypoglycemia
Neoplasms
Molecular Weight
Insulin-Like Growth Factor I
Growth Hormone
Serum
IGF Type 2 Receptor
Peptides
Reoperation
Radioimmunoassay
Hydrocortisone
Thorax
Gels

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Daughaday, W. H., Emanuelle, M. A., Brooks, M. H., Barbato, A. L., Kapadia, M., & Rotwein, P. (1988). Synthesis and secretion of insulin-like growth factor II by a leiomyosarcoma with associated hypoglycemia. New England Journal of Medicine, 319(22), 1434-1440.

Synthesis and secretion of insulin-like growth factor II by a leiomyosarcoma with associated hypoglycemia. / Daughaday, W. H.; Emanuelle, M. A.; Brooks, M. H.; Barbato, A. L.; Kapadia, M.; Rotwein, P.

In: New England Journal of Medicine, Vol. 319, No. 22, 1988, p. 1434-1440.

Research output: Contribution to journalArticle

Daughaday, WH, Emanuelle, MA, Brooks, MH, Barbato, AL, Kapadia, M & Rotwein, P 1988, 'Synthesis and secretion of insulin-like growth factor II by a leiomyosarcoma with associated hypoglycemia', New England Journal of Medicine, vol. 319, no. 22, pp. 1434-1440.
Daughaday WH, Emanuelle MA, Brooks MH, Barbato AL, Kapadia M, Rotwein P. Synthesis and secretion of insulin-like growth factor II by a leiomyosarcoma with associated hypoglycemia. New England Journal of Medicine. 1988;319(22):1434-1440.
Daughaday, W. H. ; Emanuelle, M. A. ; Brooks, M. H. ; Barbato, A. L. ; Kapadia, M. ; Rotwein, P. / Synthesis and secretion of insulin-like growth factor II by a leiomyosarcoma with associated hypoglycemia. In: New England Journal of Medicine. 1988 ; Vol. 319, No. 22. pp. 1434-1440.
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AU - Daughaday, W. H.

AU - Emanuelle, M. A.

AU - Brooks, M. H.

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AU - Kapadia, M.

AU - Rotwein, P.

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N2 - We describe a case of recurrent hypoglycemia apparently caused by secretion of insulin-like growth factor II (IGF-II) by a leiomyosarcoma. A 67-year-old woman presented with recurrent severe hypoglycemia and a large mass in the thorax. During hypoglycemia, plasma cortisol was elevated, but insulin and growth hormone levels were low. After resection of a large leiomyosarcoma, the hypoglycemia resolved. After an eight-year remission, both the tumor and symptomatic hypoglycemia recurred. During a second operation a second large tumor was removed, with relief of the patient's hypoglycemia. The tumor contained high concentrations of IGF-II mRNA and 2100 ng of IGF-II immunoreactive peptide per gram. Filtration through a BioGel P-60 gel column established that 77 percent of the IGF-II was present as a larger molecule, demonstrating incomplete processing of the pro-IGF-II peptides. A similar fraction of high-molecular-weight IGF-II was present in the serum, indicating that the tumor was the chief source of IGF-II. The high-molecular-weight IGF-II found in both the tumor and serum was fully reactive with the IGF-II receptor. Radioimmunoassay showed that the concentrations of insulin-like growth factor I (IGF-I) in tumor and serum were low, suggesting feedback inhibition of growth hormone secretion by IGF-II. Eight months after reoperation, plasma concentrations of IGF-I and IGF-II were normal, and high-molecular-weight IGF-II was virtually undetectable. We conclude that the most likely cause of this patient's recurrent hypoglycemia was IGF-II produced by the leiomyosarcoma.

AB - We describe a case of recurrent hypoglycemia apparently caused by secretion of insulin-like growth factor II (IGF-II) by a leiomyosarcoma. A 67-year-old woman presented with recurrent severe hypoglycemia and a large mass in the thorax. During hypoglycemia, plasma cortisol was elevated, but insulin and growth hormone levels were low. After resection of a large leiomyosarcoma, the hypoglycemia resolved. After an eight-year remission, both the tumor and symptomatic hypoglycemia recurred. During a second operation a second large tumor was removed, with relief of the patient's hypoglycemia. The tumor contained high concentrations of IGF-II mRNA and 2100 ng of IGF-II immunoreactive peptide per gram. Filtration through a BioGel P-60 gel column established that 77 percent of the IGF-II was present as a larger molecule, demonstrating incomplete processing of the pro-IGF-II peptides. A similar fraction of high-molecular-weight IGF-II was present in the serum, indicating that the tumor was the chief source of IGF-II. The high-molecular-weight IGF-II found in both the tumor and serum was fully reactive with the IGF-II receptor. Radioimmunoassay showed that the concentrations of insulin-like growth factor I (IGF-I) in tumor and serum were low, suggesting feedback inhibition of growth hormone secretion by IGF-II. Eight months after reoperation, plasma concentrations of IGF-I and IGF-II were normal, and high-molecular-weight IGF-II was virtually undetectable. We conclude that the most likely cause of this patient's recurrent hypoglycemia was IGF-II produced by the leiomyosarcoma.

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