Glucocorticoid therapy suppresses abnormal secretion of big IGF-II by non-islet cell tumours inducing hypoglycaemia (NICTH)
OBJECTIVE To assess the relative efficacy of hGH and glucocorticoids in the treatment of non‐islet cell tumour hypoglycaemia (NICTH) by examination of their influence on the composition of the various molecular species involving tumour and mature forms of IGF‐II in association with IGFBP‐3. DESIGN T...
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Published in | Clinical endocrinology (Oxford) Vol. 49; no. 4; pp. 491 - 498 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Oxford BSL
Blackwell Science Ltd
01.10.1998
Blackwell |
Subjects | |
Online Access | Get full text |
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Summary: | OBJECTIVE
To assess the relative efficacy of hGH and glucocorticoids in the treatment of non‐islet cell tumour hypoglycaemia (NICTH) by examination of their influence on the composition of the various molecular species involving tumour and mature forms of IGF‐II in association with IGFBP‐3.
DESIGN
Two groups each of 4 patients, all diagnosed as cases of NICTH, were treated with either hGH or glucocorticoids. Through the use of acidic size exclusion chromatography serum levels of tumour (big) and mature IGF‐II were evaluated. Neutral size exclusion chromatography was used in the separation of molecular species before assay for immunoreactive IGF‐II and IGFBP‐3 content.
RESULTS
High‐dose hGH treatment produced increases in serum levels of big and mature IGF‐II and IGFBP‐3 but without generation of high molecular weight complexes. Glucocorticoid treatment suppressed big IGF‐II permitting re‐establishment of normal IGF/IGFBP association patterns.
CONCLUSION
Glucocorticoid therapy has been demonstrated to consistently reverse the biochemical abnormalities caused by tumour‐derived big IGF‐II compared with the potentially adverse stimulatory effects of hGH treatment in causing increases in serum levels of big IGF‐II. |
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Bibliography: | ark:/67375/WNG-W6Z5CCPP-V ArticleID:CEN564 istex:D01E47607E63B54394B7050889859CCE227A56F4 ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 ObjectType-News-3 content type line 23 |
ISSN: | 0300-0664 1365-2265 |
DOI: | 10.1046/j.1365-2265.1998.00564.x |