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The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.

Endocrine consequences of anorexia nervosa

Open access
Misra, Madhusmita, Klibanski, Anne·2014·The Lancet Diabetes & Endocrinology

Abstract

Summary Anorexia nervosa (AN) is prevalent in adolescents and young adults, and endocrine changes include hypothalamic amenorrhea, a nutritionally acquired growth hormone resistance with low insulin like growth factor-1 (IGF-1), relative hypercortisolemia, decreases in leptin, insulin, amylin and incretins, and increases in ghrelin, PYY and adiponectin. These changes in turn have deleterious effects on bone, and may affect neurocognition, anxiety, depression and eating disorder psychopathology. Low bone density is particularly concerning; clinical fractures occur and changes in both bone microarchitecture and strength estimates have been reported. Recovery causes improvement of many, but not all, hormonal changes, and deficits in bone accrual may persist despite recovery. Physiologic, primarily transdermal, estrogen replacement increases bone density in adolescents, although catch-up is incomplete. In adults, oral estrogen co-administered with rhIGF-1 in one study, and bisphosphonates in another increased bone density, though not to normal. More studies are necessary to determine the optimal therapeutic approach in AN.

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Metadata

Authors
Misra, M., & Klibanski, A.
Venue
The Lancet Diabetes & Endocrinology
Publisher
Elsevier BV
Published
2014-07
Volume
2
Issue
7
Pages
581-592
ISSN
2213-8587 (ISSN-L)
OpenAlex
W2063273990
Cited by
341
References
12
FWCI
28.51
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Endocrine consequences of anorexia nervosa. https://app.cochat.ai/papers/10.1016/s2213-8587(13)70180-3
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Misra, M., & Klibanski, A. (2014). Endocrine consequences of anorexia nervosa. The Lancet Diabetes & Endocrinology. https://doi.org/10.1016/s2213-8587(13)70180-3

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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