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10.1016/S2213-8587(13)70180-3

http://scihub22266oqcxt.onion/10.1016/S2213-8587(13)70180-3
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C4133106!4133106!24731664
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suck abstract from ncbi

pmid24731664      Lancet+Diabetes+Endocrinol 2014 ; 2 (7): 581-92
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  • Endocrine Consequences of Anorexia Nervosa #MMPMID24731664
  • Misra M; Klibanski A
  • Lancet Diabetes Endocrinol 2014[Jul]; 2 (7): 581-92 PMID24731664show ga
  • 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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