PMID 19579890. Alkatib AA, Cosma M, Elamin MB, Erickson D, Swiglo BA, Erwin PJ, Montori VM (October 2009). "A systematic review and meta-analysis of randomized placebo-controlled trials of DHEA treatment effects on quality of life in women with adrenal insufficiency". J. Clin. Endocrinol. Metab. 94 (10): 3676–81. doi:10.1210/jc.2009-0672. PMID 19773400. Panjari M, Davis SR (June 2010). "DHEA for postmenopausal women: a review of the evidence". Maturitas. 66 (2): 172–9. doi:10.1016/j.maturitas.2009.12.017. PMID 20089375. Oberbeck R, Kobbe P (2010). "Dehydroepiandrosterone (DHEA): a steroid with multiple effects. Is there any possible option in the treatment of critical illness?". Curr. Med. Chem. 17 (11): 1039–47. doi:10.2174/092986710790820570. PMID 20156161. Prati A, Santagni S, Rattighieri E, Campedelli A, Ricchieri F, Chierchia E, Despini G, Genazzani AR, Genazzani AD (June 2014). "[The putative role and use of DHEA and its association with the hormone replacement therapy]". Minerva Ginecol (in Italian). 66 (3): 313–24. PMID 24971788. Genazzani AR, Pluchino N (August 2010). "DHEA therapy in postmenopausal women: the need to move forward beyond the lack of evidence". Climacteric. 13 (4): 314–6. doi:10.3109/13697137.2010.492496. PMID 20540592. S2CID 5578070. Luci M, Valenti G, Maggio M (September 2010). "[Dehydroepiandrosterone [DHEA(S)]: anabolic hormone?]". Recenti Prog Med (in Italian). 101 (9): 333–44. hdl:11381/2436727. PMID 21268370. Gleicher N, Barad DH (May 2011). "Dehydroepiandrosterone (DHEA) supplementation in diminished ovarian reserve (DOR)". Reprod. Biol. Endocrinol. 9: 67. doi:10.1186/1477-7827-9-67. PMC 3112409. PMID 21586137. Davis SR, Panjari M, Stanczyk FZ (June 2011). "Clinical review: DHEA replacement for postmenopausal women". J. Clin. Endocrinol. Metab. 96 (6): 1642–53. doi:10.1210/jc.2010-2888. PMID 21411558. Panjari M, Davis SR (September 2011).
The American Society of Health-System Pharmacists guideline recommends against the practice of stress ulcer prophylaxis in non-critically ill patients. Mechanisms
Location
The ulcerations may be superficial and confined to the mucosa, in which case they are more appropriately called erosions, or they may penetrate deeper into the submucosa. The former may cause diffuse mucosal oozing of blood, whereas the latter may erode into a submucosal vessel and produce frank hemorrhage. Lesions
The characteristic lesions may be multiple, superficial mucosal erosions similar to erosive gastroduodenitis. Occasionally, there may be a large acute ulcer in the duodenum (Curling’s ulcer).Generally, there are multiple lesions located mainly in the stomach and occasionally in the duodenum. They range in depth from mere shedding of the superficial epithelium (erosion) to deeper lesions that involve the entire mucosal thickness (ulceration). Formation
The pathogenic mechanisms are similar to those of erosive gastritis.The pathogenesis of stress ulcer is unclear but probably is related to a reduction in mucosal blood flow or a breakdown in other normal mucosal defense mechanisms in conjunction with the injurious effects of acid and pepsin on the gastroduodenal mucosa. Diagnosis
Stress ulcer is suspected when there is upper gastrointestinal bleeding in the appropriate clinical setting, for example, when there is upper gastrointestinal bleeding in elderly patients in a surgical intensive care unit (ICU) with heart and lung disease, or when there is upper gastrointestinal bleeding in patients in a medical ICU who require respirators.Stress ulcer can be diagnosed after the initial management of gastrointestinal bleeding, the diagnosis can be confirmed by upper GI endoscopy.