Tsushima Yumiko, Munshi Lubna Bashir, Taneja Charit, Kim Se-Min
AACE Clin Case Rep. 2019 Jun 7;5(5):e290-e293. doi: 10.4158/ACCR-2019-0097. eCollection 2019 Sep-Oct.
Glaucoma is a well-recognized side effect of corticosteroids. However, steroid-induced glaucoma typically refers to that caused by exogenous corticosteroid administration. Glaucoma secondary to endogenous overproduction of corticosteroids has only been reported in a few case reports. We aim to bring attention to glaucoma as a rare but important manifestation of endogenous hypercortisolism.
Patient history, physical exam, laboratory results, and imaging studies were reviewed.
We report a case of glaucoma as the initial presentation of Cushing disease (CD). The patient was diagnosed with glaucoma 16 months prior to his endocrinology evaluation. At our initial encounter, the patient had a cushingoid appearance. Levels of 24-hour urinary cortisol and late-night salivary cortisol were elevated. Serum cortisol was not suppressed by 1 mg of dexamethasone overnight, but it was suppressed by 8 mg of dexamethasone. Adrenocorticotropic hormone was also elevated. All other pituitary hormone axes were unremarkable (thyroid-stimulating hormone, free thyroxine, follicle-stimulating hormone, luteinizing hormone, growth hormone, prolactin, and insulin-like growth factor). Pituitary magnetic resonance imaging suggested a small adenoma (2 to 3 mm); therefore, the patient underwent inferior petrosal sinus sampling. The results were consistent with CD. Transsphenoidal resection was performed and final pathology confirmed an adrenocorticotropic hormone-positive adenoma. Hypercortisolism and intraocular pressures improved after the surgery.
Glaucoma can lead to irreversible blindness if left untreated or uncontrolled. However, endogenous hypercortisolism-induced glaucoma can be reversed with treatment of the underlying CD. Thus, heightened awareness of extraocular manifestations of secondary causes of glaucoma such as endogenous hypercortisolism is necessary in order to promote prompt evaluation and treatment.
青光眼是皮质类固醇激素一种公认的副作用。然而,类固醇诱导的青光眼通常是指外源性给予皮质类固醇激素所导致的。内源性皮质类固醇激素过度产生继发的青光眼仅在少数病例报告中有所记载。我们旨在引起人们对青光眼作为内源性皮质醇增多症一种罕见但重要表现的关注。
回顾患者病史、体格检查、实验室检查结果及影像学研究。
我们报告一例青光眼作为库欣病(CD)首发表现的病例。该患者在内分泌科评估前16个月被诊断为青光眼。在我们初次接诊时,患者呈库欣样面容。24小时尿皮质醇和午夜唾液皮质醇水平升高。血清皮质醇未被1毫克地塞米松过夜抑制,但被8毫克地塞米松抑制。促肾上腺皮质激素也升高。所有其他垂体激素轴均无异常(促甲状腺激素、游离甲状腺素、促卵泡激素、促黄体生成素、生长激素、催乳素和胰岛素样生长因子)。垂体磁共振成像提示一个小腺瘤(2至3毫米);因此,患者接受了岩下窦采血。结果与CD相符。进行了经蝶窦切除术,最终病理证实为促肾上腺皮质激素阳性腺瘤。术后高皮质醇血症和眼压均有所改善。
青光眼若不治疗或控制,可导致不可逆性失明。然而,内源性皮质醇增多症所致青光眼可通过治疗潜在的CD而逆转。因此,提高对青光眼继发原因如内源性皮质醇增多症眼外表现的认识,对于促进及时评估和治疗是必要的。