Graves' Disease in Hypopituitarism Due to Pituitary Apoplexy.

Chiara Mura, Rebecca Sonnino, Laura Crispino, Carlo Antonio Rota, Alfredo Pontecorvi
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Abstract

Background: Central hypothyroidism and autoimmune hyperthyroidism are contrasting pathologies requiring careful hormone monitoring for restoring euthyroidism. Their coexistence is rare and challenging for clinicians [1, 2].

Case report: We have, herein, presented the case of a 41-year-old female patient with an unremarkable clinical history except for chronic autoimmune thyroiditis in euthyroidism. At the 21st week of gestation, she experienced a spontaneous abortion. The patient underwent an assessment of the uterine cavity, which was complicated by bleeding and hypotensive shock. In the postoperative course, the patient presented worsening headache, and after an MRI, the diagnosis of pituitary apoplexy due to an ischemic-hemorrhagic base was made. Laboratory tests showed anterior panhypopituitarism. Multiaxial replacement therapy was initiated with hydrocortisone, levothyroxine (LT4), and subsequently estrogen-progestin and GH. After two years of good recovery with stable LT4 dosage, the patient experienced palpitations and fine tremors; blood tests showed hyperthyroidism with suppressed Thyroid-stimulating Hormone (TSH) levels and elevated free thyroid fractions and anti-TSH receptor antibodies. Diagnosis of Graves' disease was made, and therapy with methimazole was initiated. During antithyroid therapy, TSH remained persistently suppressed, consistent with the underlying central hypothyroidism. This condition required close follow-up, with monitoring based solely on free thyroid hormone levels. After six months of antithyroid therapy, disease remission was achieved, with negative antibodies and mild hypothyroxinemia. Therefore, methimazole was discontinued and replacement therapy gradually resumed until optimal hormone levels were reached.

Conclusion: This case is unique demonstrating autoimmune hyperthyroidism to coexist with central hypothyroidism, rendering TSH a misleading disease progression indicator. Consequently, managing Graves' disease has become more complex and challenging.

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垂体性脑瘫导致的垂体功能减退症中的巴塞杜氏病
背景:中枢性甲状腺功能减退症和自身免疫性甲状腺功能亢进症是两种截然不同的病症,需要仔细监测激素才能恢复甲状腺功能正常。它们同时存在的情况非常罕见,对临床医生来说具有挑战性[1, 2]:病例报告:我们在此报告了一名 41 岁女性患者的病例,除了甲状腺功能正常的慢性自身免疫性甲状腺炎外,她的临床病史并无特殊之处。在妊娠第 21 周时,她经历了一次自然流产。患者接受了宫腔评估,评估过程因出血和低血压休克而变得复杂。术后,患者头痛加剧,经核磁共振检查后,诊断为缺血出血性脑垂体骤停。实验室检查显示患者患有垂体前叶功能减退症。开始使用氢化可的松、左甲状腺素(LT4)以及随后的雌激素-孕激素和 GH 进行多轴替代治疗。在使用稳定剂量的左旋甲状腺素(LT4)两年后,患者恢复良好,但又出现了心悸和细微震颤;血液检查显示患者患有甲状腺功能亢进症,促甲状腺激素(TSH)水平受到抑制,游离甲状腺分数和抗TSH受体抗体升高。诊断结果为巴塞杜氏病,并开始使用甲巯咪唑治疗。在抗甲状腺治疗期间,促甲状腺激素仍持续受到抑制,这与潜在的中枢性甲状腺功能减退症一致。这种情况需要密切随访,仅根据游离甲状腺激素水平进行监测。经过 6 个月的抗甲状腺治疗后,疾病得到缓解,抗体呈阴性,甲状腺素血症轻微降低。因此,停用了甲巯咪唑,并逐渐恢复替代疗法,直到达到最佳激素水平:本病例的独特之处在于,自身免疫性甲状腺功能亢进与中枢性甲状腺功能减退并存,使促甲状腺激素成为误导疾病进展的指标。因此,巴塞杜氏病的治疗变得更加复杂和具有挑战性。
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