Du Jianyang, Ji Hang, Jin Jiaqi, Gao Shuai, Yan Xiuwei, Hu Shaoshan
Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Medicine (Baltimore). 2020 Feb;99(8):e19222. doi: 10.1097/MD.0000000000019222.
Primary hypothyroidism is characterized by loss of thyroxine feedback inhibition and overproduction of thyrotropin-releasing hormone, which might result in reactive pituitary hyperplasia. However, pituitary adenoma secondary to primary hypothyroidism is extremely rare and usually underdiagnosed, and the pathogenic mechanism remains unclear. Herein, we reported two cases with pituitary adenoma secondary to primary hypothyroidism.
Case 1: A 35-year-old man presented to the local clinic with a 2-year history of fatigue, puffiness in the bilateral lower extremities and facial region, and coarseness of facial features. Additionally, his relatives also supplemented that he suffered from hypomnesis and hypophrenia.Case 2: A 56-year-old, postmenopausal woman presented to the local clinic with fatigue, dry skin, and sluggishness.
The pathological diagnosis of two patients was plurihormonal pituitary adenoma.
A microscopical tumorectomy was performed when the two patients were admitted to our hospital. Thyroid hormone replacement therapy (thyroxine 50 μg/day) was prescribed after microsurgery.
After 32 months (Case 1) or 43 months (Case 2) follow-up respectively, there was no recurrence, and the symptoms were completely relieved.
Pituitary hyperplasia caused by primary hypothyroidism responds well to thyroid hormone replacement therapy. It is worth noting that repeated detection of serum T3, T4, and thyroid-stimulating hormone (TSH) should be performed 3 months after replacement therapy. If the results showed that TSH level decreased partly, while thyroid function did not improve significantly, long-term increased secretion of pituitary TSH adenoma should be considered. And microsurgical resection via a transsphenoidal approach could be ordered. If the optic nerve or optic chiasm were pressed by the adenoma, microsurgery should be performed to relieve the pressure immediately. And then, thyroxine tablet substitute therapy should be performed after surgery.
原发性甲状腺功能减退症的特征是甲状腺素反馈抑制丧失和促甲状腺激素释放激素分泌过多,这可能导致垂体反应性增生。然而,原发性甲状腺功能减退症继发垂体腺瘤极为罕见,通常诊断不足,其发病机制仍不清楚。在此,我们报告了2例原发性甲状腺功能减退症继发垂体腺瘤的病例。
病例1:一名35岁男性到当地诊所就诊,有2年疲劳、双侧下肢和面部浮肿以及面部特征粗糙的病史。此外,他的亲属还补充说他有记忆力减退和智力低下的症状。病例2:一名56岁绝经后女性到当地诊所就诊,有疲劳、皮肤干燥和行动迟缓的症状。
两名患者的病理诊断均为多激素垂体腺瘤。
两名患者入院后均进行了显微镜下肿瘤切除术。显微手术后给予甲状腺激素替代治疗(甲状腺素50μg/天)。
分别随访32个月(病例1)或43个月(病例2)后,无复发,症状完全缓解。
原发性甲状腺功能减退症引起的垂体增生对甲状腺激素替代治疗反应良好。值得注意的是,替代治疗3个月后应反复检测血清T3、T4和促甲状腺激素(TSH)。如果结果显示TSH水平部分下降,而甲状腺功能无明显改善,则应考虑垂体TSH腺瘤长期分泌增加。可考虑经蝶窦入路显微手术切除。如果腺瘤压迫视神经或视交叉,应立即进行显微手术减压。然后,术后应进行甲状腺素片替代治疗。