Mika Ladies Clinic, Sapporo Medical University, School of Medicine, Sapporo, Japan.
Int J Womens Health. 2012;4:427-31. doi: 10.2147/IJWH.S33386. Epub 2012 Aug 24.
Follicle-stimulating hormone (FSH)-secreting pituitary adenoma is usually a nonfunctioning tumor, but in rare cases it may develop into ovarian hyperstimulation. Several reports have revealed that serum FSH levels are normal to slightly high in patients with combined FSH-secreting pituitary adenoma with ovarian hyperstimulation. This finding is different from iatrogenic ovarian hyperstimulation syndrome (OHSS), which is associated with extremely high levels of FSH.
To describe the clinical course of two patients who developed OHSS from FSH-secreting pituitary adenoma.
Endocrine studies of the two cases revealed that FSH levels were normal or slightly increased, but luteinizing hormone levels were low to undetectable. Their estradiol (E2) levels were intriguing: levels fluctuated drastically over 6 weeks in Case 1, but stayed flat in Case 2. Ultrasonographic examinations showed bilaterally enlarged multicystic ovaries, and magnetic resonance imaging indicated pituitary tumors. Transsephenoidal resection of the tumors ameliorated the symptoms and pathological diagnosis revealed FSH-secreting pituitary adenomas.
As is not the case in iatrogenic OHSS, even a small to moderate amount of FSH stimulation, which is continuously secreted by a pituitary adenoma, can cause ovarian hyperstimulation. Although FSH-secreting pituitary adenoma can cause ovarian hyperstimulation, an extremely high amount of E2 biosynthesis from granulosa cells seldom occurs.
促卵泡激素(FSH)分泌性垂体腺瘤通常为无功能性肿瘤,但在极少数情况下,它可能发展为卵巢过度刺激。有几项报道表明,在伴有卵巢过度刺激的 FSH 分泌性垂体腺瘤患者中,血清 FSH 水平正常或略高。这一发现与与 FSH 水平极高相关的医源性卵巢过度刺激综合征(OHSS)不同。
描述两例因 FSH 分泌性垂体腺瘤而发生 OHSS 的患者的临床经过。
对这两例患者的内分泌研究表明,FSH 水平正常或略有升高,但黄体生成素(LH)水平低至无法检测。他们的雌二醇(E2)水平很有意思:第 1 例患者的 E2 水平在 6 周内急剧波动,而第 2 例患者的 E2 水平则保持平坦。超声检查显示双侧卵巢多囊性增大,磁共振成像(MRI)提示垂体肿瘤。肿瘤经蝶窦切除术改善了症状,病理诊断为 FSH 分泌性垂体腺瘤。
与医源性 OHSS 不同,即使是由垂体腺瘤持续分泌的少量至中等量的 FSH 刺激,也可引起卵巢过度刺激。虽然 FSH 分泌性垂体腺瘤可引起卵巢过度刺激,但很少发生来自颗粒细胞的大量 E2 生物合成。