George Jyothis T, Thow Jonathan C, Matthews Bruce, Pye Maurice P, Jayagopal Vijay
Department of Endocrinology, York Hospital, York, UK.
J Med Case Rep. 2008 Feb 28;2:67. doi: 10.1186/1752-1947-2-67.
Hyperthyroidism is a well established cause of atrial fibrillation (AF). Thyroid Stimulating Hormone-secreting pituitary tumours are rare causes of pituitary hyperthyroidism. Whilst pituitary causes of hyperthyroidism are much less common than primary thyroid pathology, establishing a clear aetiology is critical in minimising complications and providing appropriate treatment. Measuring Thyroid Stimulating Hormone (TSH) alone to screen for hyperthyroidism may be insufficient to appropriately evaluate the thyroid status in such cases.
A 63-year-old Caucasian man, previously fit and well, presented with a five-day history of shortness of breath associated with wheeze and dry cough. He denied symptoms of hyperthyroidism and his family, social and past history were unremarkable. Initial investigation was in keeping with a diagnosis of atrial fibrillation (AF) with fast ventricular response leading to cardiac decompensation.TSH 6.2 (Normal Range = 0.40 - 4.00 mU/L), Free T3 of 12.5 (4.00 - 6.8 pmol/L) and Free T4 51(10-30 pmol/L). Heterophilic antibodies were ruled out. Testosterone was elevated at 43.10 (Normal range: 10.00 - 31.00 nmol/L) with an elevated FSH, 18.1 (1.0-7.0 U/L) and elevated LH, 12.4 (1.0-8.0 U/L). Growth Hormone, IGF-1 and prolactin were normal. MRI showed a 2.4 cm pituitary macroadenoma. Visual field tests showed a right inferotemporal defect.While awaiting neurosurgical removal of the tumour, the patient was commenced on antithyroid medication (carbimazole) and maintained on this until successful trans-sphenoidal excision of the macroadenoma had been performed. AF persisted post-operatively, but was electrically cardioverted subsequently and he remains in sinus rhythm at twelve months follow-up off all treatment.
This case reiterates the need to evaluate thyroid function in all patients presenting with atrial fibrillation. TSH-secreting pituitary adenomas must be considered when evaluating the cause of hyperthyroidism. Early diagnosis and treatment of such adenomas is critical in reducing neurological and endocrine complications.
甲状腺功能亢进是心房颤动（AF）的一个公认病因。分泌促甲状腺激素的垂体瘤是垂体性甲状腺功能亢进的罕见病因。虽然垂体性甲状腺功能亢进的病因比原发性甲状腺病变少见得多，但明确病因对于将并发症降至最低并提供适当治疗至关重要。仅通过测量促甲状腺激素（TSH）来筛查甲状腺功能亢进可能不足以在此类病例中准确评估甲状腺状态。
一名63岁的白种男性，既往身体健康，出现了为期五天的气短症状，伴有喘息和干咳。他否认有甲状腺功能亢进的症状，其家族史、社会史和既往史均无异常。初步检查符合心房颤动（AF）伴快速心室反应导致心脏失代偿的诊断。促甲状腺激素（TSH）为6.2（正常范围 = 0.40 - 4.00 mU/L），游离三碘甲状腺原氨酸（Free T3）为12.5（4.00 - 6.8 pmol/L），游离甲状腺素（Free T4）为51（10 - 30 pmol/L）。排除了嗜异性抗体。睾酮升高至43.10（正常范围：10.00 - 31.00 nmol/L），促卵泡生成素（FSH）升高至18.1（1.0 - 7.0 U/L），促黄体生成素（LH）升高至12.4（1.0 - 8.0 U/L）。生长激素、胰岛素样生长因子-1（IGF-1）和催乳素正常。磁共振成像（MRI）显示一个2.4厘米的垂体大腺瘤。视野检查显示右侧颞下象限缺损。在等待神经外科手术切除肿瘤期间，患者开始服用抗甲状腺药物（卡比马唑），并持续服用直至成功经蝶窦切除大腺瘤。术后心房颤动仍持续存在，但随后通过电复律成功转复，在停止所有治疗后的十二个月随访中，他一直维持窦性心律。
该病例再次强调了对所有心房颤动患者评估甲状腺功能的必要性。在评估甲状腺功能亢进的病因时，必须考虑分泌促甲状腺激素的垂体腺瘤。早期诊断和治疗此类腺瘤对于减少神经和内分泌并发症至关重要。
