Abucham J, Castro V, Maccagnan P, Vieira J G
Neuroendocrine Unit, Escola Paulista de Medicina, Universidade Federal de Sáo Paulo (UNIFESP), Brazil.
Clin Endocrinol (Oxf). 1997 Nov;47(5):515-22. doi: 10.1046/j.1365-2265.1997.2381042.x.
Since panhypopituitarism in patients with Sheehan's syndrome is due to massive pituitary necrosis with only minor hypothalamic involvement, we hypothesized that serum TSH levels would be low but its circadian rhythm preserved in these patients.
Basal and TRH-stimulated mean afternoon (1500-1700 h) and nocturnal (0100-0300 h) TSH levels were determined in 10 patients with Sheehan's syndrome before and during T4/glucocorticoid replacement and in seven controls.
Serum concentrations of T3, T4, free T4 (fT4) and cortisol were measured by radio-immunoassay; TSH, GH, PRL and LH were determined by immunofluorimetric assay.
Afternoon TSH levels were markedly increased in Sheehan's syndrome patients compared with controls (3.3 +/- 1.0 vs 0.5 +/- 0.15 mU/l, respectively, P = 0.002). At night, TSH levels remained unchanged in Sheehan's syndrome patients (3.3 +/- 1.1 mU/l) but rose significantly in controls (1.1 +/- 0.34 mU/l, P = 0.016). The nocturnal TSH increment was significantly higher in controls than in patients (143 vs approximately 4.9%, respectively, P = 0.0001). In eight patients with normal serum fT4 levels during treatment, basal TSH levels decreased to 0.16 +/- 0.05 mU/l (P < or = 0.008), being barely detectable or undetectable in four patients. In the six patients with detectable TSH during treatment, nocturnal TSH increments were normal in four and blunted in two. There was a strong correlation between pre- and post-treatment basal TSH (r = 0.82, P = 0.012) and between pre- and post-treatment peak TSH after TRH (r = 0.91, P = 0.0017), but no significant correlation between TSH and thyroid hormone levels. The per cent ratio of peak TSH after TRH between treated patients and controls, an estimate of the relative size of the functional thyrotroph pool in Sheehan's syndrome patients, was 7%.
Loss of TSH rhythm in Sheehan's syndrome is usually secondary to hormonal deficiency and results from maximally increased secretory activity of a decreased pool of thyrotrophs. The paradox of increased TSH levels and decreased thyroid function in Sheehan's syndrome could result from decreased TSH bioactivity and/or from a critically reduced thyrotroph population that fails to sustain sufficient TSH secretion in the face of rising serum thyroid hormone levels.
由于席汉综合征患者的全垂体功能减退是由垂体大量坏死所致，仅伴有轻微下丘脑受累，我们推测这些患者血清促甲状腺激素（TSH）水平会降低，但昼夜节律仍保留。
在10例席汉综合征患者进行甲状腺素/糖皮质激素替代治疗前及治疗期间，以及7名对照者中，测定基础及促甲状腺激素释放激素（TRH）刺激后的午后（15:00 - 17:00时）和夜间（01:00 - 03:00时）TSH水平。
采用放射免疫分析法测定血清三碘甲状腺原氨酸（T3）、甲状腺素（T4）、游离甲状腺素（fT4）和皮质醇浓度；采用免疫荧光分析法测定TSH、生长激素（GH）、催乳素（PRL）和促黄体生成素（LH）。
与对照组相比，席汉综合征患者午后TSH水平显著升高（分别为3.3±1.0与0.5±0.15 mU/L，P = 0.002）。夜间，席汉综合征患者TSH水平保持不变（3.3±1.1 mU/L），而对照组显著升高（1.1±0.34 mU/L，P = 0.016）。对照组夜间TSH增加值显著高于患者（分别为143%与约4.9%，P = 0.0001）。在8例治疗期间血清fT4水平正常的患者中，基础TSH水平降至0.16±0.05 mU/L（P≤0.008），4例患者中TSH水平几乎检测不到或无法检测。在6例治疗期间TSH可检测到的患者中，4例夜间TSH增加值正常，2例降低。治疗前和治疗后基础TSH之间（r = 0.82，P = 0.012）以及TRH刺激后治疗前和治疗后TSH峰值之间（r = 0.91，P = 0.0017）存在强相关性，但TSH与甲状腺激素水平之间无显著相关性。治疗患者与对照者TRH刺激后TSH峰值的百分比比值（席汉综合征患者功能性促甲状腺细胞池相对大小的估计值）为7%。
席汉综合征中TSH节律丧失通常继发于激素缺乏，是由促甲状腺细胞池减少但分泌活性最大程度增加所致。席汉综合征中TSH水平升高与甲状腺功能降低的矛盾现象可能是由于TSH生物活性降低和/或促甲状腺细胞数量严重减少，导致面对血清甲状腺激素水平升高时无法维持足够的TSH分泌。
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