Mason J, Southwick S, Yehuda R, Wang S, Riney S, Bremner D, Johnson D, Lubin H, Blake D, Zhou G
National Center for Posttraumatic Stress Disorder, Veterans Affairs Medical Center, West Haven, Conn.
Arch Gen Psychiatry. 1994 Aug;51(8):629-41. doi: 10.1001/archpsyc.1994.03950080041006.
This study was designed to assess both central and peripheral aspects of thyroid function in combat-related posttraumatic stress disorder (PTSD), with the particular purpose of finding a mechanistic explanation for an imbalance between serum levels of free thyroxine (T4) and total T4 previously observed in pilot work.
A total of 96 male combat veterans with PTSD diagnosed by DSM-III-R (72 from the West Haven, Conn, Veterans Affairs Medical Center and 24 from the Menlo Park, Calif, Veterans Affairs Medical Center) were compared with 24 male control subjects. One or more serum samples were analyzed by radioimmunoassays for levels of total T4, free T4, total triiodothyronine (T3), free T3, T4-binding globulin, and thyrotropin.
The pilot observation of moderately elevated total T4 levels with no elevation in free T4 levels in patients with PTSD was confirmed, suggesting the hypotheses that (1) there may be an increased peripheral conversion of free T4 by deiodination to T3 or (2) there may be an increased binding of T4 secondary to elevated T4-binding globulin levels. Our findings support both hypotheses. The PTSD groups all showed a marked and sustained elevation in levels of both total T3 and free T3, as well as elevated T3/T4 ratios, supporting the increased T3 conversion hypothesis. The PTSD groups also showed a marked and sustained increase in T4-binding globulin levels, supporting the increased binding hypothesis. Thyrotropin levels did not differ between PTSD and control groups.
These findings demonstrate an unusual pattern of thyroid alterations, featuring substantial elevations in total T3, free T3, and T4-binding globulin levels, in combat-related PTSD that differs from established endocrinopathies, such as classic hyperthyroidism, T3 thyrotoxicosis, or chronic T4-binding globulin elevation.
本研究旨在评估与战斗相关的创伤后应激障碍(PTSD)中甲状腺功能的中枢和外周方面,特别目的是为先前在前期研究中观察到的血清游离甲状腺素(T4)水平与总T4水平之间的失衡找到一个机制性解释。
将总共96名经DSM-III-R诊断为PTSD的男性退伍军人(其中72名来自康涅狄格州韦斯特黑文退伍军人事务医疗中心,24名来自加利福尼亚州门洛帕克退伍军人事务医疗中心)与24名男性对照受试者进行比较。通过放射免疫分析法分析一份或多份血清样本中的总T4、游离T4、总三碘甲状腺原氨酸(T3)、游离T3、T4结合球蛋白和促甲状腺激素水平。
PTSD患者总T4水平适度升高而游离T4水平未升高的前期观察结果得到证实,提示以下假设:(1)游离T4可能通过脱碘作用在外周转化为T3的过程增加;(2)由于T4结合球蛋白水平升高,T4的结合可能增加。我们的研究结果支持这两个假设。PTSD组总T3和游离T3水平均显著且持续升高,以及T3/T4比值升高,支持T3转化增加的假设。PTSD组T4结合球蛋白水平也显著且持续升高,支持结合增加的假设。PTSD组和对照组之间促甲状腺激素水平无差异。
这些发现表明,与战斗相关的PTSD中甲状腺改变呈现出一种不寻常的模式,其特征是总T3、游离T3和T4结合球蛋白水平大幅升高,这与已确定的内分泌疾病不同,如经典甲亢、T3甲状腺毒症或慢性T4结合球蛋白升高。