Free Thyroid-stimulating Hormone Research Articles

The thyroid axis and desipramine treatment in depression

Although there has been much recent investigation of the role of thyroid function in affective illness, few studies have addressed the effects of the tricyclic antidepressants on the pituitary-thyroid axis. In the present study, thyroid functions (TFTs) and thyrotropin-releasing hormone (TRH) stimulation of thyroid-stimulating hormone (TSH) were measured before and after treatment with desipramine (DMI) in 13 men with a diagnosis of major depressive disorder. All subjects had normal TFTs and baseline TSH measured in a drug-free state at the initiation of the study. Both mean free thyroxine index and baseline TSH decreased after DMI treatment. The amount of decrease in baseline TSH correlated with increase in ATSH. Four subjects had blunted ATSH (ATSH ⩽5 μIU/ml); three of these subjects “normalized” with treatment (ΔTSH ⩽5 μIU/ml; ⩾20 μI/JU/ml). Two subjects had a high ATSH, and both “normalized” during treatment. The decrease in both free T 4 index and TSH suggests a down-regulation of the thyroid axis at the hypothalamic level. “Normalization” of subtle dysregulation of the thyroid axis is suggested as a mechanism of antidepressant therapy in the treatment of some depressions.

Prevalence of abnormal thyroid function test results in patients with acute medical illnesses

We measured serum total and free thyroxine (T 4) and triiodothyronine (T 3) concentrations, free T 4 and T 3 indexes, thyroid-stimulating hormone (TSH), thyroxine-binding globulin (TBG) and thyroxinebinding prealbumin (TBPA) concentrations in 98 patients hospitalized for acute medical illnesses. The free thyroxine index (FT 4I) or TSH level was abnormal in 16 percent, but only 3 percent had thyroid disease. Serum free T 4 measurements by equilibrium dialysis were abnormal in 25 percent, but no additional patients who initially had abnormal concentrations of serum free T 4 were subsequently proved to have thyroid disease. Patients with supranormal serum free T 4 concentrations (21 percent) had higher serum T 4, lower serum T 3, and higher serum reverse T 3 (rT 3) concentrations than other patients, but the measured changes in serum T 4, TBG and TBPA levels could only partly account for the magnitude of the free T 4 elevation. In these acutely ill patients, an accurate diagnosis of thyroid disease could be achieved by determination of FT 4I and TSH level and a history of medication usage. We conclude that other tests are rarely necessary for this purpose in a patient population such as this.