Elevated prolactin to cortisol ratio and polyclonal autoimmune activation in Hashimoto's thyroiditis

Citation
I. Legakis et al., Elevated prolactin to cortisol ratio and polyclonal autoimmune activation in Hashimoto's thyroiditis, HORMONE MET, 33(10), 2001, pp. 585-589
Citations number
37
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
HORMONE AND METABOLIC RESEARCH
ISSN journal
00185043 → ACNP
Volume
33
Issue
10
Year of publication
2001
Pages
585 - 589
Database
ISI
SICI code
0018-5043(200110)33:10<585:EPTCRA>2.0.ZU;2-P
Abstract
Cortisol and prolactin, which are considered to have an immunomodulatory ef fect, and selected autoantibodies were determined in Hashimoto's thyroiditi s. 37 patients (8 males and 29 females) (54 +/- 13.8 years) and an equal nu mber of sex- and age-matched normal subjects (52.6 +/- 14.2 years) were stu died. None of the 74 subjects suffered from any other immunological, infect ious, hepatic, renal or malignant diseases. Patients with Hashimoto's thyro iditis exhibited significantly higher (p <0.016) prolactin values (14.0 +/- 3.8 ng/ml) than did control subjects (6.5 1.3 ng/ml). In contrast, cortisol levels were lower in Hashimoto's thyroiditis (13.5 +/-3.2 mug/dl) vs. norm al state (16.0 +/- 1.13 mug/dl), (p <0.05). The prevalence of anti-TPO and anti-Tg antibodies was 100% and 43% in the patients with Hashimoto's diseas e. In contrast, no subject of the control group was positive for anti-TPO, although 9 subjects (24%) were positive for anti-Tg autoantibodies. The per centage of positive autoantibodies to nucleous, smooth-muscle, and parietal cells in the patients (36.0,10.9 and 18.5%, respectively) was higher than that in healthy group (11.0 and 0% respectively). Notably, neither group wa s positive for antibodies against double-stranded DNA or mitochondria. In c onclusion, our results provide evidence for a polyclonal activity in Hashim oto's thyroiditis, an organ-specific autoimmune disease, associated with an altered prolactin-adrenocortical status. Such information should initiate longitudinal studies to clarify the exact time sequence of these events rel ated to the disease's activity.