Horm Metab Res 2001; 33(10): 585-589
DOI: 10.1055/s-2001-17904
Original Clinical
© Georg Thieme Verlag Stuttgart · New York

Elevated Prolactin to Cortisol Ratio and Polyclonal Autoimmune Activation in Hashimoto’s Thyroiditis

I. Legakis1 , V. Petroyianni2 , A. Saramantis2 , G. Tolis1
  • 1 Department of Endocrinology, “Hippokrateion” General Hospital, Athens, Greece
  • 2 Laboratory of Biopathology, Institute of Medical Technology, Athens, Greece
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Publikationsverlauf

Publikationsdatum:
18. Oktober 2001 (online)

Cortisol and prolactin, which are considered to have an immunomodulatory effect, and selected autoantibodies were determined in Hashimoto’s thyroiditis. 37 patients (8 males and 29 females) (54 ± 13.8 years) and an equal number of sex- and age-matched normal subjects (52.6 ± 14.2 years) were studied. None of the 74 subjects suffered from any other immunological, infectious, hepatic, renal or malignant diseases. Patients with Hashimoto’s thyroiditis 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 µg/dl) vs. normal state (16.0 ± 1.13 µg/dl), (p < 0.05). The prevalence of anti-TPO and anti-Tg antibodies was 100 % and 43 % in the patients with Hashimoto’s disease. In contrast, no subject of the control group was positive for anti-TPO, although 9 subjects (24 %) were positive for anti-Tg autoantibodies. The percentage 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 was positive for antibodies against double-stranded DNA or mitochondria. In conclusion, our results provide evidence for a polyclonal activity in Hashimoto’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 related to the disease’s activity.

References

Dr. I. Legakis

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