Η επίδραση των βιολογικών παραγόντων θεραπείας ρευματικών νοσημάτων στη θυρεοειδική λειτουργία και η επαγωγή αυτοάνοσης θυρεοειδίτιδας
Κακλαμάνος Μιχαήλ
(EL)
Biological anti-rheumatic agents (BAA) may induce autoimmune phenomena.
Evidence on thyroid-specific effects of these agents is relatively limited. We
studied prospectively, over 3 years, 36 rheumatic patients treated with BAA (18
Infliximab and 18 Rituximab) and no prior exposure to biological therapies
(group-1), with respect to their thyroid function, thyroid antibody titers, and
thyroid ultrasonographic parameters, such as left inferior thyroid artery peak
systolic velocity (ITA PSV), left thyroid lobe vascularity index (TL VI), and
echogenicity. Twenty-eight rheumatic patients treated with diseasemodifying
anti-rheumatic drugs and/or glucocorticoids (group-2), 21 rheumatic patients
not receiving any treatment (group-3), and 49 healthy individuals (group-4)
were used for comparison. Thyroid function and autoantibody titers were not
significantly altered at any stage irrespectively of the administered BAA,
previously unknown autoimmune thyroid disease (AITD) status, and/or concomitant
treatment with glucocorticoids. Left ITA PSV was significantly increased in
group-1 patients (mean±SD start: 25.5±14.1 cm/s vs. end: 29.8±11.1 cm/s,p=0.038
and p=0.001, respectively). Six group-1, 7 group-2, and 3 group-3 patients
developed reduced thyroid echogenicity during follow-up (start: p=0.003 and
end: p=0.001). Left ITA PSV, left TL VI, and echogenicity changes were not
related to alterations in thyroid volume, thyrotropin hormone levels, and/or
underlying AITD. Infliximab and Rituximab do not cause any alterations in
thyroid function and/or autoimmunity, even in patients with previously
undiagnosed AITD. Elevated left ITA PSV and reduced thyroid echogenicity may be
early features signaling progression to AITD in patients treated with BAA.
(EN)
