Psychiatric patients on long-term lithium (Li) therapy frequently deve
lop goiter and/or hypothyroidism. It has also been suggested that Li m
ay trigger/exacerbate thyroid autoimmunity. Previous studies provided
evidence that underlying thyroid diseases represent important predispo
sing factors for the development of Li-induced thyroid dysfunction. Th
e aim of the present paper was to assess the value of thyroid ultrasou
nd - a simple and reliable tool to detect subtle thyroid abnormalities
- in the longitudinal evaluation of 23 Li-treated psychiatric patient
s without evidence of biochemical thyroid abnormalities before therapy
. For this purpose, thyroid ultrasound was associated with a clinical
and laboratory (serum thyroxine, serum triiodothyronine, serum TSH, an
tithyroglobulin (AbTg), antithyroid microsomal (AbM) and antithyroid p
eroxidase autoantibodies) evaluation prior to and at 6- to 12-month in
tervals during Li treatment. On the basis of thyroid ultrasound before
Li, patients were subdivided into two groups: group A (n = 15, 7 male
s, 8 females) with a normal echography and group B (n = 8, 5 males, 3
females) with mild ultrasound abnormalities. In group A the developmen
t of a small diffuse goiter was confirmed by physical examination duri
ng Li therapy; 2 patients displayed a transient increase of serum TSH
concentration and none developed detectable serum antithyroid autoanti
bodies. Beside the small volumetric increase, no other ultrasound abno
rmalities were observed during the entire follow-up. In all group B pa
tients a mild diffuse goiter was clinically detected before and on Li
administration and no significant Volumetric changes were observed dur
ing follow-up. Two patients developed high titers of AbM and AbTg 12 a
nd 1 s months after the beginning of Li, respectively; in 1 a persiste
nt increase of serum TSH concentration was also observed. Thyroid echo
graphy before Li displayed different degrees of scattered or diffuse h
ypoechogenicity and a further decrease in echogenicity was detected du
ring Li therapy in 2 patients. In conclusion, we provided further evid
ence that longterm Li administration is not associated with de novo ap
pearance of thyroid autoimmune phenomena in humans, but rather with an
exacerbation of underlying thyroid autoimmunity. In addition to thyro
id autoantibody and TSH measurements, thyroid echography appears to be
a sensitive tool in the identification of patients at risk of develop
ing autoimmune hypothyroidism during long-term Li therapy.