Pj. Drinka et al., LOW TSH LEVELS IN NURSING-HOME RESIDENTS NOT TAKING THYROID-HORMONE, Journal of the American Geriatrics Society, 44(5), 1996, pp. 573-577
BACKGROUND: Many practitioners perform a thyroid stimulating hormone (
TSH) assay as a screening test in older patients. The introduction of
sensitive TSH assays with lower normal limits has created a laboratory
abnormality that is often of uncertain significance. Mechanisms inclu
de autonomous overproduction of thyroid hormone, nonthyroidal illness
including medication effects, and hypothalamic/pituitary dysfunction.
OBJECTIVE: To characterize the clinical status and course of nursing h
ome residents with low TSH and normal total T-4 levels in the absence
of treatment with thyroid hormone. DESIGN: Retrospective chart review
was performed to determine participants status at the time of the low
TSH level, with additional recording of follow-up thyroid hormone leve
ls, cardiac rhythm, and mortality. Mortality was compared with that of
a control group matched for age and sex. SETTING: A nursing home for
veterans and their spouses. MAIN RESULTS: Forty subjects with low TSH
and initially normal total T-4 were identified. Only three subjects we
re subsequently diagnosed as hyperthyroid. TSH levels of 18 subjects s
ubsequently normalized, and four additional subjects had low total T-3
levels suggesting a nonthyroidal mechanism. Seven subjects died durin
g the first 4 months of follow-up compared with three in a control gro
up (P < .001). Nine of the 40 subjects had a history of or current atr
ial fibrillation. No new atrial fibrillation was documented during 388
months of EKG follow-up. CONCLUSIONS: Low total T-3 levels, TSH norma
lization, and excess mortality suggest that nonthyroidal illness plays
a role in the pathogenesis of low TSH determinations in the nursing h
ome. Autonomous production of thyroid hormone also plays a role. We be
lieve that the term ''subclinical hyperthyroidism'' should be used onl
y if the clinician believes that autonomous overproduction of thyroid
hormone is the cause of a low TSH level. If subsequent research shows
correctable adverse consequences associated with subclinical hyperthyr
oidism from autonomous overproduction of thyroid hormone, a more aggre
ssive diagnostic approach will be needed to define the mechanism of a
low TSH level at the time of its discovery.