Abstract
Sub clinical hyperthyroidism (SCH) is characterized by normal free thyroid hormone concentrations along with a low or undetectable serum TSH (thyrotropin) level. The increased use of TSH as a screening measure and improved assay sensitivity is contributing to the diagnosis of sub clinical hyperthyroidism more frequently than ever in our clinical practise leading to the increased prevalence of the disease. The significance of SCH remains uncertain for most patients as some will revert to normal thyroid status over time whereas others will either remain static or progress to overt thyroid disease in the future. The detrimental effects of a persistently suppressed TSH has now been extensively studied and its effect on the cardiovascular system, the skeleton, mood disturbance, quality of life is quite significant leading to considerable morbidity and mortality. Majority of the patients are asymptomatic and lack overt features but the relevance of treatment is more focussed in elderly patients where the risk of developing cardiac arrhythmia and loss of bone mineral density is much more than young people in whom a conservative approach is usually preferred. The issue is contentious, the situation is challenging and the benefits of treatment are debatable. The consensus for who, when and how to treat is growing but still hasn’t been universally accepted. We attempt to review the recent literature available for sub clinical hyperthyroidism and suggest an analytical approach to its investigations and management.
Highlights
Sub clinical hyperthyroidism is characterized by a lower undetectable concentration of serum TSH with free triodothyronine (FT3) & free thyroxine (FT4) levels within laboratory reference ranges
The increased use of TSH as a screening measure and improved assay sensitivity is contributing to the diagnosis of sub clinical hyperthyroidism more frequently than ever in our clinical practise leading to the increased prevalence of the disease
There has been an explosion of published data regarding sub clinical hyperthyroidism and its clinical relevance, which has provoked the inevitable debate about screening and treatment
Summary
Sub clinical hyperthyroidism is characterized by a lower undetectable concentration of serum TSH with free triodothyronine (FT3) & free thyroxine (FT4) levels within laboratory reference ranges. Sub clinical hyperthyroidism may be caused by exogenous thyroid hormone therapy, endogenous thyroid disease, drug effects and non-thyroidal illness and the intrinsic disorders are same as those that cause overt hyperthyroidism [4,5,6]. When the lower limit of TSH is less than 0.4 mIU/L, 3.2% of the population is defined as having sub clinical hyperthyroidism [28] but if patients with known thyroid diseases are excluded, the prevalence decreases to 2%. An autonomous functioning adenoma or multi-nodular goitre, early or mild graves disease, silent or post-partum thyroiditis, sub-acute thyroiditis are common causes of endogenous sub clinical hyperthyroidism [29] whereas the exogenous form is usually related to TSH suppression therapy with thyroxine for single thyroid nodule, multi-nodular goitre or differentiated carcinoma [21]. Subnormal TSH levels may be related to pituitary or hypothalamic insufficiency, or non-thyroid pathological conditions or consequent to administration of glucocorticoids, dopamine or amiodarone [30]
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