In overt hyperthyroidism, serum levels of free thyroxine (free T4) and triiodothyronine (T3) or T3 levels alone are elevated, while serum TSH levels are suppressed. In subclinical hyperthyroidism, the levels of free T4 and T3 are normal (usually in the middle to upper range of normal), TSH levels are suppressed. The prevalence of overt hyperthyroidism is 0.7 to 1.8% in populations with sufficient iodine and 2 to 15% in people with mild iodine deficiency. Between 65% and 75% of people with subclinical hyperthyroidism have serum TSH levels of 0.1 to 0.4 μUI / ml (referred to here as mild subclinical hyperthyroidism), and the rest have TSH levels <0,1 μUI/ml (severe subclinical hyperthyroidism).
What are the causes of subclinical hyperthyroidism?
These are the same as those of overt hyperthyroidism. The common endogenous causes are toxic multinodular goiter or toxic adenoma, and Graves’ disease. The latter is responsible for 40% of cases in populations with sufficient iodine intake.
Exogenous subclinical hyperthyroidism, resulting from excessive intake of levothyroxine, liothyronine or dried thyroid, may reflect an involuntary overtreatment; excessive voluntary consumption on the part of the patient or, the intentional use to suppress the production of TSH.
Exogenous subclinical hyperthyroidism is much more common than endogenous subclinical hyperthyroidism. In endogenous cases, serum T3 levels are usually normal or are at the upper end of the reference range, while in patients receiving levothyroxine, T3 levels are usually in the middle or lower part of the reference range.
It is not known whether differences in the patterns of thyroid hormone levels between endogenous subclinical hyperthyroidism and exogenous hyperthyroidism produce disparate effects on the cardiovascular and skeletal systems.
What are the important characteristics of subclinical hypothyroidism?
Subclinical hyperthyroidism, in which serum thyroid hormone levels are within the reference range but serum TSH levels are subnormal (≤0.4 μUI/ml), may be due to an overproduction of endogenous thyroid hormone or excessive intake of exogenous thyroid hormone.
It can progress to overt hyperthyroidism, especially when serum TSH levels are <0.1 μUI/ml. Even without progression to overt hyperthyroidism, subclinical hyperthyroidism may be associated with adverse outcomes, such as cardiovascular disease (eg, atrial fibrillation, heart failure and coronary artery disease, bone loss, fractures, and dementia, especially in people> 65 years with severe disease). .
Although data from randomized clinical trials are lacking to guide therapeutic decisions, professional organizations recommend the treatment of subclinical hyperthyroidism in> 65 years and postmenopausal women, especially when serum TSH levels are <0.1 μUI/ml.
What are the clinical consequences?
The possible clinical consequences of subclinical hyperthyroidism are:
• Progression to manifest hyperthyroidism.
• Emergence of cardiovascular diseases.
• Bone loss.
• Fractures.
• Dementia.
How is the evaluation of a patient with subclinical hyperthyroidism?
Older patients with subclinical hyperthyroidism are usually asymptomatic, while younger patients may have mild adrenergic symptoms. The test may reveal an enlarged or nodular thyroid or Graves’ ophthalmopathy, but there may be no tachycardia, tremor, and other adrenergic signs caused by thyroid hyperactivity.
The diagnosis of subclinical hyperthyroidism is based on laboratory results, but there are several common clinical situations that are associated with similar laboratory findings. In patients with a serum TSH level <0.1 μUI/ml, free T4 and T3 levels should be evaluated quickly to rule out overt hyperthyroidism.
In the absence of overt disease, it is reasonable not to repeat the tests until 2 to 3 months later; Subnormal TSH serum levels are transient in up to 50% of patients, especially those with mild disease. If the subnormal serum TSH level persists, then additional tests will be required to determine the cause.
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