Subclinical hypothyroidism

Subclinical hypothyroidism is an analytical rather than a clinical concept. As the name implies, it is “subclinical” or without clinical manifestations. However, those of us who do clinical workup often encounter patients with certain symptoms compatible with clinical hypothyroidism. When they are tested, they have a normal T4l and a TSH slightly above the reference range, i.e., between 4.5 and 10mIU/L. They cannot be typed as having a normal T4l and a TSH slightly above the reference range.

So they cannot be typed as having primary hypothyroidism, since in primary hypothyroidism a decrease in T4l and an increase in TSH above 10 mIU/L is mandatory. TSH is a hormone of variable concentration depending on the production of thyroxine by the thyroid gland. But it is necessary to know which other conditions are also capable of modifying the plasma TSH concentration. Thus, they also have high TSH:

  • Transient high TSH in the evolution or recovery from severe disease.
  • During recovery from subacute thyroiditis.
  • During and after treatment with Thyrogen® (recombinant TSH).
  • In untreated primary adrenal insufficiency.
  • Others.

In NHANES III with a study population of 13,344 subjects free of thyroid pathology, the range of normal TSH was 0.45 to 4.12 mIU/L. The available data from the United States of America, for the adult population, give a range between 4 and 8.5% of subclinical hypothyroidism in patients without thyroid pathology. The prevalence increases with age, and thus, for women over 65 years of age, it is established at 20%. There are no valid data for men, but it is known that in the black race it is present in a third part than in the white race and that it is also more frequent in persons with autoimmune diseases or who have received radiation to the head, neck and thorax.

Approximately 2 to 5% of people with subclinical hypothyroidism progress annually to clinical hypothyroidism, this progression being directly proportional to the existence of antithyroid antibodies. However, approximately 5% of patients with subclinical hypothyroidism return to normal after approximately one year of evolution. This is known as transient hypothyroidism. In the rest it remains elevated and progresses.

Subclinical hypothyroidism is asymptomatic. However, some patients consult for symptoms compatible with mild hypothyroidism, which is sometimes also present in people with strictly normal hormones. Although in this last group the presence of hypothyroid symptoms is exceptional. Elevations of LDLc, cardiac dysfunction such as decreased myocardial contractility, and the appearance of neuropsychiatric symptoms have been described, but all in a very mild form.

Diagnosis

A normal T4free and TSH above 4.5mIU/L should be sufficient for diagnosis, although it would be convenient to separate the group that already has TSH above 10mIU/L. In these patients it is necessary to have a determination of antithyroid antibodies (AAT), especially anti-TPO. The positivity of these indicates the progression of the disease and helps to make the decision to treat the condition.

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Treatment

Treatment of a person with normal free T4 and TSH between 4.5-10mIU/L and TAA (-) is not necessary. It is advisable to repeat the analysis in a period between 2 and 6 months to compare the analytical evolution with a possible appearance of symptoms. The same patient, but with TSH>10 mIU/L would have to be evaluated whether or not to treat it.

In recent years I have seen some cases of patients in whom the cause of subclinical hypothyroidism has been the abandonment of iodized salt. Here administration of iodine (200 mcg/day) and a return to iodized salt may be sufficient for normalization of thyroid function. If the patient in addition to TSH >10mIU/L presents TAA (+), thyroxine treatment can be started to control the progressive thyroid dysfunction. Some rare patients with anti-TPO (-) may present with a condition known as idiopathic thyroid atrophy.

Thyroid palpation is of a firmer consistency than usual, generally resembling Hashimoto’s disease. When the decision is made to start treatment, the dose of thyroxine should never be higher than 50 mcg/day, it being advisable to start with 25 mcg/day and evaluate after 2 months. Lipid-lowering agents should not be added until it is verified that dyslipidemia persists with thyroid control returned to normal.

The relationship between hormonal normalization and clinical improvement, if symptomatology exists, is doubtful, although there is some study of double-blind treatment of subclinical hypothyroidism, thyroxine/placebo, improving the symptomatology of affected patients. In my case, I treat patients with subclinical hypothyroidism with TSH>10mIUI/L and AAT (-) with doses of thyroxine that leave TSH between 1 to 3 mIU/L, and I reevaluate them 2 to 6 months later.