Clinical Practice Guidelines For Hypothyrodism


• Hypothyroidism may be either subclinical or overt.

• Subclinical hypothyroidism is characterized by a serum TSH above the upper reference limit in combination with a normal free thyroxine (T4).

• An ele¬vated TSH, usually above 10 mIU/L, in combination with a subnormal free T4 characterizes overt hypothyroidism.

• Environmental iodine deficiency is the most common cause of hypothyroidism on a worldwide basis . In areas of iodine sufficiency, such as the United States, the most common cause of hypothyroidism is chronic autoim¬mune thyroiditis (Hashimoto’s thyroiditis). Autoimmune thyroid diseases (AITDs) have been estimated to be 5-10 times more common in women than in men.

• One of the keys to diagnosing AITDs is determin¬ing the presence of elevated anti-thyroid antibody titers which include antithyroglobulin antibodies (TgAb), anti-microsomal/anti-thyroid peroxidase antibodies (TPOAb), and TSH receptor antibodies (TSHRAb).

• The presence of elevated TPOAb titers in patients with subclinical hypothyroidism helps to predict progression to overt hypothyroidism.

• When adrenal insufficiency is present, the diagnosis of subclinical hypothyroidism should be deferred until after glucocorticoid therapy has been instituted because TSH levels may be elevated in the presence of untreated adrenal insufficiency and may normalize with glucocorticoid therapy. Check the side effects!

• In monitoring patients with hypothyroidism on L-thyroxine replacement, blood for assessment of serum free T4 should be collected before dosing because the level will be transiently increased by up to 20% after L-thyroxine administration.

• A subnormal assessment of serum free T4 serves to establish a diagnosis of hypothyroidism, whether primary, in which serum TSH is elevated, or central, in which serum TSH is normal or low.

• However, serum T3 measurement, whether total or free, has limited utility in hypothyroidism because levels are often normal due to hyperstimulation of the remaining functioning thyroid tissue by elevated TSH

• Although there is general agreement that patients with primary hypothyroidism with TSH levels above 10 mIU/L should be treated (106,115-117), which patients with TSH levels of 4.5-10 mIU/L will benefit is less certain.

• Although there is general agreement that patients with primary hypothyroidism with TSH levels above 10 mIU/L should be treated,which patients with TSH levels of 4.5-10 mIU/L will benefit is less certain.

• A number of studies, following a 1999 report cit¬ing the benefit of L-thyroxine (T4)and L-triiodothyronine (T3)com¬bination therapy , have re-addressed the benefits of synthetic L-thyroxine and Ltriiodothyronine combination therapy but have largely failed to confirm an advantage of this approach to improve cognitive or
mood outcomes in hypothyroid individuals treated with L-thyroxine alone

• It is not known if those who responded positively to L-thyroxine and L-triiodothyronine combina¬tion therapy will have long-term benefit and whether geno¬typing patients with hypothyroidism who are clinically and biochemically euthyroid will ultimately reliably identify patients with hypothyroidism who are most likely to ben¬efit from combination therapy.

• However, patients with subclinical hypo¬thyroidism do not require full replacement doses . Doses of 25-75 μg daily are usually sufficient for achieving euthyroid levels , with larger doses usually required for those presenting with higher TSH values . One randomized control trial assigned L-thyroxine doses on the basis of the initial serum TSH values as follows: 25 μg for TSH 4.0-8.0 mIU/ L, 50 μg for TSH 8-12 mIU/L, and 75 μg for TSH >12 mIU/L. After 2 months only minimal further adjustments were required to achieve euthyroidism (162).

• study showed that taking it 60 minutes before breakfast on an empty stomach was better.

• Patients with normal thyroid tests. Patients with symp¬toms of hypothyroidism, but normal thyroid hormone lev¬els do not benefit from treatment with L-thyroxine . Moreover, treatment confers a substantial risk of subclini¬cal or overt hyperthyroidism.

• The diagnosis of subclinical or overt hypothyroidism must be considered in every patient with depression. In fact, a small proportion of all patients with depression have primary hypothyroidism—either overt or subclinical.

September 30, 2018

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