Primary and central hypothyroidism are differentiated by TSH, which is elevated in primary hypothyroidism while central or pituitary causes yield an inappropriately normal or decreased TSH. FT4 is low or low-normal in both cases. Euthyroid sick syndrome may manifest with a variety of laboratory values.
In euthyroid sick syndrome, T4 is often normal though T3 is decreased; TSH decreases to normal or low values with prolonged non-thyroidal illness. Subclinical hypothyroidism is characterized by an elevation in TSH with normal levels of thyroid hormones. In the hospital setting there are only a few occasions when thyroid function testing is necessary beyond TSH, fT4, and perhaps thyroid antibodies. Given the changes in thyroid function tests during acute illness, further evaluation is indicated only in critically ill patients in whom true thyroid disease needs to be differentiated from euthyroid sick syndrome.
Emergencies in hypothyroidism are uncommon with the main exception being myxedema crisis which is treated with thyroid hormone replacement as well as hydrocortisone intravenously until adrenal insufficiency can be ruled out. Intravenous loading of T4 with mcg bolus is followed by continued intravenous T4 therapy daily until oral therapy can safely be initiated mcg, depending on underlying cardiovascular risk factors and age.
Though somewhat controversial, recommendations are also generally for intravenous therapy with T3 as it is the biologically active form for approximately 48 hours mcg every 8 hours. Concurrent supportive therapy addresses precipitants such as infection, medications, and cerebrovascular disease as well as symptoms such as hypothermia and hypotension.
Aggressive antibiotics, gradual passive re-warming to avoid cardiac complications of vasodilation , and blood pressure support are all appropriate. Hypotension not responsive to fluids should be treated with pressors until thyroid hormone levels rise.
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Hyponatremia is often present so care when administering fluids is needed to avoid worsening that state. Caution needs to be used in administering opioids as the underlying myxedema crisis makes patients exquisitely sensitive such that normal dosages may be fatal.
Whether in the hospital or outpatient setting, standard long-term treatment of hypothyroidism is with levothyroxine to replace the decreased fT4. Like in the acute cases, addressing possible adrenal insufficiency is important and should be ruled out before initiation of therapy. Starting doses of levothyroxine are weight-based and lower for elderly patients or those with underlying coronary artery disease 1. Dosages are titrated up every weeks until the patient is asymptomatic with goal TSH between 0. Level of T4 should peak by weeks of appropriate therapy. Truter, I. S Afr Pharm J.
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Pages Bogner, U. Krogh et al. He had occasional dry skin. Family history was remarkable for maternal grandmother and mother with hypothyroidism. His midparental target height was On physical examination, the patient measured The patient was well appearing without dysmorphic features and had a normal affect. He had cherubic facies and fundi appeared normal.
His thyroid was palpable and smooth with right and left lobe each measuring 4 cm with no lymphadenopathy. His chest, heart, and abdomen were normal. He had Tanner stage 1 genital development with 3 cc testes and no pubic hair.
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Skin examination was negative for rash, acanthosis, or striae. A thyroid ultrasound showed an enlarged heterogeneous thyroid consistent with autoimmune thyroiditis. Normalization of thyroid levels was achieved on levothyroxine mcg daily with TSH 0. His growth parameters dramatically improved on treatment Figure 1. His weight decreased from By 7 months post initiation of treatment, his height increased from Table 1.
Thyroid function tests at presentation and months post levothyroxine initiation. Figure 1. A Boys Stature-for-age and Weight-for-age Curve. Linear Growth Curve reveals a crossing of percentiles from the 90th to the 25th percentile prior to levothyroxine initiation. Weight curve shows excessive weight gain and subsequent weight loss after levothyroxine initiation. B Body mass index-for-age Curve. BMI shows a significant decline from severe obesity to overweight status after levothyroxine initiation. This case highlights that pediatric patients presenting with excessive weight gain and a declining growth velocity with crossing of height percentiles should be evaluated for hypothyroidism, even in the absence of other associated features of hypothyroidism including constipation, declining school performance, or cold intolerance.
Acquired hypothyroidism can be related to thyroid disease primary hypothyroidism or hypothalamic-pituitary disease central hypothyroidism. However, most childhood cases of hypothyroidism are primary and are caused by chronic autoimmune thyroiditis. It usually presents in adolescence and has a female predilection, affecting females three to five times more commonly than males 1. Other rare causes of acquired hypothyroidism include excess iodine ingestion, anti-thyroid drugs and thyroid injury secondary to external radiation, thyroidectomy or infiltrative diseases.
Iodine deficiency also remains an important cause of acquired hypothyroidism worldwide.
Autoimmune hypothyroidism is characterized by antibodies against thyroglobulin and thyroperoxidase TPO and by lymphocytic infiltration of the thyroid gland, which can result in thyromegaly 2. In cases of seronegative autoimmune thyroiditis, thyroid ultrasound examination is considered the cornerstone for diagnosis as well as for differentiating this chronic inflammatory condition from other forms of non-autoimmune hypothyroidism of genetic origin 3.
In has been reported in adult literature that patients with Hashimoto's thyroiditis and negative thyroid antibodies have a milder form of the disease; however, pediatric literature regarding the clinical course of seronegative thyroiditis is sparse 3. Our patient presented with significant effects on growth parameters. Hashimoto's disease may be associated with a euthyroid state, hypothyroidism or transient hyperthyroidism.
Patients with anti-TPO antibodies are at risk for developing hypothyroidism, however, it is known that some individuals with large goiters and high antibody levels can remain euthyroid for many years 4.
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A concurrent diagnosis of celiac disease, an elevated baseline TSH and higher antithyroid antibody titers have been associated with an increased risk of progression to hypothyroidism 5. The most common presentation of thyroiditis is thyroid gland enlargement, followed by clinical symptoms of hypothyroidism and then those found incidentally as part of routine screening or a work up for an unrelated condition 1 , 6. The most common clinical manifestation of hypothyroidism in children is actually declining growth velocity, which can also be accompanied by increased and sometimes excessive weight gain.
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The growth delay is usually insidious in onset, and may be present for a few years before other symptoms occur 1. Unfortunately, prolonged juvenile acquired hypothyroidism that is undiagnosed can result in incomplete catch up growth and the severity of the height deficit is proportionate to the duration of the hypothyroidism 7.
The signs and symptoms of hypothyroidism in children are often elusive and depend on severity and duration.