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Subject: Hashimoto Disease
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Hashimoto thyroiditis (HT), also called lymphocytic thyroiditis or chronic autoimmune thyroiditis, is characterized by autoimmune destruction of the thyroid gland that can result in progression to overt hypothyroidism or goiter formation.
Lymphocytic infiltration of the thyroid gland and presence of antibodies to thyroid peroxidase (TPO) and thyroglobulin (TG) are hallmark features.
Clinical presentation can vary and includes asymptomatic disease, atrophic thyroid, transient hyperthyroidism (also known as hashitoxicosis), as well as transient conditions such as silent (or painless) thyroiditis and postpartum thyroiditis that may progress to thyroid failure years later.
Hashimoto encephalopathy (HE) is a rare condition associated with high TPO titers. The neurologic manifestations are not related to the underlying thyroid status and are thought to be related to autoimmune vasculitis.
Most common etiology of hypothyroidism in iodine sufficient areas. In the United States, prevalence of subclinical and overt hypothyroidism can be as high as 5% and 2%, respectively.
Five times more common in women than men
10% of the general population has antibodies to TPO and TG.
Both genetic predisposition and environmental factors contribute to the development of HT.
Characterized by lymphocytic infiltration of the thyroid tissue resulting in B- and T-cell–mediated destruction of the thyroid follicles and hypothyroidism.
Early in the course, disruption of the thyroid gland can result in thyroid hormone release and transient hyperthyroidism or hashitoxicosis.
Extent of the infiltration, fibrosis, and TSH–mediated follicular cell hyperplasia determines a goitrous or atrophic presentation.
Nearly all patients with HT have TPO and TG antibodies. High titer in postpartum/silent thyroiditis or in subclinical disease indicates progression to overt hypothyroidism in later years.
High TPO antibody titers can also be associated with autoimmune vasculitis and present as encephalopathy.
Presence of other autoimmune conditions
Family history of autoimmune disorders
Turner and Down syndrome
Postpartum thyroiditis or painless thyroiditis
Although asymptomatic in some cases, most patients will present with symptoms specific for hypothyroidism:
Mild weight gain
Early in the course, some patients can present with symptoms of hyperthyroidism (hashitoxicosis) including palpitation, weight loss, and tremors.
Patients with HE present with mental status changes, seizures, and myoclonus.
Typically, patients will present with exam findings specific for hypothyroidism:
Goiter or atrophy on thyroid exam
Skin is cool and dry
Coarse or thin hair, brittle nails
Loss of lateral eyebrows
Slow speech and macroglossia
Pericardial and/or pleural effusion
Delayed deep tendon reflexes (DTR)
Slow movement and thought process
Nonpitting edema involving hands and feet
Patients with hashitoxicosis may present with tachycardia, weight loss, tremors, and brisk DTR.
Myxedema coma: severe hypothyroidism characterized by change in mental status, hypothermia, respiratory failure, hemodynamic instability, and death. Precipitated by stress, sepsis, and trauma.
Other causes of hypothyroidism including thyroidectomy, radioiodine treatment, neck radiation, iodine, medications such as amiodarone and tyrosine kinase inhibitors, and pituitary/hypothalamic disorders
Other causes of encephalopathy need to be ruled out to make the diagnosis of HE.
Initial screening with TSH is recommended. If TSH is abnormal, then check serum free thyroxine (FT4) (1)[A].
Overt hypothyroidism: elevated TSH and decreased FT4
Subclinical hypothyroidism: elevated TSH and normal FT4
Hashitoxicosis: transient decrease in TSH and increase in FT4
Silent or postpartum thyroiditis: Initially, patients present with thyrotoxicosis followed by hypothyroidism and eventually reach a euthyroid state after 3–6 months. Some patients progress to permanent Hashimoto hypothyroidism. Depending on the stage of illness, thyroid function results can vary.
Consider checking TPO and TG antibodies in individuals with subclinical disease and silent or postpartum thyroiditis to determine risk of progression to overt hypothyroidism and need for thyroid hormone replacement (1,2).
Ultrasound (US) of the gland can show diffuse, patchy hypoechoic areas (i.e., “leopard skin pattern” or “moth-eaten appearance”). US is not warranted for the diagnosis of HT. However, a US can be used to characterize thyroid nodules that can develop to HT.
Consider evaluation for other autoimmune conditions (e.g., adrenal insufficiency) in patients with HT, as clinically indicated.
Hypothyroidism can be associated with hyperlipidemia, hyperprolactinemia, and hyponatremia.
Gradual loss of thyroid function is noted in HT with subclinical disease progressing to overt hypothyroidism at a rate of 5% per year.
30–50% of individuals with silent or postpartum thyroiditis can progress to permanent hypothyroidism and/or goiter development.
Therefore, monitor TSH in high-risk patients (i.e., history of silent/postpartum thyroiditis, other autoimmune disorders, family history, radiation exposure, etc.) and treat when abnormal TSH is noted (1)[A].
Excluding other causes of hypothyroidism, an elevated TSH with low or normal FT4 is diagnostic of HT, although reversion of mild TSH elevation to normal is common, especially with “subclinical” hypothyroidism. Repeat TSH testing at regular intervals in those with subclinical hypothyroidism is warranted.
High TG and TPO antibodies titers can identify individuals at high risk for developing overt hypothyroidism or at risk for HE.
The goal of treatment is to alleviate symptoms and to bring blood levels of TSH into the normal range.
Oral thyroid hormone replacement should be considered in all patients with subclinical or overt HT. Thyroxine (T4), triiodothyronine (T3), or a combination of T4 and T3 can be prescribed (1)[A].
IV thyroid hormone replacement (i.e., T4) is recommended for patients at risk for myxedema coma.
Levothyroxine, synthetic T4, is recommended for the treatment of HT (1)[A].
Patients with HT generally require smaller doses early in the disease process and progress to higher doses as the disease evolves.
Starting doses of levothyroxine is between 25 and 75 μg/day based on age, weight, and comorbid conditions such as coronary artery disease.
Levothyroxine 1.6 μg/kg/day estimates full replacement.
Certain foods and medications including calcium supplements can affect levothyroxine absorption. For this reason, levothyroxine should be administered on an empty stomach and separate from other medications.
Glucocorticoid treatment is recommended for HE (prednisone 50–150 mg/day for 3–6 months). Dose titrated by symptoms.
Liothyronine sodium (Cytomel) is a synthetic preparation of T3. It can be given alone or in combination with T4. It has a shorter onset and duration of action than T4.
Desiccated thyroid preparations (Armour Thyroid, Nature-Thyroid, Westhroid) are animal-derived thyroid hormone products containing both T3 and T4 and generally not recommended.
Majority of studies have failed to show benefit of combined T4 plus T3. More research is needed to identify if any subgroups of patients with HT benefit from this combination.
Potential cardiac complications noted with treatment (i.e., arrhythmias) limit the use of these agents.
Start elderly patients with cardiac problems on a low dose (e.g., levothyroxine 25–50 θg daily) and titrate up every 4–6 weeks (1)[B].
Euthyroid pregnant women with high TPO antibodies titers
Increased risk for fetal loss, perinatal mortality, and large for gestational age infants. Thyroid hormone replacement may improve miscarriage rates.
Increased risk for subclinical hypothyroidism in the 1st trimester and thyroiditis in the postpartum period. Recommend universal screening of all pregnant women at risk for HT in the 1st trimester and postpartum period. Treatment started if appropriate.
Replacement doses of thyroid hormone increases by as much as 50% during pregnancy. TSH should be monitored every 4 weeks until target goals are achieved and then at least once per trimester. The goal of therapy is to keep TSH <2.5 mU/L during 1st trimester, <3 mU/L during 2nd trimester, and <3.5 mU/L during 3rd trimester. After delivery, thyroid hormone replacement doses can generally be reduced to prepregnancy doses (2)[A].
In patients with HT, always consider coexisting autoimmune adrenal insufficiency. Thyroid hormone replacement can trigger adrenal crisis. Therefore, adrenal insufficiency needs to be ruled out prior to thyroid hormone replacement and stress steroids started in individuals at high risk for underlying adrenal insufficiency.
Severe hypothyroidism/myxedema coma is an endocrine emergency and requires admission to the intensive care unit.
Treatment consists of IV levothyroxine and corticosteroids together with hemodynamic support.
TSH can be monitored every 4–6 weeks and dose titrated to achieve target goals.
Once target goal is achieved, then TSH should be monitored yearly or based on symptoms.
Education should focus on the importance of patient compliance, as it relates to frequency and manner of dosing (i.e., empty stomach).
Maternal hypothyroidism especially in the 1st trimester has been linked to impaired psychomotor/cognitive deficits in the child. Therefore, women of childbearing years with or at risk for HT need to notify their physician when planning pregnancy and when they become pregnant so that timely monitoring of labs and T4 dose adjustments can occur.
245.2 Chronic lymphocytic thyroiditis
244.9 Unspecified acquired hypothyroidism
240.9 Goiter, unspecified
E06.3 Autoimmune thyroiditis
E03.9 Hypothyroidism, unspecified
E04.9 Nontoxic goiter, unspecified
21983002 Hashimoto thyroiditis (disorder)
40930008 Hypothyroidism (disorder)
3716002 Goiter (disorder)
HT progresses from asymptomatic to overt hypothyroidism. Thyroid hormone replacement is recommended for both overt and subclinical Hashimoto hypothyroidism.
Pregnant women who are at risk for HT should have TSH checked in the 1st trimester and postpartum period. Thyroid hormone replacement started and monitored to maintain TSH goal of <2.5 mU/L in pregnancy.