Chronic Autoimmune Thyroiditis (Hashimoto Thyroiditis)

Chapter: Chronic Autoimmune Thyroiditis (Hashimoto Thyroiditis)
McMaster Section Editor(s): Victor M. Montori, Juan P. Brito
Section Editor(s) in Interna Szczeklika: Barbara Jarząb, Ewa Płaczkiewicz-Jankowska
McMaster Author(s): Juan P. Brito
Author(s) in Interna Szczeklika: Andrzej Lewiński, Ewa Płaczkiewicz-Jankowska
Additional Information

Definition, Etiology, Pathogenesis Top

Chronic autoimmune (lymphocytic) thyroiditis (Hashimoto thyroiditis) is a painless thyroiditis associated with antibodies against thyroid peroxidase (TPO) and—in some cases—against thyroglobulin (Tg), presenting with thyroid lymphocytic infiltrates and slow-onset hypothyroidism. The pathogenesis is primarily attributed to the activity of cytotoxic T cells, which are responsible for the destruction of the follicular thyroid cells.

Clinical Features and Natural History Top

The disease may take one of two clinical forms: with a normal thyroid volume (atrophic form) or with a goiter (painless enlargement and increased density of the thyroid gland). Both forms may present with either subclinical or overt hypothyroidism. The course of the disease is chronic, indolent, and usually results in permanent hypothyroidism. Exacerbations with sudden enlargement and tenderness of the thyroid gland and general features of inflammation (elevated C-reactive protein levels and erythrocyte sedimentation rate, rarely with fever) are very rare; they may be accompanied by the clinical features of thyrotoxicosis (Hashitoxicosis, hyperthyroiditis) caused by excessive release of the thyroid hormones from the affected gland. These symptoms resolve spontaneously and are followed by the development of hypothyroidism.

Diagnosis Top

Diagnostic Tests

1. Laboratory tests:

1) Increased titers of antibodies to TPO and—in some cases—to Tg.

2) Elevated serum thyroid-stimulating hormone (TSH) levels (they may be decreased in the rarely observed hyperthyroid phase).

3) Decreased serum free thyroxine (FT4) levels (in subclinical hypothyroidism, FT4 levels are normal, whereas in the rare hyperthyroid phase, the levels of free thyroid hormones may be elevated).

2. Imaging studies: Results of ultrasonography and 131I radionuclide thyroid imaging are frequently not conclusive. Ultrasonography shows a heterogeneous hypodense parenchyma both in patients with a goiter and with thyroid atrophy; if nodular lesions are found, consider the indications for fine-needle biopsy (FNB) [see Nontoxic Multinodular Goiter].

3. FNB and morphology studies: Cytologic findings may vary from mild fibrosis to massive lymphocytic and plasmacytic infiltrates with the formation of lymphoid follicles and oncocytic metaplasia of the follicular epithelium.

Diagnostic Criteria

The key diagnostic criterion is an elevated level of TPO antibodies in a patient who presents with a goiter, with a reduced size of the thyroid gland (atrophic thyroid), or with hypothyroidism. The diagnostic importance of Tg antibodies is considerably lower than that of TPO antibodies due to their lower specificity. In patients with concomitant hypothyroidism and elevated levels of TPO antibodies, FNB should not be performed to confirm the diagnosis.Evidence 1Strong recommendation (downsides clearly outweigh benefits; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence lowered due to imprecision. Haberal AN, Toru S, Ozen O, Arat Z, Bilezikçi B. Diagnostic pitfalls in the evaluation of fine needle aspiration cytology of the thyroid: correlation with histopathology in 260 cases. Cytopathology. 2009 Apr;20(2):103-8. doi: 10.1111/j.1365-2303.2008.00594.x. Epub 2008 Aug 18. PubMed PMID: 18713250.

Differential Diagnosis

1. Other thyroid diseases causing hypothyroidism: History, different morphologic features.

2. Differentiation of Hashitoxicosis from other causes of hyperthyroidism: History, elevated TPO antibody levels, negative thyrotropin-stimulating hormone receptor [TSH-R] antibodies, and different morphologic features.

Treatment Top

There are no effective methods of treating the cause of the disease. Patients with overt hypothyroidism should receive levothyroxine (L-T4) replacement therapy (see Hypothyroidism). In subclinical hypothyroidism, L-T4 replacement is suggested when TSH levels are >10 mIU/LEvidence 2Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to the observational nature of data on risk. Rodondi N, den Elzen WP, Bauer DC, et al; Thyroid Studies Collaboration. Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA. 2010 Sep 22;304(12):1365-74. doi: 10.1001/jama.2010.1361. PubMed PMID: 20858880; PubMed Central PMCID: PMC3923470. Gencer B, Collet TH, Virgini V, et al; Thyroid Studies Collaboration. Subclinical thyroid dysfunction and the risk of heart failure events: an individual participant data analysis from 6 prospective cohorts. Circulation. 2012 Aug 28;126(9):1040-9. Epub 2012 Jul 19. PubMed PMID: 22821943; PubMed Central PMCID: PMC3884576. or in pregnancy. Uncertainty exists regarding the management of patients with subclinical hypothyroidism and TSH levels between 5 and 10 mIU/L; thus, the decision of treatment with L-T4 replacement is based on the presence of symptoms suggestive of hypothyroidism and age of the patient (TSH values between 5 and 10 mIU/L may be normal in elderly people). In the rare cases of Hashitoxicosis, the use of antithyroid drugs is not mandatory and usually accelerates the development of hypothyroidism.

Prognosis Top

The disease usually leads to permanent hypothyroidism, which requires a lifelong hormone replacement therapy (with adequate treatment, the disease causes no sequelae). The risk of developing overt hypothyroidism in patients with subclinical hypothyroidism increases with age. Very rarely, thyroiditis may progress to primary lymphoma of the thyroid gland; transformation of Hashimoto thyroiditis into Graves disease is also rare and is caused by the development of TSH-R antibodies early in the course of the disease along with the subsequent overstimulation of the thyroid gland.

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