Hashimoto Thyroiditis

Hashimoto thyroiditis is an autoimmune inflammatory condition of the thyroid gland. It is the commonest cause of hypothyroidism in iodine sufficient populations.

It is characterised by lymphocytic infiltration of the thyroid gland with progressive destruction of thyroid follicular cells. Both humoral autoimmunity (thyroid peroxidase and thyroglobulin antibodies) and cell mediated cytotoxic mechanisms contribute.

It typically produces a gradual, progressive decline in thyroid function over years. This is occasionally preceded by a transient hyperthyroid (hashitoxicosis) phase. The phase reflects release of preformed hormone from the actively inflamed gland before the more characteristic, sustained hypothyroid phase becomes established.

Pathophysiology

• Loss of normal immune tolerance to thyroid specific antigens, principally thyroid peroxidase and thyroglobulin, drives a sustained lymphocytic and plasma cell infiltration of the gland.
• Follicular cell destruction and fibrosis progress over time. This accounts for the gradual decline in thyroid hormone production and the typically firm, sometimes nodular or irregular texture of the gland on examination.
• A transient early hyperthyroid phase (hashitoxicosis) occurs in a proportion of patients. It reflects release of preformed thyroid hormone from the actively inflamed, damaged gland. It is generally self limiting and typically followed by the sustained hypothyroid phase, as ongoing follicular destruction outpaces residual functional capacity.
• The aetiology is multifactorial. There is a strong genetic predisposition, together with recognised environmental triggers (including excess iodine intake, certain infections, and pregnancy or the postpartum period).
• Association with other autoimmune conditions is frequent: type one diabetes, coeliac disease and other autoimmune endocrinopathies. In some patients these form part of the broader autoimmune polyendocrine syndrome spectrum.

• The typical, dominant presentation is the general hypothyroid symptom constellation, addressed in detail under hypothyroidism. It develops gradually over months to years as the autoimmune destructive process progresses.
• A goitre is common though not universal. It is typically firm, sometimes nodular or irregular in texture, and generally painless, distinguishing it from the painful, tender goitre of subacute thyroiditis.
• Some patients instead have a normal sized or even atrophic gland, particularly in longstanding disease with extensive fibrous replacement of thyroid tissue.
• A transient period of mild hyperthyroid symptoms may occur early in the disease course in a proportion of patients (hashitoxicosis). It is generally self limiting and typically evolves into the sustained hypothyroid phase over subsequent weeks to months.
• Because of the strong association with other autoimmune conditions, specifically explore relevant symptoms or family history suggesting coexisting autoimmune disease (type one diabetes, coeliac disease, vitiligo, pernicious anaemia, Addison disease). This is particularly relevant in younger patients or those with a personal or family history suggesting a broader autoimmune predisposition.

• Thyroid function testing shows the characteristic pattern of primary hypothyroidism. In overt disease thyroid stimulating hormone is elevated with reduced free thyroxine; in subclinical disease there is isolated thyroid stimulating hormone elevation.
• Elevated thyroid peroxidase antibodies confirm the diagnosis in the appropriate clinical context. They are positive in the great majority of patients and are the most sensitive and widely used diagnostic marker. Thyroglobulin antibodies are elevated in a proportion.
• Thyroid ultrasound, where performed, typically shows a diffusely heterogeneous, hypoechoic gland texture, supporting the diagnosis.
• Ultrasound is also useful for characterising and monitoring any coexisting discrete thyroid nodule. Hashimoto thyroiditis does not preclude a separate, clinically significant nodule, which requires its own workup according to standard thyroid nodule evaluation principles.
• Fine needle aspiration cytology is not routinely required to diagnose Hashimoto thyroiditis itself, given the reliable biochemical and serological approach. It remains appropriate for any discrete, sonographically suspicious nodule within a background of Hashimoto thyroiditis, following standard thyroid nodule assessment principles.

• Levothyroxine replacement, following the principles detailed under hypothyroidism, is standard treatment once overt hypothyroidism is confirmed. Regular thyroid function monitoring and dose titration are as detailed under that condition.
• Subclinical hypothyroidism with confirmed Hashimoto thyroiditis (positive thyroid peroxidase antibodies) is more likely to progress to overt disease than subclinical hypothyroidism from other or unclear causes.
• This supports a somewhat lower threshold for starting treatment in this population. Where treatment is deferred, monitor more closely and regularly for progression.
• The transient hyperthyroid (hashitoxicosis) phase, where it occurs, is managed with beta blockade alone for symptomatic relief. This follows the same principles as thyroiditis related hyperthyroidism addressed under hyperthyroidism generally, because there is no genuine excess ongoing hormone synthesis and the phase is generally self limiting.
• Screen for coexisting autoimmune conditions, particularly in younger patients or those with suggestive symptoms or family history.
• Reassess thyroid function periodically, even in patients with initially normal or subclinical biochemistry, given the progressive natural history.
• Regular clinical review monitors symptomatic and biochemical progression of thyroid dysfunction, and the size and characteristics of any associated goitre. This underpins ongoing management of a common, generally readily managed chronic autoimmune condition once appropriately diagnosed and, where indicated, treated.