The key clinical features differentiating Hashimoto's thyroiditis from subacute thyroiditis primarily involve the presence of pain, the typical course of thyroid function, and specific laboratory markers [1, 2, Synoracki et al. 2016].
Subacute thyroiditis (also known as De Quervain's thyroiditis) is characterised by a **painful and tender thyroid gland**, which is a hallmark differentiating feature [1, Synoracki et al. 2016]. This pain can often radiate to the jaw, ear, or chest NICE CKS. Its onset is typically acute or subacute, often following a viral illness, and patients may also experience fever, malaise, and myalgia [1, Synoracki et al. 2016]. Thyroid function in subacute thyroiditis commonly follows a triphasic course: an initial hyperthyroid phase due to the release of preformed hormones, followed by a transient hypothyroid phase, and usually culminating in a return to euthyroidism [1, Synoracki et al. 2016]. Laboratory tests typically show markedly elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), while thyroid antibodies are usually negative or present at low titres [1, Synoracki et al. 2016]. The condition is generally self-limiting, resolving within months [1, Synoracki et al. 2016].
In contrast, Hashimoto's thyroiditis is typically a **painless condition** NICE CKS. It is an autoimmune disorder with a gradual onset, often presenting with symptoms of hypothyroidism such as fatigue, weight gain, and cold intolerance NICE CKS. While a goitre may be present, it is usually firm and non-tender NICE CKS. Hashimoto's thyroiditis primarily leads to chronic hypothyroidism, although a transient hyperthyroid phase (Hashitoxicosis) can occur NICE CKS. The presence of high titres of thyroid peroxidase (TPO) antibodies and/or thyroglobulin antibodies is characteristic of Hashimoto's thyroiditis NICE CKS. Inflammatory markers like ESR and CRP are not typically elevated to the same extent as in subacute thyroiditis NICE CKS,NICE CKS.