Thyroiditis
- Inflammation of the thyroid gland
Infectious thyroiditis
- May be acute or chronic
- Can reach the thyroid by haematogical spread or by direct seeding such as via a fistula from the piriform sinus adjacent to the larynx
- Mycobacterial, fungal and Pneumocystis infections are more chronic and occur more commonly in immunocompromised patients
- May cause sudden onset pain and tenderness in the thyroid region and be accompanied by fever and chills
- Thyroid function is generally not affected and there are few residual affects apart from perhaps some small foci of scarring
Hashimoto Thyroiditis
- Also called chronic lymphocytic thyroiditis
- The most common cause of hypothyroidism in areas of the world with sufficient iodine levels
- Occurs age 45-65 F>M 10:1
- Increased risk of developing disease in people with Down syndrome and Turner syndrome
- May be some association with polymorphisms in HLA-DR3 and HLA-DR5 alleles
Pathogenesis
- Autoimmune disease against a variety of thyroid antigens
- Results in progressive depletion of thyroid epithelial cells which are replaced by mononuclear cell infiltrate and fibrosis
- Sensitisation of autoreactive CD4 T cells appears to be an initiating event
- The effector mechanisms of thyrocyte death include;
- CD8 cytotoxic T cell mediated death
- Cytokine mediated cell death; CD4 T cells produce IFNg which activated macrophages resulting in follicle damage
- Binding of anti-thyroid antibodies followed by ADCC. Antibodies can recognise the TSH receptor, thyroglobulin and thyroid peroxidase
Morphology
- Thyroid is generally diffusely enlarged
- Microscopically there is extensive mononuclear infiltration containing lymphocytes, plasma cells and well formed lymphoid follicles
- The thyroid follicles are atrophic and are lined by epithelial cells with an abundant eosinophilic cytoplasm called Hürthle cells which are a metaplastic response to ongoing injury
- There may be increased interstitial connective tissue
- Unlike Reidel thyroiditis the fibrosis does not extend beyond the capsule of the gland
Clinical course
- Painless enlargement of the thyroid usually associated with some degree of hypothyroidism
- Enlargement is generally symmetrical or diffuse
- May be proceeded by a transient thyrotoxicosis caused by disruption of the thyroid follicles and release of thyroid hormone
- Patients are at increased risk of developing other autoimmune disorders and B cell Non-Hodkins lymphoma
Subacute (Granulomatous) Thyroiditis
- Can also be referred to as De Quervain thyroiditis
- Occurs far less commonly than Hashimoto disease
- Occurs age 30-50 F>M 3:1
Pathogenesis
- Believed to be caused by a viral infection of a postviral inflammatory process
- Most patients have a previous history of an upper respiratory tract infection and there is a seasonal incidence with cases peaking in the summer
- Associated viruses include coxsackievirus, mumps, measles, adenovirus
- One model of pathogenesis is that viral infection result in the release of antigen (possible viral or thyroid) secondary to virus induced host tissue damage
- Stimulates cytotoxic T cells
- As the disease is virus initiated it is self limiting (in contract to autoimmune disease)
Morphology
- Gland may be unilateral or bilaterally enlarged with an intact capsule
- Early in the inflammatory process, follicles may be disrupted and replaced by neutrophils forming microabscesses. Later there may be aggregrates of lymphocytes, macrophages and plasma cells
- Multinucleated giant cells may be present hence the term granulomatous thyroiditis
- In later stages fibrosis may be present
Clinical course
- Presentation may be sudden or gradual
- It is characterised by pain in the neck which may radiate to the jaw, throat or ears particularly when swallowing
- There may be varying enlargement of the thyroid
- May be accompanied by fever, fatigue, malaise, anorexia and myalgia
- There is a transient hyperthyroidism followed by a period of hypothyroidism that is generally asymptomatic
Subacute lymphocytic (painless) Thyroiditis
- May also be called silent thyroiditis
- Uncommon cause of hyperthyroidism
- Seen in middle age, most commonly in postpartum women
- Pathogenesis is unknown, possibly autoimmune
Morphology
- Mild symmetrical enlargement
- Lymphocytic infiltration with hyperplastic germinal centres within the thyroid parenchyma, patchy disruption and collapse of thyroid follicles
- Hürthle cells are not commonly seen
Clinical course
- Hyperthyroidism, usually developing over 1-2 weeks and lasting from 2-8 weeks before subsiding
- Thyroid gland is normally non tender and minimally and diffusely enlarged
- Patients who develop it after one pregnancy are at increased risk of developing it in subsequent pregnancies
- A minority progress to hypothyroidism
- Infiltrative opthalmopathy is not present
Reidel thyroiditis
- Rare and of unknown aetiology (possibly autoimmune)
- Characterised by extensive fibrosis of the thyroid and other neck structures
- Presents as a hard fixed thyroid mass, similar to a carcinoma
- May be associated with idiopathic fibrosis in other sites of the body including the retroperitoneum
Palpation thyroiditis
- Caused by vigorous clinical palpation of the thyroid gland
- Result in multifocal follicular disruption and occasional giant cell formation
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