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Thyroiditis is a general term for inflammation of the thyroid gland. The most common forms of thyroiditis encountered by family physicians include Hashimoto, postpartum, and subacute. Most forms of thyroiditis result in a triphasic disease pattern of thyroid dysfunction. Patients will have an initial phase of hyperthyroidism (thyrotoxicosis) attributed to the release of preformed thyroid hormone from damaged thyroid cells. This is followed by hypothyroidism, when the thyroid stores are depleted, and then eventual restoration of normal thyroid function. Some patients may develop permanent hypothyroidism. Hashimoto thyroiditis is an autoimmune disorder that presents with or without signs or symptoms of hypothyroidism, often with a painless goiter, and is associated with elevated thyroid peroxidase antibodies. Patients with Hashimoto thyroiditis and overt hypothyroidism are generally treated with lifelong thyroid hormone therapy. Postpartum thyroiditis occurs within one year of delivery, miscarriage, or medical abortion. Subacute thyroiditis is a self-limited inflammatory disease characterized by anterior neck pain. Treatment of subacute thyroiditis should focus on symptoms. In the hyperthyroid phase, beta blockers can treat adrenergic symptoms. In the hypothyroid phase, treatment is generally not necessary but may be used in patients with signs and symptoms of hypothyroidism or permanent hypothyroidism. Nonsteroidal anti-inflammatory drugs and corticosteroids are indicated for the treatment of thyroid pain. Certain drugs may induce thyroiditis, such as amiodarone, immune checkpoint inhibitors, interleukin-2, interferon-alfa, lithium, and tyrosine kinase inhibitors. In all cases of thyroiditis, surveillance and clinical follow-up are recommended to monitor for changes in thyroid function.

Riedel's thyroiditis (RT) is a rare chronic inflammatory disease of the thyroid gland. It is characterized by a fibroinflammatory process that partially destroys the gland and extends into adjacent neck structures. Its clinical manifestation can mask an accompanying thyroid neoplasm and can mimic invasive thyroid carcinoma. Therefore, diagnosis can be difficult prior to surgical removal of the thyroid, and histopathologic examination of the thyroid is necessary for a definite diagnosis. The concurrent presence of RT and other thyroid diseases has been reported. However, to our knowledge, the association of RT with acute suppurative thyroiditis and micropapillary carcinoma has not been reported. We report a rare case of concurrent RT, acute suppurative thyroiditis, and micropapillary carcinoma in a 48-year-old patient.

Riedel's thyroiditis, known as invasive fibrous thyroiditis, is a very rare form of chronic thyroiditis. It is hard to make the diagnosis without surgical biopsy. We present a case of Riedel's thyroiditis in a 52-year-old female with past history of Hashimoto's thyroiditis. She suffered from bilateral neck pain, which radiated to both lower jaws. The erythrocyte sedimentation rate was 125 mm/hour. Subacute thyroiditis superimposed on Hashimoto's thyroiditis was diagnosed and treated with steroid. However the response was poor and she had a history of severe peptic ulcer. To avoid inducing the peptic ulcer by steroid, she received bilateral subtotal thyroidectomy. During surgery, the thyroid had severe adhesion to surrounding soft tissue and the pathology showed Riedel's thyroiditis. The neck pain improved after thyroidectomy. Tamoxifen has been given for 8 months and the size of remnant thyroid decreased to 8 mm. We concluded that combined thyroidectomy and tamoxifen successfully cured a patient with Riedel's thyroiditis., (Copyright © 2012. Published by Elsevier B.V.)

Thyroiditis is an inflammation of the thyroid gland that may be painful and tender when caused by infection, radiation, or trauma, or painless when caused by autoimmune conditions, medications, or an idiopathic fibrotic process. The most common forms are Hashimoto's disease, subacute granulomatous thyroiditis, postpartum thyroiditis, subacute lymphocytic thyroiditis, and drug-induced thyroiditis (caused by amiodarone, interferon-alfa, interleukin-2, or lithium). Patients may have euthyroidism, hyperthyroidism, or hypothyroidism, or may evolve from one condition to another over time. Diagnosis is by clinical context and findings, including the presence or absence of pain, tenderness, and autoantibodies. In addition, the degree of radioactive iodine uptake by the gland is reduced in most patients with viral, radiation-induced, traumatic, autoimmune, or drug-induced inflammation of the thyroid. Treatment primarily is directed at symptomatic relief of thyroid pain and tenderness, if present, and restoration of euthyroidism.

We review the pathophysiology, clinical features and therapy of acute thyroiditis. Four cases are reported stressing the role of fine needle aspiration for the diagnosis of this clinical entity.

Postpartum thyroiditis is a syndrome of transient or permanent thyroid dysfunction occurring in the first year after delivery and based on an autoimmune inflammation of the thyroid. The prevalence ranges from 5-7%. We discuss the role of antibodies (especially thyroid peroxidase antibodies), complement, activated T cells, and apoptosis in the outbreak of postpartum thyroiditis. Postpartum thyroiditis is conceptualized as an acute phase of autoimmune thyroid destruction in the context of an existing and ongoing process of thyroid autosensitization. From pregnancy an enhanced state of immune tolerance ensues. A rebound reaction to this pregnancy-associated immune suppression after delivery explains the aggravation of autoimmune syndromes in the puerperal period, e.g., the occurrence of clinically overt postpartum thyroiditis. Low thyroid reserve due to autoimmune thyroiditis is increasingly recognized as a serious health problem. 1) Thyroid autoimmunity increases the probability of spontaneous fetal loss. 2) Thyroid failure due to autoimmune thyroiditis-often mild and subclinical-can lead to permanent and significant impairment in neuropsychological performance of the offspring. 3) Evidence is emerging that as women age subclinical hypothyroidism-as a sequel of postpartum thyroiditis-predisposes them to cardiovascular disease. Hence, postpartum thyroiditis is no longer considered a mild and transient disorder. Screening is considered.

Thyroiditis is a group of inflammatory thyroid disorders. Patients with chronic lymphocytic thyroiditis (also referred to as Hashimoto's thyroiditis) present with hypothyroidism, goiter, or both. Measurement of serum thyroid autoantibodies and thyroglobulin confirms the diagnosis. Subacute granulomatous thyroiditis (sometimes referred to as de Quervain's disease) is a self-limited but painful disorder of the thyroid. Physical examination, elevated erythrocyte sedimentation rate, elevated thyroglobulin level and depressed radioactive iodine uptake (RAIU) confirm the diagnosis. Subacute lymphocytic thyroiditis (silent thyroiditis) is considered autoimmune in origin and commonly occurs in the postpartum period. Symptoms of hyperthyroidism and depressed RAIU predominate. Acute (suppurative) thyroiditis is a rare, infectious thyroid disorder caused by bacteria and other microbes. The rare, invasive fibrous thyroiditis (Riedel's thyroiditis) presents with a slowly enlarging anterior neck mass that is sometimes confused with a malignancy.

Immunization of mice with 50 micrograms human thyroglobulin (TG) in complete Freund's adjuvant leads to histological thyroiditis; production of IgG, IgA, and IgM anti-TG antibodies; and in vitro proliferative responses after incubation of lymphocytes with TG. Oral administration of 500 micrograms TG at four intervals before Tg immunization and once afterward causes up to 80% suppression of these responses. The effect is antigen specific and dose dependent. Feeding TG after immunization produces a 40% reduction in responses. We wished to define the mechanism of this antigen-specific oral tolerization. Popliteal lymph nodes (PLN) of orally tolerized animals (T) are reduced in size compared to those in immunized (I) animals not fed TG. PLN and mesenteric lymph nodes (MLN) of I animals produce interleukin-2 (IL-2) and interferon-gamma (IFN gamma) after in vitro incubation with TG, typical of an inflammatory immune response. PLN and MLN of tolerized animals do not proliferate in response to antigen, do not produce IL-2 or IFN gamma, but do not produce the cytokines IL-4 and transforming growth factor-beta (TGF beta). Mixing in vitro of spleen cells from T and I animals causes a reduction in the immune response when incubated with TG, but no reduction in response to purified protein derivative (PPD) (the antigen in complete Freund's adjuvant). When T splenocytes are incubated with TG and PPD together, the response to TG and PPD is suppressed. Partially purified CD8+ cells from tolerized animals produce IL-4 and TGF beta after exposure to human TG and induce suppression, whereas partially purified CD4+ cells produce IL-2 and IFN gamma and do not cause suppression. MLN cells do not proliferate in response to antigen, but do produce inhibitory cytokines. T animals appear to shift the immune response from a Th-1 helper cell subset response to a Th-2 helper cell immunosuppressive response. In this model, oral tolerization produces a dramatic reduction in the immune response. Exposure of MLN to oral TG appears to cause the production of regulatory cells that migrate to spleen and PLN. In vitro studies demonstrate that on exposure to antigen, these regulatory cells produce IL-4 and TGF beta, which suppress all aspects of specific immune responsiveness and nonspecifically suppress other ongoing immune responses (bystander effect). Oral tolerization may include some element of T cell deletion or anergy. This model defines an experimental system with possible relevance to immunosuppression of human autoimmune thyroid disease.

Thyroiditis may be categorized as acute (suppurative), subacute (granulomatous or lymphocytic), or chronic (invasive fibrous or lymphocytic). Acute suppurative thyroiditis is typically caused by a bacterial infection and resolves with appropriate antibiotic treatment. The subacute thyroiditides are characterized by spontaneously resolving hyperthyroidism associated with low radioiodine uptake, often followed by transient hypothyroidism. Neck pain is the initial symptom in subacute granulomatous thyroiditis, and the disorder recurs only in a minority of patients. Subacute lymphocytic thyroiditis is typically painless, often occurs in the postpartum period, and is being increasingly recognized in the Great Lakes area of the United States. Invasive fibrous thyroiditis (Riedel's struma) is exceedingly rare, often mimics carcinoma, and is associated with extracervical foci of fibrosclerosis. Chronic lymphocytic (Hashimoto's) thyroiditis, an organ-specific autoimmune disease, occurs in at least 2% of women. Although the disorder often produces hypothyroidism, the type of thyroid dysfunction present in patients with Hashimoto's disease reflects the character of the dominant thyroid autoantibody--that is, destructive, blocking, or stimulatory.

Clinical and laboratory characteristics of 224 patients with thyroidal infection reported since 1900 are reviewed. Much of the prior literature on this subject has assumed that most instances of thyroiditis are infectious and that all lymphomatous thyroiditis is tuberculous. Similarly, thyroiditis occurring with syphilis was often equated with treponemal invasion of the gland. Acute bacterial thyroiditis is rapid in onset and more likely than tuberculous infection to produce fever, pain, and tenderness. Suppurative and mycobacterial infections are most common among women with preexisting thyroid disorders. Mortality due to infectious thyroiditis is lower in cases covered by this review than has been previously reported. Gummatous and fungal infections of the thyroid are generally diagnosed only at biopsy or necropsy. Frequent thyroidal involvement in disseminated aspergillosis warrants careful investigation of the gland in patients with this infection. Echinococcosis of the thyroid is a chronic process that is generally diagnosed only following excision.