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Thyroiditis is a frequent and mostly benign disease that can sometimes disrupt the thyroid balance. Their diagnosis, as well as their aetiology, is a necessary step in the management of the patients. Painful thyroiditis includes acute thyroiditis of infectious origin and subacute thyroiditis. The first one can be treated by antibiotics or antifungals depending on the germ found. The second one will be treated with non-steroidal anti-inflammatory drugs or corticosteroids. In cases of Hashimoto's thyroiditis with overt hypothyroidism, replacement therapy with L-thyroxine will be adapted to the TSH level. As amiodarone treatment provides dysthyroidism, the thyroid status should be monitored regularly. Hypothyroidism will be treated using thyroid replacement therapy. Hyperthyroidism imposes a stop of amiodarone when it is possible. Treatment with synthetic antithyroid drugs (propyl-thio-uracil) or corticosteroids could be used whether there is an underlying thyroid disease or not. Immunotherapies with anti-PD-1/PDL1 or anti-CTLA-4 can also provide dysthyroidism. A monitoring of the thyroid assessment needs to be done in these patients, even if there are no clinical signs, which are not very specific in this context. The treatment of hypothyroidism will be based on thyroid replacement therapy according to the TSH level and the presence or absence of anti-TPO antibodies. Treatment of symptomatic hyperthyroidism may involve a prescription of beta-blockers, or synthetic antithyroid drugs in case of positive anti-TSH receptor antibodies. In all cases, it is desirable to contact an endocrinologist to confirm the diagnosis hypothesis and to decide on a suitable treatment., (Copyright © 2020 Société Nationale Française de Médecine Interne (SNFMI). Published by Elsevier Masson SAS. All rights reserved.)

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.

The approach to the evaluation of a neck mass requires careful history and physical examination to determine if the mass is thyroidal or non-thyroidal. Thyromegaly can be classified as diffuse or nodular, painless or painful, or associated with a solitary or multiple nodules. While the most common cause of diffuse enlargement is chronic lymphocytic thyroiditis, the presence of nodularity should prompt consideration of cancer. Results of a radionuclide scan, ultrasonogram, and/or a fine-needle aspiration of a cystic nodule should help guide the physician to those patients in need of an open thyroid biopsy.

Inflammatory diseases of the thyroid are collectively the commonest thyroid disorder. Individually, they range from the rare case of acute bacterial thyroiditis to the other end of the spectrum, the even rarer Riedel's thyroiditis. Relatively common thyroid inflammatory diseases include the subacute thyroiditis syndromes. Of particular interest to endocrinologists is that both subacute granulomatous (painful) thyroiditis and subacute lymphocytic (painless) thyroiditis are very similar in terms of clinical course, although most likely have different etiologies. Nevertheless, their similarities suggest the possibility that there may be etiologic heterogeneity for the syndromes. From a clinical standpoint, it is essential to differentiate subacute painless thyroiditis from Graves' disease, because these two disorders also may mimic each other, yet only Graves' disease requires specific therapy. Chronic lymphocytic (Hashimoto's) thyroiditis, the commonest of the thyroiditides, presents with goiter and either hyperthyroidism (uncommon), hypothyroidism (common), or euthyroidism (most common). When L-T4 therapy is used in the treatment of Hashimoto's thyroiditis, the physician must be alert to the possibility of excess thyroid hormone administration. Sensitive TSH measurements help to avoid this therapeutic pitfall.

In this review, the major types of immune mediated thyroiditis are described and the etiology explained in the light of current theories of autoimmunity. Hashimoto's thyroiditis is a common autoimmune disease. The onset is gradual with patients presenting with symptoms of hypothyroidism, nonspecific symptoms of the autoimmune process itself, or symptoms relating to a goitre. The disease is usually relentless and, except in young patients, permanent replacement with thyroxine is eventually required. Silent thyroiditis is another autoimmune disease of more acute onset. The initial, thyrotoxic, phase lasting several weeks is due to release of thyroid hormone from damaged follicles, and radionuclidic scans show absent uptake. There often follows a hypothyroid phase with final recovery in most patients. Post partum thyroiditis is due to silent thyroiditis, or, less commonly, Hashimoto's thyroiditis, occurring three to six months after delivery. Subacute thyroiditis often follows a viral infection and is not thought to be an autoimmune disease. It presents with severe thyroid pain and tenderness with marked non-specific symptoms such as myalgia and fatigue. The initial, thyrotoxic, phase is also due to release of thyroid hormone, and radionuclidic scans show absent uptake. A hypothyroid phase often follows and recovery is complete. Hashimoto's thyroiditis appears to be due to a congenitally present, antigen specific, T suppressor lymphocyte defect. It is proposed that in silent thyroiditis there is a less severe Ts defect and a correspondingly greater decompensating factor. In post partum thyroiditis, this factor appears to be a general decline in T suppressor lymphocyte function after delivery. Subacute thyroiditis is not an autoimmune disease. The thyroid appears to be an "innocent bystander" in an immune mediated antiviral attack.

From indirect and circumstantial evidence it would appear that subacute thyroiditis is probably a viral infection of the thyroid gland. The thyroid may respond in the stereotyped manner to any one of a number of viruses. Despite the available evidence, however, the viral theory has yet to be finally proven. Autoimmunity does not appear to be a primary factor in the initiation of subacute thyroiditis, although transient immunologic responses occur as a secondary phenomenon. Autoimmune thyroiditis, on the other hand, is almost certainly a primary immunologic disease, and likely is due to a specific inherited defect in immunologic control. It would appear that both cell-mediated immunity and humoral immunity (i.e., T and B lymphocytes) are necessary for the full expression of this disorder.

In summary thyroiditis runs a complete spectrum of diseases, from the potentially life-threatening to the indolent, from hyperthyroidism to hypothyroidism, from localized to diffuse disease. Because many features are shared by several different forms of thyroiditis, the clinical picture may be confusing. Overlapping hyperthyroid syndromes add complexity. Nevertheless, by careful evaluation and judicious testing, the correct diagnosis and therapy can be established.

Focal or diffuse infiltration of lymphoid cells in auto-immune thyroiditis destroys the parenchyma. In the diffuse form (Hashimoto's disease), the clinical picture is characterized by fatigue and thyroid enlargement. The diagnosis is settled by cytology. All patients must be treated with thyroid hormones to avoid myxoedema. Loss of immunological tolerance and cytotoxic immune reactions is discussed.

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.