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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Thyroiditis. 293 21

Silent thyroiditis is an increasingly recognized cause of transient thyrotoxicosis. Inflammatory destruction of thyroid follicles results in release of preformed thyroxine and triiodothyronine. Patients present with symptoms of thyrotoxicosis, but unlike subacute thyroiditis, lack thyroid pain or tenderness. The thyrotoxic state spontaneously resolves in 2 to 12 weeks at which time the patient either returns to a euthyroid state or passes through a transient hypothyroid phase. Diagnostic laboratory findings include elevations of thyroxine and triiodothyronine and a markedly depressed radioactive iodine uptake. It is imperative for the primary care physician to distinguish silent thyroiditis from chronic causes of hyperthyroidism, eg, Graves' disease, since treatment must be palliative rather than definitive. Long-term prognosis is usually excellent.
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PMID:Silent thyroiditis. 376 Aug

Silent thyroiditis and subacute thyroiditis are important causes of transient thyrotoxicosis from rapidly progressive tissue injury, followed by the release of thyroid hormone into the circulation. The most striking differences between them are severe pain and extreme tenderness in the thyroid region. Although the etiology of these diseases is not clarified, silent thyroiditis is basically occurred in autoimmune thyroiditis. The most difficult differential diagnosis of silent thyroiditis is Graves' disease. TSH receptor antibody (TRAb) is useful, but TRAb is rarely positive in silent thyroiditis. A low thyroid radioiodine uptake value is most useful in identified silent thyroiditis.
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PMID:[Silent thyroiditis and subacute thyroiditis]. 2321 66