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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.

Tuberculosis (TB) of the thyroid gland, either in its primary or secondary form, is an extremely rare occurrence. It is infrequent even in countries with high incidence and prevalence of pulmonary and extrapulmonary TB. We report here a case of primary tuberculosis of thyroid presenting to us with sudden onset thyroid swelling since 20 days., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Background: Riedel's thyroiditis (RT) is a rare, fibroinflammatory condition which induces gradual thyroid gland destruction and adjacent soft-tissue fibrous infiltration. About one- seventh of RT cases are associated with hypoparathyroidism, necessitating long-term therapy for symptomatic hypocalcemia. The reversibility of the parathyroid hormone deficit has not been fully described., Patient Findings: A 40-year-old woman with no prior history of thyroid disease presented with a six month history of progressive thyroid enlargement complicated by worsening dysphagia and positional dyspnea. Her past medical history was remarkable only for retroperitoneal fibrosis. Physical examination revealed a large, hard, non-mobile goiter. Thyroid indices while maintained on levothyroxine were normal, but marked asymptomatic hypocalcemia with an inappropriately normal parathyroid hormone level was noted. Thyroid imaging and fine needle aspiration were consistent with RT. Isthmectomy and subsequent serial corticosteroid and tamoxifen treatment led to rapid symptom improvement. Serum calcium and parathyroid hormone levels returned to the reference range within three months., Summary: We describe a case of RT in which hypoparathyroidism resolved after treatment targeted the mechanical compression and the fibroinflammatory milieu of the patient's thyroidal disease., Conclusions: RT can be associated with hypoparathyroidism that is clinically silent at presentation. Mechanical decompression of the goiter and immunomodulatory therapy can reverse the fibrosclerotic process and lead to rapid recovery of parathyroid gland function, as in this patient. However, in most cases hypoparathyroidism is persistent and requires continued treatment to prevent symptomatic hypocalcemia.

Purpose: To report an unusual case of IgG4-related Mikulicz's disease associated with thyroiditis., Case Report: We describe a 25-year-old Chinese man who presented with bilateral, painless swellings of the lachrymal glands, parotid glands, and thyroid nodules. The patient underwent left-sided dacryoadenectomy and the diagnosis of IgG4-related Mikulicz's disease was pathologically confirmed. The size of the right-sided lachrymal gland and parotid glands recovered fundamentally after one month of glucocorticoid therapy., Conclusion: IgG4-related Mikulicz's disease associated with thyroiditis should be considered in the differential diagnosis of bilateral swellings of lachrymal glands, salivary glands, and thyroid nodules. Surgical excision is recommended in order to treat the tumor and to ensure the pathological diagnosis. Glucocorticoid therapy should be considered in association with surgery after removal.

Background: Interferon-alpha (IFNα)-induced thyroid dysfunction occurs in up to 20% of patients undergoing therapy for hepatitis C. The diversity of thyroid disease presentations suggests that several different pathological mechanisms are involved, such as autoimmunity and direct toxicity. Elucidating the relationships between risk factors and disease phenotype provides insight into the mechanisms of disease pathophysiology., Methods: We studied 869 euthyroid patients from the ACHIEVE 2/3 trial, a randomized international clinical trial comparing pegylated-IFNα2a weekly or albumin-IFNα2b every 2 weeks for up to 24 weeks in patients with hepatitis C, genotype 2 or 3, from 136 centers. The study population was 60% male and 55% white. Serum thyrotropin (TSH) and free thyroxine were measured before therapy, monthly during treatment from week 8, and at 4- and 12-week follow-up visits., Results: Overall, 181 (20.8%) participants had at least one abnormal TSH during the study. Low TSH occurred in 71 (8.2%), of whom 30 (3.5%) had a suppressed TSH below 0.1 mU/L. Hypothyroidism occurred in 53 patients (6.1%), with peak TSH above 10 mU/L in 12 patients (1.4%). Fifty-seven patients had a biphasic thyroiditis (6.6%), with extreme values for the nadir and/or peak TSH in all but one. Medical therapy was given to one thyrotoxic patient, four hypothyroid patients, and 26 biphasic thyroiditis patients. Multivariate logistic regression analysis demonstrated that biphasic thyroiditis is associated with being female and higher pretreatment serum TSH, whereas being Asian or a current smoker decreased the risk of thyroiditis. Hypo- and hyperthyroidism are most strongly predicted by the pretreatment TSH., Conclusions: Biphasic thyroiditis accounted for the majority (58%) of clinically relevant IFNα-induced thyroid dysfunction. We confirmed our recent findings in a related cohort that female sex is a risk factor for thyroiditis but not hypothyroidism. Further, in this large multiethnic study, the risk of thyroiditis is dramatically increased, specifically for white women. Smoking was found to be protective of thyroiditis. These results support closer monitoring of women and those with a serum TSH at the extremes of the normal range during therapy so that prompt intervention can mitigate the consequences of thyroid dysfunction associated with IFNα treatment.

Introduction: Hyperthyroidism is characterized by increased synthesis and release of thyroid hormones by the thyroid gland. Thyrotoxicosis refers to the clinical syndrome resulting from excessive circulating thyroid hormones, secondary to hyperthyroidism or due to other causes. This article describes evidence-based guidelines for the clinical management of thyrotoxicosis., Objective: This consensus, developed by Brazilian experts and sponsored by the Department of Thyroid Brazilian Society of Endocrinology and Metabolism, aims to address the management, diagnosis and treatment of patients with thyrotoxicosis, according to the most recent evidence from the literature and appropriate for the clinical reality of Brazil., Materials and Methods: After structuring clinical questions, search for evidence was made available in the literature, initially in the database MedLine, PubMed and Embase databases and subsequently in SciELO - Lilacs. The strength of evidence was evaluated by Oxford classification system was established from the study design used, considering the best available evidence for each question., Results: We have defined 13 questions about the initial clinical approach for the diagnosis and treatment that resulted in 53 recommendations, including the etiology, treatment with antithyroid drugs, radioactive iodine and surgery. We also addressed hyperthyroidism in children, teenagers or pregnant patients, and management of hyperthyroidism in patients with Graves' ophthalmopathy and various other causes of thyrotoxicosis., Conclusions: The clinical diagnosis of hyperthyroidism usually offers no difficulty and should be made with measurements of serum TSH and thyroid hormones. The treatment can be performed with antithyroid drugs, surgery or administration of radioactive iodine according to the etiology of thyrotoxicosis, local availability of methods and preferences of the attending physician and patient.

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.

Objective: Hepatitis C virus (HCV) infection is one of the major epidemics afflicting young people in both developed and developing countries. The most common endocrine disorder associated with this infection, especially in conjunction with interferon-α (IFN-α)-based therapy, is thyroid disease (TD). This review examines the development of TD before, during, and after the completion of treatment with combination IFN-α and ribavirin (RBV) for chronic HCV infection. We also summarize the current understanding of the natural history of the condition and propose management and follow-up guidelines., Methods: PubMed was searched up to June 30, 2011 for English-language publications that contained the search terms "hepatitis C virus," "chronic hepatitis C," "HCV," "thyroid disease," "thyroiditis," "autoimmunity," "interferon-alpha," and "ribavirin." Additional publications were identified from the reference lists of identified papers. The included studies were original research publications and included combination IFN-α and RBV use in patients that developed TD., Results: The prevalence of TD before combination IFN-α and RBV therapy ranges from 4.6 to 21.3%; during therapy, 1.1 to 21.3%; and after therapy, 6.7 to 21.3%. The most common TD is thyroiditis. Thyroid function testing (TFT) frequency and diagnostic criteria for various thyroid conditions are not standardized, and many of the existing studies are retrospective., Conclusion: Patients undergoing this therapy should be assessed with a standardized protocol to appropriately detect and manage developed TD. Based on the currently available literature, we recommend that patients receiving combination interferon-α and RBV therapy undergo monthly thyrotropin (TSH) level testing.

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.)

Objective: The aim was to update the guidelines for the management of thyroid dysfunction during pregnancy and postpartum published previously in 2007. A summary of changes between the 2007 and 2012 version is identified in the Supplemental Data (published on The Endocrine Society's Journals Online web site at http://jcem.endojournals.org)., Evidence: This evidence-based guideline was developed according to the U.S. Preventive Service Task Force, grading items level A, B, C, D, or I, on the basis of the strength of evidence and magnitude of net benefit (benefits minus harms) as well as the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system to describe both the strength of recommendations and the quality of evidence., Consensus Process: The guideline was developed through a series of e-mails, conference calls, and one face-to-face meeting. An initial draft was prepared by the Task Force, with the help of a medical writer, and reviewed and commented on by members of The Endocrine Society, Asia and Oceania Thyroid Association, and the Latin American Thyroid Society. A second draft was reviewed and approved by The Endocrine Society Council. At each stage of review, the Task Force received written comments and incorporated substantive changes., Conclusions: Practice guidelines are presented for diagnosis and treatment of patients with thyroid-related medical issues just before and during pregnancy and in the postpartum interval. These include evidence-based approaches to assessing the cause of the condition, treating it, and managing hypothyroidism, hyperthyroidism, gestational hyperthyroidism, thyroid autoimmunity, thyroid tumors, iodine nutrition, postpartum thyroiditis, and screening for thyroid disease. Indications and side effects of therapeutic agents used in treatment are also presented.

Background: Severe hypercalcemia has rarely been reported in patients with hyperthyroidism. Although the pathogenesis is not clear; it is believed to be due to activation of osteoclasts resulting in excessive bone resorption., Objective: To recognize the unusual cause of hypercalcemia from painless thyroiditis, which could manifest with transient hyperthyroidism in the early stage., Case Report: A 70-year-old woman presented with watery diarrhea, nausea and vomiting and significant weight loss for two months. Initially, she was misdiagnosed as having Graves'disease from her clinical presentation and thyroid function tests. Oral propylthiouracil was given to treat hyperthyroidism. However two weeks after discharge, she developed altered consciousness due to severe hypercalcemia. After combined treatment of hypercalcemia and severe hyperthyroidism, her symptoms resolved quickly. Later on, her thyroid function tests switched to subclinical hypothyroid at two months after initial presentation. No concurrent pathological conditions could be found to explain the other causes of hypercalcemia. Therefore, painless thyroiditis complicated with severe hypercalcemia was subsequently diagnosed based on her clinical course., Conclusion: Hypercalcemic encephalopathy is an uncommon manifestation of hyperthyroidism that should be kept in mind in patients who demonstrated clinical pictures of hyperthyroidism and alteration of consciousness. Moreover the present case emphasizes the consideration of painless thyroiditis as a differential diagnosis of hyperthyroidism because anti-thyroid medications were not indicated in this condition.

Context: Riedel's thyroiditis is a rare inflammatory process involving the thyroid and surrounding cervical tissues and is associated with various forms of systemic fibrosis. Riedel's presentation is complex, including a thyroid mass associated with local symptoms, characteristic biochemical abnormalities such as hypocalcemia and hypothyroidism, as well as the involvement of a wide range of other organ systems. Diagnosis of Riedel's thyroiditis requires histopathological confirmation, but due to high complication rates, the role of surgical intervention is limited to airway decompression and diagnostic tissue retrieval. Unique among processes of the thyroid, Riedel's is commonly treated with long-term antiinflammatory medications to arrest progression and maintain a symptom-free course. Due to its rarity, Riedel's may not be immediately diagnosed, so clinicians benefit from recognizing the constellation of findings that should make prompt diagnosis possible., Evidence Acquisition: A review of print and electronic reviews was conducted. Source references were identified, and available literature was reviewed. A search of the PubMed database using the search term "Riedel's thyroiditis" was cross-referenced with associated clinical findings, systemic fibrosis diagnoses, and therapeutic search terms. Because most of the literature consisted of case reports and very small series, inclusion of identified articles was based on clinical descriptions of the subjects included and the criteria for diagnosis reported. More weight was attributed to series, using contemporary criteria for diagnosis. Case reports were included if the diagnosis was clear and clinical presentation was unique to illustrate the spectrum of disease., Evidence Synthesis: Because the majority of therapeutic intervention data were based upon case reports and very small series, an evidence-based approach was problematic, but information is presented as objectively and with as much balance as the limited quality of the data allows., Conclusions: Clinical awareness of the characteristic presentations of Riedel's thyroiditis should enhance our ability to make this diagnosis in a timely and focused manner. Recognition of certain clinical finding patterns will increase the likelihood of recognizing Riedel's thyroiditis promptly. Local restrictive or infiltrative symptoms out of proportion to a demonstrable mass or simultaneous biochemical deficiencies especially of calcium should lead the clinician to consider this diagnosis. Likewise in this setting, the surgeon alert to this possibility may minimize overly aggressive surgical intervention, thus avoiding complications. Once Riedel's thyroiditis is diagnosed, the application of antiinflammatory therapies may greatly enhance the clinical outcome. Understanding the pathophysiological relationship of this entity with other forms of systemic fibrosis and the role that IgG4 may play in this process should result in enhanced diagnostic and therapeutic tools in the future.

Autoimmune thyroid diseases (AITD) are postulated to develop as a result of a complex interplay between several genetic and environmental influences. The pathogenesis of AITD is still not clearly defined. However, among the implicated triggers (e.g. iodine, infections, medications), more recent data confirmed strong associations of AITD with the hepatitis C virus (HCV) infection and interferon-α (IFNα) therapy. Moreover, it is likely that HCV and IFN act in synergism to trigger AITD in patients. Indeed, approximately 40% of HCV patients develop either clinical or subclinical disease while receiving IFNα. Interferon induced thyroiditis (IIT) can manifest as non-autoimmune thyroiditis (presenting as destructive thyroiditis, or non-autoimmune hypothyroidism), or autoimmune thyroiditis [presenting with clinical features of Graves' disease (GD) or Hashimoto's thyroiditis (HT)]. Although not yet clearly understood, it is thought that IFNα can induce thyroiditis via both immune stimulatory and direct toxic effects on the thyroid. In view of the high frequency of IIT, routine screening and surveillance of HCV patients receiving IFNα is recommended to avoid the complications, such as cardiac arrhythmias, associated with thyrotoxicosis. In summary, IIT is a common clinical problem that can be readily diagnosed with routine thyroid function screening of HCV patients receiving IFN. The treatment of IIT consists of the standard therapy for differing clinical manifestations of IIT such as GD, HT, or destructive thyroiditis. However, anti-thyroid medications are not recommended in this setting since they can potentially be hepatotoxic.

Interferons are currently the major treatment modality for several malignant and non-malignant diseases such as chronic hepatitis C and B, multiple sclerosis, hematological malignancies, malignant melanoma, renal cell carcinoma, etc. Thyroid disorders develop in some of the interferon-treated patients with the incidence ranging from 1% to 35%. These complications may often result in dose reduction or discontinuation of interferon therapy. Interferon induced thyroid disorders can be classified as autoimmune and non-autoimmune thyroiditis. There are many studies on the development of thyroid dysfunction in interferon-alpha treated patients with chronic hepatitis C and in patients with multiple sclerosis treated with interferon-beta. There is a dearth of information about the incidence and characteristics of thyroid abnormalities in patients with hematological malignancies receiving interferon-alpha. A number of genetic determinants are discussed as causes for thyroid impairment (sex, age, ethnic group, genes involved in the thyroid immune regulation), as well as non-genetic factors (related to the underlying disease--hepatitis C virus; multiple sclerosis; therapeutic regimens of interferon administration, iodine concentration in the environment, presence of thyroid autoantibodies at the start of treatment, etc.). In this article we summarize the relevant data about the frequency and characteristics of thyroid disorders in patients treated with interferons, the risk factors and the mechanisms for their development and the peculiarities of the course, detection and treatment of these complications. The review of the literature motivates studying the thyroid function of specific groups of patients receiving interferon in order to clarify the influence of the factors drug and disease on the thyroid gland. Early detection and adequate treatment of thyroid dysfunction in these patients is important to avoid complications that may compromise treatment.

Interferon alpha (IFN alpha) is the cornerstone therapeutic agent for chronic hepatitis C virus (HCV) infection. Prospective studies have shown that up to 15% of HCV patients receiving IFN alpha develop clinical thyroid disease, and up to 40% become thyroid antibody positive. In some cases IFN-induced thyroiditis (IIT) may result in discontinuation of interferon therapy; thus, IIT represents a major clinical problem for hepatitis C patients receiving IFN alpha therapy. Recently, the mechanisms leading to the development of IIT have begun to be unraveled. It is now clear that HCV itself plays a role in the disease. Moreover, recent data suggest the IFN alpha precipitates thyroiditis by both immune modulatory mechanisms and direct thyroid toxic effects. Genetic factors also play a major role in the etiology of IIT. IIT can manifest both as clinical autoimmune thyroiditis (ie, Hashimoto's thyroiditis and Graves' disease) and as nonautoimmune thyroiditis (ie, destructive thyroiditis). Early detection and therapy of these conditions are important to avoid complications of thyroid disease such as cardiac arrhythmias. This article reviews the epidemiology and clinical manifestations of IIT and the mechanisms causing IIT, focusing on the role of HCV.

If an abscess is not able to establish drainage through the skin surface or into the oral cavity, it may spread diffusely through fascial planes of the neck's soft tissue. Once the infection descends into the submandibular space, it may extend to the lateral pharyngeal space, and then to the retro-pharyngeal space. From here, it may reach the thyroid gland. The authors here describe a case of submandibular phlegmon derived from a periapical abscess of inferior premolar, which has reached the thyroid gland. The damage caused to the gland resulted in the release of a conspicuous quantity of thyroid hormones, thus causing a thyrotoxic pattern: temperature, cutaneous pallor, excessive perspiration, tremor, tiredness, weight loss, increased appetite, and tachycardia. Additionally, the gland's edema caused dysphagia and dysphonia commonly seen with thyroid gland enlargement. After dental drainage and appropriate anti-inflammatory and antibiotic therapy, administration of oral beta-blockers and corticosteroid therapy were performed to counteract thyrotoxicosis in order to prevent recurrences. Finally, a root canal was performed once the thyrotoxicosis had been resolved.

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.

Inflammatory thyroid disorders encompass a broad spectrum of diseases that are generally self-limited, and relatively easy to diagnose and manage. Autoimmune subtypes are by far the most commonly encountered diagnoses and create the most confusion because of simultaneous overlap and the potential for interconversion among the subtypes. The otolaryngologist will frequently see these disorders and provide valued consultative care and surgical intervention as needed.

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.

High prevalence of thyroid autoantibodies, with or without overt thyroiditis, has been described in hepatitis C patients, particularly in those undergoing alpha-interferon treatment. The aim of this study was to describe the frequency and clinical outcome of thyroid disease in a cohort of HCV carriers before and during combination therapy with interferon plus ribavirin. Between May, 1997, and May, 1999, 111 previously untreated (naive) patients were treated with a-interferon plus ribavirin for 6 or 12 months. Of those, 67 (60%) patients were male and 44 (40%) female. Thyroid function was evaluated in all patients by testing free T4, TSH and antiTPO within 30 days prior to treatment, 90 days after treatment was initiated, and 6 months after treatment was concluded. Abnormal thyroid tests were observed in 4 (3.6%) patients--1 male and 3 female--before the onset of antiviral treatment. Three patients were already undergoing T4 replacement due to Hashimoto thyroiditis and 1 patient had positive antiTPO with normal free T4 and TSH. All 4 patients completed the treatment regime for HCV, but required hormone replacement. Among the patients with a normal thyroid function test prior to treatment (107 cases), 5 (4.6%) developed thyroid test abnormalities; 2 patients had hypothyroidism due to autoimmune thyroiditis; 1 patient became positive for antiTPO antibodies but thyroid function remained normal, and 2 patients had subacute thyroiditis. Four of these patients (80%) were female and 1 was male (20%). A family history of thyroid disease was strongly predictive of thyroid abnormalities during antiviral treatment. In conclusion, there is a low prevalence of thyroid function abnormalities in HCV carriers with no prior antiviral treatment. Family history of thyroid disease reinforces the special attention to thyroid abnormality development before considering antiviral therapy. Subacute thyroiditis during combination therapy was observed, but its pathogenesis is still unknown. Evaluation of thyroid function during and after antiviral treatment is strongly recommended because thyroid related symptoms can be easily misinterpreted as medication side effects.

Postpartum thyroiditis is the most common endocrinologic disorder, with an incidence that varies geographically from 5% to 10%. It has important clinical sequelae including symptoms of hyperthyroidism, hypothyroidism, and depression. Long-term follow-up of women who experience postpartum thyroiditis reveals a high recurrence rate in subsequent pregnancies. Postpartum thyroiditis is an autoimmune disorder, and thyroid antibody-positive women in the first trimester have a 33% to 50% chance of developing thyroiditis in the postpartum period. Whether or not to screen for postpartum thyroiditis remains controversial.

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.

Riedel's thyroiditis is a rare condition in which the thyroid gland is replaced by fibrous tissue. Fibrosis in various distant sites is a possible concomitant event. We report a case of Riedel's thyroiditis complicated by mediastinal fibrosis, a tumefactive fibro-inflammatory lesion of the neck and primary hypothyroidism. A review of the literature in which only 8 previous cases of hypoparathyroidism secondary to Riedel's thyroiditis have been recounted concludes the report.

Postpartum thyroiditis (PPT) is a syndrome of transient thyroid dysfunction occurring in the first postpartum year. A thyrotoxic phase may be brief and unnoticed before a more long-lasting hypothyroid phase occurs. The incidence is variably reported, ranging from 1.9% to 16.7%, perhaps reflecting racial or geographical differences in the distribution of genetic or environmental risk factors such as the titre of thyroid antibodies and the dietary intake of iodine. The syndrome is an autoimmune disorder, strongly associated with the presence of thyroid microsomal antibody in serum. The thyrotoxic phase may be distinguished from Graves' disease by the finding of low, rather than high, uptake of radioactive iodine or technetium in the thyroid. Screening may be valuable in women with other autoimmune disorders such as Type 1 diabetes mellitus. Treatment should be tailored to the symptoms. Significant thyrotoxic problems should be managed with beta-blocking agents, but severe hypothyroid symptoms should be treated with the short-term replacement thyroxine. A small proportion of affected women will remain permanently hypothyroid. There is also a significant risk of recurrent disease after a subsequent pregnancy.

Two cases of acute suppurative thyroiditis occurring in a normal thyroid gland secondary to a demonstrable primary focus at a distant site are described and the role of interventional radiology in the management is discussed.

The authors present a unique case of actinomycosis occurring in a 10-year-old girl who presented with a painless, noninflammatory left neck mass of 3 weeks duration. Physical examination findings showed a firm, nontender mass within the left thyroid lobe, and a presumptive diagnosis of thyroid neoplasm was made. Inflammatory changes subsequently occurred and surgical drainage was performed revealing sulphur granules. Histological examination confirmed actinomycosis of the thyroid gland.

This article presents current knowledge about common childhood thyroid gland disorders. Included are congenital and acquired hypothyroidism, hyperthyroidism, disorders due to iodine deficiency, tumors and miscellaneous conditions. The significance of early diagnosis by screening and institution of treatment of congenital hypothyroidism is emphasized. Etiology, pathogenesis, clinical signs and symptoms, diagnosis and treatment are discussed.

We report a case of amiodarone-induced thyrotoxicosis of protracted duration, unresponsive to conventional thionamide therapy, with therapy limited by severe adverse drug reactions. Other treatment modalities included high dose corticosteroids, plasmapheresis, lithium and perchlorate. Temporary amelioration was achieved following plasmapheresis; however, this and other measures were unsuccessful in controlling the thyrotoxicosis, which deteriorated to thyroid storm. Histopathologically, a degenerative, inflammatory thyroiditis was evident. We discuss the limitations of conventional drug therapy and the lack of a sustained response to plasmapheresis. The failure of high doses steroids to alter the course of illness and to completely suppress the thyroidal inflammatory process is highlighted. A potential role for renal and hepatic impairment in the observed protracted course of amiodarone-induced thyrotoxicosis is suggested.

Inflammatory disorders of the thyroid, including autoimmune thyroiditis, are among the most common endocrine abnormalities encountered in clinical practice. The association of pain with these disorders, however, is relatively uncommon. Despite this observation, painful thyroid disorders comprise a significant component of the spectrum of thyroid disease. A rational approach to such patients, including history, physical examination, laboratory evaluation, radionuclide or ultrasonographic imaging, and fine needle aspiration biopsy, will allow the appropriate diagnosis to be made in the vast majority of cases.

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.

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.

Thyroiditis is a spectrum of diseases that includes acute, subacute and chronic thyroiditis, all of which demonstrate the histologic findings of inflammation, fibrosis or lymphocytic infiltration. Acute thyroiditis is an infectious disease characterized by the abrupt onset of anterior neck pain and swelling. Subacute thyroiditis can have a viral or autoimmune etiology and may present with or without thyroid pain. Chronic thyroiditis is one of the most common causes of asymptomatic goiter and hypothyroidism. Each type of thyroiditis has a distinct clinical presentation and laboratory profile that allows the clinician to identify the disease and provide proper management.

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.