eMedicine Specialties > Endocrinology > Thyroid

De Quervain Thyroiditis

Author: Ildiko Lingvay, MD, MPH, Assistant Professor, Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Texas Southwestern Medical Center at Dallas
Coauthor(s): Daniel Matei Brailita, MD, Chief of Infectious Diseases, Mary Lanning Memorial Hospital; Joseph E Loewenstein, MD, Retired; James Burks, MD, FACP, FACE, Professor of Medicine, Program Director, Department of Medicine, Texas Tech University Health Sciences Center; KoKo Aung, MD, MPH, FACP, Associate Professor, Department of Medicine, University of Texas Health Science Center; Adjunct Assistant Professor of Public Health, University of Texas School of Public Health
Contributor Information and Disclosures

Updated: Dec 16, 2008

Introduction

Background

De Quervain thyroiditis was first reported in 1825, but de Quervain recorded its pathological description in 1904.

De Quervain (subacute granulomatous) thyroiditis is the most common cause of a painful thyroid gland. It is a transient inflammation of the thyroid, the clinical course of which is highly variable. Most patients have pain in the region of the thyroid, which is usually diffusely tender, and some have systemic symptoms. Hyperthyroidism often occurs initially, sometimes followed by transient hypothyroidism. Complete recovery in weeks to months is characteristic.

Some authors use the term subacute thyroiditis for this disease. However, subacute thyroiditis is a generic term that may be used for all types of thyroiditis with a subacute course, including subacute granulomatous thyroiditis (de Quervain disease), subacute lymphocytic (painless) thyroiditis, and some forms of postpartum thyroiditis and drug-induced thyroiditis.

Pathophysiology

A viral infection or a postviral inflammatory response is presumed to cause de Quervain thyroiditis. Serial studies of viral antibody titers have implicated many viruses (including coxsackievirus, Ebstein-Barr, mumps, measles, adenovirus, echovirus, and influenza), but the changes could be attributed equally to nonspecific anamnestic responses. Viral inclusion bodies are not observed in thyroid tissue.

A strong association exists with human leukocyte antigen (HLA)-B35 in most ethnic groups. A proposed mechanism is that the disease results from a viral infection that provides an antigen, either viral or resulting from virus-induced host tissue damage, that uniquely binds to HLA-B35 molecules on macrophages. The antigen–HLA-B35 complex activates cytotoxic T lymphocytes that damage thyroid follicular cells because they have some structural similarity with the infection-related antigen. The transient presence of autoantibodies (eg, inhibitory immunoglobulins that bind to thyrotropin [TSH], antibodies that block thyroid stimulation, thyroid antimicrosomal antibodies, thyroglobulin [TGB] antibodies) has been noted in the acute phase of the disease, but their presence is attributed to a virally induced autoimmune response and is not implicated in the pathological process. In contrast with autoimmune thyroid disease, the immune response is not self-perpetuating; therefore, the process is limited.

Destruction of follicular epithelium and loss of follicular integrity are the primary events in the pathophysiology of de Quervain thyroiditis. TGB, thyroid hormones, and other iodinated compounds are released into the blood, often in quantities sufficient to elevate the serum thyroxine (T4) and triiodothyronine (T3) concentrations and suppress TSH secretion. This state lasts until the stores of TGB are exhausted or until healing occurs. New hormone synthesis temporarily ceases because of the low TSH. As inflammation subsides, the thyroid follicles regenerate and thyroid hormone synthesis and secretion resume. In some patients, several months are required for thyroid hormone synthesis to return to a normal rate; during that period, clinical hypothyroidism may be evident.

Frequency

United States

De Quervain thyroiditis occurs in less than 5% of all patients with thyroid pathology. It tends to have seasonal and geographical distribution and is most common during the summer and fall. It tends to follow viral epidemics.

A systematic review of all cases diagnosed between 1960 and 1997 in Olmsted County, Minnesota revealed an age- and sex-adjusted incidence of 4.9 cases per 1000,000 per year.1

International

International frequency is approximately the same as US frequency.

Mortality/Morbidity

De Quervain thyroiditis is a benign self-limited disease. Morbidity is caused during the initial phase by pain, which usually prompts the patient to consult a physician. Mild and transient hyperthyroidism occurs, and, in as many as 50% of patients, hypothyroidism may occur later. Recurrence of thyroiditis up to 21 years following the initial episode has been reported.

Sex

As is the case for most thyroid diseases, de Quervain thyroiditis appears more frequently in females, with a female-to-male ratio of 3-5:1.

Age

De Quervain thyroiditis has a peak incidence in the fourth and fifth decades of life. It is rare in the first decade and relatively infrequent in people older than 50 years, although it has been reported in extreme age groups.2 Occurrence during pregnancy has been reported as well.3

Clinical

History

Some patients experience a flulike prodromal episode 1-3 weeks prior to the onset of clinical disease. The natural course of the disease can be divided into the following 4 phases that usually unfold over a period of 3-6 months:

  1. The acute phase, lasting 3-6 weeks, presents primarily with pain. Symptoms of hyperthyroidism also may be present.
  2. The transient asymptomatic and euthyroid phase lasts 1-3 weeks.
  3. The hypothyroid phase lasts from weeks to months, and it may become permanent in 5-15% of patients.
  4. The recovery phase is characterized by normalization of thyroid structure and function.

Characteristic Course of de Quervain Thyroiditis

Open table in new window

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Table
ParametersStage 1Stage 2Stage 3Stage 4
SymptomsHyperthyroidEuthyroidHypothyroidEuthyroid (recovery)
T4, T3ElevatedNormalDecreasedNormal
TSHDecreasedNormalElevatedNormal
ParametersStage 1Stage 2Stage 3Stage 4
SymptomsHyperthyroidEuthyroidHypothyroidEuthyroid (recovery)
T4, T3ElevatedNormalDecreasedNormal
TSHDecreasedNormalElevatedNormal

The diagnosis is made based on clinical findings. Prodromal flulike symptoms or known infectious disease, such as pharyngitis, measles, mumps, Q fever, or typhoid fever, may occur. In young patients, de Quervain thyroiditis may develop following an episode of Henoch-Schönlein purpura. However, a history of prodromal symptoms often cannot be obtained.

  • Local symptoms
    • Pain over the thyroid area that is gradual or of sudden onset; that usually involves both lobes (in 30% of cases, it starts on one side and then migrates contralaterally within a few days); that radiates to the neck, ear, jaw, throat, or occiput; and is aggravated by swallowing and head movement; pain is the presenting symptom in over 90% of cases
    • Dysphagia
    • Hoarseness (uncommon)
  • Constitutional symptoms (often absent)
    • Fever
    • Malaise
    • Anorexia
    • Fatigue
    • Muscle aches
  • Symptoms of hyperthyroidism (palpitations, tremulousness, heat intolerance, sweating, nervousness) occurring in the initial phase of the disease
    • Hyperthyroidism that usually is mild and rarely is severe
    • Transient symptoms, usually lasting 3-6 weeks
  • Symptoms of hypothyroidism, occurring in the late phase of the disease in as many as half the cases
    • Mostly mild or moderate
    • Transient hypothyroidism in 90-95% of cases
    • Hypothyroidism lasts weeks to months
  • Atypical presentations (extremely rare, documented as case reports)
    • Thyroid storm4
    • Fever of unknown origin
    • Painless subacute granulomatous thyroiditis
    • Occult de Quervain disease mimicking giant cell arteritis
    • Prominent prostration and confusion lasting several weeks
    • Solitary painless nodule

Physical

  • Thyroid tenderness is usually symmetrical, but, occasionally, it starts in one lobe and then involves the contralateral lobe. Often, the pain is so severe that the patient cannot tolerate palpation of the neck.
  • Thyroid enlargement is usually symmetric and mild, occasionally with areas of localized firmness.
  • Erythema and hyperesthesia of the overlying skin may be present at the onset of severe cases.
  • Cervical lymphadenopathy is uncommon.
  • Hyperthyroidism
    • Hyperthyroidism is present in approximately half the patients.
    • Signs of hyperthyroidism consist of tremor, tachycardia, warm skin, and a rapid relaxation phase of tendon reflexes
    • Lid retraction is rare; exophthalmos does not occur.

Causes

See Pathophysiology.

A viral infection or a postviral inflammatory response in genetically predisposed individuals is presumed to cause de Quervain thyroiditis. Serial studies of viral antibody titers have implicated many viruses (including coxsackievirus, Ebstein-Barr, mumps, measles, adenovirus, echovirus, and influenza), but the changes could be attributed equally to nonspecific anamnestic responses. Recent studies failed to demonstrate significant changes in serum antiviral antibody titers, or to detect viral DNA in the thyroid specimens.

More on De Quervain Thyroiditis

Overview: De Quervain Thyroiditis
Differential Diagnoses & Workup: De Quervain Thyroiditis
Treatment & Medication: De Quervain Thyroiditis
Follow-up: De Quervain Thyroiditis
References
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Further Reading

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Keywords

subacute nonsuppurative thyroiditis, subacute granulomatous thyroiditis, subacute thyroiditis, giant cell thyroiditis, subacute painful thyroiditis

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Contributor Information and Disclosures

Author

Ildiko Lingvay, MD, MPH, Assistant Professor, Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Texas Southwestern Medical Center at Dallas
Ildiko Lingvay, MD, MPH is a member of the following medical societies: Endocrine Society and Texas Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Daniel Matei Brailita, MD, Chief of Infectious Diseases, Mary Lanning Memorial Hospital
Daniel Matei Brailita, MD is a member of the following medical societies: HIV Medicine Association of America and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Joseph E Loewenstein, MD, Retired
Joseph E Loewenstein, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Diabetes Association, Endocrine Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

James Burks, MD, FACP, FACE, Professor of Medicine, Program Director, Department of Medicine, Texas Tech University Health Sciences Center
James Burks, MD, FACP, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, American Diabetes Association, and Endocrine Society
Disclosure: Nothing to disclose.

KoKo Aung, MD, MPH, FACP, Associate Professor, Department of Medicine, University of Texas Health Science Center; Adjunct Assistant Professor of Public Health, University of Texas School of Public Health
KoKo Aung, MD, MPH, FACP is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Medical Editor

Amir E Harari, MD, Staff Physician, Endocrinology Division, Instructor, Department of Clinical Medicine, Naval Medical Center at San Diego
Amir E Harari, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Clinical Endocrinologists, American College of Physicians, and Endocrine Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Don S Schalch, MD, Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics
Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

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