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De Quervain Thyroiditis

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Last Update: March 14, 2019.

Introduction

In general, thyroiditis is defined as an inflammation of the thyroid gland. There are several kinds of thyroiditis, and they can be associated with either increased, decreased, or normal thyroid function. Furthermore, they can be classified as painful or painless, depending on the etiology. Differentiating between the different kinds is dependent on the clinical setting, medical and family history, how fast the symptoms progressed, and most importantly, the presence or absence of neck pain.[1]

Typically, painful thyroiditis is caused by radiation, trauma or infection while painless thyroiditis is caused by autoimmune diseases or medications. Painful thyroiditis can be further divided into subacute granulomatous (de Quervain) thyroiditis, suppurative thyroiditis, and thyroiditis caused by radiation/trauma.

Painless thyroiditis can be subdivided into Hashimoto thyroiditis, postpartum thyroiditis, subacute lymphocytic thyroiditis, drug-induced (amiodarone, interferon-alpha, interleukin 2, lithium) thyroiditis, and Riedel (fibrosis) thyroiditis. [1]

This article will be focusing on subacute granulomatous thyroiditis, also known as subacute thyroiditis, giant cell thyroiditis, or de Quervain thyroiditis.

Etiology

De Quervain thyroiditis is the most common cause of thyroid/neck pain and typically occurs a few weeks after a viral infection. Some studies have suggested that the seasonal distribution of thyroiditis coincides with the peak incidences of coxsackievirus (groups A & B) as well as echovirus infections. Other studies have found associations with mumps, measles, influenza and other viruses. [2][3]

Epidemiology

This disease affects women almost four times as often as men and typically occurs between the ages of 40 and 50 years. It also appears to be seasonal, as most cases occur in the summer and fall. [1]

History and Physical

It is important to elicit from the patient the timing and duration of any symptoms, any sick contacts, any family or medical history pertinent to the patient's chief complaint, and any recent illness the patient has experienced. If there are family members present, they may be good sources of information to help in narrowing down a differential, especially if the patient's mental status is altered or confused.

Patients most often will present with fatigue, low-grade fever, myalgias along with neck pain (that can switch over to the opposite side before settling), and diffuse goiter. Pain can frequently radiate to the jaw, ears, or chest and can be aggravated by swallowing or turning the head. A thorough physical exam should include a full HEENT (head, eyes, ears, nose, and throat) exam to rule out any other causes of neck pain. [1]

Evaluation

Diagnosis is made by a combination of clinical context, physical findings, and laboratory testing, including the presence or absence of neck pain/ tenderness, and autoantibodies. Common tests that are ordered in the emergency department are thyroid studies (including free thyroxine (T4) and thyroid-stimulating hormone levels (TSH), erythrocyte sedimentation rate (ESR), and C-reactive protein along with other tests as needed based on patient presentation. Patients with de Quervain thyroiditis will often have elevated ESR and CRP levels, along with a mild leukocytosis. Levels of antithyroid peroxidase and antithyroglobulin antibodies are generally normal. Because patients often present with a fever, a septic workup is usually done. If tachycardia is noted, it may be helpful to get an EKG and consider a cardiac workup as well. [4]

Patients with this disease go through different phases over a period of weeks to months. Initially, they will be hyperthyroid and then transition to a brief euthyroid phase. This is followed by a hypothyroid phase before eventually returning to being euthyroid. Hyperthyroidism, in this case, is caused by the follicular cells being attacked by cytotoxic T lymphocytes which causes the release of large amounts of T4 and T3 into the circulation. Patients will remain hyperthyroid for weeks until their thyroid stores are diminished. Laboratory values during this period will likely reflect accordingly, with low TSH levels and elevated free T4.

The hyperthyroidism found in de Quervain can be differentiated from Graves disease by the lack of exophthalmos and pretibial myxedema. These are typically not found in de Quervain thyroiditis but are common in patients with Graves disease. Bedside ultrasound can also be useful as it can show increased vascularity in Graves disease. This finding is absent in de Quervain disease. [1]

In the hypothyroid phase, TSH levels are elevated, and free T4 is low. During the transition period from hyper- to hypothyroidism, low TSH and T4 levels can be found; this finding can lead to the mistaken diagnosis of central hypothyroidism.

Treatment / Management

Treatment for de Quervain thyroiditis is fairly straightforward, with anti-inflammatory treatment being the key. Salicylates or NSAIDs can be used for patients with the mild or moderate disease. For more advanced cases, corticosteroids can be started with doses ranging from 15 to 20 mg a day tapered over 4 to 6 weeks. There is usually a marked improvement of symptoms within 48 hours.

Steroids, while reducing the pain associated with de Quervain, do not necessarily prevent the thyroid dysfunction that can occur during the course of the disease. Symptoms of hyperthyroidism may need to be treated with propranolol or atenolol with close follow up. Additionally, in some cases, patients may even need a short course of levothyroxine (started and monitored by their primary care provider) during the hypothyroid phase.

Therapy with antithyroid drugs in patients with subacute granulomatous thyroiditis is not indicated because the disorder is caused by the release of preformed thyroid hormone from destroyed follicles instead of synthesis of new T3 and T4. [4]

Differential Diagnosis

The differential for de Quervain is vast and can include dental pain, pharyngitis, otitis, abscess, thyrotoxicosis or Graves disease among others and is often mistaken for an upper respiratory infection. There have been cases where patients present with a fever of unknown origin, and the workup only reveals subacute thyroiditis. [5]

Prognosis

De Quervain thyroiditis is generally self-limited with patients returning to a euthyroid state within a few months. Recurrence is uncommon but can occur in up to 2% of patients. Hypothyroidism may also become permanent in 5% of cases. [4]

Complications

Subacute thyroiditis has been known to cause thyroid storm in rare cases. If there is any concern for this, admission to the intensive care unit is strongly recommended due to the danger of decompensation. [6]

Consultations

Endocrinology consult should be considered. In moderate to severe cases, inpatient admission should be considered, depending on clinical gestalt and patient presentations.

Deterrence and Patient Education

Patients can be advised that their condition will likely last a few weeks barring any complications and to follow up with their primary care provider as soon as possible for continued monitoring of TSH levels and radioactive iodine uptake (RAIU) testing. [4]

Pearls and Other Issues

Pregnant patients will need immediate obstetric and endocrine consultation.

It is important to remember that a small number of cases can recur, and a small minority of cases can progress to thyrotoxicosis. Patient presentation, history, physical exam, and labs should help in the diagnosis of thyrotoxicosis if suspected.

Enhancing Healthcare Team Outcomes

The majority of patients with De Quervain thyroiditis will present to the primary care provider and nurse practitioner. Unfortunately, the diagnosis not always straight forward and a consult from an endocrinologist is recommended. If the patient is pregnant, then a consult from an obstetrician is recommended. Most patients can be treated with NSAIDs and recovery occurs within 2-12 weeks. Serial thyroid levels are necessary because some patients may be rendered hypothyroid. Recurrence is known to occur in about 2% of patients. The condition is benign and does not reduce life expectancy.[7][8][9]

Questions

To access free multiple choice questions on this topic, click here.

References

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Bindra A, Braunstein GD. Thyroiditis. Am Fam Physician. 2006 May 15;73(10):1769-76. [PubMed: 16734054]
2.
Martino E, Buratti L, Bartalena L, Mariotti S, Cupini C, Aghini-Lombardi F, Pinchera A. High prevalence of subacute thyroiditis during summer season in Italy. J. Endocrinol. Invest. 1987 Jun;10(3):321-3. [PubMed: 3624803]
3.
Michas G, Alevetsovitis G, Andrikou I, Tsimiklis S, Vryonis E. De Quervain thyroiditis in the course of H1N1 influenza infection. Hippokratia. 2014 Jan;18(1):86-7. [PMC free article: PMC4103053] [PubMed: 25125962]
4.
Slatosky J, Shipton B, Wahba H. Thyroiditis: differential diagnosis and management. Am Fam Physician. 2000 Feb 15;61(4):1047-52, 1054. [PubMed: 10706157]
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Karachalios GN, Amantos K, Kanakis KV, Deliousis A, Karachaliou IG, Zacharof AK. Subacute thyroiditis presenting as fever of unknown origin. Int. J. Clin. Pract. 2010 Jan;64(1):97-8. [PubMed: 17956558]
6.
Salih AM, Kakamad FH, Rawezh QS, Masrur SA, Shvan HM, Hawbash MR, Lhun TH. Subacute thyroiditis causing thyrotoxic crisis; a case report with literature review. Int J Surg Case Rep. 2017;33:112-114. [PMC free article: PMC5387892] [PubMed: 28399492]
7.
Alfadda AA, Sallam RM, Elawad GE, Aldhukair H, Alyahya MM. Subacute thyroiditis: clinical presentation and long term outcome. Int J Endocrinol. 2014;2014:794943. [PMC free article: PMC3996955] [PubMed: 24803929]
8.
Sarkar SD. Benign thyroid disease: what is the role of nuclear medicine? Semin Nucl Med. 2006 Jul;36(3):185-93. [PubMed: 16762609]
9.
Ishihara T, Mori T, Waseda N, Ikekubo K, Akamizu T, Imura H. Histological, clinical and laboratory findings of acute exacerbation of Hashimoto's thyroiditis--comparison with those of subacute granulomatous thyroiditis. Endocrinol. Jpn. 1987 Dec;34(6):831-41. [PubMed: 3450505]
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Bookshelf ID: NBK526066PMID: 30252322

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