A 53-year-old woman presented with a fever of 38oC in the evening for 8 days, intense asthenia and altered ESR (sedimentation erythrocyte sedimentation rate).
Before 48 hours after the onset of symptoms, he had visited a private physician, who explored it by ruling out serious pathology and requested laboratory tests.
The patient, on receiving laboratory tests 6 days after the onset of symptoms, comes to the health center due to persistent symptoms.
Blood count with formula and count within normal limits, general biochemistry, hepatic profile and coagulation were normal, and ESR (globular sedimentation rate) was 110 mm/1h.
The patient has intense symptoms of anxiety (angustia), due to fear and suspicion of having a possible occult neoplasia, since her mother recently died of breast cancer.
In the anamnesis, in addition to the previously mentioned symptoms, she complained of discomfort in the anterior area of the neck and sometimes a misdefined feeling of pressure or “return” in the precordial region.
She has no medical history of interest, and does not take drugs regularly.
The physical examination revealed: —Nerviosism and — Palm perhydrosis. —French disease: 90 beats per minute. — Thyroid distress without right coronary artery stenosis, cardiac diseased gland.
It is explained to the patient that the process presented has characteristics of correspond to an acute disease, which may be due to different processes: inflammation of the thyroid gland, viral infection: EBV (but autoimmune CMV disease).
Blood count, ESR (globular sedimentation rate), thyroid hormones: T3 L (triyodothyronine) and T4 L (thyroid thyroxine) and TSH (thyroxine) were repeated.
I.L.T. (transient work disability) begins due to the disabling symptoms the patient has.
A diagnostic approach of subacute thyroiditis is performed and as treatment initially diclofenac 50 mg every 8 hours is prescribed to control symptoms.
Establishment plan
After 10 days, the patient comes to the health center with the new complementary tests requested and others that he provides at the request of his private doctor.
The patient continues to present with MEG (general malaise), fever, nervousness, hyperhidrosis and intense asthenia, with little response to treatment (diclofenac 50 mg every 8 hours).
Physical examination showed no change compared to the previous one, except for a heart rate of 98 beats per minute.
The result of the new complementary tests performed is the following: —Although with formula and count without pathological stimulant alterations. —SGA: 120 mm/h. —ml. Normal thyroid hormone < 5260 μg.
It is explained to the patient that the disease presented may correspond to a benign inflammation of the thyroid gland of subacute type and that the evolution is toward the total remission of the condition in a period of time between 1-2 months.
Pharmacological treatment is changed by the persistence and intensity of symptoms: oral corticosteroids (prednisone 40 mg in the morning, decreasing 5 mg every 3 days) and beta-blockers every other week (8 hours).
The patient attends a week, reporting significant improvement of symptoms 48 hours after starting the new treatment.
Corticosteroid tapering continues faster and after two weeks, they are completely suppressed together with beta-blockers.
Complementary tests are repeated one month to assess response to treatment and the result is the following: complete blood count with no changes compared to previous performed, thyroid T4 L (free thyroxine): 1.2 ng/yr TSH, thyroid hormone gamma μdl
Differential diagnosis process performed: discussion
In our case, it is important to note that the diagnosis was made quickly because the patient provided initial complementary tests: complete blood count, ESR (globular sedimentation rate), biochemical, liver profile, coagulation and subsequent determination of thyroid gamma antibodies.
The differential diagnosis was made according to the following scheme: —For the symptoms (asthenia, fever, pain in the anterior face of the neck) and elevated ESR.
The diseases that were initially suspected were: acute viral disease (infectious mononucleosis, cytomegalovirus), rheumatic polymyalgia with or without vasculitis (temporal arteritis), onset of an acute connective tissue disease SLE.
Anxiety and nervousness symptoms may correspond to an anxiety disorder (cancerophobia distress disorder), or to a hyperthyroid state.
An isolated distress disorder was ruled out due to the rest of the symptoms present in the patient and subsequently due to the result of the new complementary tests requested.
—Friendly speaking: polymyalgia rheumatica with or without vasculitides (temporal arteritis), although there was no correlation with the exploratory data: age of the patient and absence of more typical signs in the abdomen.
The otorhinolaryngological examination and glanglia non-viral corresponded to an infectious mononucleosis or cytomegalovirus type viral infection, although it could not be ruled out until the results of the 2 complementary tests were obtained.
The rapid onset of symptoms and the absence of reumatism and cutaneous symptoms also ruled out connective tissue disease, even without laboratory confirmation (ANAS, ANOES).
painful thyroiditis in the anterior face of the neck and increased thyroid gland, made suspicion in pathology with hyperthyroidism (Graves-Based disease, multitoxic goiter).
—Because of the complementary tests: The laboratory data that most led to suspicion of subacute thyroiditis and rule out the rest of the possible thyroiditis (bacterial acute, silent thyroiditis, autoimmune sedimentation phase)
The absence of antithyroid antibodies ruled out processes such as thyroid abnormality, toxicosis or silent thyroiditis.
The decrease in radioactivity I uptake in thyroid scintigraphy was more compatible with subacute thyroiditis than with the rest of thyroiditis and other thyroid diseases (Graves-Based disease).
QUERVAIN ISSUED TREATMENT
Quervain's granulomatous subacute thyroiditis is an entity that encompasses a large number of synonymous terms such as Quervain's thyroiditis, subacute thyroiditis, and painful giant cell thyroiditis.
Etiology
The most common cause of Quervain's subacute thyroiditis is a viral thyroid infection secondary to upper respiratory tract infection.
It usually occurs in shoots, with prodomes of viral type and seasonal distribution, more frequent in summer and fall.
Thanks to viral cultures in the affected thyroid tissue, some of these have been related as potential pathogens of this disease: adenovirus, thighckievirus, mononucleosis and influenza virus, virus of the paper.
On the other hand, it seems that there may be greater genetic susceptibility to the disease in patients with HLA-Bw 35 and HLA-DR36.
In some cases, transient thyroid autoimmunity (almost always in the acute phase of anti-myosomal disease), and anti-thyroglobulin antibodies (peroxidase receptor) have been observed.
Although it is believed that the origin of this autoimmunity is more related to the release of antigens during inflammation than to a primary phenomenon7.
There are very few cases in the literature of Graves' disease after an episode of subacute thyroiditis8.
Histopathology
Histological examination, which is not necessary to establish the diagnosis, is obtained by needle aspiration biopsy and initially reveals destruction of glandular epithelium, with polymorphonuclear infiltrates and partial or complete loss of basal membrane.
Subsequently, follicular lesion is typically characterized by a central nucleus of colloid surrounded by multinucleated giant cells that eventually progress to granulomas.
Characteristically these histological lesions of subacute thyroiditis are reversible.
Clinical manifestations
The most common symptom in patients with Quervain's subacute thyroiditis is neck pain that can radiate to ears, occiput, jaw, and throat.
The onset of pain may be abrupt or last several weeks before suspecting the diagnosis and may include the entire gland, a lobe or part of a lobe.
Although pain is initially unilateral, usually within a few days or weeks it will extend to the contralateral side.
Initially, there is usually a viral prodromal syndrome of the upper respiratory tract that includes myalgia, fever, asthenia, foreign body sensation in the throat and dysphagia.
Depending on the degree of destruction of the glandular parenchyma, symptoms and signs of thyrotoxicosis may appear in the acute phase (50% of cases), which are usually transient and smooth, and may be followed by transient hypothyroidism9.
On other occasions the disease may manifest in a less typical way as fever of unknown origin, constitutional syndrome, simulate a chronic inflammatory disease (such as temporal arteritis) or a malignant disease secondary to edema and in very severe cases can manifest
Thyroid thickening usually reveals a hard, painful and enlarged thyroid, either diffuse, unilateral or nodular.
Generally, the overlying skin is usually erythematous.
Complementary tests
The most characteristic laboratory finding of subacute thyroiditis is transient hypersensitivity pneumonitis with an elevation of 100 mm in the first hour, which allows for the differentiation from other types of chronic silent microbial thyrotoxicosis, such as chronic thyroid
The white series is usually normal or slightly elevated and normocytic normochromic anemia is frequent11.
The concentration of thyroid hormones T3 and T4 are elevated due to inflammation and follicular inflammation, causing a discharge of these hormones and a decrease in TSH, which can be undetectable glandular destruction.
There is usually a disproportionate increase in T4 compared to T3.
Imaging tests and in this case thyroid scintigraphy is more useful than in other thyroid diseases.
In subacute thyroiditis is typical the absence of visualization of the thyroid gland after performing scintigraphy with radioactive iodine, by the destruction of tissue secondary to glandular inflammation.
In most cases, the uptake is less than 2% in the first 24 hours.
The thyroid scan shows patchy or very low uptake of contrast (although the disease is localized and TSH levels are not very low, a single affected area may be seen).
It can also provide evolutionary information of the process according to changes in the radiological pattern.
Another fact to consider is the absence in most cases of antithyroid antibodies, although there are series of studies showing their presence in 2-5%.
Differential diagnosis
The differential diagnosis should initially be made with pathologies requiring neck pain (Table I), a process that involves an elevated ESR and the rest of the thyroiditis (Table II).
The differential diagnosis of subacute thyroiditis and other diseases that can cause neck pain is made based on differences in the rest of the clinical presentation and complementary tests.
Thus, for example, the presence of acute hemorrhage within a cistern or nodule usually manifests more suddenly than subacute thyroiditis, with severe unilateral anterior cervical thyroid pain and always predates a nodule.
Imaging techniques (radioiodine scan) will provide us with a differential diagnosis, since the non-affected areas of the gland present normal function.
Acute suppurative thyroiditis is extremely rare14, and usually presents with more leukocytosis and a more striking febrile syndrome than subacute thyroiditis.
In this pathology the uptake of tracer in gammagraphy is not usually reduced, being FNA the definitive procedure for the diagnosis of thyroiditis Voxithyroxine, white globulin and thyroid subacute, to high titers.
Graves' disease is characterized by the presence of normal or elevated RAIU, so it is difficult to confuse it with other causes.
1.
In the case of thyroid carcinoma, although it may also present pain in the cervical region due to rapid growth and decreased tracer uptake, the rest of the clinic and laboratory findings make these two rare confounders.
Globus histericus is an anxious reaction characterised by a sensation of laryngeal constriction that the patient often refers to as “a lump in the throat”, related to processes of emotional stress or menstrual cycles.
It has been tried to relate this fact with a greater blood supply to the gland, without finding evidence on this fact, so the diagnosis will always be exclusion.
Thyroid amyloidosis is a disease that may present with clinical manifestations similar to granulomatous thyroiditis, significant increase in SGV, decrease in scintigraphic uptake and spectacular response to corticosteroids.
There are antiarrhythmic drugs rich in iodine, such as amiodarone, which can produce iodine-induced thyrotoxicosis (Jodbasedow's disease) and less frequently thyroiditis.
The clinical history will be key to diagnosis.
Pneumocisti carinii infection may present with neck pain and low tracer uptake, but the clinical history as in the previous case will establish the diagnosis.
Other causes of thyroiditis may be thyroiditis secondary to treatment with interferon α 2a16 and postvaccination thyroiditis of hepatitis B17.
Ev
The evolution of this process is generally towards spontaneous remission in about 4 to 6 months18, presenting in its most typical evolution four characteristic phases: —Acute phase: characterized by the presence of thyroid pain and transient thyrotoxicosis lasting approximately 6 weeks.
In 5% of cases, patients may become permanently hypothyroid. —Final recovery phase: in which functional thyroid tests normalize.
It is a disease that usually does not recur, although some authors have published in case series that recurrence may occur in 5%19.
1.
Treatment
Initial treatment consists of administering nonsteroidal anti-inflammatory drugs (acetyl salicylic acid 500-1,000 mg every 8 hours) to reduce thyroid pain and general malaise.
Occasionally, it is necessary to administer oral corticosteroids (prednisone administration 20 mg every 24 hours) when symptoms do not develop after taking NSAIDs (those not responding to steroids), resulting in clinical improvement after oral
Corticosteroid therapy should be performed on a descending pattern until withdrawal within 2-4 weeks to prevent recurrence (20% of cases).
It is important not to administer oral corticosteroids initially if the patient does not present very intense symptoms, since cases of autoimmune thyroiditis have been observed more frequently in subacute thyroiditis treated with oral corticosteroids alone.
RAIU (uptake of radioactive iodine by the thyroid) may be of great help in determining patients at risk of relapse, so in those patients in whom the uptake continues to be low, corticosteroid treatment should be prolonged.
Beta-blockers are needed when symptoms of hyperthyroidism are very severe.
Establishment plan
There is no evidence of the benefit of treatment with antithyroid drugs, since the mechanism of this disease is more related to the release of thyroid pre-hormone than to the synthesis of new T3 and T4.
There are some published cases of late hypothyroidism in those subacute thyroiditis in which antithyroid drugs were administered as the base treatment.
BACKGROUND: Carmelo Prieto Zacundo C/ Cobos de Segovia 7, portal 4, piso 5oA 28005 Madrid e-mail: cprieto@nexo.es
