Introduction
In contrast to subacute thyroiditis, which typically results in thyroid discomfort, the phrase 'silent' refers to the absence of thyroid tenderness. A self-limiting, subacute condition known as silent lymphocytic thyroiditis, it most frequently affects women after giving birth. Initial hyperthyroidism symptoms are followed by hypothyroidism. In most cases, a return to the euthyroid condition. A beta-blocker is used to treat the hyperthyroid phase. If hypothyroidism is chronic, thyroxine supplementation is required lifelong.
What Are the Causative Agents for Silent Lymphocytic Thyroiditis?
The disease's origin is a mystery. However, it is connected to the immune system attacking the thyroid. More often than men, women are affected by the condition.
Women who have recently given birth are susceptible to the sickness. It can also be brought on by immune system-altering drugs like Interferon, Amiodarone, and some forms of chemotherapy.
What Is the Clinical Course of Silent Lymphocytic Thyroiditis?
The clinical progression of the illness often consists of an initial hyperthyroid period, followed by repeated hypothyroid and recovery stages. About 50 percent of the patients exhibit this pattern.
On the other hand, the remaining individuals never go through the hypothyroid phase and instead enter the euthyroid or recovery phase. As a result, the disease's pattern resembles that of subacute thyroiditis almost exactly.
Each phase's duration varies greatly. On average, the hyperthyroid phase lasts three to four months, but it might last one month or twelve months. The hypothyroid phase can continue from one to eight months when it is present, with a typical duration of three months. Recovery often happens in six months, although it can take up to 21 months.
Although it has not been shown that any patients have a persistent hypothyroid phase, some have developed permanent hypothyroidism after recovering from the initial episode; nonetheless, this development is unusual. The second episode of transitory hyperthyroidism is possible, although it happens less frequently. The postpartum patient, in particular, may face increased incidence with subsequent pregnancies.
What Are the Symptoms and Signs Associated With Silent Lymphocytic Thyroiditis?
The disease normally starts to manifest within 12 to 16 weeks after giving birth. The hallmark of silent lymphocytic thyroiditis is a variable degree of painless thyroid enlargement with a hyperthyroid phase lasting several weeks, which is frequently followed by brief hypothyroidism caused by depleted thyroid hormone stores, but which typically recovers to the euthyroid state eventually (as noted for painful subacute thyroiditis). The self-limiting hyperthyroid phase may be short-lived or disregarded. When a woman develops hypothyroidism, which can sometimes be permanent, she is diagnosed with this illness frequently.
Patient symptoms include:
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Heat intolerance.
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Palpitations.
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Exhaustion.
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Nervousness.
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Irritability.
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Weight loss.
Other systemic signs and symptoms of high thyroid hormone. Sometimes the beginning or worsening of angina prompts older persons to seek medical attention. Another common issue is insomnia. Patients may occasionally have hypothyroidism symptoms. The absence of thyroidal discomfort is crucial to the diagnosis.
Clinical examination reveals the symptoms of excess thyroid hormone:
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A fine tremor of the upper extremities and tongue.
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Moist warm skin.
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Signs of elevated sympathetic tone in the eyes (stare and lid lag).
How Is Silent Lymphocytic Thyroiditis Diagnosed?
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Clinical assessment.
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TSH (thyroid-stimulating hormone), triiodothyronine (T3), and serum thyroxine (T4) levels.
It is common for silent lymphocytic thyroiditis to go undetected.
Laboratory testing of patients at the time of initial presentation supports the clinical picture of excess thyroid hormones.
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Serum values of thyroxine (T4), triiodothyronine (T3), and thyrotropin (TSH) are all much higher than they would normally be.
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Anomalies of thyroid hormone binding proteins are therefore not taken into account further because of the greatly elevated free T4 index and T3 resin absorption.
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Acute follicular cell injury is evident in the noticeably reduced radioiodine uptake by the thyroid. This is further supported by the finding that exogenous TSH delivery results in a subnormal thyroidal response.
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All patients with clinical or biochemical hyperthyroidism should undergo radioiodine uptake studies because the hyperthyroidism of silent thyroiditis represents follicular cell destruction rather than autoantibody-mediated activation of the thyroid gland in Grave's disease.
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In patients with silent thyroiditis, increasing urinary iodide excretion and blood thyroglobulin concentrations also signal follicular destruction and the release of hormone from storage.
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The erythrocyte sedimentation rate and white blood cell count are often normal, unlike subacute thyroiditis.
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Complement fixation technique evaluations of antithyroid anti-microsomal antibodies are typically negative. Among those that are positive, most turn negative a few months after healing.
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When a thyroid biopsy is conducted during the hyperthyroid phase, lymphocytic infiltration is frequently evident.
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Infiltration can mimic the histological features of chronic lymphocytic thyroiditis, including the development of lymphoid follicles, and can be localized or diffuse.
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Most individuals who had thyroid biopsies done after recovery showed almost full histologic remission.
What Are the Treatment Modalities for Silent Lymphocytic Thyroiditis?
1. Beta-blockers.
2. Replenishment of thyroid hormone can occur.
The only medication typically needed during the hyperthyroid phase of silent lymphocytic thyroiditis is a beta-blocker (such as Propranolol), as the condition only lasts a few months. Surgery, radioiodine therapy, and antithyroid medications are not advised.
In the hypothyroid period, replacement thyroid hormones could be necessary. Although some patients remain hypothyroid permanently, the majority of patients regain normal thyroid function. As a result, thyroid function should be reevaluated after 9 to 12 months of thyroxine therapy. Thyroid function should be reevaluated; Thyroxine replacement is then halted for five weeks, and thyroid stimulating hormone is again tested. After subsequent pregnancies, this issue frequently reappears.
Conclusion
Silent lymphocytic thyroiditis is also known as transient hyperthyroidism, which is defined by the sudden emergence of symptoms in a patient with a normal to slightly enlarged and hard thyroid gland and is frequently caused by silent or painless thyroiditis. The disease's distinguishing features are absent thyroidal discomfort or tenderness and a noticeably decreased radioiodine uptake. Histologically, the gland is distinguished by a significant lymphocytic infiltration, which can occasionally progress to the development of lymphoid follicles. Other signs of an autoimmune cause, however, are typically lacking. The postpartum period seems to be the disease's preferred time to spread. Relapses could happen with later pregnancies. Otherwise, the course is typically benign and brief, requiring only little symptomatic relief from adrenergic-blocking medications. Although no known pathogenetic factors exist, the illness could theoretically have an autoimmune origin, particularly in postpartum patients.
