Lecture_5

Laboratory tests

Leucocytosis with a left shift, increased ESR are usually present. Thyroid hormone concentrations in blood are normal, although hyperthyroxinemia has been reported.

Treatment

Patient should be treated at surgical department. Parental antibiotics should be administered according to the specific pathogen identified. If fluctuance is present, incision and drainage might be required. Bacterial thyroiditis must be treated early and aggressively, since abscess formation can occasionally dissect downward into the mediastinum. Recurrences of the disorder are very rare.

(Duration of the treatment must be nearly 1,5-2 month).

Subacute thyroiditis

It is an acute inflammatory disease of the thyroid probably caused by a virus. Subacute granulomatous thyroiditis (giant cell thyroiditis) SAT.

Etiology

SAT is most likely viral in origin .The specific agent responsible for the disorders is not known, although coxsackie virus, adenovirus and the mumps, echovirus, influenza and Epstein-Barr viruses have been implicated in the etiology.

A genetic predisposition is likely because of the association of HLA-BW 35 histocompatibility antigens.

Clinical features

The most common symptom is unilateral anterior neck pain, often associated with unilateral radiation of pain to the ear or mandible. Pain is often proceeded by a few weeks prodrome of myalgias, low-grade fever, malaise and sore throat. Dysphagia is also common. Symptoms of hyperthyroidism (such as tachycardia, weight loss, nervousness, and diaphoresis occur in up to 50% of patients as the disorder processes, pain can migrate to the contralateral side.

Physical examination discloses an exquisitely tender, very hard, nodular enlargement, which is most often unilateral. Tenderness is often so extreme that palpation is limited. Bilateral tenderness and goiter can occur as well.

Tachycardia, a widened pulse pressure, warm skin and diaphoresis are also observed when hyperthyroidism is present.

Laboratory findings.

Early in the disease we can find an increase in T4, a decrease in RAI uptake (often 0), leucocytosis and a high ESR. After a several weeks, the T4, is decreased and the RAI uptake remains low. Full recovery is the rule; rarely, patients may become hypothyroid.

Treatment

An acute phase lasts from 4-8 weeks, during which treatment is symptomatic (aspirin 600 mg q 3-4 h, prednisolone 10-20 mg orally tid; after 1 week prednisolone can be tapered by 5 mg every 2-3 days; thus glucocorticoids are usually not required for longer than several weeks. Symptoms of hyperthyroidism are effectively controlled by the use of beta-blockers).

Following the acute phase euthyroidism is restored, and the thyroid becomes depleted of stored hormone. Patients can either remain euthyroid or progress to hypothyroid phase. It rarely lasts longer than 2-3 months, and during this phase thyroid hormone replacement in the form of levothyroxine 0,10-0,15 mg/day should be given. After several months of treatment T4 can be discontinued.

Following the hypothyroid phase recovery occurs, and the normal histologic features and secretory capacity of the thyroid are restored.

Subacute lymphocytic thyroiditis (silent thyroiditis)

A subacute disorder occurring most commonly in women , often in the postpartum period, characterized by a variable, but mild degree of thyroid enlargement, absence of thyroid tenderness, and self-limited hyperthyroid phase of several weeks to several months, often followed by transient hypothyroidism but with eventual recovery to the euthyroid state.

Etiology

Recent evidence suggests on:

1)autoimmune component (because of autoantibodies observed);

2)genetic predisposition (this is a significant prevalence of HLA-DRW3 and HLA-DRW5 histocompatibility agents);

3) viral etiology (viral antibody titers are rarely elevated);

Clinical features.

Hyperthyroid symptoms are frequent and vary from mild to normal. (Postpartum thyroiditis occur 6 weeks to 3 months after delivery).

Physical examination usually discloses a mildly enlarged, diffuse, firm, nontender goiter it has been reported that up to 50 % of patients do not have goiter.

Laboratory findings

Serum total and free T4 and T3 are elevated. Biopsies reveal lymphocytic infiltration as seen in Hashimotos thyroiditis.

Thyroid autoantibodies are positive in greater than 50 % of patients.

Treatment

Hyperthyroid phase lasts from 6 weeks to 3 month. Treatment is conservative, usually requiring only B-adrenergic blockers with propranolol.

Euthyroid interval lasts for 3-6 weeks.

During hypothyroid period (it usually lasts no longer than 2-3 months thyroid hormone supplementation with T4 0,10-0,15 mg/day may be required. Following the hypothyroid phase patients usually remain clinically euthyroid.)

Chronic thyroiditis.

Hashimoto thyroiditis (chronic lymphocytic thyroiditis) HT

Etiology

HT is an organ - specific autoimmune disorder, a chronic inflammation of the thyroid with lymphocytic infiltration of the gland generally though to be caused by autoimmune factors.

It is mire prevalent (8:1) in woman than men and is most frequent between the ages of 30 and 50 . A family history of thyroid disorders is common, and incidence is increased in patients with chromosomal disorders, including Turners, Down and Klinefelters syndromes. Histologic studies reveal extensive infiltration of lymphocytes in the thyroid.

The basic defect underlying this disease suggests an abnormality in suppressor T lymphocytes that allows helper T lymphocytes to interact with specific antigens directed against the thyroid cell. A genetic predisposition is

suggested because of the frequent occurrence of the HLADR5 histocompatibility antigen in patients with HT.

Clinical features

HT is characterized by a wide spectrum of clinical features, ranging from

no symptoms and the presence of small goiter to frank myxedema.

Occasionally patients complain of a vague sensation of tightness in the area of the anterior neck or mild dysphagia. In general, however, thyroid enlargement is insidious and asymptomatic. Symptoms of hypothyroidism may or may not be present, depending on the presence or absence of biochemical

hypothyroidism.

Physical examination usually discloses a symmetrically enlarged, very firm goiter, a smooth or knobby consistency is common. Occasionally patients

present with a single thyroid nodule.

A small group of patients have a form of HT termed primary idiopathic

hypothyroidism, goiter is usually absent in this group.(atrophic form of HT).

Yet a small subset of patients(probably 2-4%) present with

hyperthyroidism and have so-called hashitoxicosis (hypertrophy from of HT).

Laboratory findings

1) early in the disease a normal T and high titers of antithyroid

(antimicrosomal) antibodies can be detected. Late in the disease, the patient develops hypothyroidism with a decreased in T and antibodies in this stage are usually no longer detectable;

2)the thyroid scan typically shows a irregular pattern of iodine uptake;

3)fine-needle biopsy of the nodule or enlarging area should be done to rule out a coexistent neoplasm.

Treatment

1)treatment of HT requires lifelong replacement with thyroid hormone to correct and prevent hypothyroidism. The average oral replacement dose with l-thyroxine is 100 to 150 mkg/day;

2)glucocorticoids have been reported to be effective in HT when true is a rapidly enlarging goiter associating with pressure symptoms;

3)symptomatic therapy