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264 Thyroid and Parathyroid Glands
Prevention common cause of hyperthyroidism in childhood. The condition is an
The supply of adequate iodine in the diet and the elimination of goitro- autoimmune disease caused by the presence of immunoglobulin (Igs)
gens are the means used to prevent endemic goiter. Global iodisation of of the IgG class directed against components of the thyroid plasma
salt has been successfully introduced with remarkable results worldwide. membrane, possibly including the TSH receptor. These autoantibod-
Thyroiditis ies stimulate the thyroid follicles to increase iodide uptake and cyclic
adenosine monophosphate production, leading to thyroid growth and
Hashimoto’s disease inducing the production and secretion of increased thyroid hormones.
Hashimoto’s disease (chronic lymphocytic thyroiditis) is an uncom- TSH receptor antibodies are present in more than 95% of patients
mon entity in young patients. This is a common cause of diffuse with active Graves’ disease. The inciting event eliciting the antibody
enlargement of the thyroid gland, occurring frequently in female ado- response against TSH is unknown. Reports have suggested the
lescents. This condition is part of the spectrum of autoimmune thyroid possibility of bacterial infection eliciting antibodies that react with the
disorders. It is thought that CD T cells are activated against thyroid 20
4 TSH receptor.
antigens and recruit cytotoxic CD T cells, which kill thyroid cells,
8 Graves’ disease is seen in girls more than boys, with a ratio of 5:1.
to cause hypothyroidism. In this autoimmune self-destructive state of The incidence steadily increases throughout childhood, peaking in the
lymphadenoid goiter, the gland is firm and uniformly enlarged, usu- adolescent years. Thyrotoxicosis is uncommon in African children;
18
ally pebbly and granular in nature. Children are initially euthyroid and a relative incidence of a case or two per year is recorded. A study in
2
slowly progress to become hypothyroid. About 10% of children are conjunction with the British Paediatric Surveillance Unit (BPSU) that
18
hyperthyroid (hashitoxicosis). Ninety-five percent of patients with analysed data collected between September 2004 and September 2005
chronic lymphocytic thyroiditis have elevated antithyroid microsomal from the UK and Ireland reported 110 cases of acquired congenital
antibodies or antithyroid peroxidase antibodies. The plasma level of childhood thyrotoxicosis. This incidence (0.9 cases per 100,000
thyroid hormones is normal or low, and TSH levels are elevated in 70% individuals younger than 15 years of age) is lower than has previously
18
of patients. This condition may also be associated with Down syn- been reported in European studies. Data from Hong Kong report an
drome, Turner syndrome, Noonan syndrome, juvenile diabetes, treated even higher incidence of thyrotoxicosis: 6.5 cases per 100,000 per year
Hodgkin’s disease, and phenytoin therapy. 19 between 1994 and 1998. Ninety-six percent of the cases were due to
Thyroid imaging may not be necessary if clinical and laboratory autoimmune thyrotoxicosis, and the incidence increased with age for
findings are strongly suggestive of the diagnosis. both males and females. The incidence in females was significantly
An ultrasound finding is not specific, showing diffuse thyroid higher than in males in the 10–14 year age group. 21
hypoechogenicity. Congenital Graves’ disease, resulting from transplacental passage of
A radionuclide scan usually shows patchy uptake of the tracer and maternal antibodies, occurs in about 1% of babies born to women with
may mimic the findings in Graves’ disease or multinodular goiter. active Graves’ disease. The onset may be delayed until 2 to 3 weeks
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Fine needle aspiration may be needed to confirm the diagnosis. after birth. In most children, the onset of Graves’ disease develops
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Histology usually reveals the characteristic Askanazy cells. 2 over several months. The clinical manifestations of Graves’ disease
Treatment include goiter (virtually 100%), thyrotoxicosis, and exophthalmus
Thyroiditis resolves spontaneously in about one-third of adolescent (Figure 40.2). The systemic manifestations of thyrotoxicosis can be
patients, with the gland becoming normal and the antibodies disappear- classified as initial and later presentations:
ing. Exogenous thyroid hormone should be given in the hypothyroid • Early: Nervousness, emotional lability, decline in school performance.
patient, but it is not effective in reducing the size of the gland in euthy- • Late: Weight loss, sweating, palpitations, heat intolerance, staring
roid children. 18
gaze, increase in appetite, diarrhoea, and general malaise.
Subacute Thyroiditis Amenorrhea and a swelling above the ankles called pretibial
Subacute (de Quervain’s) thyroiditis is a viral inflammation of the myxoedema may sometimes be present. Above all, thyrotoxicosis must
thyroid gland. It is unusual in children. The thyroid is swollen, pain-
ful, and tender. Mild thyroitoxicosis results from injury to the thyroid
follicles, with release of thyroid hormone into circulation. Serum T
3
and T levels are elevated and TSH is decreased. Findings of reduced
4
radioactive iodine uptake due to thyroid follicle dysfunction differenti-
ate it from Graves’ disease. Histologically, granulomas and epitheliod
cells may be seen. 18
The treatment of subacute thyroiditis is symptomatic, consisting
of nonsteroidal anti-inflammatory agents or steroids. The condition
typically lasts 2 to 9 months, and complete recovery is expected.
Acute Suppurative Thyroiditis
Acute suppurative thyroiditis is a bacterial infection of the thyroid
glands. The gland is acutely inflamed, and the patient is septic. Patients
are usually euthyroid. The patient may have a preexisting multinodular
14
goiter. Staphylococci or mixed aerobic and anerobic flora are com-
mon causative agents, and a pharyngeal sinus tract may predispose the
patient to infection.
Management consists of intravenous antibiotics. Drainage of the
abscess may be needed. The thyroid gland may recover completely.
Hyperthyroidism: Graves’ Disease
Primary hyperthyroidism (thyrotoxicosis) is a disease associated
with an elevation in the circulating long-acting thyroid stimulating
(LATS) hormones. Graves’ disease, or diffuse toxic goiter, is the most Figure 40.2: Thyrotoxicosis in an 8-year-old girl.