Thyrotoxicosis

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Thyrotoxicosis is a clinical syndrome that results from exposure to increased levels of circulating thy

Figure 1-13. In follicular neoplasms, cytology and frozen section examinations are of limited to no value in differentiating between follicular adenoma and adenocarcinoma. Permanent histology with the demonstration of capsular or vessel invasion is necessary to diagnose cancer. A, Photomicrograph showing invasion into but not through the capsule consistent with an atypical follicular adenoma. B, Photomicrograph revealing vascular invasion into a capsular venule. It appears as a tumor thrombus attached to the wall of the blood vessel and is consistent with follicular adenocarcinoma (hematoxylin and eosin; x40 original magnification).

Figure 1-13. In follicular neoplasms, cytology and frozen section examinations are of limited to no value in differentiating between follicular adenoma and adenocarcinoma. Permanent histology with the demonstration of capsular or vessel invasion is necessary to diagnose cancer. A, Photomicrograph showing invasion into but not through the capsule consistent with an atypical follicular adenoma. B, Photomicrograph revealing vascular invasion into a capsular venule. It appears as a tumor thrombus attached to the wall of the blood vessel and is consistent with follicular adenocarcinoma (hematoxylin and eosin; x40 original magnification).

Ivus Malignant Vascular Wall Invasion

Figure 1-14. Nuclear scanning can be helpful in a patient with a follicular neoplasm. A, A "cold" nodule has a 20% chance of being malignant, whereas a "hot" or "autonomous" thyroid nodule is rarely malignant. B, A hemithyroidectomy specimen of a follicular neoplasm. Note the smooth outer surface of the neoplasm. C, In contrast to B, the irregular appearance of a benign solitary nodule presenting as part of a multinodular architecture is demonstrated here.

Figure 1-14. Nuclear scanning can be helpful in a patient with a follicular neoplasm. A, A "cold" nodule has a 20% chance of being malignant, whereas a "hot" or "autonomous" thyroid nodule is rarely malignant. B, A hemithyroidectomy specimen of a follicular neoplasm. Note the smooth outer surface of the neoplasm. C, In contrast to B, the irregular appearance of a benign solitary nodule presenting as part of a multinodular architecture is demonstrated here.

roid hormone, which results in an exaggerated autonomic response. Major causes of thyrotoxicosis are listed in Table 1-2.

Graves' Disease

Graves' disease is an autoimmune disease of the thyroid gland that results in a diffuse goiter and overproduction of thyroid hormones (Figure 1-15). Patients sometimes develop a characteristic ophthalmopathy and dermopathy as part of the extrathyroidal autoimmune process. Graves' disease is more common in women of child-bearing age (ie, the third and fourth decades of life). The disease has a bimodal distribution with a smaller peak between 11 and 16 years of age. About 5% of patients with Graves' disease develop thyroid nodules, of which 20% are malignant.

The etiology of Graves' disease remains unclear. Possible explanations include impaired humoral mediated immunity that results in overproduction of different immunoglobulins such as the thyroid-stimulating immunoglobulins (TSIs) or antibodies that are capable of binding TSH receptors, which, in turn, stimulate the thyroid gland to grow and produce excessive amounts of T3 and T4. Antibodies against thyroperoxidase have also been isolated and result in lymphocytic infiltration of the thyroid gland. In addition, high antibody titers against Yersinia enterocolitica in Graves' disease patients suggest cross-reactivity between the bacteria and the TSH receptors. Recently, linkage analysis has confirmed two chromosomal susceptibility loci (14q31 and 20q11.2) that may explain the strong family predisposition in Graves' disease patients, but precipitating factors such as hormonal changes seen in puberty and pregnancy or psychological stress may initiate the disease in susceptible individuals.

The clinical manifestations of Graves' disease are summarized in Table 1-3. The goiter is usually symmetric and firm, and there is often a bruit. About 15% of patients, especially the elderly, pre-

Cause

Table 1-2. CAUSES OF HYPERTHYROIDISM

Relative Frequency

Characteristics

Increased thyroid hormone production (increased iodine uptake)

Graves'disease 60-85%

Plummer's disease 5-15%

TSH-secreting pituitary tumors Very rare

Functional thyroid cancer metastasis Very rare

Trophoblastic disease (choriocarcinoma Very rare or molar pregnancy)

Decreased thyroid hormone production (decreased iodine uptake often with increased release)

Thyroiditis 5-25%

Thyroiditis factitia Uncommon

Struma ovarii Very rare

Ophthalmopathy, dermopathy, increased uptake Elderly, solitary or multiple palpable nodules clinically or on scan with variable uptake Elevated alpha subunit TSH, CNS manifestations Clinically evident Elevated HCG

Pain, tenderness, low uptake

Absent goiter, low uptake, intentional from eating raw thyroid Decreased thyroid but increased ovarian uptake

CNS = central nervous system; HCG = human chorionic gonadotropin; TSH = thyroid-stimulating hormone.

sent with normal-size thyroid glands. Some patients present with apathetic thyrotoxicosis and appear to be clinically hypothyroid rather than hyperthyroid. Apathetic hyperthyroidism is more

Figure 1-15. A profile of a patient with Graves' disease. Note the classic appearance of a smooth diffuse enlarged goiter.

common in patients with Plummer's disease than in patients with Graves' disease. All patients with new-onset atrial fibrillation should have a blood test for TSH and T3.

Noninfiltrative eye signs such as lid retraction or staring gaze result from sympathetic overstimulation of the levator palpebre superioris muscle and disappear with successful treatment. Infiltrative ophthalmopathy results from mucopolysaccharide deposition and cellular infiltration of the orbit and ocular muscles. It causes acutely swollen inflamed red eyes that sometimes become ulcerated, leading to loss of visual acuity. Muscle involvement results in lid lag, squint with double vision. Infiltrative dermopathy, pretibial myxedema, is defined as plaques or confluent areas of violacious pretibial induration. Uncommonly, pretibial myxedema may arise many years after the onset or treatment of the disease (Figure 1-16).

A classic triad of tachycardia with palpitation, weight loss, and heat intolerance is usually diagnostic of Graves' disease in a patient with a diffuse goiter. The goiter is usually symmetrically enlarged, with a smooth rubbery consistency. Elevated T3 and T4 and reduced TSH levels confirm the diagnosis and establish a baseline for follow-up. High antibody titers against TSH, also called TSI, are present in about 80% of patients with Graves' disease. A radionuclide uptake scan may be unnecessary, but it is essential if one suspects subacute thyroiditis; the

Table 1-3. MANIFESTATION OF THYROTOXICOSIS 1

Symptoms

Signs

Nervousness and sweating

Palnitatinn

Tachycardia

Diffuse» noitpr

raiui icnit-H I

Skin changes

Weight loss

Rri lit

n\icnr\Qa MnninfiItrati\/o cinnc*

Dyspnea noiiiiiiimauve eye signs

\ /1 cm nl £>»/mr»lnmt> Unorl rJi r no pa

v louai oy 111pl^i i io

Infiltrative dermopathy*

Menstrual disturbance

Atrial fibrillation

raihoioyic iiaciuies osteoporosis

*Extrathyroidal manifestation specific to Graves' disease.

*Extrathyroidal manifestation specific to Graves' disease.

scan would reveal increased uptake in Graves' patients (Figure 1-17) and low uptake in the thyroid bed in patients with thyroiditis. Furthermore, Plum-mer's disease and toxic adenoma have a characteristic appearance on a radionuclide scan with increased uptake in the nodule and suppression of the rest of the thyroid gland (Figure 1-18).

Ideally, successful treatment should aim at prompt restoration and maintenance of a euthyroid state with minimal complications and reasonable cost. Surgical treatment and radioactive ablation have been superior to medical therapy in avoiding recurrence. Indicators of a favorable response to medical treatment include the following:

• A small thyroid gland

• Reduction in the goiter size with medical treatment

• Biochemical euthyroidism with normalization of TSH

• Decreased antibody titers

Medical Treatment

Medical treatment is most effective as definitive treatment in patients with small diffusely toxic goiters or T3 thyrotoxicosis. It is also used for preparation prior to treatment with surgery or radioidine and for those who refuse other modalities of therapy. The incidence of relapse correlates inversely with the duration of therapy in some but not all investigations, in which as many as 65% of the patients relapse after a year of medical therapy, and even after 4 years of treatment, around 25% relapse once the medications

Thyrotoxicosis

Figure 1-16. Graves' disease can usually be differentiated from other causes of thyrotoxicosis by the presence of extrathyroidal manifestations. A, Early pretibial myxedema. (Note the confluency of the violacious pigmented lesions often mistaken for insect bites.) B, Advanced pretibial myxedema. (Note the chronicity evident by the appearance of raised indurated plaques.) C, Acute red eye as part of Graves' ophthalmopathy. (Note the scleral injection and periorbital edema that is partly caused by the inflammation and partly by the proptosis of the eyeball.) D, Thyroid acropachy is a rare extrathy-roidal manifestation of Graves' disease that results from subperi-osteal bone formation and swelling. Reproduced with permission from Clark OH. Endocrine surgery of the thyroid and parathyroid glands. St. Louis: Mosby; 1985.

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