hyperthyroidism :::: The clinical manifestations of hyperthyroidism are largely independent of its cause (see Disorders that cause hyperthyroidism). However, the disorder that causes hyperthyroidism may have other effects. In particular, Graves disease, the most common cause of hyperthyroidism, causes unique problems that are not related to the high serum thyroid hormone concentrations. These include Graves ophthalmopathy and infiltrative dermopathy (localized or pretibial myxedema). Most patients with Graves hyperthyroidism have a diffuse goiter, but so do patients with other, less common causes of hyperthyroidism such as painless thyroiditis and thyrotropin (TSH)-secreting pituitary tumors. The major clinical manifestations of hyperthyroidism (thyrotoxicosis) will be briefly reviewed here. More detailed discussions of its effects on specific organ systems as well as the diagnostic approach to patients with hyperthyroidism are discussed separately. (See Diagnosis of hyperthyroidism.) SKIN — The skin is warm (and may rarely be erythematous) in hyperthyroidism due to increased blood flow; it is also smooth because of a decrease in the keratin layer [1]. Other changes include: ●Sweating, which increases due to increased calorigenesis; this is often associated with heat intolerance ●Onycholysis (loosening of the nails from the nail bed, Plummers nails) and softening of the nails ●Hyperpigmentation, which can occur in severe cases; it appears to be mediated by accelerated cortisol metabolism, leading to increased corticotropin (ACTH) secretion [2] ●Pruritus and hives, which are occasional findings, primarily in patients with Graves hyperthyroidism [3] ●Vitiligo and alopecia areata, which can occur in association with autoimmune disorders ●Thinning of the hair Infiltrative dermopathy occurs only in patients with Graves hyperthyroidism. The most common site is the skin overlying the shins, where it presents as raised, hyperpigmented, violaceous, orange-peel-textured papules. (See Pretibial myxedema (thyroid dermopathy) in autoimmune thyroid disease.) EYES — Stare and lid lag occur in all patients with hyperthyroidism. They are due to sympathetic overactivity, possibly mediated by increased alpha-adrenergic receptors in some tissues [4]. Lid lag is evaluated by having the patient follow the examiners finger as it is moved up and down. The patient has lid lag if sclera can be seen above the iris as the patient looks downward. As noted above, only patients with Graves disease have ophthalmopathy. It is characterized by inflammation of the extraocular muscles and orbital fat and connective tissue, which results in proptosis (exophthalmos), impairment of eye-muscle function, and periorbital and conjunctival edema. Ophthalmopathy is more common in patients who smoke cigarettes. (See Pathogenesis and clinical features of Graves ophthalmopathy (orbitopathy).) Patients with ophthalmopathy may have gritty feeling or pain in their eyes, and may have diplopia due to extraocular muscle dysfunction. Corneal ulceration can occur as a result of proptosis and lid retraction, and severe proptosis can cause optic neuropathy and even blindness. CARDIOVASCULAR — Patients with hyperthyroidism have an increase in cardiac output, due both to increased peripheral oxygen needs and increased cardiac contractility. Heart rate is increased, pulse pressure is widened, and peripheral vascular resistance is decreased [5]. Systolic hypertension is common [6]. The left ventricular ejection fraction does not increase appropriately during exercise, suggesting the presence of a true cardiomyopathy [7]. High- or normal-output congestive heart failure can occur in patients with severe hyperthyroidism and congestive heart failure worsens in patients who already have it. (See Cardiovascular effects of hyperthyroidism.) Atrial fibrillation occurs in 10 to 20 percent of patients with hyperthyroidism, and is more common in elderly patients. In one study, 8 percent of all patients and 15 percent of patients between ages 70 to 79 developed atrial fibrillation within 30 days of the diagnosis of hyperthyroidism [8]. Even subclinical hyperthyroidism is associated with an increased rate of atrial ectopy and a threefold increased risk of atrial fibrillation (figure 1) [9]. In 60 percent of hyperthyroid patients with atrial fibrillation, the rhythm converts spontaneously to sinus rhythm when the hyperthyroidism is treated; in one study, all who spontaneously converted did so within four months after becoming euthyroid [10]. Among those who do not convert spontaneously to sinus rhythm and who undergo successful electrical cardioversion, the two-year risk of recurrent atrial fibrillation was 59 percent compared with 83 percent of patients whose atrial fibrillation was not associated with hyperthyroidism [11]. The role of anticoagulation is controversial in hyperthyroid patients with atrial fibrillation. In several studies, 10 to 40 percent of patients with hyperthyroidism and atrial fibrillation had an arterial embolus [12]. Left atrial enlargement, which is a risk factor for thrombus formation, is present in about 90 percent of hyperthyroid patients with atrial fibrillation and two percent of hyperthyroid patients with sinus rhythm. Based on these results, we usually anticoagulate hyperthyroid patients with atrial fibrillation. This recommendation is in agreement with guidelines published in 2006 by the American College of Cardiology/American Heart Association/European Society of Cardiology [13]. Other abnormalities, including mitral valve prolapse, mitral regurgitation, and an increase in left ventricular mass index have also been reported. (See Cardiovascular effects of hyperthyroidism.) METABOLIC / ENDOCRINE Serum lipids — Patients with hyperthyroidism tend to have low serum total and high-density lipoprotein (HDL) cholesterol concentrations and a low total cholesterol/HDL cholesterol ratio. These values increase after treatment [14]. Hyperglycemia — Although thyroxine is not a counterregulatory hormone, hyperthyroidism can interfere with glucose metabolism. It is associated with both increased sensitivity of pancreatic beta cells to glucose, resulting in increased insulin secretion, and antagonism to the peripheral action of insulin [15]. The latter effect usually predominates, leading to impaired glucose tolerance in untreated patients [16]. Adrenal function — Interpretation of the cortisol response to ACTH stimulation testing may be misleading in patients with hyperthyroidism because cortisol binding globulin (CBG) levels decrease, resulting in lower total serum cortisol concentrations. In one report of 49 hyperthyroid patients undergoing ACTH testing, 35 percent had subnormal total serum cortisol values (
Posted on: Mon, 17 Nov 2014 01:50:03 +0000