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Hyperthyroidism subclinical

Hyperthyroidism can be differentiated into overt and subclinical hyperthyroidism. Overt hyperthyroidism is diagnosed when the TSH level is suppressed, with free thyroxine (T4) and/or tri-iodothyronine (T3) levels above the normal reference range, in a person with symptoms of hyperthyroidism. Subclinical hyperthyroidism is diagnosed when the TSH level is suppressed, with free T4 and T3 levels within the normal reference range. The prevalence of overt hyperthyroidism is about 20 per 1000 women and 2 per 1000 men (including previously treated cases) with the annual incidence of overt hyperthyroidism is about 1 per 1000 women and is negligible for men. The prevalence of subclinical hyperthyroidism is 2% in adults, and 3% in those older than 80 years. [Pg.759]

Discuss the prevalence of thyroid disorders, including subclinical (mild) and overt (typical signs and/or symptoms present) hypothyroidism and hyperthyroidism. [Pg.667]

Hyperthyroidism is much less common than hypothyroidism. In NHANES III,1 1.3% of the population was hyperthyroid (0.5% overt, 0.8% subclinical), with the highest incidences in women overall and in men and women in the 20 to 39 and over 80 years of age groups. The Colorado Thyroid Health Study2 showed a hyperthyroid incidence of 2.2% (2.1% subclinical). [Pg.676]

Subclinical or mild thyrotoxicosis is defined as a low TSH with a normal FT4 level. While there may be few or no symptoms in these patients, there are several areas of concern.31,32 Many patients will progress to overt thyrotoxicosis. Patients with subclinical hyperthyroidism have been shown to suffer long-term cardiovascular and bone sequelae. In a 10-year follow-up of 2007 patients over age 60,33 patients with an undetectable TSH level had a 3.1-fold increased risk of atrial fibrillation versus those with a normal TSH. In a different 10-year follow-up study34 of... [Pg.677]

The growth and spread of thyroid carcinoma is stimulated hy TSH. An important component of thyroid carcinoma management is the use ofLT4 to suppress TSH secretion. Early in therapy, patients receive the lowest LT4 dose sufficient to fully suppress TSH to undetectable levels. Controlled trials show that suppressive LT4 therapy reduces tumor growth and improves survival. These patients are purposefully overtreated with LT4 and rendered subclinically hyperthyroid. Postmenopausal women should receive aggressive osteoporosis therapy to prevent LT4-induced bone loss. Other thyrotoxic complications, such as atrial fibrillation, should be monitored and managed appropriately. [Pg.681]

In the adult population, the prevalence of overt hypothyroidism is 19 per 1000 women and 1 per 1000 men with annual incidence of overt hypothyroidism is 4 per 1000 women and 0.6 per 1000 men. Subclinical hypothyroidism is also more common in women, the incidence increases with age, with up to 10% of women older than 60 years having an increased thyroid-stimulating hormone concentration. Subclinical hypothyroidism is more common in people who have been treated for hyperthyroidism with radioactive iodine or surgery, and in those with organ-specific autoimmune diseases, such as pernicious anaemia, type 1 diabetes mellitus, or Addison s disease. [Pg.762]

Subclinical hyperthyroidism is defined as a suppressed TSH level (below the normal range) in conjunction with normal thyroid hormone levels. Cardiac toxicity (eg, atrial fibrillation), especially in older persons, is of greatest concern. The consensus of thyroid experts concluded that hyperthyroidism treatment is appropriate in those with TSH less than 0.1 mlU/L, while close monitoring of the TSH level is appropriate for those with less TSH suppression. [Pg.870]

Faber J, Galloe AM. Changes in bone mass during prolonged subclinical hyperthyroidism due to L-thyroxine treatment a meta-analysis. Eur J Endocrinol 1994 130(4) 350-6. [Pg.354]

Patients with beta-thalassemia major have an increased risk of primary hypothyroidism. In 23 patients with beta-thalassemia amiodarone was associated with a high risk of overt hypothyroidism (33 versus 3% in controls) (43). This occurred at up to 3 months after starting amiodarone. The risk of subclinical hypothyroidism was similar in the two groups. In one case overt hypothyroidism resolved spontaneously after withdrawal, but the other patients were given thyroxine. After 21-47 months of treatment three patients developed thyrotoxicosis, with remission after withdrawal. There were no cases of hyperthyroidism in the controls. The authors proposed that patients with beta-thalassemia may be more susceptible to iodine-induced hypothyroidism, related to an underlying defect in iodine in the thyroid, perhaps associated with an effect of iron overload. [Pg.576]

Thyroid function and thyroid antibodies were not modified in 20 breast cancer patients (451), and only one case of hypothyroidism with increased thyroid antibodies has been reported (SEDA-20, 337). G-CSF had no effect on thyroid function in 33 patients with cancer, even in patients with pre-existing antibodies (452). Subclinical and spontaneously reversible hyperthyroidism occurred in eight patients without thyroid antibodies and with normal thyroid function before treatment, but this was felt to be related to stressful procedures. [Pg.604]

Of 42 bipolar patients who had taken lithium for 4-156 months, three had subclinical hypothyroidism, three had subclinical hyperthyroidism, and one was overtly hyperthyroid (623). Ultrasonography showed that goiter was present in 38% and mild thyroid dysfunction was suggested in 48% because of an apparent increased conversion of free T4 to free T3. There was no correlation between the duration of lithium therapy and thyroid abnormalities. [Pg.616]

Biondi B, Palmieri FA, Klain M, et al. Subclinical hyperthyroidism clinical features and treatment options. Eur J Endocrinol. 2005 152 1-9. [Pg.472]

Of 42 bipolar patients who had taken lithium for 4—156 months, three had subclinical hypothyroidism, three had subclinical hyperthyroidism, and one was overtly hyperthyroid (256). Ultrasonography showed that goiter... [Pg.138]

Pohlenz J, Pfarr N, Kruger S et al (2006) Subclinical hyperthyroidism due to a thyrotropin receptor (TSHR) gene mutation (S505R). Acta Paediatr 95 1685-1687... [Pg.182]

In a population-based study of 68-year-old people living in Iceland and in Jutland, subclinical hypothyroidism was much more prevalent in Iceland, with sufficient to excessive iodine intake, than in an area of Jutland, with moderate iodine deficiency (Figure 47.4) (Laurberg et al., 1998). Subclinical hyperthyroidism was much more common in Jutland, as discussed above (Figure 47.4). [Pg.451]

The therapeutic dosage of iodine is in the range of 100— 200 tg/day. Side-effects of low doses are rare and minor, consisting mainly of iodine-induced acne. Contraindications for the use of iodine are all states of subclinical or overt hyperthyroidism, thyroid autoimmune diseases and the rare dermatological disease Dermatitis herpetiformis Duhring. [Pg.797]


See other pages where Hyperthyroidism subclinical is mentioned: [Pg.669]    [Pg.669]    [Pg.677]    [Pg.763]    [Pg.281]    [Pg.294]    [Pg.870]    [Pg.347]    [Pg.611]    [Pg.272]    [Pg.651]    [Pg.706]    [Pg.707]    [Pg.1833]    [Pg.3411]    [Pg.2061]    [Pg.1371]    [Pg.1374]    [Pg.1380]    [Pg.1388]    [Pg.142]    [Pg.349]    [Pg.121]    [Pg.583]    [Pg.789]    [Pg.791]    [Pg.807]    [Pg.807]    [Pg.807]    [Pg.817]    [Pg.817]   
See also in sourсe #XX -- [ Pg.706 ]




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