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Evaluation
Hashimoto thyroiditis is an autoimmune disorder of inadequate thyroid hormone production. The biochemical picture indicates raised thyroid-stimulating hormone (TSH) in response to low free T4. A low total T4 or free T4 level in the presence of an elevated TSH level confirms the diagnosis of primary hypothyroidism.
Integrative and functional medicine practitioners may also assess free T3 and reverse T3 levels, however, Western medicine does not use this approach.
The presence of anti-thyroid peroxidase and anti-thyroglobulin antibodies suggests Hashimoto thyroiditis. However, 10% of patients may be antibody negative.
Anemia is present in 30 to 40%.
There can be decreased glomerular filtration rate (GFR), renal plasma flow, and renal free water clearance with resultant hyponatremia.
Creatine kinase is frequently elevated.
Prolactin levels may be elevated.
Elevated total cholesterol, LDL, and triglyceride levels can occur.
A thyroid ultrasound assesses thyroid size, echotexture, and whether thyroid nodules are present, however, it is usually not necessary for diagnosing the condition in the majority.[9][10]
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Epidemiology
After age six, Hashimoto is the most common cause of hypothyroidism in the United States and in those areas of the world where iodine intake is adequate. The incidence is estimated to be 0.8 per 1000 per year in men and 3.5 per 1000 per year in women. Twin studies have shown an increased concordance of autoimmune thyroiditis in monozygotic twins as compared with dizygotic twins. Danish studies have demonstrated concordance rates of 55% in monozygotic twins, compared with only 3% in dizygotic twins.[7] This data suggests that 79% of predisposition is due to genetic factors, allotting 21% for environmental and sex hormone influences. The prevalence of thyroid disease, in general, increases with age.
The development of Hashimoto disease is thought to be of autoimmune origin, with lymphocyte infiltration and fibrosis as typical features. The current diagnosis is based on clinical symptoms correlating with laboratory results of elevated TSH with normal to low thyroxine levels. It is interesting to note, however, that there is little evidence demonstrating the role of antithyroid peroxidase (anti-TPO) antibody in the pathogenesis of autoimmune thyroid disease (AITD). Anti-TPO antibodies can fix complement and, in vitro, have been shown to bind and kill thyrocytes. However, to date, there has been no correlation noted in human studies between the severity of disease and the level of anti-TPO antibody concentration in serum. We do, however, know that positive serum anti-TPO antibody concentration is correlated with the active phase of the disease.[8] Other theories implicated immune complexes, containing thyroid directed antibodies, as culprits of thyroid destruction.
Histopathology
On pathologic examination, there is a diffuse, symmetric enlargement of the thyroid. The capsule is often intact with a prominent pyramidal lobe. When cut, the surface is similar to that of lymph nodes, with a pale brown to yellow color. Interlobular fibrosis may or may not be present. Atrophy may also occur, and in some patients, the gland may become nodular or asymmetric. However, necrosis or calcification does not occur and would suggest a different diagnosis.
The organ system manifestations of Hashimoto thyroiditis are varied due to the nature of the disease. Initially, patients may have bouts of hyperthyroid symptoms, as the initial destruction of thyroid cells may lead to the increased release of thyroid hormone into the bloodstream. Eventually, when enough destruction has been caused by the antibody response, patients exhibit symptoms of hypothyroidism. These symptoms are insidious and variable and may affect almost any organ system in the body.
The rate of hair growth slows, and hair can be dry, coarse, dull, and brittle. Diffuse or partial alopecia is not uncommon.
Decreased thyroid function can increase peripheral vascular resistance by as much as 50% to 60% and reduce cardiac output by as much as 30% to 50%. Bradycardia may result from a loss of chronotropic action of thyroid hormone directly on the sinoatrial cells. However, most patients have a few symptoms directly attributable to the cardiovascular system.
Fatigue, exertional dyspnea, and exercise intolerance are likely associated with a combination of limited pulmonary and cardiac reserve in addition to decreased muscle strength or increased muscle fatigue. Hypothyroid rats have been shown to have decreased endurance. Biochemical changes in this population have shown decreased muscle oxidation of pyruvate and palmitate, increased utilization of glycogen stores, and diminished fatty acid mobilization. Muscle weakness and myopathy are important features.
