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Thyroid Disease I – Hypothyroidism and Hyperthyroidism

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					Thyroid Disease I – Hypothyroidism and Hyperthyroidism Caroline Christopher March 22, 2004

Case 1:

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What is your diagnosis? With the given lab values this patient is most likely having panic attacks. The important point in this case is that the repeat TSH value was normal. A variety of non-thyroidal illnesses can cause mild abnormalities in measurements of TSH and FT4 values, so it is reasonable to repeat lab tests after 2-3 months if the suspicion of true thyroid disease is low. Also, keep in mind that the mean TSH value for the population is closer to 1.0 whereas the normal range (at MCLNO) is reported as 0.5-5.0. A value as low as 0.2-0.3 may be statistically normal, though not within 2 standard deviations of the mean. If the TSH had remained low with a normal free T4, what would you consider? Other considerations include subclinical hyperthyroidism, or T3 thyrotoxicosis. A measurement of free T3 (triiodiothyronine) is indicated. If this is high, the dx of T3 thyrotoxicosis can be made and treatment initiated for hyperthyroidism. If the FT3 value is normal, then subclinical hyperthyroidism may indicate that the pt may develop Graves’ disease or toxic nodular goiter. Be more aggressive with patients in their 20s or 60s, the two age ranges when Graves’ disease will present. Note that free T3 assays are not always accurate, so total T3 may be more useful, depending on the lab.

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What other laboratory and/or imaging studies could you do to confirm your results? Imaging modalities for studying thyroid disease include radionuclide uptake and scans, and thyroid ultrasound. The radionuclide test involves an iodine tracer which can denote activity of the gland, whereas the ultrasound can only suggest the anatomical features of the gland. In this case, a radionuclide scan and uptake would be most useful if you had a suspicion for true thyroid disease.

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How frequently would this patient need follow-up? In this case, TSH and FT4 values can be checked every 6 months for surveillance if subclinical hyperthyroidism is suspected.

Case 2. What is your differential? What further testing will help you confirm a diagnosis? Graves’ disease, toxic multinodular goiter, toxic adenoma (also, consider thyrotropin (TSH)-secreting pituitary adenomas, and resistance to thyroid hormone.) The diagnosis of Graves’ disease can be made based on clinical and biochemical features, with a low TSH and high FT4 as a confirmatory test. T3 should be measured when FT4 is normal, but clinical suspicion is high and TSH is low/suppressed. Measurements of TSH-receptor antibodies are indirect, and can reflect stimulatory or inhibitory antibodies. A high level of anti-thyroid peroxidase (anti-TPO) antibodies can be found in 75% of Graves’ patients. A thyroid radionuclide uptake and scan can be performed in patients with an unclear diagnosis or a nodular goiter. However, due to the intake of iodine in the USA, 50% of hyperthyroidism cases may have normal radionuclide uptake/scans b/c of the saturation of the gland with iodine (ref 1, page 1070). Thyroid ultrasound can also verify the anatomy of the goiter, which is useful if the patient has a nodular goiter as in this case.

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What are the treatment options for this patient? Antithyroid drugs include methimazole and propylthiouracil, which can be used in patients with severe symptoms from Graves’ as a temporary treatment or as a definitive treatment alone. For severe cases, drug therapy can be used to prepare patients for radioablative therapy or surgery. Patients with Graves’ disease can go into remission on drug therapy alone and can be given a trial period of up to 18-24 months on antithyroid drugs with close follow-up. The reason for remission is unclear – it may be the natural course of the disease, or it may the consequence of new antibody development such as TSH-receptor inhibitory antibodies or anti-TPO antibodies. In the USA, the most common treatment is radio-ablation (dose 10-12mCi), though throughout the rest of the world drug therapy is usually attempted first. There is some evidence that treatment with anti-thyroid treatment makes patients “radio-resistant” when ablative therapy is attempted after failure of drug therapy, though this is not statistically significant. For patients with toxic MNG, remission does not occur and definitive treatment must occur with radioiodine ablation, or with surgery for patients with obstructive symptoms. Again, temporary anti-thyroid drug therapy can be useful to control symptoms and prepare for surgery or ablation. In both conditions, beta-blockers have a role for controlling symptoms, and should be used after radioablative therapy to prevent symptoms from the remaining thyroxine.

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What is she at risk for without treatment of this disorder? Atrial tachyarrhythmias, congestive heart failure, and increased bone resorption are long-term complications of hyperthyroidism. Thyroid storm or thyrotoxicosis could arise as an acute complication of any etiology of hyperthyroidism.

Case 3. What are the possible etiologies of this diagnosis? Are there any clinical/physical clues which are more suggestive of any specific diagnosis? Primary hypothyroidism can be due to Hashimoto’s thyroiditis, post-partum (lymphocytic), or acquired causes such as post-operative, irradiation, hemochromatosis, drugs (lithium, interferon alpha, stavudine). Transient causes can also include de Quervain’s subacute thyroiditis, which would involve a painful thyroid gland and a preceding viral syndrome. Secondary causes of hypothyroidism include post-treatment sequlae from pituitary adenomas or hypothalamic tumours, or infiltrative/infectious processes such as hemochromatosis, tuberculosis, histoplasmosis, sarcoidosis, syphilis, fungal infections, toxoplasmosis, etc.

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In addition to TSH and FT4 what other labs will help confirm a diagnosis? Anti-microsomal antibodies or anti-thyroid peroxidase antibodies. Is there a role for imaging in this case? Radionuclide scan/uptake would be useful for patients with suspected transient subacute thyroiditis during the thyrotoxic phase. If nodules are palpated, then imaging is also indicated.

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How would you start treatment, and how often should she follow-up? Without risk factors for cardiac disease, an appropriate dose of replacement thyroxine is 1.0-2.0 micrograms/kg body weight, on average between 88-112 micrograms/day. Repeat TSH values should be done after 6 weeks, and can be followed every three months once they are normalized. Assuming this patient is without significant cardiac risk for ischemia or arrhythmias, the dose can be initiated at 75-88mcg and titrated. In older patients with cardiac risk factors or known ischemia, starting at 25mcg and slowly titrating the dose until euthyroid is reasonable.

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What is she at risk for without treatment? Hypothyroidism leads to dyslipidemia and atherosclerosis. Myxedema coma is an acute complication of hypothyroidism is the face of other extreme stress or illness.


				
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posted:11/13/2009
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