Thyroid ablation for therapeutic purposes is a common cause of primary hypothyroidism in the adult. Thyroid failure is an obvious consequence of total or subtotal thyroidectomy for thyroid cancer, goitre, or Graves’ disease, but clinical hypothyroidism does not develop as long as substitutive therapy is started shortly after surgery. Similarly, ¹³¹I therapy for Graves’ disease is directed to destroy thy roid tissue. However, the success rate of radioiodine therapy and the time of onset of hypothyroidism are not fully predictable; they depend on several factors including the dose of radiation delivered, the size of the goitre, and the underlying autoimmune phenomena. Drug- induced hypothyroidism is also common. Excessive inhibition of thyroid hormone synthesis commonly occurs during therapy for hyperthyroidism with antithyroid agents. Furthermore, primary hypothyroidism may develop as a side effect of several drugs administered for different purposes.

Postoperative Hypothyroidism

Total thyroidectomy is performed for thyroid cancer, Graves’ disease, and large diffuse or multinodular goitres, occasionally also harbouring Hashimoto’s thyroiditis. However, hypothyroidism does not develop as long as L- thyroxine replacement therapy is started soon after thyroidectomy. In the past, patients with thyroid cancer had to discontinue thyroid hormone therapy before ¹³¹I scanning and therapy. The availability of recombinant human TSH has greatly reduced the need for thyroid hormone withdrawal before radioiodine administration.

The frequency of hypothyroidism after subtotal thyroidectomy varies depending on the mass of remaining tissue and the degree of its autonomous function. A small thyroid residue may be sufficient for maintenance of the euthyroid state in Graves’ disease. On the other hand, a large residue of a multinodular or Hashimoto’s goitre may not be enough for adequate thyroid hormone secretion. Partial thyroidectomy or lobectomy for multinodular goitres or solitary nodules are usually not associated with permanent hypothyroidism, although L- thyroxine is usually administered to prevent relapse of the goitre.

Post- Irradiation Hypothyroidism

 Among different radioactive isotopes of iodine, ¹³¹I is the agent of choice in the treatment of thyroid hyperfunction. After oral administration, radioiodine is completely absorbed, rapidly concentrated, oxidized, and organified by thyroid follicular cells. The biological effects of radioiodine include necrosis of follicular cells, shorter survival and impaired replication of undestroyed cells, and vascular occlusion, leading to atrophy and fibrosis of thyroidal tissue.

The goal of radioiodine therapy for hyperthyroidism is to destroy sufficient thyroid tissue to cure the hyperthyroidism with one dose of ¹³¹I. This dose is calculated on the basis of thyroid size and up take of 1³¹I. Because of radiation safety restrictions, in some centres small repeated doses of radioiodine are administered. In other centres standard fixed doses are given. Small glands are destroyed more readily by radioiodine than larger ones, and toxic adenoma or toxic multinodular goitre are usually more radioresistant than Graves’ glands. Radioiodine has a delayed effect and several months may be required for the complete control of hyperthyroidism.

In the case of Graves’ disease, the goal of radioiodine should be to destroy as much thyroid tissue as possible. This strategy has been adopted because residual tissue, necessary to ensure euthyroidism, is responsible for the relapse of hyperthyroidism in a large proportion of patients. A strict control of thyroid function is required during the first 6– 12 months following ¹³¹I therapy for Graves’ disease to avoid the appearance of symptoms of hypothyroidism, which may be rapidly progressive and severe. Early post- radioiodine hypothyroidism may be transient, and hyperthyroidism may relapse during L- thyroxine replacement therapy.

Radioiodine- induced hypothyroidism is less frequent after treatment for toxic adenoma or multinodular goitre because non- functioning thyroid tissue should not receive the radioisotope. Yet, hypothyroidism may develop whenever TSH is not completely sup pressed at the time 131I is administered. Furthermore, a small degree of iodine uptake is maintained in normal thyroid cells even in the absence of TSH stimulation, and this may be the cause of hypothyroidism many years after radioiodine administration.

External irradiation to the neck for non- thyroidal neoplasias (lymphomas, tumours of the head and neck, spinal tumours, or metastases) may produce hypothyroidism in up to 50% of patients. T hyroid failure may develop after a variable interval, depending on the dose of radiation that has been administered. Hypothyroidism after total body irradiation for acute leukaemia or aplastic anaemia has also been reported. An increased risk of hypothyroidism has been found in breast cancer patients treated with radiation, since a portion of the thyroid gland may be included in the treatment fields.

Drug- Induced Hypothyroidism

Transient hypothyroidism is common in the course of medical treatment for hyperthyroidism with thionamides, and quickly sub sides with adjustment of the dose. Excess iodide, such as in dis infectants, radiographic contrast agents, and seaweed- containing preparations, may precipitate hypothyroidism in autoimmune chronic thyroiditis, due to failure of the thyroid to escape from the Wolff– Chaikoff effect. Animal studies suggest that excessive iodide increases the incidence of thyroid autoimmunity but evidence in humans is controversial. Amiodarone is an antiarrhythmic agent containing about 37 mg iodine per 100 mg drug. Amiodarone may produce hypothyroidism by the excess iodine released with metabolism of the drug. As in other cases of excess iodine administration, an underlying autoimmune thyroid disease is a prerequisite. Amiodarone may also induce destructive thyroiditis in another wise normal thyroid gland. The prevalence of overt hypothyroidism may be as high as 5% of amiodarone- treated patients, with no clear association between the occurrence of hypothyroidism and the dose of the drug. Substitutive L- T4 can be administered with no need to discontinue amiodarone, if the antiarrhythmic drug is essential for the underlying cardiac disease. Mild (subclinical) hypothyroidism is more common and does not necessarily progress to overt hypothyroidism. Treatment of mild hypothyroidism may be avoided in patients at high risk of cardiovascular events.

Lithium inhibits thyroid hormone synthesis and secretion, and lithium therapy for psychiatric disorders is associated with an increased risk of hypothyroidism, with a hazard ratio of 2.31. The risk is increased in patients with positive antithyroid antibodies or with minor thyroid abnormalities, which reduce the ability of the thy roid gland to override the inhibitory effects of lithium. Goitre is also common in lithium- treated patients, even when serum thyroid hormones and TSH are within normal limits. If hypothyroidism appears, LT4 therapy should be initiated and lithium therapy may be continued.

Tyrosine kinase inhibitors are newly developed drugs approved for the treatment of several tumours. The first observation of hypothyroidism after sunitinib treatment has been reported in 2006. Since then several studies have been published and have confirmed that various tyrosine kinase inhibitors can affect thyroid function tests through different physiopathological mechanisms impairing thyroid function or thyroid hormone metabolism.

Targeted manipulation of immune checkpoints by monoclonal antibodies against molecules that are critical for immune regulation, has been recently introduced as an effective anticancer therapy for its ability to enhance the immune responses against malignant cells. Triggering of autoimmunity due to disruption of immunological tolerance to self- antigens may induce immune- related adverse events, with primary hypothyroidism scoring among the most frequent, usually associated with appearance of thyroid autoantibodies.

Several other drugs have been reported to be capable of inducing primary hypothyroidism. Treatment with interferon- α  or interleukin- 2 may produce hypothyroidism, thyrotoxicosis, or the biphasic pattern of silent thyroiditis. Pre- existent thyroid auto immunity increases the risk of thyroid dysfunction during treatment with these agents. Other medications occasionally reported to induce hypothyroidism include tricyclic antidepressants, selective serotonin reuptake inhibitors, rifampin, sulphonamides, sulphonylureas, ethionamide, p- aminosalicylic acid, phenylbuta zone, and nicardipine, but the antithyroid potential of these drugs is weak and an underlying thyroid abnormality or concurrent iodine deficiency are usually associated.

اخر الاخبار

اخبار العتبة العباسية المقدسة

سماحة السيد الصافي: عهد الإمام علي (عليه السلام) لمالك الأشتر ضرورة لكل قيادي وإداري في المجتمعات

قسم المعارف: كتاب (الكواكب السماوية) يقدم مادة علمية تخدم الباحثين في مجالات الأدب والعقيدة والبلاغة

قسم الصيانة يجري أعمال الإدامة الدورية لجدران حرم مرقد أبي الفضل العباس (عليه السلام) وصحنه الشريف

قسم الشؤون الفكرية يعلن انضمام الجامعة العراقية لمشروع حفظ النتاج العلمي العراقي

المزيد

الآخبار الصحية

السجائر الإلكترونية والإقلاع عن التدخين.. نتائج متباينة تثير الجدل العلمي

مصر تحقق إنجازاً دولياً جديداً في منظمة الصحة العالمية

دراسة: السباحة فعّالة أكثر من الجري في الحفاظ على صحة القلب

عامل خطر في بداية الحمل يؤخر تطور الكلام والمهارات الحركية لدى الرضع

المزيد

الآخبار التكنلوجية

أحلامك ليست عشوائية.. إليك ما يفعله دماغك أثناء نومك

روسيا.. العلماء يضاعفون الاستقرار الحراري للألواح الشمسية ثلاث مرات

علماء يكشفون سر سرعة الدلافين في السباحة

سلمي أو دموي.. هكذا تنتقل السلطة في مجتمع الجرذان

المزيد

مواضيع ذات صلة

Severe Iodine Deficiency and natural Goitrogens

Pathobiology of Sickle Cell Disease: The Basis of Phenotypic Diversity

The Unique Systems Biology of Sickle Cell Anemia

Abnormalities of Sickle Red Blood Cells

Abnormal Molecular Behaviors of Sickle Hemoglobin

Clinical Assessment and Systemic Manifestations of Hypothyroidism: Diagnostic Accuracy

Clinical Aspects of Hypothyroidism due to Different Aetiologies

Clinical Aspects of Hypothyroidism at Different Ages

Thalassemic Structural Variants

Chronic Care of the Adult Patient With Thalassemia : Novel Therapeutic Approaches

Chronic Care of the Adult Patient With Thalassemia : Hematopoietic Stem Cell Transplantation

Survival in Patients With Thalassemia Major