Diagnosis Of Subclinical Hyperthyroidism Research Articles

Аналіз впливу субклінічного гіпертиреозу на параметри кісткового метаболізму

Стан субклінічного гіпертиреозу можна розглядати як оптимальну модель для оцінки значення тиреотропного гормона (ТТГ) для кісткової тканини у клінічній практиці. Мета дослідження: здійснити порівняльний аналіз впливу субклінічного гіпертиреозу різного генезу на показники мінеральної щільності кісткової тканини (МЩКТ) і параметри кісткового обміну. Матеріали і методи. У дослідження в амбулаторних умовах було включено 112 жінок з діагнозом «субклінічний гіпертиреоз» і тривалістю менопаузи принаймні 5 років. Із числа обстежених ендогенний субклінічний гіпертиреоз спостерігався у 78 жінок (група I), екзогенний субклінічний гіпертиреоз на тлі супресивної терапії левотироксином (група II) — у 34. До контрольної групи (група III) увійшло 20 жінок без порушення функції щитоподібної залози. Результати. У дослідженні вперше проведений порівняльний аналіз стану кісткового метаболізму, показників МЩКТ, а також показників фосфору і кальцію, ліпідного спектру крові у жінок із субклінічним гіпертиреозом різної етіології. Позитивна кореляція маркерів кісткового метаболізму і вільного трийодтироніну (вТ3) як гормонів, необхідних для розвитку скелета і підтримки його гомеостазу, вказує на фізіологічний вплив паратгормона і вТ3 на кісткову тканину. Показано, що стан кісткового метаболізму і МЩКТ залежить не лише від вмісту ТТГ, але й від причин розвитку субклінічного гіпертиреозу. Висновки. У жінок постменопаузального періоду з ендогенним субклінічним гіпертиреозом спостерігається вірогідне зниження показників МЩКТ, більш виражене в кістках із кортикальною будовою. Виявлена негативна кореляційна залежність між маркерами кісткового метаболізму і ТТГ серед усіх пацієнтів, включених у дослідження.

Subclinical Hyperthyroidism: Diagnostic Criteria and Principles of Treatment

This article presents the European Thyroid Association guidelines for diagnosis and treatment of subclinical hyperthyroidism, 2015. Determination of thyroid1stimulating hormone levels can help to diagnose a variety of pathological conditions: hypertension, cardiac fibrillation, atrial fibrillation, mineral density reduction in bones, menstrual irregularities, infertility, which require specific treatment after detection of hormonal status disorders (subclinical, overt), taking into account the patient’s age.
 Diagnosis of endogenous subclinical hyperthyroidism is based solely on the results of laboratory tests, not clinical criteria. Endogenous subclinical hyperthyroidism is defined by the presence of sub-normal levels of thyroid-stimulating hormone with normal levels of free thyroxine, total triiodothyronine, and/or free triiodothyronine. There are two categories of endogenous subclinical hyperthyroidism: stage 1 – the level of thyroid-stimulating hormone is 0,1–0,39 mIU/l; stage 2 – the level of thyroid-stimulating hormone is <0.1 mIU/l. The levels of free thyroxine and free triiodothyronine, as a rule, are medium-high value at a subclinical level of thyroid hormone and can help differentiate between endogenous subclinical hyperthyroidism from overt hyperthyroidism.
 It is recommended to study the thyroid-stimulating hormone level as the first test for the diagnosis of subclinical hyperthyroidism. In identifying low levels of thyroid-stimulating hormone it is necessary to investigate the level of free thyroxine, free or bound triiodothyronine. Patients with primary sub-normal levels of thyroid-stimulating hormone with concentration of thyroid hormones in the upper limit or in normal range should be evaluated within 2-3 months.
 It is recommended to perform scintigraphy and possible 24-hour test the absorption of radioactive iodine if in patient with 2nd degree endogenous subclinical hyperthyroidism there is nodular goiter to determine treatment strategy.
 Ultrasonography with color Doppler can be informative for patients with endogenous subclinical hyperthyroidism and nodular goiter.
 Determining the level of antibodies to thyroid-stimulating hormone receptors can confirm the etiology of autoimmune-induced hyperthyroidism.

Субклинический гипертиреоз: диагностические критерии и принципы лечения (Обзор руководства европейской тиреоидной ассоциации 2015 года «Diagnosis and Treatment of endogenous subclinical hyperthyroidism»)

This article presents the European Thyroid Association guidelines for diagnosis and treatment of subclinical hyperthyroidism, 2015. Determination of thyroid-stimulating hormone levels can help to diagnose a variety of pathological conditions: disorders of sexual development, amenorrhea (primary or secondary), infertility, miscarriage, which require specific treatment after detection of hormonal status disorders (subclinical, overt), taking into account the patient’s age. Diagnosis of endogenous subclinical hyperthyroidism is based solely on the results of laboratory tests, not clinical criteria. Endogenous subclinical hyperthyroidism is defined by the presence of sub-normal levels of thyroid-stimulating hormone with normal levels of free thyroxine, total triiodothyronine, and/or free triiodothyronine. There are two categories of endogenous subclinical hyperthyroidism: Class 1 – the level of thyroid-stimulating hormone is 0.1–0.39 mIU/l; class 2 – the level of thyroid-stimulating hormone is < 0.1 mIU/l. The levels of free thyroxine and free triiodothyronine, as a rule, are medium-high value at a subclinical level of thyroid hormone and can help differentiate between endogenous subclinical hyperthyroidism from overt hyperthyroidism. Recommended to study the thyroid-stimulating hormone level as the first test for the diagnosis of subclinical hyperthyroidism. In identifying low levels of thyroid-stimulating hormone it is necessary to investigate the level of free thyroxine, free and bound triiodothyronine. Patients with primary sub-normal levels of thyroid-stimulating hormone with concentration of thyroid hormones in the upper limit or in normal range should be evaluated within 2-3 months. It is recommended to perform scintigraphy and possible 24-hour test the absorption of radioactive iodine if in patient with 2nd degree endogenous subclinical hyperthyroidism there is nodular goiter to determine treatment strategy. Ultrasonography with color Doppler can be informative in patients with endogenous subclinical hyperthyroidism and nodular goiter. Determining the level of antibodies to thyroid-stimulating hormone receptors can confirm the etiology of autoimmune-induced hyperthyroidism. Key words: thyroid, thyroid stimulating hormone, hyperthyroidism, thyrotoxicosis, subclinical hyperthyroidism, Graves’ disease, toxic multinodular goiter.

Subclinical Hyperthyroidism: Diagnostic Criteria and Principles of Treatment

This article presents the European Thyroid Association guidelines for diagnosis and treatment of subclinical hyperthyroidism, 2015. Determination of thyroid1stimulating hormone levels can help to diagnose a variety of pathological conditions: hypertension, cardiac fibrillation, atrial fibrillation, mineral density reduction in bones, menstrual irregularities, infertility, which require specific treatment after detection of hormonal status disorders (subclinical, overt), taking into account the patient’s age.
 Diagnosis of endogenous subclinical hyperthyroidism is based solely on the results of laboratory tests, not clinical criteria. Endogenous subclinical hyperthyroidism is defined by the presence of subnormal levels of thyroid-stimulating hormone with normal levels of free thyroxine, total triiodothyronine, and/or free triiodothyronine. There are two categories of endogenous subclinical hyperthyroidism: stage 1 – the level of thyroid1stimulating hormone is 0,1–0,39 mIU/l; stage 2 – the level of thyroid1stimulating hormone is <0.1 mIU/l. The levels of free thyroxine and free triiodothyronine, as a rule, are medium-high value at a subclinical level of thyroid hormone and can help differentiate between endogenous subclinical hyperthyroidism from overt hyperthyroidism.
 It is recommended to study the thyroid-stimulating hormone level as the first test for the diagnosis of subclinical hyperthyroidism. In identifying low levels of thyroid1stimulating hormone it is necessary to investigate the level of free thyroxine, free or bound triiodothyronine. Patients with primary subnormal levels of thyroid-stimulating hormone with concentration of thyroid hormones in the upper limit or in normal range should be evaluated within 2-3 months. It is recommended to perform scintigraphy and possible 24-hour test the absorption of radioactive iodine if in patient with 2nd degree endogenous subclinical hyperthyroidism there is nodular goiter to determine treatment strategy.
 Ultrasonography with color Doppler can be informative for patients with endogenous subclinical hyperthyroidism and nodular goiter. Determining the level of antibodies to thyroid-stimulating hormone receptors can confirm the etiology of autoimmune-induced hyperthyroidism.

Clinical Implications and Management of Sub Clinical Hyperthyroidism: A Review

Sub clinical hyperthyroidism (SCH) is characterized by normal free thyroid hormone concentrations along with a low or undetectable serum TSH (thyrotropin) level. The increased use of TSH as a screening measure and improved assay sensitivity is contributing to the diagnosis of sub clinical hyperthyroidism more frequently than ever in our clinical practise leading to the increased prevalence of the disease. The significance of SCH remains uncertain for most patients as some will revert to normal thyroid status over time whereas others will either remain static or progress to overt thyroid disease in the future. The detrimental effects of a persistently suppressed TSH has now been extensively studied and its effect on the cardiovascular system, the skeleton, mood disturbance, quality of life is quite significant leading to considerable morbidity and mortality. Majority of the patients are asymptomatic and lack overt features but the relevance of treatment is more focussed in elderly patients where the risk of developing cardiac arrhythmia and loss of bone mineral density is much more than young people in whom a conservative approach is usually preferred. The issue is contentious, the situation is challenging and the benefits of treatment are debatable. The consensus for who, when and how to treat is growing but still hasn’t been universally accepted. We attempt to review the recent literature available for sub clinical hyperthyroidism and suggest an analytical approach to its investigations and management.

Disfunción tiroidea en los pacientes con carcinoma de células renales avanzado en tratamiento con sunitinib: un problema multifactorial

Objective Several studies have reported the substantial prevalence of sunitinib-induced thyroid dysfunction. However, the underlying mechanism and the benefit of thyroid hormone replacement therapy remain to be determined. To evaluate the effect of sunitinib on thyroid function, we carried out a descriptive study in patients with advanced renal cell carcinoma. Patients and methods A total of 24 patients treated by sunitinib between 2006 and 2008 at Hospital Clínico San Carlos were included. The data were collected retrospectively and analyzed with SPSS 15.0. Results Treatment duration was 30 weeks (18–42) [median (IQR)]. Five patients (20.8%) developed subclinical hypothyroidism and three (12.5%) developed overt hypothyroidism. The number of weeks needed to observe an increase in thyroid-stimulating hormone (TSH) values in these patients was 15 (6–20) [median (IQR)]. TSH levels were below the normal range in five patients (20.8%) before or during the treatment period, but the diagnosis of subclinical hyperthyroidism could not be established because of concomitant factors. Fourteen patients (58.3%) showed sunitinib adverse events, but these were not related to the development of hypothyroidism (p=0.388). Conclusions Because of the high prevalence of sunitinib-induced hypothyroidism, thyroid function should be systematically monitored in patients with renal cell carcinoma treated with this drug. However, several pathophysiological and pharmacological factors may interfere with monitoring. Consequently, it might be useful to determine not only TSH and free T4 but also free T3 and, ideally, reverse T3. Evidence-based recommendations to manage hypothyroidism in oncology patients are not available at present.

Subclinical Thyroid Disease

Subclinical Thyroid Disease