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Amiodarone, a medicine frequently used in the treatment of supraventricular and ventricular arrhythmias, has a similar structure with F4 thyroid hormone. The usual dose of amiodarone is 200-600 mg/day, which determines the daily release of 7-21 mg of iodine. Because there is recommended a daily iodine intake of 150-200 μg, a constant treatment with amiodarone determines a 50-100 fold increase of the iodine level in the organism. It is essential to establish the thyroid status of the patients who are about to be treated with amiodarone in the long term. Thus, there are recommended the dosage of basal serum values of TSH, fT4, T4, fT3, T3, the investigation for antithyroid antibodies and an ultrasound ecography of the thyroid gland before the initiation of amiodarone therapy. Also, it must be taken into consideration that, in the case of positive antithyroidperoxidase antibodies (ATPO), the patients are at risk for developing amiodarineinduced hypothyroidism in the first year of treatment, therefore levothyroxine treatment is recommended. [ABSTRACT FROM AUTHOR]

Introduction: Amiodarone (AMI), a class III anti-arrhythmic drug, is associated with a number of side effects, including thyroid dysfunction (both hypo- and hyperthyroidism), which is due to amiodarone's high iodine content and its direct toxic effect on the thyroid. Objective: To evaluate the incidence of Amiodarone induced thyrotoxicosis (AIT) (type, rate of occurrence) and to identify the risk factors involved in its occurrence. Material and method: We examined patients treated with amiodarone, between January 2002 and December 2011, who presented to our Department of Endocrinology Târgu Mures for thyroid dysfunctions. Results: The retrospective study included 87 patients with thyroid dysfunctions; 58 (66.7%) patients had AIT and 29 (33.3%) had Amiodarone induced hypothyroidism (AIH). In the AIT group: 35 were women (60.3%), 23 were men (39.7%); the average age was 61.60 ± 12.39 years. Risk factors identified for the AIT group were male gender (RR = OR = 3.8; Chi-squer = 5.7, p = 0.004) and pre-existing thyroid abnormalities (RR = 2.5, Chi-square = 4.1, p = 0.005). The thyroid dysfunction occurrence was heterogeneous (0.2-183 months). The patients with previous thyroid abnormalities developed earlier thyroid dysfunction compared to those with an apparently normal thyroid gland (22.25 ± 4.14 months versus 32.09 ± 7.69 months, p = 0.02, T test). Conclusion: In the context of the specific iodine geoclimatic intake and the area of origin, amiodarone - induced thyroid dysfunction spectrum is dominated by thyrotoxicosis. Screening and monitoring of thyroid function for patiens under chronic amiodarone treatment is necessary. [ABSTRACT FROM AUTHOR]

Prader-Willi syndrome (PWS) is a genetic disorder characterized by absence of the active genes on chromosome 15. Symptoms appear since intrauterine development with decreased fetal movements, low birth weight and persist after birth with hypotonia, feeding difficulties and failure to thrive in the neonatal period. From infancy until adulthood, patients have short stature, become severely obese, with an insatiable appetite and food-seeking behavior. They also have psychiatric disorders, behavioral problems and learning disabilities. Treatment of these patients is multidisciplinary and several drugs have been studied in order to control appetite and reduce the morbidity of obesity, including cardiovascular and metabolic side-effects. The following paper offers an insight in the difficult management of the co-morbidities of Prader-Willi syndrome. [ABSTRACT FROM AUTHOR]

Introduction: The relationship between rhGH treatment and thyroid function has been the subject of numerous studies. Some say that rhGH treatment unmasks central hypothyroidism, other say that rhGH induces subclinical primary hypothyroidism., Aim: To assess the changes in thyroid function in short stature children in the first year of treatment with rhGH and the impact on growth velocity., Material and Methods: We evaluated 37 patients treated with rhGH, 5 were excluded because developed side effects during treatment. We measured height, height velocity, and height standard deviation gain during treatment and thyroid function during the first year of treatment., Results: We observed a slight increase in the TSH level and no significant change in the f T4 level after the first 3-6 months of treatment in all the groups; in GH deficiency (GHD) patients, we observed a statistically significant decrease of the f T4 level after the first 3-6 months, without a significant increase of the TSH level. After the first year, thyroid function returned to baseline. There were no differences between height velocities in all the groups, except from the GHD patients., Conclusions: The slight increase in the TSH level and the decrease of f T4 level might unmask a transient subclinical primary hypothyroidism but these changes do not influence the growth velocity in first year of rhGH treatment.