A miodarone, an effective iodine-rich antiarrhythmic drug, frequently causes either changes in thyroid function tests or clinical thyroid dysfunction. Both amiodarone-induced THYROTOXICOSIS (AIT) and amiodarone-induced hypothyroidism (AIH) have an overall incidence of approximately 14- 18%, and AIT being most common in iodinedeficient areas, AIH in iodine-sufficient areas. Both dysfunctions may develop either in apparently normal thyroid glands or in glands with preexisting abnormalities (either nodular goiter or thyroid autoimmune disease). The most important pathogenic mechanisms of AIT include excess iodine-induced thyroid hormone synthesis (type I AIT) and amiodarone (or iodine) - related destructive thyroiditis (type II AIT), but mixed forms involving both pathogenic mechanisms are likely more frequent than previously believed. AIT is a therapeutic challenge, because rapid restoration of euthyroidism is warranted in patients with underlying cardiac disorders. Treatment of choice for type I AIT is represented by the concomitant administration of thionamides and potassium perchlorate, whereas steroids are the most useful tool for type II AIT. Mixed (or, better, undefined) forms of AIT should be treated with a combination of thionamides, potassium perchlorate and glucocorticoids. Radioiodine therapy is usually not feasible owing to low thyroidal radioiodine uptake due to iodine load, while thyroidectomy can be performed in cases resistant to medical therapy or in those patients requiring a rapid control of THYROTOXICOSIS after a short course with iopanoic acid to restore normal serum T3 levels. Thyroid ablation is usually required in type I and undefined AIT, also because this allows safe reinstitution of amiodarone treatment, if needed; follow-up without treatment is sufficient in most patients with type II AIT, who usually remain euthyroid or may develop hypothyroidism after reexposure to iodine load.

Background and objective-In THYROTOXICOSIS, changes in urine output and serum creatinine (Cr) concentration has been related to increased glomerular filtration rate (GFR). The aim of this study is to clarify the mechanism of these changes. Methods-Forty-one thyrotoxic patients, 9 male and 32 female with the age range of 16-62 years were selected and body weight, 24-h urine output, serum and urine Cr concentration, and GFR were measured in the thyrotoxic state and two months after treatment. The data was analyzed by student ‘t’ test and paired ‘t’ test. Results-The following parameters were measured and are compared in thyrotoxic and euthyroid states respectively. Body weight: 58.4±10.6 Kg and 61.6±10.4 Kg after receiving anti-thyroid therapy (p<0.001). 24-h urine output: 1430±420 ml, and 1165±450 ml (p <0.001). Serum creatinine concentration: 0.7±0.11 mg/dl, and 0.84±0.13 mg/dl (p<0.001). 24-h urine creatinine concentration: 906±225 mg/l and 1081±285 mg/l (p<0.001). The change in GFR was not statistically significant, being 90.1 ml/min before therapy and 89.5 ml/min in the euthyroid state. Conclusion-Increased urine output and decreased serum creatinine concentration in THYROTOXICOSIS is not GFR related.

BACKGROUND AND OBJECTIVE: Diagnosis of hyperthyroidism and graves disease are not difficult due to typical symptoms. Sometimes manifestations of this disease are unusual. So final clinical diagnosis is important. CASE: In this study, 10 cases with THYROTOXICOSIS along with unusual manifestations were surveyed. Of these, 6 cases were male and 4 cases were female. They were at the 17-68 age groups with the mean of 48.2. The frequency of unusual symptoms were as follows: general pruritis without skin lesion (3 cases), anorexia and vomiting (3 cases), hypokalemic paralysis (2 cases), dysphagia with recurrent pulmonary aspiration (1 case), pretibial myxedema (1 case) and means lerman scratch (1 case). This interval between the beginning of symptoms and final diagnosis was different from 10 to 120 days. The thyroid function test showed hyperthyroidism in all cases. Another underlying disorder was not detected. All symptoms of patients were removed after antithyroid drugs therapy except pretibial myxedema (1case) and exophthalmos (2 cases). There was no complication during 18 month antithyroid therapy after interruption of drug, relapse of disease was seen in 3 cases.CONCLUSION: With regard to different manifestation of THYROTOXICOSIS, this disease should be considered in differential diagnosis, especially in older age groups with gastrointestinal, cardiac, cutaneous and musculoskeletal complaints.

Background and Aim: Poorly treated or untreated maternal overt hyperthyroidism may affect pregnancy outcome. Thyroid dysfunction and hyperthyroidism is present in about 0.3% and 2-3% of pregnancies respectively. Thyroid hyperfunction and hypofunction are more prevalent and usually go unrecognized. If thyroid dysfunction remained undiagnosed and has not been treated appropriately, would result in serious adverse pregnancy outcomes and treat both mother and her fetus. The aim of this review is to mention many aspects of hyperthyroidism in pregnancy and lactation in depth. Materials and Methods: Literature review was performed using MEDLINE between years 1960 and 2010, with the terms “Hyperthyroidism and pregnancy”, “Anti-thyroid drug and pregnancy”, “Radioiodine and pregnancy”, “Hyperthyroidism and lactation”, “Anti-thyroid drug and lactation”, both separately and in conjunction with the terms “fetus”, “neonate” and “maternal”. We selected Proper study design of survey, case control and cohort studies, and clinical trials and review papers if the authors had at least four articles of their own in the list of references of review paper. The strategy used to search for articles was developed with the assistance of a research librarian. Results: Antithyroid drugs are the main therapy of maternal hyperthyroidism during the lactation. All forms of antithyroid drugs can be used in pregnancy. As there are some reports regarding teratogenicity of methimazole (MMI), Propylthiouracil (PTU) is preferred in the first trimester and should be replaced by MMI after this trimester. Radioiodine is absolutely contraindicated for treatment of hyperthyroidism in pregnancy. Subtotal thyroidectomy in second trimester is indicated if hyperthyroidism is uncontrolled. MMI is the mainstay of the treatment of postpartum hyperthyroidism, in particular during lactation.Conclusion: Management of hyperthyroidism during pregnancy requires special considerations because maternal thyroid disease could have adverse effects on the mother, fetus and neonate.

Background: Insulin resistance and abnormal glucose metabolism are the main characteristics of THYROTOXICOSIS and gestational diabetes mellitus (GDM). However, it remains unclear whether THYROTOXICOSIS increases the risk of GDM. Therefore, this research aimed to explore the causality between THYROTOXICOSIS and GDM by using a Mendelian randomization (MR) analysis. Methods: A MR analysis was conducted to explore the causal effects of THYROTOXICOSIS on GDM. Summary statistics data of THYROTOXICOSIS (3115 THYROTOXICOSIS cases and 187684 controls) and GDM (13039 cases and 197831 controls) were derived from genome-wide association study. We selected MR Egger, Weighted median, Inverse-variance weighted, Simple mode and Weighted mode to evaluate the causal effect between THYROTOXICOSIS and GDM. Results: By using a two-sample MR analysis, we found a strong causal relationship between THYROTOXICOSIS and GDM as indicated by Inverse-variance weighted (OR=1.069; beta=0.067; 95%CI=1.023-1.118; P=0.003), Weighted median (OR=1.087; beta=0.084; 95%CI=1.040-1.137; P=0.0002), Simple mode (OR=1.102; beta=0.097; 95%CI= 1.038-1.170; P=0.013) and Weighted mode (OR=1.089; beta=0.085; 95%CI=1.033-1.147; P=0.013). No significant pleiotropy, heterogeneity, genetic correlations or bi-directional causal relationship was existed in this study. Bayesian colocalization suggested that THYROTOXICOSIS colocalized with GDM on rs10830963 (PP.H4 = 1.000), where rs10830963 was located on MTNR1B gene locus. Conclusion: THYROTOXICOSIS had a causal effect on the risk of developing GDM, and the exposure of THYROTOXICOSIS increased the risk of GDM.

Introduction: None of the current available long-term therapies for THYROTOXICOSIS is ideal, and the choice for each patient must be made individually. The purpose of the present study is to compare the two choices of treatment, the radioiodine and antithyroid drug therapy. Materials and Methods: The study population were thyrotoxic patients treated in Shaheed Beheshti Hospital of Babol between April 1997 to May 2000. Diagnosis of THYROTOXICOSIS was based on the clinical features and assessment of serum TSH, T4 and T3 levels. Patients with thyroiditis and patients non compliant to regular treatment were excluded. Standard antithyroid drug therapy was started for all patients and continued until the occurence of remission, then tapered off and discontinued. Patients unresponsive to at least six months of drug therapy or patients with disease recurrence after, at least, a three month remission period, were treated with 8-15 mci, of radioiodine and continuation of antithyroid therapy until reaching a euthyroid state. All patients were followed during the treatment period and for at least one year after the beginning of remission. Results: 30 patients (20 females, 10 males) with a mean age of 46±11 years and 44 patients (22 females, 22 males) with a mean age of 37±14 were treated by radioiodine and antithyroid drugs. The disease duration in the two age groups was 14±33 and 10.5±15 months respectively (p=NS), and causes of THYROTOXICOSIS in the two groups were: Graves’ disease in 63% and 79.5%, toxic multinodular goiter in 27% and 11.5% (p<0.05), toxic nodular goiter in 10 and 9% of patients. After a mean follow-up of 19.7±21 months, 60% of patients achieved remission by radiodine and 40% became hypothyroid, whereas 45% of patients achieved remission by antithyroid drugs and 55% remained hyperthyroid for as long as 28±19 months. The duration of antithyroid drug therapy in each group was 3.3±4.8 and 13.3±8.3 months, respectively. No drug reaction or recurrence was observed during the remission period of 17.5±19 and 21±18 months. Conclusion: On a short term basis, the outcome of THYROTOXICOSIS for remission is similar either by radioiodine or antithyroid drug therapy, but development of hypothyroidism in the former and persistance of hyperthyroid state in the latter, gives radioiodine therapy priority.