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      Incidence and Pattern of Thyroid Dysfunction in Patients on Chronic Amiodarone Therapy: Experience at a Tertiary Care Centre in Oman

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          Abstract

          Objective:

          To determine the incidence and pattern of thyroid dysfunction (TD) in patients on chronic amiodarone therapy.

          Methods:

          A retrospective study which evaluated 59 patients who had received amiodarone therapy regularly for at least 12 months from a period of 3 years from October 2007 to October 2010. The patients were followed-up at the cardiac clinic at Sultan Qaboos University Hospital, Muscat, Oman.

          Results:

          The mean age of the cohort was 63 ± 13 years ranging from 27 to 98 years. Fifty-one percent (n = 30) of the patients were female. There were 11 (19%) cases of thyroid dysfunction (TD). Seven (12%) patients were hypothyroid, 3 (5%) had hyperthyroidism and 1 (2%) patient had sub-clinical hypothyroidism; no cases of sub-clinical hyperthyroidism were noted. Female gender and presence of anti-thyroid peroxidase antibodies were significantly associated with amiodarone-induced hypothyroidism (p = 0.001) while age, amiodarone dose and duration of therapy were not correlated with the development of TD (all p-values > 0.05).

          Conclusion:

          Amiodarone-induced thyroid dysfunction is prevalent. Hypothyroidism was more frequent and seen more in female patients and those who had positive anti-thyroid peroxidase antibodies. Initial screening and periodic monitoring of thyroid function is mandatory for all patients on amiodarone therapy.

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          Most cited references38

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          Subclinical thyroid disease: scientific review and guidelines for diagnosis and management.

          Patients with serum thyroid-stimulating hormone (TSH) levels outside the reference range and levels of free thyroxine (FT4) and triiodothyronine (T3) within the reference range are common in clinical practice. The necessity for further evaluation, possible treatment, and the urgency of treatment have not been clearly established. To define subclinical thyroid disease, review its epidemiology, recommend an appropriate evaluation, explore the risks and benefits of treatment and consequences of nontreatment, and determine whether population-based screening is warranted. MEDLINE, EMBASE, Biosis, the Agency for Healthcare Research and Quality, National Guideline Clearing House, the Cochrane Database of Systematic Reviews and Controlled Trials Register, and several National Health Services (UK) databases were searched for articles on subclinical thyroid disease published between 1995 and 2002. Articles published before 1995 were recommended by expert consultants. A total of 195 English-language or translated papers were reviewed. Editorials, individual case studies, studies enrolling fewer than 10 patients, and nonsystematic reviews were excluded. Information related to authorship, year of publication, number of subjects, study design, and results were extracted and formed the basis for an evidence report, consisting of tables and summaries of each subject area. The strength of the evidence that untreated subclinical thyroid disease is associated with clinical symptoms and adverse clinical outcomes was assessed and recommendations for clinical practice developed. Data relating the progression of subclinical to overt hypothyroidism were rated as good, but data relating treatment to prevention of progression were inadequate to determine a treatment benefit. Data relating a serum TSH level higher than 10 mIU/L to elevations in serum cholesterol were rated as fair but data relating to benefits of treatment were rated as insufficient. All other associations of symptoms and benefit of treatment were rated as insufficient or absent. Data relating a serum TSH concentration lower than 0.1 mIU/L to the presence of atrial fibrillation and progression to overt hyperthyroidism were rated as good, but no data supported treatment to prevent these outcomes. Data relating restoration of the TSH level to within the reference range with improvements in bone mineral density were rated as fair. Data addressing all other associations of subclinical hyperthyroid disease and adverse clinical outcomes or treatment benefits were rated as insufficient or absent. Subclinical hypothyroid disease in pregnancy is a special case and aggressive case finding and treatment in pregnant women can be justified. Data supporting associations of subclinical thyroid disease with symptoms or adverse clinical outcomes or benefits of treatment are few. The consequences of subclinical thyroid disease (serum TSH 0.1-0.45 mIU/L or 4.5-10.0 mIU/L) are minimal and we recommend against routine treatment of patients with TSH levels in these ranges. There is insufficient evidence to support population-based screening. Aggressive case finding is appropriate in pregnant women, women older than 60 years, and others at high risk for thyroid dysfunction.
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            Plasma inorganic iodide as a homeostatic regulator of thyroid function.

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              Adverse effects of low dose amiodarone: a meta-analysis.

              We sought to assess the odds of experiencing adverse effects with low dose amiodarone therapy compared with placebo. An estimate of the likelihood of experiencing amiodarone-related adverse effects with exposure to low daily doses of the drug is lacking in the published reports, and little information is available on adverse effect event rates in control groups not receiving the drug. Data from four published trials involving 1,465 patients were included in a meta-analysis design. The criteria for inclusion were 1) double-blind, placebo-controlled design; 2) absence of a crossover design between patient groups; 3) mean follow-up of at least 12 months; 4) maintenance amiodarone dose < or = 400 mg/day; and 5) presence of an explicit description of adverse effects. Data were pooled after testing for homogeneity of treatment effects across trials, and summary odds ratios were calculated by the Peto-modified Mantel-Haenszel method for each adverse effect. The mean amiodarone dose per day ranged from 152 to 330 mg; 738 patients were randomized to receive amiodarone and 727 placebo. Exposure to amiodarone in this dose range, for a minimal duration of 12 months, resulted in odds similar to those of placebo for hepatic and gastrointestinal adverse effects, but in significantly higher odds than those of placebo (p < 0.05) for experiencing thyroid (odds ratio [OR] 4.2, 95% confidence interval [CI] 2.0 to 8.7), neurologic (OR 2.0, 95% CI 1.1 to 3.7), skin (OR 2.5, 95% CI 1.1 to 6.2), ocular (OR 3.4, 95% CI 1.2 to 9.6) and bradycardic (OR 2.2, 95% CI 1.1 to 4.3) adverse effects. A trend toward increased odds of pulmonary toxicity was noted (OR 2.0, 95% CI 0.9 to 5.3), but this did not reach statistical significance (p = 0.07). The unadjusted total incidence of drug discontinuation was 22.9% in the amiodarone group and 15.4% in the placebo group. The odds of discontinuing the drug in the amiodarone group was approximately 1.5 times that of the placebo group (OR 1.52, 95% CI 1.2 to 1.9) (p = 0.003). Compared with placebo, there is a higher likelihood of experiencing several amiodarone-related adverse effects with exposure to low daily doses of the drug. Thus, although low dose amiodarone may be well tolerated, it is not free of adverse effects.
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                Author and article information

                Journal
                Open Cardiovasc Med J
                Open Cardiovasc Med J
                tocmj
                The Open Cardiovascular Medicine Journal
                Bentham Open
                1874-1924
                29 November 2013
                2013
                : 7
                : 122-126
                Affiliations
                [1 ]Department of Medicine, Sultan Qaboos University Hospital, Oman
                [2 ]Department of Pharmacy, Sultan Qaboos University Hospital, Oman
                [3 ]Department of Clinical Biochemistry, Sultan Qaboos University Hospital, Oman
                [4 ]Department of Pharmacology & Clinical Pharmacy, College of Medicine & Health Sciences, Sultan Qaboos University, Muscat, Oman
                [5 ]Gulf Health Research, Muscat, Oman
                Author notes
                [* ]Address correspondence to this author at the Department of Medicine, Sultan Qaboos University Hospital, PO Box: 35: post code: 123, Al-khod, Muscat, Sultanate of Oman; Tel: +968 98517982; Fax: +968 24144430; E-mail: dr.albulushi@ 123456gmail.com
                Article
                TOCMJ-7-122
                10.2174/1874192401307010122
                3866614
                5820837e-6f33-4242-b8a2-f5ee2be5086e
                © Farhan et al.; Licensee Bentham Open.

                This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                : 1 November 2013
                : 4 November 2013
                Categories
                Article

                Cardiovascular Medicine
                amiodarone,thyrotoxicosis,hyperthyroidism,oman,thyroid diseases,hypothyroidism
                Cardiovascular Medicine
                amiodarone, thyrotoxicosis, hyperthyroidism, oman, thyroid diseases, hypothyroidism

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