Amiodarone (AM), a potent class III anti-arrhythmic drug, is an iodine-rich compound with a structural resemblance to thyroid hormones triiodothyronine (T3) and thyroxine (T4). At the commonly employed doses, AM causes iodine overload up to 50-100 times the optimal daily intake, which may be responsible of a spectrum of effects on thyroid function often counterbalancing its heart benefits. Although most patients on chronic AM treatment remain euthyroid, a consistent proportion may develop thyrotoxicosis (AM-induced thyrotoxicosis, AIT) or hypothyroidism. AIT is more prevalent in iodine-deficient areas and is currently subdivided in two different clinico-pathological forms (AIT I and AIT II). AIT I develops in subjects with underlying thyroid disease, and is caused by an exacerbation by iodine load of thyroid autonomous function; AIT II occurs in patients with no underlying thyroid disease and is probably consequent to a drug-induced destructive thyroiditis. Mixed or indeterminate forms of AIT encompassing several features of both AIT I and AIT II may be also observed. The differential diagnosis between AIT I and AIT II (which is important for the choice of the appropriate therapy) is currently made on radioiodine uptake (RAIU), which may be high, normal or low but detectable in AIT I, while is consistently very low or undetectable in AIT II and on colour-flow Doppler sonography (CFDS) showing normal or increased vascularity in AIT I and absent vascularity in AIT II. Quite recently, studies carried out in our Units at the University of Cagliari (Italy) showed that sestaMIBI thyroid scintigraphy may represent the best single test to differentiate AIT I (showing increased MIBI retention) from AIT II (displaying no significant uptake). Treatment of AIT is dependent from its etiology. AIT usually responds to combined thionamides and potassium perchlorate (KClO4) therapy, AIT II generally responds to glucocorticoids, while indeterminate forms may require both therapeutic approaches. In patients with AIT I definitive treatment of hyperthyroidism by administration of (131)I, initially not feasible for the low RAIU and/or the risk of thyrotoxicosis exacerbation, is advised after normalization of iodine overload. To control severe AIT additional treatment with lithium carbonate, the use of short course of iopanoic acid and plasmapheresis have been also proposed. In cases resistant to medical treatment and/or in patients with severe cardiac diseases who cannot interrupt AM or require quick AM reintroduction, total thyroidectomy (possibly carried out by minimally invasive video-assisted technique) may be proposed after rapid correction of thyrotoxicosis with combination of thionamides, KClO4, corticosteroids and a short course of iopanoic acid.
[Show abstract][Hide abstract] ABSTRACT: The American Society for Apheresis (ASFA) Apheresis Applications Committee is charged with a review and categorization of indications for therapeutic apheresis. This elaborate process had been undertaken every 7 years resulting in three prior publications in 1986, 1993, and 2000 of "The ASFA Special Issues." This article is the integral part of the Fourth ASFA Special Issue. The Fourth ASFA Special Issue is significantly modified in comparison to the previous editions. A new concept of a fact sheet has been introduced. The fact sheet succinctly summarizes the evidence for the use of therapeutic apheresis. A detailed description of the fact sheet is provided. The article consists of 53 fact sheets devoted to each disease entity currently categorized by the ASFA. Categories I, II, and III are defined as previously in the Third Special Issue. However, a few new therapeutic apheresis modalities, not yet approved in the United States or are currently in clinical trials, have been assigned category P (pending) by the ASFA Clinical Categories Subcommittee. The diseases assigned to category IV are discussed in a separate article in this issue.
[Show abstract][Hide abstract] ABSTRACT: To compare thyroid imaging using Tc-99m sestamibi with the standard Tc-99m pertechnetate scintigraphy in patients on chronic use of amiodarone.
A total of 23 patients on oral amiodarone for at least 4 months had thyroid scintigraphy and uptake measurement using Tc-99m pertechnetate and Tc-99m sestamibi. Thyroid function was evaluated by measuring serum concentrations of thyrotropin, free thyroxine, and free triiodothyronine, and antithyroglobulin and antithyroperoxidase antibodies.
Ten of the 23 patients were euthyroid, 9 hypothyroid, and 4 hyperthyroid, with normal, increased, and decreased serum thyrotropin, respectively. All euthyroid patients had markedly decreased thyroid Tc-99m pertechnetate uptake and normal or slightly increased Tc-99m sestamibi uptake, except for one patient who had increased uptake of both radiotracers. One of the 4 hyperthyroid patients had Graves' disease and markedly increased thyroid uptake of both tracers. The other 3 hyperthyroid patients had normal or decreased Tc-99m pertechnetate uptake and increased Tc-99m sestamibi uptake. Differently than expected, all 9 hypothyroid patients had normal or increased uptake of both radiopharmaceuticals.
This study suggests that Tc-99m sestamibi may be an alternative tracer for thyroid scintigraphy and uptake measurement of patients on chronic use of amiodarone. Tc-99m sestamibi seems to be better than Tc-99m pertechnetate for the scintigraphic evaluation of the thyroid of euthyroid and hyperthyroid patients.
Clinical nuclear medicine 04/2010; 35(4):223-7. DOI:10.1097/RLU.0b013e3181d18e8e · 3.93 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The neuroendocrine response to critical illness is key to the maintenance of homeostasis. Many of the drugs administered routinely in the intensive care unit significantly impact the neuroendocrine system. These agents can disrupt the hypothalamic-pituitary-adrenal axis, cause thyroid abnormalities, and result in dysglycemia. Herein, we review major drug-induced endocrine disorders and highlight some of the controversies that remain in this area. We also discuss some of the more rare drug-induced syndromes that have been described in the intensive care unit. Drugs that may result in an intensive care unit admission secondary to an endocrine-related adverse event are also included. Unfortunately, very few studies have systematically addressed drug-induced endocrine disorders in the critically ill. Timely identification and appropriate management of drug-induced endocrine adverse events may potentially improve outcomes in the critically ill. However, more research is needed to fully understand the impact of medications on endocrine function in the intensive care unit.
Critical care medicine 06/2010; 38(6 Suppl):S219-30. DOI:10.1097/CCM.0b013e3181dda0f2 · 6.31 Impact Factor
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