Glucocorticoids amiodarone

Patients with hypothyroidism who are taking levothyroxine may become hypothyroid if given drugs that decrease T4 absorption (cholestyramine, iron salts, calcium carbonate, aluminum hydroxide, sucralfate, raloxifene, omeprazole, dietary soy and fiber), increase its clearance (phenytoin, car-bamazepine, phenobarbital, rifampin), or decrease T4 to T3 conversion (amiodarone, glucocorticoids, propranolol). 

Others Acetaminophen, amiodarone, carbamazepine, delavirdine, efavirenz, nevirapine, quinidine, repaglinide, sildenafil, tadalafil, trazodone, vardenafil Amiodarone, amprenavir, atazanavir, ciprofloxacin, cisapride, clarithromycin, diltiozem, erythromycin, fluconazole, fluvoxamine, grapefruit juice (in high ingestion), indinavir, itraconazole, ketoconazole, nefazodone, nelfinavir, norfloxacin, ritonavir, telithromycin, troleandomycin, verapamil, voriconazole Carbamazepine, efavirenz, glucocorticoids, macrolide antibiotics, nevirapine, phenytoin, phenobarbital, rifabutin, rifapentine, rifampin, St. John s wort... 

Several drugs (for example amiodarone, androgens, glucocorticoids, phenytoin, and salicylates) interfere with the transport or metabolism of thyroid hormones and thereby alter thyroid function tests. These have been reviewed (90). In patients taking levothyroxine serum TSH rises after treatment with sertraline (91) and antimalarial prophylaxis with chloroquine and proguanil... 

It has been suggested that potassium perchlorate should be used in the treatment of type 1 hyperthyroidism and glucocorticoids in the treatment of type 2 (SEDA-21, 199). Since hypothyroidism due to amiodarone tends to occur in areas in which there is sufficient iodine in the diet, it has been hypothesized that an iodinated organic inhibitor of hormone synthesis is formed and that the formation of this inhibitor is inhibited by perchlorate to a greater extent than thyroid hormone iodination is inhibited, since the iodinated lipids that are thought to be inhibitors require about 10 times more iodide than the hormone. However, there is a high risk of recurrence after treatment with potassium perchlorate, and it can cause serious adverse effects (SED-13,1281). 

The management of hyperthyroidism due to amiodarone has been reviewed in the light of the practices of 101 European endocrinologists (60). Most (82%) treat type I amiodarone-induced hyperthyroidism with thionamides, either alone (51%) or in combination with potassium perchlorate (31%) the preferred treatment for type II hyperthyroidism is a glucocorticoid (46%). Some initially treat all cases, before the type has been established, with a combination of thionamides and glucocorticoids. After restoration of normal thyroid function, 34% recommend ablative therapy in type I hyperthyroidism and only 8% in type II. If amiodarone therapy needs to be restarted, 65% recommend prophylactic thyroid ablation in type I hyperthyroidism and 70% recommend a wait-and-see strategy in type II. 

Thyroid function tests were measured before and after treatment of amiodarone-induced hyperthyroidism (n = 12) and the response to combined antithyroid and glucocorticoid treatment (n = 11) was recorded (61). One patient had type 1 hyperthyroidism, nine had type 2, and two probably had a mixed form. Six patients had diffuse hypoechoic goiters. The median time to euthyroidism (defined as a normal free T3 concentration) with a thionamide + prednisolone (starting dose 20-75 mg/day) was... 

A 40 year-old patient with severe amiodarone-induced hyperthyroidism after heart transplantation did not respond to high doses of antithyroid drugs combined with glucocorticoids (62). A low dose of lithium carbonate resulted in normalization of thyroid function. 

The antithyroid effect of lithium has occasionally been used to benefit patients. In a case of amiodarone-induced thyrotoxicosis that did not respond to antithyroid drugs and glucocorticoids, low-dose lithium normalized thyroid function (62). 

A4 Acetaminophen, alfentanil, amiodarone, astemizole, cocaine, cortisol, cyclosporine, dapsone, diazepam, dihydroergotamine, dihydropyridines, diltiazem, ethinyl estradiol, gestodene, indinavir, lidocaine, lovastatin, macrolides, methadone, miconazole, midazolam, mifepristone (RU 486), paclitaxel, progesterone, quinidine, rapamycin, ritonavir, saquinavir, spironolactone, sulfamethoxazole, sufentanil, tacrolimus, tamoxifen, terfenadine, testosterone, tetrahydro-cannabinol, triazolam, troleandomycin, verapamil Barbiturates, carbamazepine, macrolides, glucocorticoids, pioglitazone, phenytoin, rifampin Erythromycin, 613-hydroxy cortisol... 

Clinically important, potentially hazardous interactions with alcohol, amiodarone, amphotericin B, cisapride, clonidine, digitalis, diltiazem, disopyramide, erythromycin, glucocorticoids, halofantrine, haloperidol, hypokalemic diruretics, imipramine antidepressants, levodopa, lithium, pentamidine, pimozide, quinidine, sotalol, stimulant laxatives, tetracosactides, thioridazine... 

A number of medications have been shown to alter thyroid function and thyroid function tests.Few drugs are associated with the development of clinically significant thyroid disease (amiodarone may be an exception), but difficulty in the interpretation of thyroid function tests results when patients are placed on medications that affect thyroid function testing. In general, drugs do not interfere chemically with the assays for thyroid hormones or TSH. The medications most likely to affect TSH concentrations are glucocorticoids and dopamine (reduced TSH concentrations) and amiodarone (increased TSH concentrations). The most commonly encountered variations in thyroid hormone measurements induced by medications are reduced peripheral conversion of T, to T3 or altered binding of T4 and T3 to carrier proteins. Some of the medications that affect thyroid function tests are shown in Table 52-2. 

Bogazzi F, Bartalena L, Cosci C, et al. Treatment of type 11 amiodarone-induced thyrotoxicosis by either iopanoic acid or glucocorticoids A prospective, randomized study. J Clin Endocrinol Metab 2003 88 1999-2002. 

The management of amiodarone-induced thyrotoxicosis has been extensively reviewed [42 ]. For type 1 thyrotoxicosis, thionamides are the best treatment (possibly associated with potassium perchlorate) for type 2, glucocorticoids are the treatment of choice. However, if rapid restoration of euthyroidism is necessary, a short course of iopanoic acid followed by total thyroidectomy is an option. Radioactive iodine has a marginal role. The authors addressed some important controversies, practical problems, and unanswered questions. 

Management Glucocorticoids are the first-line treatment in type 2 amiodarone-induced thyrotoxicosis, and thionamides play no role. In a matched retrospective cohort comparison of the ejficacy of a thionamide (methimazole) or a glucocorticoid (prednisone) for 40 days in type 2 amiodarone-induced thyrotoxicosis, in 42 patients, 23% of those who took prednisone were still thyrotoxic, compared with 86% of those who took methimazole [39 ]. When those who had taken methimazole were then given prednisone, 94% achieved euthyroidism within another 40 days. 

Withdrawal of amiodarone is more often considered unnecessary by North American thyroidologists in type 1 amiodarone-induced thyrotoxicosis (which occurs in patients with latent disease, due to the iodine contained in amiodarone) than in type 2 amiodarone-induced thyrotoxicosis (which is due to destructive thyroiditis in a previously normal gland) 21% versus 10% in Europe in type 1 34% versus 20% in type 2. In type 1 thyrotoxicosis thionamides represent the treatment of choice in North America and Europe, but as monotherapy in 65% compared with 51% European thyroidologists more often consider potassium perchlorate as a useful addition (31% versus 15%). Glucocorticoids are the selected treatment for type 2 thyrotoxicosis, either alone (62% V5. 46% in Europe) or in association with thionamides (16% versus 25%). After restoration of euthyroidism, thyroid ablation in the absence of recurrent thyrotoxicosis is recommended in type 1 less often in North America. If amiodarone needs to be restarted, prophylactic thyroid ablation is advised by 76% in type 1 thyrotoxicosis, while a wait-and-see strategy is adopted by 61% in type 2, as in Europe. This survey shows differences in therapeutic attitudes, which reflect the frequent uncertainty of the underlying mechanism that leads to amiodarone-induced thyrotoxicosis. 

Bogazzi F, Tomisti L, Rossi G, DeirUnto E, Pepe P, Bartalena L, Martino E. Glucocorticoids are preferable to thionamides as first-line treatment for amiodarone-induced thyrotoxicosis due to destructive thyroiditis a matched retrospective cohort study. J Clin Endocrinol Metab 2009 94(10) 3757-62. 

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