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Endocrine Diseases
Published in Miriam Orcutt, Clare Shortall, Sarah Walpole, Aula Abbara, Sylvia Garry, Rita Issa, Alimuddin Zumla, Ibrahim Abubakar, Handbook of Refugee Health, 2021
Thyrotoxic crisis is an emergency; management is shown in Table 11.3.4. Three treatment options are available: thionamides, radioactive iodine ablation and surgery. Thionamide treatment with carbimazole is most feasible in humanitarian aid or low-resource settings: starting dose is 20 mg daily, increased to 40 mg daily after four weeks, if needed; once stable, 10–20 mg daily for 12–18 months is usual. There is a risk of neutropenia and agranulocytosis associated with carbimazole. It is also associated with an increased risk of congenital malformations, especially in the first trimester and at high doses (daily dose of 15 mg or more). Therefore, women of childbearing potential should use effective contraception, and it should only be considered during pregnancy after a thorough benefit–risk assessment, and at the lowest effective dose. Cases of acute pancreatitis have been reported so carbimazole should be stopped immediately if acute pancreatitis occurs.1–17
Clinical Pharmacology of the Anti-Tuberculosis Drugs
Published in Lloyd N. Friedman, Martin Dedicoat, Peter D. O. Davies, Clinical Tuberculosis, 2020
Gerry Davies, Charles Peloquin
Thioamides are teratogenic in animal studies and few data human data exist. Concentrations in breast milk have not been studied. The recommended dose in children is 10–20 mg/kg per day in 2–3 divided doses. In severe renal impairment (CrCl <30 mL/min) the dose interval should be not more than daily. ETH is not significantly removed by dialysis (2%).179 Thioamides are contraindicated in severe liver disease.
Benign Thyroid Disease
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Christopher M. Jones, Kristien Boelaert
The thionamides (carbimazole, its active metabolite methimazole [not available in the UK] and propylthiouracil) are the most effective antithyroid drugs and represent the mainstay of drug treatment of thyrotoxicosis.57 They act by blocking the synthesis of T4 and T3 early in their biosynthetic pathway by disrupting the organification and oxidation of iodide through inhibition of the thyroperoxidase enzyme. Propylthiouracil (PTU) additionally acts to inhibit the conversion of T4 to T3 but this is not thought to be of clinical relevance. Thionamides have also been associated with a possible immunomodulatory effect, although this is of doubtful clinical significance given that most patients relapse following drug withdrawal.62 Carbimazole can be dosed as a once-daily preparation in order to improve compliance and results in fewer adverse effects than propylthiouracil.63 It is therefore generally given in preference, with propylthiouracil reserved for use in pregnancy, women attempting to conceive or patients who have developed an adverse reaction (other than agranulocytosis) to carbimazole or methimazole.64
A practical approach to the management of thyroid dysfunction during pregnancy
Published in Gynecological Endocrinology, 2022
Costanzo Moretti, Natalia Lazzarin, Elena Vaquero, Alessandro Dal Lago, Luisa Campagnolo, Herbert Valensise
Thyrotoxicosis in pregnancy is usually treated by reducing TH synthesis using antithyroid drugs (ATD). The main ATD are thionamides, such as propylthiouracil (PTU), carbimazole (CBZ), and the active metabolite of the latter, methimazole (MMI). Thionamides inhibit the coupling of iodothyronines, reducing the biosynthesis of TH [53]. All inhibit the function of thyroperoxidase, reducing oxidation and the organification of iodide. Moreover, MMI determines the inhibition of the production of TRABs, by inhibiting the activity of lymphocytes that mediate the intrathyroidal inflammatory process. Propylthiouracil is considered the first-choice treatment for pregnant patients. Although the embryo toxic effects of methimazole have not been confirmed, it is not recommended as a first-choice option in pregnancy [54]. The suggested initial doses are of 200 mg of PTU daily.
Usefulness of plasmapheresis in patients with severe complicated thyrotoxicosis
Published in Baylor University Medical Center Proceedings, 2021
Myrian Vinan-Vega, Barbara Mantilla, Nusrat Jahan, Cabandugama Peminda, Kenneth Nugent, Joaquin Lado-Abeal, Ana Rivas
The prevalence of hyperthyroidism in the United States is 1.3%; thyroid storm occurs in 0.22% of all thyrotoxic patients, with an overall mortality of 8% to 30%.5 Treatment strategies include thionamides, iodine solution, bile acid sequestrants, hydrocortisone, and beta-adrenergic receptor blockers (Figure 2).2 Minor side effects of thionamides occur in about 5% of patients and include pruritus, arthralgia, and gastrointestinal distress.6,7 Agranulocytosis is a rare but life-threatening side effect and generally occurs within 90 days after initiation of therapy.8 Hepatotoxicity occurs in 0.1% to 0.2% of patients, mainly in the first 3 months of therapy, and most commonly presents as hepatitis. Acute liver failure is rare and is more frequently associated with propylthiouracil.9,10
Safety of antithyroid drugs in pregnancy: update and therapy implications
Published in Expert Opinion on Drug Safety, 2020
Thanuya Francis, Niroshan Francis, John H. Lazarus, Onyebuchi E. Okosieme
The thionamide antithyroid drugs are 5–6 ringed sulfur containing thiourea derivatives that inhibit thyroid hormone synthesis by preventing thyroid peroxidize (TPO) catalyzed iodination and coupling of thyroglobulin-linked tyrosine residues [22,23]. The thionamides also have immunosuppressive effects which over time leads to a reduction in TRAb levels but it is unclear whether these immunosuppressive effects are as a result of direct actions on humoral and cellular mechanisms or an indirect effect of hyperthyroidism control [22]. In addition, PTU in large doses blocks peripheral thyroxine (T4) to triiodothyronine (T3) conversion through inhibition of the type 1 deiodinase [22,23]. Lastly, the thionamides may exhibit antioxidant properties but it is also unclear if this action occurs through direct effects or through control of hyperthyroidism.