alexa Rectal and Liver Metachronous Cancers and Sorafenib-Induced Thyroid Dysfunction.
ISSN: 2165-7920

Journal of Clinical Case Reports
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Case Report

Rectal and Liver Metachronous Cancers and Sorafenib-Induced Thyroid Dysfunction.

Ancuta Augustina Gheorghisan Galateanu1,2, Mara Carsote2,3*, Dan Peretianu4, Cristina Iosif5,6, Dana Terzea2,5 and Catalina Poiana2,3
1Department of Cellular and Molecular Medicine, “Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania
2“C.I.Parhon” National Institute of Endocrinology, Bucharest, Romania
3Department of Endocrinology, “Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania
4SCM Povernei Medical Centre, Bucharest, Romania
5OncoTeam Monza Hospital, Bucharest, Romania
6“Sfanta Maria” Hospital, Bucharest, Romania
Corresponding Author : Mara Carsote
C.I.Parhon National Institute of Endocrinology
Bucharest, Romania, Aviatorilor Ave 34-36
postal cod 011863, Romania
Tel: +40744851934
Fax: +40213170607
E-mail: [email protected]
Received May 16, 2015; Accepted May 26, 2015; Published May 27, 2015
Citation: Gheorghisan Galateanu AA, Carsote M, Peretianu D, Iosif C, Terzea D, et al. (2015) Rectal and Liver Metachronous Cancers and Sorafenib-Induced Thyroid Dysfunction. J Clin Case Rep 5:530.doi:10.4172/2165-7920.1000530
Copyright: © 2015 Gheorghisan Galateanu AA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 

Abstract

Background: The tyrosine kinase inhibitor, a new treatment option in hepatic carcinoma, may associate thyroid dysfunction like spontaneously remitting thyrotoxicosis followed by hypothyroidism. Case report: A 66-year Caucasian female was first diagnosed and operated for a moderately differentiated rectal adenocarcinoma of 5 centimeters. Immunohistochemistry showed positive VEGF receptor 2 (Flk-1, KDR), VEGF receptor 1(Flt-1), and a Ki67 of 30%. 4 years later a hepatic adenocarcinoma (clear cells variant) was diagnosed. After surgery, daily 400 mg of sorafenib was introduced. Three months later mild symptomatic thyrotoxicosis was seen: palpitations, fatigue, and mild bilateral pedal clonus. Thyroid-stimulating hormone (TSH) was suppressed (0.044 μIU/mL, normal levels between 0.4 and 4.5 μIU/mL), and free levothyroxine (fT4) elevated. The TSH receptor antibody, the antithyreoglobulin and antithyreoperoxidase antibodies were negative. Thyroid ultrasound pointed hypoechogenic, inhomogeneous aspects. She received beta-blocker and within two months thyrotoxicosis remitted but TSH progressively increased suggesting hypothyroidism with level less 5 μIU/mL so no replacement levothyroxine therapy was added yet. Discussions: The exact mechanism of the tyrosine kinase inhibitors-related thyroid malfunction is not fully understood. Non-autoimmune destructive thyroiditis of unknown trigger causes thyrotoxicosis and later hypothyroidism as seen in our case. The clinical features vary from one person to another. The hormone replacement is rarely necessary. The baseline cancer seems irrelevant for thyroid toxicity. In our unusual case the patient had a history of two metachronous cancers. The thyroid follow up is essential during each patient therapy yet a specific pattern of follow-up is not precisely designed. Conclusion: The tyrosine kinase inhibitor-induced thyroid dysfunction includes both thyrotoxicosis and hypothyroidism. We emphasize the idea of periodic endocrine evaluation in oncologic patient treated with this class of drugs.

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