Hypothyroidism in patients with colorectal carcinoma treated with fluoropyrimidines

Yutaka Fujiwara1, Naoko Chayahara, Toru Mukohara

  • 1Division of Internal Medicine and Thoracic Oncology, National Cancer Center Hospital, Tokyo 104-0045, Japan.

Oncology Reports
|August 1, 2013
PubMed

Insights

Fluoropyrimidines, used in colorectal cancer chemotherapy, can cause thyroid dysfunction. Bevacizumab did not impact thyroid function in this study, but further research is needed on fluoropyrimidine mechanisms.

Area of Science:

  • Oncology
  • Endocrinology
  • Pharmacology

Background:

  • Targeted therapies, including tyrosine kinase inhibitors, are known to cause hypothyroidism and thyroid dysfunction.
  • Thyroid dysfunction in cancer patients may be underdiagnosed and undertreated.
  • Colorectal cancer patients receiving chemotherapy require monitoring for thyroid function.

Purpose of the Study:

  • To evaluate thyroid function in colorectal cancer patients undergoing fluoropyrimidine-based chemotherapy with or without bevacizumab.
  • To determine the impact of bevacizumab and fluoropyrimidines on thyroid function.
  • To identify the incidence of chemotherapy-induced thyroid dysfunction.

Main Methods:

  • Thyroid function was assessed at baseline and monthly in colorectal cancer patients.
  • Thyroid-stimulating hormone (TSH) levels were monitored.
  • Patients received fluoropyrimidine-based chemotherapy with or without bevacizumab.

Main Results:

  • 11.1% of patients developed TSH levels >10 µU/ml, and 48.1% had elevated TSH.
  • No significant difference in TSH elevation was observed between the bevacizumab and chemotherapy-alone groups.
  • Three patients developed TSH >10 µU/ml; two with hypothyroidism received thyroid hormone replacement.

Conclusions:

  • Bevacizumab does not appear to affect thyroid function in colorectal cancer patients.
  • Fluoropyrimidines may induce thyroid dysfunction in patients with colorectal cancer.
  • Further research is necessary to elucidate the mechanism of fluoropyrimidine-induced thyroid dysfunction.

Related Concept Videos

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Drugs for Treatment of Ulcerative Colitis in IBD01:29

Drugs for Treatment of Ulcerative Colitis in IBD

Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide generation. 
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids01:21

Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids

Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2 (COX-2),...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...