Diagnosis and Treatment > Signs and Symptoms > Vocal cord paresis

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Alex González Bóssolo Endocrinology, Diabetes and Metabolism

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Michelle Mangual Garcia Endocrinology

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Paula Jeffs González Endocrinology, Diabetes and Metabolism, San Juan City Hospital, Hato Rey Pathologies, San Juan, Puerto Rico

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Miosotis Garcia Endocrinology, Diabetes and Metabolism

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Guillermo Villarmarzo Endocrinology, Diabetes and Metabolism, San Juan City Hospital, Hato Rey Pathologies, San Juan, Puerto Rico

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Jose Hernán Martinez Endocrinology, Diabetes and Metabolism

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Summary

Classical papillary thyroid microcarcinoma (PTMC) is a variant of papillary thyroid carcinoma (PTC) known to have excellent prognosis. It has a mortality of 0.3%, even in the presence of distance metastasis. The latest American Thyroid Association guidelines state that although lobectomy is acceptable, active surveillance can be considered in the appropriate setting. We present the case of a 37-year-old female with a history of PTMC who underwent surgical management consisting of a total thyroidectomy. Although she has remained disease-free, her quality of life has been greatly affected by the sequelae of this procedure. This case serves as an excellent example of how first-line surgical treatment may result more harmful than the disease itself.

Learning points:

  • Papillary thyroid microcarcinoma (PTMC) has an excellent prognosis with a mortality of less than 1% even with the presence of distant metastases.

  • Active surveillance is a reasonable management approach for appropriately selected patients.

  • Patients should be thoroughly oriented about the risks and benefits of active surveillance vs immediate surgical treatment. This discussion should include the sequelae of surgery and potential impact on quality of life, especially in the younger population.

  • More studies are needed for stratification of PTMC behavior to determine if conservative management is adequate for all patients with this specific disease variant.

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Kazuyuki Oishi Kochi Health Sciences Center – Divisions of Breast & Thyroid Surgery, Kochi, Japan

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Daisuke Takabatake Kochi Health Sciences Center – Divisions of Breast & Thyroid Surgery, Kochi, Japan

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Yuichi Shibuya Kochi Health Sciences Center – Divisions of Breast & Thyroid Surgery, Kochi, Japan

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Summary

We experienced a case of an 82-year-old woman who presented to our hospital with a 1-month history of dysphagia and dyspnea. Cervical contrast-enhanced computed tomography revealed diffuse thyroid neoplasms causing significant tracheal stenosis with tumors, particularly of the superior mediastinum, which were associated with an embolism of the brachiocephalic vein and suspected invasion to the bilateral common carotid arteries. Anaplastic thyroid cancer (ATC) was diagnosed by fine-needle aspiration; thus, emergency tracheostomy and gastrostomy were performed. We made a definitive diagnosis of ATC (T4bN0M0 Stage IVB) and initiated continuous lenvatinib administration at 24 mg/day. Although several adverse events occurred, the tumor size reduced remarkably over a short period. However, the patient died from rupture of the common carotid artery 30 days after treatment initiation. Here, we report our experience with lenvatinib therapy for ATC and include a literature review.

Learning points:

  • Lenvatinib is extremely effective for ATC.

  • Lenvatinib has a much greater cytoreductive effect than traditional therapies, but it needs dose reduction or withdrawal because of treatment-related side effects.

  • Lenvatinib may cause treatment-related carotid blowout syndrome, resulting in death for patients with invasion to the carotid artery.

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Jin-Ying Lu Division of Endocrinology and Metabolism, Department of Internal Medicine, National Taiwan University Hospital, Taipei, 100, Taiwan

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Po-Ju Hung Division of Endocrinology and Metabolism, Department of Internal Medicine, National Taiwan University Hospital, Taipei, 100, Taiwan

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Pei-Lung Chen Division of Endocrinology and Metabolism, Department of Internal Medicine, National Taiwan University Hospital, Taipei, 100, Taiwan
Department of Medical Genetics, National Taiwan University Hospital, Taipei, 100, Taiwan
Graduate Institute of Medical Genomics and Proteomics, National Taiwan University, Taipei, 100, Taiwan
Graduate Institute of Clinical Medicine, National Taiwan University, Taipei, 100, Taiwan
Research Center for Developmental Biology and Regenerative Medicine, National Taiwan University, Taipei, 100, Taiwan

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Ruoh-Fang Yen Department of Nuclear Medicine, National Taiwan University, Taipei, 100, Taiwan

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Kuan-Ting Kuo Graduate Institute of Pathology, College of Medicine, National Taiwan University, Taipei, 100, Taiwan
Department of Pathology, National Taiwan University Hospital, Taipei, 100, Taiwan

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Tsung-Lin Yang Department of Otolaryngology, National Taiwan University Hospital, Taipei, 100, Taiwan

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Chih-Yuan Wang Division of Endocrinology and Metabolism, Department of Internal Medicine, National Taiwan University Hospital, Taipei, 100, Taiwan

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Tien-Chun Chang Division of Endocrinology and Metabolism, Department of Internal Medicine, National Taiwan University Hospital, Taipei, 100, Taiwan
Department of Medicine, College of Medicine, National Taiwan University, Taipei, 100, Taiwan

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Tien-Shang Huang Division of Endocrinology and Metabolism, Department of Internal Medicine, National Taiwan University Hospital, Taipei, 100, Taiwan
Department of Medicine, College of Medicine, National Taiwan University, Taipei, 100, Taiwan
Department of Social Medicine, College of Medicine, National Taiwan University, Taipei, 100, Taiwan
Department of Medicine, Cathay General Hospital, Taipei, 106, Taiwan

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Ching-Chung Chang Division of Endocrinology and Metabolism, Department of Internal Medicine, National Taiwan University Hospital, Taipei, 100, Taiwan
Department of Medicine, College of Medicine, National Taiwan University, Taipei, 100, Taiwan
Department of Internal Medicine, China Medical University Hospital, Taichung, 404, Taiwan
Department of Internal Medicine, China Medical University, Taichung, 404, Taiwan

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Summary

We report a case of follicular thyroid carcinoma with concomitant NRAS p.Q61K and GNAS p.R201H mutations, which manifested as a 13.5 cm thyroid mass with lung, humerus and T9 spine metastases, and exhibited good response to radioactive iodine treatment.

Learning points

  • GNAS p.R201H somatic mutation is an activating or gain-of-function mutation resulting in constitutively activated Gs-alpha protein and downstream cAMP cascade, independent of TSH signaling, causing autonomously functioning thyroid nodules.

  • NRAS p.Q61K mutations with GNAS p.R201H mutations are known for a good radioactive iodine treatment response.

  • Further exploration of the GNAS-activating pathway may provide therapeutic insights into the treatment of metastatic follicular carcinoma.

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