Special Collection in Recognition of Hashimoto’s Thyroiditis Awareness Month

This Special Collection of recent publications regarding Hashimoto’s Thyroiditis from the American Thyroid Association^® journals highlights current understanding and new information on this topic. The selected studies, reviews, commentaries, and videos include content related to the cognitive effects of Hashimoto’s thyroiditis in mouse models, associations of the condition with diet and oxidative stress, genetic risks, Hashimoto’s thyroiditis in pregnancy, potential use of thyroid surgery as an innovative treatment option, the rare fibrosing variant of this condition, and innovations in its sonographic assessment.

We invite you to read these articles, commentaries, and videos, selected by the Editors-in-Chief of Thyroid^®, ClinicalThyroidology^®, and VideoEndocrinology,™ free through May 15, 2021.

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Benjamin Gigliotti, MD
University of Rochester Medical Center, NY
January 15, 2021

A common clinical dilemma is the management of patients with treated hypothyroidism and/or Hashimoto’s thyroiditis who feel unwell despite normal thyroid function tests. Weight gain, fatigue, brain fog, depressed mood, cold intolerance, constipation, dry skin, joint/muscle aches, hair loss, and brittle nails may be reported. These symptoms are commonly referred to as “thyroid symptoms,” and an internet search will reveal innumerable sources that reinforce a link between these and inadequate treatment or thyroid autoimmunity itself. However, clinicians must be cautious not to reflexively infer causation from correlation since:

– Even the most classic symptoms of hypothyroidism are non-specific and are commonly found in other diseases and in the general population.
– Anti-thyroid antibodies are often ordered in patients with unexplained symptoms, so autoimmune thyroid disease is disproportionately diagnosed in this setting; it remains unclear if this causes symptoms in and of itself.
– Most online resources emphasize the voices of people with thyroid disease who feel unwell since those who feel well do not tend to seek out or contribute to these resources.

In my experience, vague symptoms in this setting often have a multifactorial explanation, and thyroid disorders are rarely the dominant or only cause. Although the severity or number of symptoms can be daunting to evaluate, it is critical to meet the patient’s frustration with compassion, longitudinal relationship-building and thoughtful inquiry. Asking the following questions may prove helpful in determining the source(s) of symptoms:

-Is the normal TSH truly reflective of the patient’s thyroid axis?

• Repeating the TSH over time can exclude spuriously or transiently normal results.
• The upper limit of the TSH reference range (4-5mIU/L for most assays) is debated and may be lower in young patients or higher in older or obese patients. Regardless, I have never seen resolution of severe symptoms from treatment of a TSH that is within (or even slightly above or below) the reference range; several studies support this observation.(1)
• Checking a free T4 level at least once can ensure concordance with the TSH and exclude assay interference (e.g. biotin or heterophile antibodies) or rare cases of central hypothyroidism).(2)
• Total T3, free T3, and reverse T3 assays perform poorly in hypothyroidism and are rarely helpful, especially if the TSH and free T4 are normal

-Could there be an alternative explanation for each symptom that warrants workup, treatment, or counseling?

• Weight gain and/or fatigue are particularly common, occurring in up to half of all adults. Inadequate or poor-quality sleep, excessive work, suboptimal diet, and inadequate exercise are common causes. Menopause can also contribute, especially if vasomotor symptoms disrupt sleep.
• Hashimoto’s is associated with a higher rate of other clinically significant autoimmune diseases (e.g. lupus, rheumatoid arthritis, celiac disease) and numerous functional disorders (e.g. depression, migraines, irritable bowel syndrome, fibromyalgia).
• Iron deficiency is common in menstruating women, a population enriched in autoimmune thyroid disease, and can cause a similar spectrum of symptoms, even without anemia or frankly low ferritin levels.

– Can thyroid hormone therapy be optimized?

• Some patients on levothyroxine report improved symptoms after targeting a “low normal” TSH, although it is increasingly unclear if this approach is effective, and caution should be used in patients at risk for harm from iatrogenic hyperthyroidism.(3)
• Many patients express interest in therapies other than standard-of-care levothyroxine (4); Dr. Shrestha recently wrote a thoughtful blog post on thyroid hormone formulations (https://www.thyroid.org/thyroid-prescription-levothyroxine/). It is prudent to consult with an experienced endocrinologist familiar with the literature and pros/cons of using T3 and T4+T3 combination therapy to determine their appropriateness on a case-by-case basis.

While there is rarely a panacea, engaging in supportive listening, initiating an appropriately comprehensive evaluation, setting realistic expectations, and seeking consultation with endocrinology (especially when questions about assay reliability or optimal thyroid hormone replacement arise) can prove beneficial.

References:
1. Biondi B 2013 The normal TSH reference range: what has changed in the last decade? J Clin Endocrinol Metab 98:3584-3587.
2. Burch HB 2019 Drug Effects on the Thyroid. N Engl J Med 381:749-761.
3. Samuels MH, Kolobova I, Niederhausen M, Janowsky JS, Schuff KG 2018 Effects of altering levothyroxine (L-T4) doses on quality of life, mood and cognition in L-T4 treated subjects. J Clin Endocrinol Metab. ePub 2018 Mar 2.
4. Jonklaas J, Bianco AC, Bauer AJ, Burman KD, Cappola AR, Celi FS, Cooper DS, Kim BW, Peeters RP, Rosenthal MS, et al. 2014 Guidelines for the treatment of hypothyroidism: prepared by the american thyroid association task force on thyroid hormone replacement. Thyroid 24:1670-1751.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

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A recent study compared thyroidectomy with medical management for persistent symptoms of Hashimoto’s thyroiditis. But is surgery really the answer? Read more on the Medscape Website…

The post ATA-Medscape Collaboration appeared first on American Thyroid Association.

Latest clinical, basic thyroid research highlighted at ATA annual meeting – September 21, 2016
Healio/Endocrine Today

Pregnancy loss, preterm delivery reduced with levothyroxine therapy – September 22, 2016
Healio/Endocrine Today

Hypocalcemia management strategies differ among physicians after thyroidectomy – September 22, 2016
Healio/Endocrine Today

Thyroid cancer overdiagnosis raises questions about overtreatment – September 22, 2016
Healio/Endocrine Today

Recommendations needed for TPOAb cut-off levels during pregnancy – September  23, 2016
Healio/Endocrine Today

Patients with Hashimoto’s thyroiditis require similar T ₄ levels regardless of body weight – September 23, 2016
Healio/Endocrine Today

The post More news from the 86th Annual Meeting of the ATA appeared first on American Thyroid Association.

“Dr. McLachlan has made an indelible mark on the field of thyroidology through her extensive contributions to our understanding of the molecular and cellular basis of thyroid autoimmunity,” said ATA President James A. Fagin, MD, of Memorial Sloan-Kettering Cancer Center.

Dr. McLachlan is Professor of Medicine and Co-Director of the Thyroid Autoimmunity Laboratory at Cedars-Sinai Medical Center. She has been investigating the molecular and cellular basis of thyroid autoimmunity for 35 years. She is internationally recognized as a leader in this field and has published over 220 peer-reviewed papers.

Dr. McLachlan’s early work includes landmark research into the interactions between T and B lymphocytes from patients with Hashimoto’s thyroiditis or Graves’ disease for their thyroid autoantibody production. Dr. McLachlan was the first to demonstrate the in vitro production of autoantoantibodies to thyroglobulin (Tg), thyroid peroxidase (TPO) and the TSHR by patients’ lymphocytes. She also established the thyroid gland as the major site of thyroid autoantibody production, providing the basis for using thyroid tissue from patients with autoimmune thyroid disease in her subsequent cloning of human autoantibodies to TPO and Tg. Additionally, she provided evidence that TPO and Tg share a T cell epitope, recently confirmed for MHC class I.

Her laboratory has been funded by the National Institutes of Health (NIH) for the past 18 years. Chief among her most recent achievements is cloning the entire repertoire of human TPO autoantibodies, an accomplishment not achieved in any other human autoimmune disease. Subsequently, a similar approach was used to clone a large panel of human autoantibodies to Tg. This resulted in the first analysis of heavy and light chain immunoglobulin genes that encode autoantibodies to TPO and Tg, the determination of the three dimensional structure of a TPO autoantibody, and inheritance of the TPO autoantibody epitopic “fingerprint” in families.

She has also made great strides in investigating disease pathogenesis and antigen specific immunotherapy using animal models of induced Graves’ and Hashimoto’s diseases. Her work includes studies demonstrating that human TSHR antibodies preferentially recognize the TSHR A-subunit rather than the full length receptor, studies determining the immunodominant epitopes recognized by T cells and linear antibody B cell epitopes in several mouse strains immunized with the TSHR, and genetic investigations of susceptibility and resistance to induced Graves’ disease in a variety of mouse strains (including HLA-DR3 humanized mice). These genetic studies in recombinant inbred mice of thyroid stimulating antibodies specific for the murine-versus the human-TSHR have provided important insights into the basis for susceptibility and resistance to induced Graves’ disease.

Dr. McLachlan is a past recipient of the ATA’s Sidney H. Ingbar Distinguished Lectureship Award. She is member of the Editorial Board of Thyroid and has served on ATA Board of Directors and as Chairperson of the ATA Awards Committee.

About the ATA Annual Meeting
The 82nd Annual Meeting of the American Thyroid Association is held Sept. 19-23, in Québec City, Québec, Canada. This four day creative and innovative scientific program, chaired by Elizabeth Pearce, MD, Boston Medical Center, and Douglas Forrest, PhD, National Institute of Diabetes and Digestive and Kidney Diseases, carefully balances clinical and basic science sessions on the latest advances in thyroidology. The ATA meeting is designed to offer continuing education for endocrinologists, internists, surgeons, basic scientists, nuclear medicine scientists, pathologists, endocrine fellows and nurses, physician assistants and other health care professionals. Visit www.thyroid.org for more information.

About the ATA
The American Thyroid Association (ATA) is the leading worldwide organization dedicated to the advancement, understanding, prevention, diagnosis and treatment of thyroid disorders and thyroid cancer. ATA is an international individual membership organization with over 1,600 members from 43 countries around the world. Celebrating its 89th anniversary, ATA delivers its mission through several key endeavors: the publication of highly regarded monthly journals, THYROID, Clinical Thyroidology and Clinical Thyroidology for Patients; annual scientific meetings; biennial clinical and research symposia; research grant programs for young investigators, support of online professional, public and patient educational programs through www.thyroid.org; and the development of guidelines for clinical management of thyroid disease. Visit www.thyroid.org for more information.

Media Contact
Bobbi Smith
Executive Director
 of the American Thyroid Association
Email: bsmith@thyroid.org
Mobile Phone: 703-772-2462 (texts preferred)

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