Dr.Guttler’s Patient Blog Post #7 What is Your Quality of Life with Hypothyroidism?

Dr.Guttler’s Patient Blog Post #7 What is Your Quality of Life with Hypothyroidism?

Dr.Guttler’s comments:

  1. 1970s treatment switched for Armour thyroid to synthetic LT4.
  2. Subclinical hypothyroidism is still debated as a treatable entity.
  3. Screening leads to over-diagnosis. Case finding is necessary for CHT patient’s family.
  4. TSH levels used to begin treatment have decreased.
  5. LT4 substitution improves, but does not always normalize quality of life.
  6. Treating Mild elevations of TSH does not improve QoL.
  7. However, neither studies combining levothyroxine and liothyronine (the synthetic form of tri-iodothyronine) nor the use of desiccated thyroid extract have shown robust improvements in patient satisfaction.
  8. Autoimmunity such as Hashimoto’s thyroiditis CHT leads to most hypothyroidism and can be a driver of patient dissatisfaction.
  9. One time that case finding is needed is CHT as it is a family disease in first degree relatives.
  10. Case finding is not screening. It is only done when a first degree relative has CHT or Graves’ disease.
  11. Long term health effects of undiagnosed CHT in family members is goiter formation nodules and cancer.
  12.  CHT is present for years before the patient becomes hypothyroid.
  13. LT4, LT3 or Armour over-treatment with suppressed TSH is a health issue and can effect QoL.
  14. Thyroid hormone therapy is a life time therapy.
  15. Approximately 10–15% of individuals with hypothyroidism treated with levothyroxine experience persistent symptoms and dissatisfaction with therapy (that might or might not be due to their hypothyroidism), which can lead to overtreatment.
  16. Are you sure you need it, and if you have CHT in the family you need to tell your first degree relatives they need testing.
  17. Call me at 310-393-8860 or thyroid.manager@thyroid.com

Nat.Rev. Endocrinol. Jan 2022

Hegedus L. et al

Primary hypothyroidism and quality of life

Abstract

In the 1970s, treatment with thyroid extract was superseded by levothyroxine, a synthetic L form of tetraiodothyronine. Since then, no major innovation has emerged for the treatment of hypothyroidism. The biochemical definition of subclinical hypothyroidism is a matter of debate. Indiscriminate screening for hypothyroidism has led to overdiagnosis and treatment initiation at lower serum levels of thyroid-stimulating hormone (TSH) than previously. Adverse health effects have been documented in individuals with hypothyroidism or hyperthyroidism, and these adverse effects can affect health-related quality of life (QOL). Levothyroxine substitution improves, but does not always normalize, QOL, especially for individuals with mild hypothyroidism. However, neither studies combining levothyroxine and liothyronine (the synthetic form of tri-iodothyronine) nor the use of desiccated thyroid extract have shown robust improvements in patient satisfaction. Future studies should focus not only on a better understanding of an individual’s TSH set point (the innate narrow physiological range of serum concentration of TSH in an individual, before the onset of hypothyroidism) and alternative thyroid hormone combinations and formulations, but also on autoimmunity and comorbidities unrelated to hypothyroidism as drivers of patient dissatisfaction. Attention to the long-term health consequences of hypothyroidism, beyond QOL, and the risks of overtreatment is imperative.

Key points

  • Epidemiological data suggest that the prevalence of (typically mild) hypothyroidism is increasing, partly owing to increased screening, which has led to a lower threshold for initiating treatment with levothyroxine.
  • Approximately 10–15% of individuals with hypothyroidism treated with levothyroxine experience persistent symptoms and dissatisfaction with therapy (that might or might not be due to their hypothyroidism), which can lead to overtreatment.
  • Health-related quality of life (QOL) is a complementary measure to morbidity and mortality; it should be measured with a validated thyroid-specific instrument for patient-related outcomes.
  • Poor QOL has been attributed to failure to achieve adequate T3 levels in tissues, polymorphisms in deiodinase and hormone transporter genes and/or symptoms unrelated to hypothyroidism such as autoimmune disease.
  • There is little evidence of durable QOL improvements with levothyroxine and liothyronine combination therapy, or from therapy with desiccated thyroid hormone, from a multitude of randomized controlled trials and meta-analyses.
  • Future research should investigate non-thyroidal causes of impaired QOL in patients with hypothyroidism as, at present, overtreatment for hypothyroidism constitutes a greater threat to health than undertreatment.
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