The Role, Rationale, Evidence and Practical Application of
Combination Therapy with DTE in Selected Patients with Hypothyroidism
A Year 2021 Hypothyroidism Update for the Endocrinology, Primary Care, Internal Medicine, and Thyroid Specialist
A Year 2021 Hypothyroidism Update for the Endocrinology, Primary Care, Internal Medicine, and Thyroid Specialist
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Can you give clinicians a sense of how many people treated for hypothyroidism with T4 monotherapy fall into a “less than optimal outcome” category and should be considered for combination approaches, including those that might include DTE?
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What percentage of patients who, for symptomatic reasons, have been switched from LT4 monotherapy to DTE, do you find actually improve on DTE, and what do they report?
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When using LT4 monotherapy, is monitoring of TSH sufficient to guide therapy? Can you elaborate on this?
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There is a subset of patients who don’t respond to or are dissatisfied with levothyroxine (T4) monotherapy. What percentage don’t respond to conventional therapy? Why is combination therapy with T3/T4 considered appropriate for this group?
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Under what circumstances would a clinician consider deploying combination T4/T3 therapy, whether adding on synthetic T3 to T4 or considering dessicated thyroid extract (DTE)? How do you identify patients who are appropriate for combination therapy?
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How would you summarize your experience with hypothyroidism, in particular, your perspective on the current role of combination therapy with DTE?
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Can you discuss the consensus report on identifying a subset of patients with hypothyroidism who fsaol to achieve optimal symptomatic resolution with LT4 monotherapy; and, therefore, should be considered for combination T4/T3 combination therapy?
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Once you commit a person with hypothyroidism to combination therapy with T4/T3, how do you follow the patient? What have you observed as far as improvements in patient status and/or their perceptions about the effects of combination T4/T3 therapy?
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What is your approach to the patient who has a TSH of 2.5—well within the normal range—but the patient still has symptoms? Is there a rationale for bringing the TSH down to, let’s say, 1. 0 or 0.7, that is, to a lower level within the normal range?