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Drs Kaniksha Desai and Laurence Katznelson discuss the complex relationship between growth hormone and the thyroid gland. https://www.medscape.com/viewarticle/... -TRANSCRIPT- Kaniksha Desai, MD: Welcome back to the Thyroid Stimulating Podcast. This podcast was created in partnership with the American Thyroid Association to discuss up-to-date diagnosis and management of a wide array of thyroid diseases. I’m your host, Dr Kaniksha Desai, and today we’re taking a closer look at the complex relationship between growth hormone and the thyroid gland. We’ll discuss how excessive growth hormone, seen in conditions like acromegaly, can lead to thyroid enlargement, nodules, and even cancer. We’ll also explore the effects of growth hormone replacement therapy, how it influences thyroid hormone metabolism, and what this means for patients on thyroid hormone replacement. It is a privilege to have with us today, Dr Laurence Katznelson, a world-renowned authority on pituitary disorders and former president of the Pituitary Society. Dr Katznelson has authored over 120 peer-reviewed publications and has delivered numerous lectures at both the national and international level, including on the topic of growth hormone and its effects. He joins us today from Cedars-Sinai Medical Center, where he currently serves as the vice dean of medical education. We look forward to having a thoughtful discussion on the relationship between growth hormone and thyroid diseases. Thank you for joining us today. Laurence Katznelson, MD: Thank you for including me. Desai: I wanted to start by doing a little bit of physiology for our listeners. Can you explain how growth hormone interacts with thyroid function in the body and how they’re interconnected? Katznelson: There are, no surprise, quite a few connections between thyroid hormone and growth hormone physiology and how they interface. We see this play out often, and I’m sure we’ll discuss this later in this podcast, with hormone replacement strategies when it comes to hypopituitarism management, and also how it plays out in managing patients who have acromegaly, which is a situation of growth hormone excess. Even at baseline, there are known connections between circulating thyroid hormone and growth hormone. I’ll give you an example of some of these. We know that growth hormone plays a role in impacting peripheral deiodination of thyroxine (T4) to triiodothyronine (T3). Depending on the ambient levels of growth hormone, there will be more or less of this impact on the peripheral deiodinase. We’ll come back later to how that plays a role in growth hormone replacement, when someone goes from zero growth hormone to normal growth hormone, and what that means in terms of thyroid physiology. It’s also true that growth hormone plays an important role in thyroid gland growth, and we’re going to come back to that a little later on as we discuss goiters that may be seen with acromegaly. Getting back to the question about other aspects of regulation, we also know that thyroid hormone influences growth hormone secretion. We know from both in vitro and clinical studies that thyroid hormone seems to have a permissive, if not stimulatory, effect on growth hormone secretion by the pituitary gland. We know that when patients are hypothyroid, for example, there is greater stimulation once thyroid hormone has been replaced vs patients who remain hypothyroid. That is secretion of the growth hormone, either at baseline or with stimulation. When we talk about stimulation tests, we talk about using glucagon or insulin-induced hypoglycemia. When you do these procedures in a patient who has little or normal levels of thyroid hormone, you’ll see differential impacts on growth hormone secretion, less or more, depending on the hypothyroid vs euthyroid state. That’s something also important to know. We think about that when we are assessing growth hormone levels in a patient. We need to ensure that patient is euthyroid because otherwise, we may have a falsely low value and think the person is growth hormone deficient when they may not be. They may just be requiring thyroid hormone normalization. Desai: Is the opposite true with hyperthyroidism? Katznelson: With hyperthyroidism, studies have shown that we may have an augmented growth hormone state. The growth hormone levels may be even higher. It doesn’t appear that this will induce an acromegaly-like state with enough growth hormone surging that can cause excessive growth hormone that may lead to elevated insulin-like growth factor 1 (IGF-1) levels; that’s our marker for acromegaly. You can see bumps and you can see increases. It does appear that, across the spectrum of low to high systemic thyroid hormone levels, you may see differential effects upon growth hormone secretion accordingly. How do you approach preoperative evaluation in your practice? https://www.medscape.com/viewarticle/...