Immunotherapy and Thyroid – NEED ADVICE

So – a level of 0.3 is not that crazy and could be due to lab variability. That said, it all certainly warrants investigation, clarification and treatment as indicated based on those findings.

In thyroiditis, which can be caused by many things, you can sometimes get a “surge” of thyroid hormone (which is not really a surge, but more of a leaking) that leads to INCREASED thyroid hormone floating around – HYPERthyroidism – sometimes symptom-less, sometimes with full blown signs and symptoms, transiently, BEFORE the gland goes kerplunk and stops producing hormone – leaving the patient with HYPOthyroidism. Here is a link that is pretty good at explaining all of that: https://www.thyroid.org/thyroiditis/

I do not have the data to demonstrate that this is the method by which the thyroid is affected by immunotherapy, but it wouldn’t surprise me. Bottom line, as you well know, until you know both the Free T4 and TSH numbers, as well as some sequential numbers of same, it will be hard to know what is happening.

Probably didn’t tell you anything you didn’t already know, Jackie. Hang in there. You are amazing! love, c

But….you basically still need more info. Now that I’ve muddied the waters completely – I hope you and your cousin get answers and help soon!! love, c

Here’s an abstract that offers some insight:

Thyroid disorders induced by checkpoint inhibitors. Ferrari SM1, Fallahi P2, Galetta F1, Citi E1, Benvenga S3,4,5, Antonelli A6.

Abstract
Immune checkpoint inhibitors are drugs that inhibit the “checkpoint molecules”. Different types of cancer immune checkpoint inhibitors have been approved recently: CTLA-4 monoclonal antibodies (as ipilimumab); anti-PD-1 monoclonal antibodies (as pembrolizumab and nivolumab); and anti-PD-L1 monoclonal antibodies (as atezolizumab, avelumab, and durmalumab). The increased immune response induced by these agents leads to immune-related adverse events (irAEs), that can vary from mild to fatal, according to the organ system and severity. Immune-related endocrine toxicities are thyroid dysfunctions, hypophysitis, adrenal insufficiency, and type 1 diabetes mellitus, and are usually irreversible in 50%. In particular, hypophysitis is the most frequent anti-CTLA-4-antibodies-related irAE, while thyroid abnormalities (as hypothyroidism, thyrotoxicosis, painless thyroiditis, or even “thyroid storm”) are more frequently associated with anti-PD-1-antibodies. The combination of anti-CTLA-4-antibodies, with anti-PD-1-antibodies, is associated with about 30% of irAEs. Clinical signs and symptoms vary according to the influenced target organ. Endocrinopathies can often be managed by the treating oncologist. However in more severe cases (i.e. in the presence of insulin-dependent diabetes, adrenal insufficiency, or disorders of gonadal hormones, or severe hyperthyroidism, or hypothyroidism, or long-lasting management of hypophysitis) an endocrinological evaluation, and a prompt therapy, are needed.

Here is a link that includes a PDF document that provides a complete algorithm for treating endocrine side effects: http://chaoticallypreciselifeloveandmelanoma.blogspot.com/2016/07/excellent-pdf-on-how-to-deal-with.html

But mrochelle’s post on this thread below, answers it even more elegantly.

Melanoma peeps and their docs do what they gotta do. Overall, decreased thyroid function due to decreased function of the thyroid itself or decreased pituitary function (from hypophysitis) are the most common thyroid problems that immunotherapy induces. c