Interferon-alpha is a major treatment modality for several malignant and nonmalignant diseases, especially Hepatitis C.
Dr Jamie Mandac and colleagues from New York reviewed the literature to assess the current evidence.
The team noted with prospective studies that up to 15% of patients with Hepatitis C receiving interferon-alpha develop clinical thyroid disease.
Up to 40% are reported to develop thyroid antibodies.
The team observed that some of these complications may result in discontinuation of interferon therapy.
Interferon induced thyroiditis is a major clinical problem for patients receiving interferon therapy, and can be classified as autoimmune and non-autoimmune.
Autoimmune interferon induced thyroiditis may manifest by the development of thyroid antibodies without clinical disease, and autoimmune thyrotoxicosis.
Non-autoimmune interferon induced thyroiditis can manifest as destructive thyroiditis or as hypothyroidism with negative thyroid antibodies.
| Genetic factors, gender, and Hepatitis C infection may play a role|
The researchers found that early detection and therapy of these conditions is important in order to avoid complications such as cardiac arrhythmias.
It is not clear which factors contribute to the susceptibility to interferon induced thyroiditis.
However, the team studied recent evidence, which suggests that genetic factors, gender, and Hepatitis C virus infection may play a role.
In contrast, viral genotype and therapeutic regimen were not found to influence susceptibility to interferon induced thyroiditis.
Dr Mandac's team concludes, “The etiology of interferon induced thyroiditis is unknown and may be secondary to immune modulation by interferon-alpha and/or direct effects of interferon on the thyroid.”
“In this review we discuss the clinical and pathophysiological aspects of interferon induced thyroiditis.”
“We are proposing a new, etiology-based classification of interferon induced thyroiditis, as well as an algorithm for diagnosis and treatment of interferon induced thyroiditis.”