Fibroadenoma under therapy with interferons in multiple sclerosis

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system with usually relapsing-remitting course of disease. Therapy with interferon-β is recommended as well in children to reduce relapse rate and to delay the progression of disease. Fibroadenomas (FA) are benign neoplasms in the mammary gland. Their growth is influenced by hormones. Changes in these neoplasms are not previously reported under therapy with interferon. We present the case of a teenager with MS and rapid progression of FA under her interferon treatment.

A 17-year-old girl with primary event of MS in April 2007 with right-sided hemiparesis; during cortisone treatment rapid reduction of complains with persistent mild hemiparesis of her right hand as residual finding. Second relapse of MS in October 2009 with the same neurological symptoms. Since October 2011, therapy with interferon-β-1a (Rebif 44 ug) is started, beneath this a stable condition of disease is achieved. Additionally, this girl has few FA in mammary glands (BIRADS 0 – 3), hirsutism, polycystic ovary and obesity. Furthermore, she has a multinodular struma with complete extirpation of thyroid gland in 2009 in case of suspected malignancy. The malignancy cannot be confirmed histologically. The measurement of hormone level repeatedly reveals normal. Under treatment with interferon-β-1a, she develops a rapid progression of FA with increased number and size, which could be confirmed both in clinical examination and radiological techniques (ultrasound, mammography). Biopsy is planned now to prove the diagnosis histologically.

For the first time, this case presents FA as a rare side effect of treatment with interferons in pediatric MS. This adverse event is especially important for female patients. Completion of therapy because of progressive course of FA remains unclear, especially in stable condition of disease. A correlation of aggressive fibromatosis and interferons is recently described in literature. This association is caused by mutation in APC-gen with increased β-catenin-mediated T cell-factor