Do hormonal contraceptives stimulate growth of neurofibromas? A survey on 59 NF1 patients

A survey was carried out on 59 female NF1 patients who are practicing or have practiced hormonal contraception to examine the effect of the various contraceptives on the growth of neurofibromas.Majority (53 out of 58) of patients who received oral estrogen-progestogen or pure progestogen preparations reported no associated tumor growth. In contrast, significant tumor growth was reported by two patients who received depot contraceptive containing high dose of synthetic progesterone.Oral contraceptives do not seem to stimulate the growth of neurofibromas in NF1 patients. High doses of progesterone might stimulate the growth of neurofibromas and deserve more caution.Neurofibromatosis type 1 (NF1) is a genetic disorder with an incidence of about 1 in 3000. Multiple neurofibromas are the most significant hallmark of NF1. These benign tumors of peripheral nerves mostly start developing at puberty and can increase in size and number during pregnancy [1]. Since decades, physicians involved in the care of NF1 patients are concerned by the dilemma if hormonal contraceptives containing estrogen and progestogen could stimulate the onset of new or the growth of the yet present neurofibromas. Recently, McLaughlin & Jacks [2] reported expression of progesterone receptors and estrogen receptors in 75% and 5% of 59 neurofibromas immunohistochemically, respectively. The authors thus inferred an important role of progesterone in neurofibroma growth and suggested that antiprogestins may be useful in the treatment of this tumor.Hormonal contraceptives contain synthetic progestogen which bind to the progesterone receptors. Depending on the formulation of the currently available preparation, combined oral contraceptives contain 0.02 to 0.05 mg synthetic estrogen and low doses of various types of synthetic progestogen. These kinds of contraceptives suppress the pituitary gonadotropin secretion and thus reduce the endogenous levels of estrogen and progesterone. The deficiency of endogenous