Corticosteroid (Topical)
PREGNANCY RECOMMENDATION: Limited Human Data—Animal Data Suggest Risk
BREASTFEEDING RECOMMENDATION: No Human Data—Potential Toxicity
PREGNANCY SUMMARY
The only report describing the use of fluocinonide in human pregnancy involved a woman in the 3rd trimester. The amount of topically applied fluocinonide reaching the systemic circulation is uncertain, but suppression of the hypothalamic–pituitary–adrenal (HPA) axis has been observed in nonpregnant patients. Use of occlusive dressings will increase the amount absorbed. Moreover, it is not known if the amounts absorbed can cause the congenital defects and growth restriction observed in humans with systemic corticosteroids. One manufacturer recommends treatment for no more than 2 weeks with a total dosage not exceeding 60 g/week (1). If a pregnant woman requires long-term topical corticosteroid therapy, the use of a less-potent agent should be considered.
FETAL RISK SUMMARY
Fluocinonide is a potent, synthetic, fluorinated corticosteroid that has anti-inflammatory, antipruritic, and vasoconstrictive properties. It is available in various topical formulations, such as creams, ointments, gels, and solutions in concentrations of 0.05% or 0.1%. Fluocinonide is indicated for the relief of the inflammation and pruritic manifestations of corticosteroid-responsive dermatoses (1). Systemic absorption does occur with topical use with the amount of absorption affected by inflammation, the integrity of the epidermal barrier, and the use of occlusive dressings. Suppression of the HPA axis is a potential complication. Application of a 0.1% cream twice daily in pediatric and adult patients has been associated with suppression of the HPA axis (1).
A number of animal reproduction studies have demonstrated that corticosteroids cause developmental toxicity (growth restriction, structural anomalies, and death) (see Hydrocortisone). Potent topical corticosteroids also can cause structural anomalies after dermal application (1).
It is not known if fluocinonide crosses the human placenta. The molecular weight (about 495) is low enough that exposure of the embryo and fetus should be expected. The placenta does contain an enzyme that degrades corticosteroids (e.g., see Betamethasone, Dexamethason, Hydrocortisone, and Prednisolone), although some active drug still crosses. The amount of fluocinonide reaching the systemic circulation apparently has not been measured, but amounts sufficient to suppress the HPA axis has been shown clinically, as indicated above.
A 2006 case report described a 21-year-old woman in the 3rd trimester with a diagnosis of food-induced acute generalized exanthematous pustulosis (2). She was successively treated with fluocinonide cream 0.05% and tapering doses of systemic methylprednisolone (doses and durations not specified). She eventually gave birth at 40 weeks’ gestation to a healthy male infant (2).
BREASTFEEDING SUMMARY
No reports describing the use of fluocinonide during human lactation have been located.
If fluocinonide reaches the systemic circulation, the molecular weight (about 495) is low enough that excretion into breast milk should be expected. The amount of topically applied fluocinonide reaching the systemic circulation is uncertain, but suppression of the HPA axis has been observed in nonpregnant patients. Because of this uncertainty, if a nursing woman requires long-term topical corticosteroid therapy, consideration should be given to a less-potent corticosteroid.
References
1.Product information. Vanos. MEDICIS, The Dermatology Company, 2007.
2.Valkova S. Food-induced acute generalized exanthematous pustulosis in a pregnant woman. Skinmed 2006;5:199–201.