Autoimmune Progesterone Dermatitis

Tami Maguire


Dermatology Nursing. 2009;21(4):190-192. 

In This Article

Evidenced-based Treatment Options

Evidence shows that various possible treatments exist for the different types of progesterone sensitivity. Symptomotology varies in each case, requiring separate courses of treatment according to the level of manifestation of progesterone sensitivity (Snyder & Krishnaswamy, 2003). Definitive treatment of APD involves using anovulatory agents to suppress progesterone secretion. In mild cases, the skin eruptions may be controlled with topical steroids and oral histamines, but is sometimes resistant to this conventional therapy (Baptist & Baldwin, 2004). Systemic glucocorticoids in high doses have been reported to control the cutaneous lesions of APD, but not in all studies. Although symptom relief has been attained with the use of systemic corticosteroids, the goal of treatment is to inhibit the secretion of endogenous progesterone by suppression of ovulation (Rodenas et al., 1998).

The 17-a-alkylated steroids such as danazol or the later generation stanozolol have been used to suppress ovulation in simple dermatologic cases. This can be complicated by elevations in liver function tests (Baptist & Baldwin, 2004). Severe cases of APD have been treated prohylactically with danazol before the expected onset of menses and continued 3 days after menses ended (Snyder & Krishnaswamy, 2003). By using this treatment regimen, there was no interference with the menstrual cycle, and the adverse effects (elevated liver function tests and masculine side effects) with danazol are avoided.

Tamoxifen, a nonsteriodal anti-estrogen agent, has also been used as a treatment modality, which has induced remission of APD. Side effects include amenorrhea and negative bone metabolism effects (Snyder & Krishnaswamy, 2003). Tamoxifen has also been associated with increased risk of deep vein thrombosis and cataract formation. Conjugated estrogens have also been used in the treatment of APD. Some improvement has been shown, although this required high doses (Baptist & Baldwin, 2004). This treatment is not commonly used today due to the increased risk of endometrial carcinoma.

Different gonadotropin-releasing hormone (GnRH)/LH - RH) agonists such as buserelin and triptore have also been used to induce remission by causing ovarian suppression (Baptist & Baldwin, 2004). Side effects include symptoms of estrogen deficiency (hot flashes, vaginal dryness, decreased bone mineral density), so estrogen supplements may be necessary. The negative effects of GnRH therapy are its expense and that estrogen supplementation is often necessary. For patients in whom these conservative therapeutic measures do not control the disease, definitive treatment appears to be surgical management with oophorectomy (Snyder & Krishnaswamy, 2003).


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