Combined oral contraceptives pills are widely prescribed throughout the world. It is likely that photosensitivity from these pills is a rare problem. There are few reports available on progesterone-induced photosensitivity disorder. Clinically, the nonpapular nature of the eruption and the symptoms of prickling were observed in this current case of contraceptive-induced photosensitivity. When the patient stopped taking the contraceptives, the abnormal phototest reaction reverted to normal4
. The mechanism of contraceptive-induced photosensitivity is uncertain. Many investigators have suggested that photosensitivity is due to the hepatotoxicity and the direct effect of the estrogen component of the pills on porphyrin synthesis5
. Two types of photosensitivity induced by estrogens, i.e., hepatic porphyria and a polymorphic light eruption-like dermatosis, have been previously observed6
. The role of progesterone in photosensitivity has not been previously reported.
Our patient showed photosensitivity to UVA and UVB on the phototest. Clinically, she showed an erythematous patch with an itching sensation on only the centrofacial area of the residual vitiliginous lesion. The intradermal testing of progesterone with UVA and UVB irradiation were positive. Yet the intradermal skin test with progesterone was negative. Unfortunately, we could not perform the skin test with the excipient (peanut oil) due to a lack of corporation. She didn't show any previous history of a cyclic skin rash in the luteal phase of her menstrual cycle. So, we diagnosed her as suffering with progesterone-induced photosensitivity in the vitiliginous area during pregnancy rather than progesterone-induced dermatitis. The low dose of UVA (1 J/cm2) and UVB (5 mJ/cm2) and the negative intradermal skin test with progesterone makes the diagnosis of phototoxicity likely rather than the diagnosis of photoallergy.
It is interesting that two critical factors in the photosensitivity of this patient must be considered. First is the hormonal effect of photosensitivity during pregnancy. The patient started the intramuscular injections of synthetic progesterone at 4 weeks of pregnancy. Physiologically, before the luteoplacental shift, the corpus luteum of the pregnant woman continues to produce progesterone and estrogen during the first 8 to 9 weeks and hormone β-HCG is released from the developing placenta7
. The corpus luteum then becomes redundant and the steroid hormone production is taken over by the placenta. The patient took an intra-musculature injection of synthetic progesterone for 3 weeks. This period increased the estrogen production of the corpus luteum. The photosensitivity of this patient may be associated with the synthetic progesterone combined with the estrogen from the corpus luteum. Second was a difference of photoprotection between the vitiliginous area and the adjacent skin. In the vitiliginous areas, because of the deficiency of melanin, the dose of ultraviolet light reaching the deepest layers of the epidermis and the underlying dermis was much greater than that in the normal skin. So, the vitiligo patient complained that the depigmented area suffered from photosensitivity, although the remaining skin reacted normally to sunlight. We think that the patient had a subclinical degree of photosensitivity to sunlight, and this was caused by the progesterone.
We report here on a case of photosensitivity that was localized in a vitiliginous facial lesion, and this photosensitivity was associated with the intramuscular injections of synthetic progesterone she had received during an in vitro fertilization-embryo transfer.