A 23-year-old man presented with an erythe- matous edematous patch with centrally grouped vesicles on the left ankle (Fig. 1). The skin lesion occurred following a coral injury while he was skin-scuba diving at the island of Hinan, China 2 days prior to his presentation. This was associated with stinging pain and mild itching. He stated that the accident had occurred near the coral reef and at the time, he had felt stinging pain on his left ankle which was not covered by the diving suit. On physical examination, there were no remarkable findings including a normal body temperature except for the skin lesion. His past medical history was not significant. Histopathologic findings re¬vealed the extensive epidermal necrosis with subepidemal blisters and neutrophils in the blister cavity (Fig. 2) and interstitial, perivascular and periadnexal inflammatory cell infiltration throughout the dermis (Fig. 3). There was also panniculitis predominantly infiltrated with neutrophils and some eosinophils and lymphohistiocytes without the evid¬ence of foreign body granulomas (Fig. 4). Radio logical examination of his left ankle showed nonspecific findings and no foreign body materials, and laboratory testing showed only leukocytosis including neutrophilia with a mildly elevated ESR. We did not perform a bacterial culture and sensitivity test.

INTRODUCTION
One of the most common injuries in the marine environment is the stings caused by Cnidarians including jellyfish, the Portuguese man of war, hydroids, sea anemones, and coral. Corals are a member of the class Anthozoa, which is composed of many calcified polyps that containing tentacles with nematocysts, venom-filled cells that are responsible for stings and lacerations. Coral injuries present with acute reactions such as pain, erythema, and swelling and may also be complicated by foreign-body reactions, secondary bacterial infections, and/or localized eczematous reactions.

The effects of CsA for the treatment of AA have been assessed in various in vitro studies. Oliver et al demonstrated that oral CsA restored hair growth in the Dundee Experimental Bald Rat Model of AA by reducing the mononuclear cell infiltrate around the hair follicles and renewing hair growth. Gafter- Gvili et al reported that CsA-induced hair growth in mice was associated with the inhibition of the calcineurin-dependent activation of NFAT in the follicular keratinocytes. They found that CsA delays the duration of the terminal differentiation of hair follicular keratinocytes and it retards catagen induction. They further demonstrated that CsA induced hair regrowth through delaying the regression of hair follicles by inhibiting the apoptosis of follicular keratinocytes.
Response
Of all the patients, 77.4% (n=24) were classified into the responder group (Table 1). Of these 24 patients, 66.6% (n=16) were cosmetically acceptable responders, and 33.3% (n=8) were satisfactory responders (Fig. 1). The initial response time ranged firom 4 to 9.5 weeks with a mean of 5.4 weeks. The mean dose of methyl prednisone during the maintenance phase was 2.9 mg/day and the dose ranged from 2 to 6 mg/day. The type with the best response was ophiasis, followed in order by patchy AA affecting more than 50% of the scalp, AU and AT/AU. The least responsive type of AA was patchy AA affecting less than 50% of the scalp.
Patients
Thirty-four patients (16 men and 18 women) with severe or refractory AA were enrolled in this study. Their mean age was 28.1 years (range: 6-54 years) and the duration of the disease ranged from 6 months to 16 years.

INTRODUCTION
Treating patients with alopecia areata (AA) remains difficult, and many treatment modalities have been used, including intralesional, topical and sys¬temic corticosteroids, ultraviolet light and contact sensitizers. Of these, systemic corticosteroids are effective for the treatment of severe AA, but to maintain hair regrowth, an increase in the dosage is inevitable. A high dose of systemic corticosteroids poses a major concern because of the side effects of systemic steroid use, such as diabetic mellitus, hypertension, acne, psychological changes, osteoporosis and the suppression of the adrenocorticotropic axis.
Although a case resembling IP was first described by Garrod in 1906, IP was characterized as a clinical syndrome by Bloch in 1926. In 1927, Sulzberger reported Bloch’s case in details, and then proposed as Bloch-Sulzberger’s disease.
In general, boys with single X chromosomal gene abnormality are so severely affected as to be lethal in utero, therefore there is an increased incidence of spontaneous abortion in affected women, presumably of male fetuses.