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erythematous plaques as in the two reported cases. Larvae with 0.2-0.5 mm in diameter are found in the water columns and penetrate the areas covered by bathing suits, including neoprene clothes, seeking shelter to metamorphose. 1-8 The fabrics of the clothes act as a filter draining the water with the trapping and disruption of the planulae against the skin activating its defence cells (cnidocytes). The toxins cause erythematous and pruriginous papules in coert areas of the body. Children are more affected than adults by staying longer in the sea.Koebner Phenomenon was described in 1871 by Heinrich Koebner in a patient with the development of psoriatic plaques in areas of multiple trauma. 10 Isomorphic phenomenon or KP can be triggered by several factors, especially trauma, and is reported in various dermatoses. 10 In this series, the linear distribution of erythematous papules resembles KP. These linear lesions are unlikely to occur at random, or by linear contact of the planulae with the skin. It is more likely that the papules with linear distribution appeared during or after the scratching and were triggered by trauma. We conclude that the observations support the inclusion of SBE in the list of KP triggering diseases.

Incontinentia pigmenti is a rare, multisystem X-linked dominant genetic disorder caused by mutations in IKBKG, the encoding inhibitor of kappa light polypeptide gene enhancer in B-cells. Almost 80% of all cases result from a recurrent intragenic deletion mutation that removes exon 4-10. At present, this mutation can be detected by a multi-primer polymerase chain reaction (PCR) technique although current protocols may preferentially amplify the wild-type allele and miss the deletion. Here, we report a female infant with incontinentia pigmenti that also affected her mother and sister, and two spontaneously aborted male siblings. We developed a modified PCR amplification method that provides more robust detection of the exon 4-10 deletion mutation, which was demonstrated in all affected females in this pedigree.

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Lucio phenomenon is an atypical reaction of leprosy, characterized by vasculitic lesions that can mimic antiphospholipid syndrome (APS) clinically. Distinguishing the two can be difficult as antiphospholipid autoantibodies may be present in patients with leprosy. We report on a 32‐year‐old female patient presenting with a sudden onset of fever, hemorrhagic bullae, and skin necrosis on her lower legs. She was treated for APS due to the presence of antiphospholipid antibodies but had an inadequate response. A skin biopsy revealed thrombotic vasculopathy and necrotizing vasculitis associated with aggregation of foam cells in the perivascular area and subcutis, with acid‐fast bacilli in the histiocytes and blood vessel walls. Direct immunofluorescence showed IgM, C3, and fibrinogen deposition in the superficial and deep dermal blood vessels. The pathology confirmed the diagnosis of Lucio phenomenon, and appropriate therapy was given. It is essential to evaluate the patient comprehensively, including clinical, serological, and pathological aspects, to obtain the correct diagnosis.

Cnidarian envenomations are common occurrences in the tropics that can affect holidaymakers. The cutaneous reactions are classified as immediate or delayed types. Delayed allergic reactions are persistently recurring dermatitis, which can occur within 1-4 weeks from the initial sting, and may last for several months. Hypertrophic scar-like or keloid-like reactions are rare, and are believed to be a type IV hypersensitivity reaction to sequestered antigens from stinging filaments. We report an unusual case of delayed allergic dermatitis with keloid-like presentation caused by Physalia utriculus.

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