Imiquimod-induced localized vitiligo-like hypopigmentation

Introduction Imiquimod is an immune response modifier,currently the 5% imiquimod cream is approved for treatment of extemal genital,perianal warts,superficial basal cell carcinoma,and actinic keratoses.Its anti-viral activity and anti-tumoral activity seem to be dependent on focal activation of the immune system with induction,synthesis,and release of cytokines,such as interferonalpha,interleukin-12 and tumor necrosis factor alpha[1-2].

Malignant and Pre-Malignant Manifestations of Xeroderma Pigmentosum in Ghanaians

Introduction: Xeroderma pigmentosum is an autosomal recessive disease with sun sensitivity, photophobia, early onset of freckling, and subsequent neoplastic changes on sun-exposed surfaces. There is cellular hypersensitivity to UV radiation and to certain chemicals in association with abnormal DNA repair. Patients with defective DNA nucleotide excision repair (NER) have defects in one of seven NER genes;xeroderma pigmentosum variants have normal NER and a defect in a polymerase gene. Study design: This is a case presentation of five patients with the features of xeroderma pigmentosum, aged 48, 26, 15, 14 and 8 years. The first and last patients were males. Each of the first four patients presented with areas of hyper- and hypo-pigmentation over sun exposed body surfaces. Each of them had a minimum of two cutaneous malignancies, distributed on the upper chest, face or scalp. The fifth patient had skin atrophy, with mottled hyperpigmentation and hypopigmentation but had no malignant lesions. Result: The first, second and fourth patients had their lesions surgically excised and the defects were skin grafted. The third patient was treated with radiotherapy. All the lesions were confirmed histologically as squamous cell carcinoma. No recurrence has been observed. Conclusion: Xeroderma pigmentosum in Ghanaians presents with squamous cell carcinoma involving the head, neck and upper trunk. A minimum period of exposure to UV radiation, not precisely known, is required for the development of the lesions. Education on sun avoidance and protective clothing is necessary to prevent morbidity and mortality.

The Disturbance of Melanogenesis and Melanosome Transfer in the Leukoderma Lesions of Extramammary Paget’s Disease

We frequently encounter characteristic color variation including hypopigmentation, hyperpigmentation, and erythema in extramammary Paget’s disease (EMPD) lesions. Owing to unclear hypopigmentation, the lesional border of EMPD can be poorly defined and it is likely insufficient to perform its complete resection. Although the existence of Toker’s cells and lack of lesional bFGF production have been reported to cause hypopigmentation inside of EMPD lesions, exact mechanisms of hypopigmentation in EMPD are not fully explored. We experienced three EMPD patients with obviously hypopigmented EMPD macules and histopathologically confirmed a reduced number of melanocytes on the hypopigmented macules and their loss on the erythematous plaques or nodules. An ultrastructural analysis on the hypopigmented lesions revealed disturbance of melanosome maturation and melanosome transfer to the adherent Pagets’ cell on the basal layer. No Paget’s cells even adhered to remaining melanocytes with dendrites contained matured melanosome and a few number of matured melanosome complexes were observed in basal keratinocytes. In the present study, we hypothesize that severe disturbance of not only melanogenesis but also melanosome transfer to surrounding Paget’s cells and basal keratinocytes may cause characteristic hypopigmentation in EMPD. Future bioanalysis would reveal molecular mechanisms for hypopigmentation in EMPD.