J. Sánchez del Río

Acneiform lesions in Becker's nevus and breast hypoplasia

An 18‐year‐old woman was referred for the evaluation of a dull gray macule on the left breast. From the age of 13 years, the patient noted breast asymmetry beginning with the development of the left breast and the presence of a pigmented stain on its border. Physical exploration revealed hypoplasia of the left breast and a homogeneous, light brown macule on the side of the breast ( Fig. 1 ) without infiltration. Papules and pustules were located mainly around the Beckers nevus on the left anterior chest wall. Biopsy specimens with Fontanas stain disclosed a hyperpigmented acanthotic epidermis. A diagnosis of Beckers nevus, acne, and hypoplasia of the breast was made.

Pigmented actinic lichen planus successfully treated with intense pulsed light

MADAM, Actinic lichen planus (ALP) is a rare clinical variant of lichen planus. Pigmented actinic lichen planus (PALP) may constitute the final stage of other ALP variants, or may be a distinctive type of ALP with clinical features similar to those of melasma, but restricted to the face. In this study, we present a patient with PALP that was successfully treated with intense pulsed light (IPL). To the best of our knowledge, this therapeutic option has not been previously used. An otherwise healthy 55-year-old white woman (Fitzpatrick skin type II) was referred to our department because of a 3-year history of a facial pigment disorder. The dermatosis started in summer, but no remarkable improvement was noticed during the winter season. The clinical findings worsened during the subsequent sunny seasons. The patient had no history of drug contact or intake. There was no family history of any similar condition. The patient had tried treating the skin condition with 4% hydroquinone preparations applied twice daily, to no avail. On physical examination, asymptomatic, large, symmetrical patches of dark brown colour with irregular borders were present in the cheeks, the chin and the neck, sparing the skin under the chin (Fig. 1, left). No further cutaneous or mucosal lesions were found. The Dermatology Life Quality Index (DLQI) score was 27. Biopsy specimens from the skin of the neck showed orthokeratosis, focal hypergranulosis and jagged epidermal hyperplasia. The patient was treated with acitretin 0Æ25 mg kg daily for 4 months, and 0Æ1% methylprednisolone ointment applied twice daily for 1 month. Protection measures against natural ultraviolet (UV) radiation were taken, and she was also instructed to avoid sun exposure. No improvement of lesions was observed during the 4 months of treatment. The patient started taking hydroxychloroquine 200 mg daily, without improvement after 2 months. Afterwards, she was treated with oral ciclosporin 3 mg kg daily for 3 months; after the treat-

Apocrine hidrocystoma on the tip of a finger

regulatory role in T-helper (Th) 1 ⁄Th2 responses by favouring the Th1 response. Thus, interferon alfa may promote a vigorous granulomatous reaction similar to that seen in sarcoidosis. Pegylated interferon alfa is the result of adding a polyethylene glycol moiety to interferon alfa. This modification extends the half-life of interferon alfa, providing a constant viral suppression which entails a more sustained virological response. Two cases of sarcoidosis in association with peginterferon (plus ribavirin) have recently been reported. In both cases the coadministration of ribavirin might have acted as a contributory factor in the development of sarcoidosis via inhibition of the Th2 response and enhancement of the Th1 immune reaction. Therefore, on the basis of these early observations it is difficult to assess the role of peginterferon in inducing sarcoidosis. By contrast, our case represents an exceptional situation in which a patient acted as his own control. He did not respond to a first course of nonpegylated interferon. However, 10 years later, peginterferon alfa led to a rapid eradication of HCV. However, the other side of the coin was the onset of sarcoidosis. The enhanced clinical efficacy of peginterferon possibly results from the development of a stronger Th1 response, favouring the appearance of sarcoidosis with a greater likelihood than with conventional interferon alfa. On the grounds of both the latter consideration and the emerging implementation of peginterferon alfa for HCV infection, we speculate that the association between sarcoidosis and this new drug will be reported with a higher frequency than with the classical agent. Skin involvement in interferon alfa induced-sarcoidosis is frequent (68%), and includes subcutaneous nodules (61%), sarcoid papules (17%), scar infiltration (17%), erythema nodosum (13%) and infiltrative plaques (9%). Intrathoracic involvement is also common (79%), with concomitant skin lesions being reported in 49% of cases. As interferon alfa causes influenza-like symptoms that can mask sarcoidosis-related malaise, and as pulmonary involvement is asymptomatic in 35% of interferon alfa-induced sarcoidosis cases, dermatologists must be aware that skin lesions appearing during peginterferon therapy may constitute the only sign of a potentially life-threatening condition. In these cases, the decision of whether or not to continue peginterferon should be made on an individual basis and after a multidisciplinary assessment.

Treatment with chemotherapy of scleredema associated with Ig A myeloma

A 70‐year‐old woman was referred to the dermatology outpatient clinic in January 1999. During the previous 12 months she had developed a progressive induration and stiffness of the skin of her face, neck, shoulders, and upper aspect of her arms. There was no history of a preceding infection or of diabetes mellitus. An examination revealed that the skin of her face, back, shoulders, arms and chest was shiny, erythematous, and diffusely indurated, with a wooden consistency and decreased range of motion. Consistent firm pressure demonstrated a brawny edema. The face lacked expression, with minimal wrinkling ( Fig. 1 ). Lymphadenopathies were not found in any location.

Treatment of hyperpigmentation component in chronic radiodermatitis with alexandrite epilation laser

lichen amyloid is an example of a disease of high prevalence in Asians. Furthermore, the use of traditional healing practices such as coining and cupping in this latter group may also be associated with specific cutaneous disorders. Finally, the cultural practice of skin bleaching is a significant problem in many individuals with skin of colour. Skin of colour also poses unique challenges in relation to dermatological therapeutics. If these are not appreciated, significant adverse reactions may occur. While superficial chemical peels and lasers may be associated with adverse reactions in this cohort, in experienced hands they can be used as adjunctive therapies for managing conditions such as pseudofolliculitis barbae. Disparities in access to healthcare may also have an impact on disease presentation in skin of colour. For example, although skin cancers are uncommon in this cohort, data from the U.S.A. demonstrate that individuals of African, Asian, Latin-American and American-Indian descent frequently present with advanced stage cutaneous malignant melanoma. Although this may reflect an aggressive tumour biology, the impact of accessibility to health services and a lack of awareness of melanoma risk in this cohort cannot be ignored. These issues are and will increasingly be addressed by skin of colour specialists. The emergence of the subspeciality of skin of colour, primarily in North America, is a significant and important milestone in dermatology. Here in the U.K., the presence of a wide variety of racial and ethnic groups, and the admixture of recent and second-generation immigrants, provide us with a unique perspective on this issue. The challenge for U.K. dermatology is using this unique resource to develop novel insights into skin of colour.