Roy Moutran

Fractional laser for vitiligo treated by 10,600 nm ablative fractional carbon dioxide laser followed by sun exposure.

Vitiligo is an acquired disorder of the skin and mucous membranes. Many patients with vitiligo remain in the refractory state despite the availability of numerous potential treatments. To the best of our knowledge, only one trial considers ablative fractional CO2 laser in the treatment of vitiligo.

Nicolau livedoid dermatitis occurring after sclerotherapy

A 53-year-old woman presented with a lesion within the left popliteal fossa 2 weeks following varicose vein sclerotherapy. Two days following the sclerotherapy (polidocanol 1%), she complained of pain within the injection site that did not respond to anti-inflammatory or analgesic medications. Clinical examination illustrated a livedoid lesion with geographic margins and a necrotic center at the site of injection of polidocanol (Panel). A duplex ultrasound documented occlusion of a small saphenous vein (SSV) tributary and incompetence within the proximal portion of the SSV proper. A diagnosis of Nicolau livedoid dermatitis (NLD) was rendered. Treatment included low-molecular weight heparin (LMWH; enoxaparin 40 mg/day), a class IV topical corticosteroid (clobetasol propionate), and a gradient compression stocking. The pain abated over several days and 10 days later the lesion resolved. NLD is a rare cutaneous reaction at subcutaneous or intramuscular injection sites characterized by intense pain followed by a violaceous livedoid plaque that may evolve to skin necrosis. It often occurs in weak areas (e.g. inguinal folds, popliteal fossa) and is due to direct arterial embolism, ischemia after perivascular compression of the injected product, and/or reflex arterial vasospasm due to para-neural or para-arterial injection. The latter mechanism was thought to underlie the pathogenesis of NLD in our subject. Until recently, it has been rarely reported with varicose vein sclerotherapy.1–4 Treatment of NLD is not well specified. Usual therapy relies on anticoagulants and prednisone.2 We used LWMH and a local potent corticosteroid, not prednisone as is the usual practice,1–4 with an excellent result. Thus, an appropriate topical glucocorticoid agent could replace systemic steroid therapy when treating a focal lesion of NLD. Images in Vascular Medicine

Depilatory laser: a potential causative factor for inguinal hyperhidrosis: Report of three cases

Abstract Hyperhidrosis has recently been described as a novel adverse effect of laser-assisted hair removal in the axillary area. Inguinal Hyperhidrosis (IH) is a localized and, typically, a primary form of hyperhidrosis affecting the groin area in individuals before age 25. IH has been reported in the literature after traumas and as a dysfunction of the central sympathetic nervous system. To the best of our knowledge, IH has never been reported as secondary to laser-assisted hair removal. Herein, we report three cases of IH following depilatory laser of the inguinal zone. Three female patients with no relevant medical history presented with the complaint of excessive sweating in the inguinal area after undergoing full bikini depilatory laser sessions. Although never described before, depilatory laser seems to trigger the occurrence of hyperhidrosis in the inguinal zone.

Etoricoxib‐induced toxic epidermal necrolysis

phages. We report a case of a 65-year-old man with Down syndrome (DS) presenting with multiple cutaneous lesions, which developed over the course of several months on his upper and lower limbs. These had been noticed by his caregivers. He was asymptomatic and otherwise well apart from learning difficulties in keeping with a diagnosis of DS. On examination, there were approximately 20–30 clinically similar lesions on the anterior and posterior aspect of his upper arms and lower legs (Fig. 1). The lesions measured up to 1 cm in diameter and were red or purple in color and firm. They appeared to be within the dermis with a positive dimple sign. Baseline biochemistry, glucose, cholesterol, immunoglobulins, protein electrophoresis, erythrocyte sedimentation rate, hepatitis and HIV serology, and a chest radiograph were within normal limits. A full blood count demonstrated a long-standing mild lymphopenia of 1.4 9 10/L (normal limits 1.5–4.0 9 10/L) likely related to his DS. Owing to the number of lesions and short clinical history, two lesions were biopsied, one on the shoulder and one on the leg, and pathology confirmed simple dermatofibromas (Fig. 2). Multiple eruptive dermatofibromas usually refers to the development of between four and eight dermatofibromas over a period of about four months, thought to be linked to immunodeficiency or autoimmune conditions. To our knowledge, there is only one previous report of patients with DS developing multiple dermatofibromas in the literature, and this report included one patient with DS who was immunosuppressed with methotrexate. The remaining two patients were found to have hypercholesterolemia and thyroid disease, both reported in association with multiple eruptive dermatofibromas. Our patient had a very mild lymphopenia but was otherwise not immunosuppressed and had no other history of autoimmune conditions. It is plausible that the development of eruptive dermatofibromas in this case is related to an altered immune system in keeping with the diagnosis of DS. It is known that patients with DS have altered antibody and cell-mediated immunity and altered phagocytic function leading to difficulty fighting infection and an increased frequency of cancers. For completeness, we therefore screened for a new immunodeficiency or malignancy, as outlined above. Consequently, multiple or eruptive dermatofibromas may be added to the list of dermatological disorders that appear with increased frequency and/or are more severe in patients with DS, including atopic eczema, seborrheic eczema, vitiligo, alopecia areata, elastosis perforans serpiginosa, psoriasis, syringomas, and milia-like calcinosis cutis.

Development of multiple nevi and lentigines in a child with Netherton's syndrome treated with narrowband ultraviolet B phototherapy.

A newborn boy presented with skin problems that his mother reported had been present since birth. The patient was born at term to consanguineous parents (seconddegree cousins). His parents described generalized exfoliative erythroderma (Fig. 1), rapidly complicated with septicemia in his first week of life. His medical record showed continuous diarrhea and a difficulty to thrive. After that, the patient did not show for his follow-up visit. He returned to our department at the age of 2 years. On physical examination, his hair was brittle and dry, with partial alopecia. His skin condition had not improved (Fig. 2). On examination of the hair under polarized light, trichorrhexis invaginata was noted. Genetic examination revealed a mutation of the gene SPINK5, mapped to chromosome 5q32. The diagnosis of Netherton syndrome was made. The patient has a phototype III. The patient’s skin condition had worsened with continuous generalized activity, refractory to topical corticosteroids, emollients, and topical pimecrolimus. We proposed narrow band ultraviolet B (NB-UVB) phototherapy. The starting dose was 350 mJ/cm, and at each visit, the dose was increased by 20% until 1700 mJ/cm (maximum dose). The patient noted a marked improvement after 18 sessions. Since then, the patient was lost to follow-up. He returned after four years for follow-up, when he was 6 years old. As he responded very well to UVB with fewer flares and less pruritus, he continued to have the sessions without medical supervision. When reviewing his record, we noticed that he has done a total of 170 sessions of NB-UVB phototherapy, with a cumulative dose of 240 J over three years. We immediately asked the patient to stop the sessions and to get a skin and ophthalmological checkup. On physical examination at that time, there was neither erythroderma nor ichthyosis. Nevertheless, over time he has developed multiple pigmented lesions all over his body. We counted more than 100 lesions over his chest and abdomen (Fig. 3). One of them was excised. The histopathologic features revealed a lentigo. Netherton syndrome is a rare autosomal recessive disorder of the skin, hair, and immune system, manifested by ichthyosis linearis circumflexa or congenital ichthyosiform erythroderma, trichorrhexis invaginata, and atopy. The underlying genetic defect of Netherton syndrome has been mapped on chromosome 5q32, and the affected gene encoding a serine protease inhibitor has been reported to be SPINK5. SPINK5 encodes a Kazal-type serine proteinase inhibitor, designated LEKTI. The possible role of LEKTI and its mutations in cutaneous neoplasia was mentioned by Krasagakis et al. On the other hand, the development of cutaneous neoplasm may be causally related to congenital ichthyosis. This was recorded in patients with keratitis–ichthyosis– deafness syndrome. Multiple skin carcinomas were also reported in patients with Netherton syndrome. Phototherapy (psoralen + UVA [PUVA] and NB-UVB) is a well-known treatment modality in the long-term management of psoriasis. It can also be used in various dermatological conditions. Among them, ichthyosis can be treated with phototherapy. Short-term side effects are commonly known (e.g., erythema). Long-term and dosedependent side effects include an increased risk of developing accelerated skin aging, actinic keratosis, atypical

Hyalinosis cutis et mucosae manifests in different features in two sisters

Hyalinosis cutis et mucosae (lipoid proteinosis or Urbach– Wiethe disease) is a rare disease of autosomal recessive inheritance, which affects mainly the skin and mucous membranes of the pharyngolaryngeal tract. Some familial cases have been described in the literature. We report observations of two sisters suffering from the disease with different symptoms and highlight the potential for variance in the penetrance and expression of the disease within the same family.

A "sexually transmitted" fixed drug reaction.

CASE A 37-year-old man presented with a 7-day history of a penile lesion. His medical history was unremarkable, and he denied taking any medications in the last 8 months. His only sexual partner, his wife, is healthy apart from the occasional self-medication using diclofenac for cervicalgia. Clinical examination showed a discrete postinflammatory hyperpigmentation. The patient reports that he had noticed the same lesion 2 months prior and was convinced that his disease was sexually transmitted. Complete blood workup and routine urinalysis revealed no abnormalities. HIV antibodies, venereal disease research laboratory test, and immunoglobulins G and M against human herpes simplex viruses were all negative. During the visit, the patient was asking about the transmissibility of his disease. After getting the explanations about the drug-induced origin of FDE, he declared that he had not taken any antibiotic before the eruption. Drug intake history showed no recent medications, but he did report that his wife had just begun a course of diclofenac for her cervicalgia. His eruption occurred 2 days after sexual contact with his wife. Surprisingly, the first episode of ‘‘erythematous pigmented glans penis that resolved spontaneously’’ 2 months ago also coincided with intake of diclofenac by his wife. Further history taking confirmed that a condom was not used for both episodes. Thus, a clinical diagnosis of FDE after sexual contact with a partner on diclofenac was made. Once the affected area was completely lesion-free, we suggested a lesional patch test with topical diclofenac. Within 2 days, an obvious dull-red, round, edematous plaque developed on his penile shaft and glans (Fig. 1). The diagnosis of FDE was confirmed.

The Case | A hemodialysis patient with bullous skin lesions

A 65-year-old woman with end-stage kidney disease secondary to diabetes on hemodialysis for 5 years presented with a several-week history of skin lesions over her face and hands. She had then noted fluid-filled lesions following minor trauma to her hands. The patient did not report any history of skin disease. On clinical examination, multiple erosions with crusting were noted over her cheeks and glabella, dorsal hands, and feet, where she also had some milia (Figure 1). There were no hypertrichosis, sclerodermoid lesions, or any other skin abnormalities. Laboratory analysis showed increased serum ferritin levels to 1735 mg/l (normal 40–250 mg/l), and normal metal screen (aluminum, zinc, and lead). Screening for hepatitis C was negative. Liver enzyme levels were elevated (AST 70 U/l; ALT 70 U/l; and AP 530 U/l).

Five cases of syphilis from an urban university hospital in Lebanon.

In Lebanon, there are no data on the incidence of syphilis because there is no mandatory reporting of cases to Public Health authorities. This is a retrospective study that interviewed all syphilitic patients who presented to the Dermatology Department in Mount Lebanon hospital between July 2011 and March 2014. Five patients were included here. The demographic consisted exclusively of men, and all cases identified themselves as men who have sex with men (MSM). Data retrieved from the interviews are detailed in Table 1. All participants had more than five sexual partners per month. They all reported receptive anal sex. Four participants reported consistent condom use during anal sex, while only one patient used condoms irregularly. All participants practised unprotected fellatio. In the previous six months, the five patients had been living in Lebanon, but all of them reported various short-term travels (New York, London, Montreal, Paris, Cairo and Dubai) during that time period with sexual contact with non-Lebanese partners. Only one participant was co-infected with HIV. All participants had a prior diagnosis of at least one sexually transmitted infection (STI) (excluding HIV). Four participants reported the use of recreational drugs, alcohol, or both, before or during sex. The clinical presentation of syphilis was primary with genital ulcer in only one patient. The four others discovered their syphilitic status on screening tests. In the Middle East and North Africa regions, the annual incidence of syphilis is 2.2 per 1000. In Saudi Arabia, among 3270 women tested at King Khalid University Hospital in Riyadh, only one was found syphilitic. The prevalence was 0.0% in women from different areas in Jordan. According to our study, all patients reported sexual intercourse while travelling in cities known to have a

Pityriasis versicolor: a case of resistance to treatment.

Pityriasis versicolor: a case of resistance to treatment Pityriasis versicolor (PV) is a common fungal skin infection affecting young adults worldwide, mainly in tropical climates. Treatment of PV infection is usually easy and effective but is becoming increasingly challenging with the emergence of resistant Malassezia species. Here we present a case of PV, which is resistant to many well conducted antifungal therapies. A 52-year-old patient consulted in April 2009 for an opinion concerning multiple white macules with fine scales on his chest and back (Fig. 1). The diagnosis of PV was clinically evident at that time and was also supported by a positive Wood’s light examination (Fig. 2). The patient was initially treated with itraconazole 200 mg/d for one week but was not cured by the end of the week. A shift to fluconazole 300 mg/week resulted in partial improvement after two weeks and total clearance after one additional month of combined systemic fluconazole 300 mg/week and local treatment (terbinafine twice daily for two weeks). Contact with the patient was lost for one year after which he came back with a recurrence of his PV. A Wood’s light examination was again positive. In contrast with the previous visit, the current PV was completely resistant to oral fluconazole (300 mg/week during two weeks). In addition, 200 mg/d of ketoconazole was prescribed for 10 days but was unsuccessful. The patient returned after nine months complaining of a persisting PV infection. A blood test (including liver function tests and immunology tests) was performed and revealed no anomalies. Again, the patient received fluconazole (300mg/week) for four weeks followed by itraconazole (200mg/d) for two weeks with topical treatment (fenticonazole cream). All treatments considered were futile, so a biopsy was done and confirmed the diagnosis of PV by showing abundant short hyphae and budding yeast forms within the stratum corneum (Fig. 3). A culture was not performed as it is not the gold standard test for the diagnosis of PV and because it was previously done by another physician in our patient without any conclusive results. A new regimen was suggested (local Brumixol with 8% salicylic acid and ketoconazole shampoo), but the patient did not adhere to the proposed treatment, and contact was again lost.