Martina Espasandín-Arias

Persisting allergic patch test reaction to minoxidil manifested as cutaneous lymphoid hyperplasia.

Keywords: allergic contact dermatitis; cutaneous lymphoid hyperplasia; minoxidil; patch test; persisting reaction

Allergic contact dermatitis due to a surgical marker

A 19-year-old female hairdressing student was referred because of hand eczema (Fig. 1a), which had developed during the 8 months she had been training. The history also showed an intense reaction following a ‘temporary henna tattoo’ when she was aged 15 years. Patch testing was performed, according to the ICDRG criteria, with the Spanish Contact Dermatitis Research Group baseline series (TRUE Test®; Marti Tor, Barcelona, Spain) extended with the local anaesthetic series (AllergEaze®; MartiTor), and the hairdressing and fragrance series (both from Chemotechnique, Vellinge, Sweden) using Curatest® chambers (Curatest®;

Photosensitivity associated with systemic triflusal therapy

To the Editor, Triflusal (2-acetyloxy-4-trifluoromethylbenzoic acid) is a fluorinated acetylsalicylic acid analogue used as an antiplatelet drug for prophylaxis of thromboembolic disease. Its main side effects are those concerning the gastrointestinal system. We report a systemic photosensitivity and a solar urticaria in a patient under triflusal therapy. A 72-year-old man, with Fitzpatrick skin phototype II and medical history of hypertension undergoing treatment with olmesartan since 2005, was diagnosed with a carotid stenosis in September 2011; therefore, triflusal (300 mg/12 h) was prescribed. Two years later, he was sent to our Photobiology Unit because of outbreaks of eczematous lesions involving the photoexposed areas of his face, neck and hands (Fig. 1a). Those lesions had appeared 1 month after the introduction of triflusal, and persisted despite the use of topical corticosteroids and oral antihistamines. He was taking no other medication. In order to rule out a systemic photosensitivity, phototesting was performed on the skin of his lower back, using a solar simulator to test UVB and UVA (Xenon arc 16S; Solar Light Co., Philadelphia, PA, USA) and a slide projector to test visible light (GAF 502 Autofocus slide projector lamp). The doses we used were from 3.7 to 24.7 mJ/cm for UVB and from 0.5 to 10 J/cm for UVA. An urticarial reaction was observed 15 min after UVB irradiation (>3.7 mJ/cm) (Fig. 1b) and UVA irradiation (>0.5 J/cm) (Fig. 1c), whereas visible light showed a negative response. These lesions were highly pruritic and cleared after 30 min. Moreover, the minimal erythema dose to UVB (UVB-MED) was 10 mJ/cm (normal value 28 4 mJ/cm, pathologic value <19 mJ/cm) (1) and response to UVA was abnormal (erythema after a single dose of 10 J/cm) (Fig. 1d). He was asked to discontinue triflusal, which was replaced by acetylsalicylic acid (ASA), with a subsequent improvement of his lesions. One week after this switch, the patient was almost asymptomatic, the UVB-MUD had risen to 13.5 mJ/cm and there was no urticarial response to UVA (up to 10 J/cm). A new phototest was performed 2 months later, showing a negative response to UVA and a UVB-MED of 24.7 mJ/cm (an increase above 70% of the previous one). Photopatch tests were also performed with the baseline series of the Spanish Group of Photobiology (MartiTor, Barcelona, Spain) being applied in duplicate to the skin of the upper back, extended with triflusal, 2-hydroxy-4-trifluoromethylbenzoic acid (HTB, the triflusal active metabolite) and ASA. All of them were prepared by the hospital pharmacy at 1% in petrolatum and were applied in triplicate to the skin of the upper back. After 2 days, one set was removed and irradiated with 5 J/cm UVA, and the set of triflusal, HTB and ASA was also removed and irradiated with a sub-UVB-MED dose (17.3 mJ/cm). Readings were done immediately, at 30 min, 60 min, days 1, 2 and 3 postirradiation. Immediate reading was negative, whereas a palpable erythemato-edematous reaction was observed at day 1 postirradiation only in triflusal and HTB UVB photopatches. A weak non-palpable erythema was also noticed in the same patches irradiated with UVA (Fig. 2). Laboratory tests were also performed in

Scrotal bullous pemphigoid in an elderly patient

Scrotal bullous pemphigoid in an elderly patient Editor, Genital bullous pemphigoid (GBP) is a clinical variant of localized bullous pemphigoid (BP). It occurs most frequently in pediatric patients and primarily in females. Localized GBP is uncommon in males, and to our knowledge, there have only been two previous cases of this condition reported, both in pediatric patients. An 89-year-old male patient was referred for dermatological assessment presenting with pruritic lesions on the scrotal skin, followed by the eruption of blisters and bleeding erosions in this area, which had lasted one month. He had been previously treated with topical antibiotics, with no notable improvement. His medical history included poliomyelitis, two ischemic strokes, and type 2 diabetes mellitus, and he denied any changes in his regular medication over the last year. Dermatological examination revealed a large erythematous and edematous plaque over the entire scrotum, with round bleeding erosive lesions measuring approximately 1 cm. Smaller, serous-filled tense blisters were also observed over the erythematous plaque (Fig. 1). Nikolsky’s and Asboe-Hansen’s sign tests were negative. No similar lesions were observed in other areas. The histopathological examination, using hematoxylin and eosin staining, revealed a subepidermal blister with an entirely epidermal roof. In the base of the blister, an intact dermis preserving dermal festooning and a predominantly lymphocytic inflammatory infiltrate with numerous eosinophils were observed. In the blister cavity, some erythrocytes and inflammatory cells (lymphocytes and eosinophils) were noticed (Fig. 2). On the periphery of the blister, superficial vacuolar dermatitis with a predominantly eosinophilic infiltrate was also observed. PAS staining revealed the basement membrane at the base of the blister. Direct immunofluorescence testing of perilesional skin showed linear deposition of IgG and C3 along the basement membrane. Routine hematological and biochemical tests only revealed elevated IgE levels (977 kIU/l). Neither eosinophilia nor circulating anti-basement membrane zone antibodies were observed. A high-strength topical corticosteroid (clobetasol propionate) was administered once daily at an approximate dose of 1 g/day on the scrotal skin. Complete clinical remission was observed in eight weeks. Scrotal pemphigoid is a rare form of localized GBP. GBP is more common in female and pediatric patients, the most frequent manifestation being vulvar or vulvovaginal pemphigoid in girls, especially those over one year old. The first case of female genital GBP in childhood was reported by DeCastro et al., and since then <20 cases have been published. Female GBP usually presents with vesiculobullous skin lesions in the vulvovaginal area. It is normally a benign condition with a rapid response to topical steroids. Localized GBP is uncommon in adult women, with only three cases reported: one vulvar, the other vaginal, and a third case affecting both areas. Localized GBP is extremely unusual in males, with only two cases reported: the first affecting the glans penis in a 7-year-old boy; and the second affecting the scrotum in a 2-year-old boy. Both responded favorably to oral prednisone (1–2 mg/kg/day) without any evidence of subsequent recurrence. A further three pediatric cases in which not only the genital area was involved have been reported. Oral prednisone (1–2 mg/kg/day) is the treatment of choice for this condition; however, a favorable response with topical corticosteroids was obtained in some cases of female genital pemphigoid. Other treatments have been used for this disease, including dapsone, sulfapyridine, Figure 1 Serous-filled tense blisters and bleeding erosions over an erythematous plaque

Erythematöser, nicht-ulzerierter Knoten im Bereich des Schulterblatts

Ein ansonsten gesunder 57-jähriger Mann stellte sich mit einem seit sechs Monaten vorliegenden asymptomatischen, erythematösen, nicht-ulzerierten Knoten im Bereich des linken Schulterblatts vor (Abbildung 1 ). Die Dermatoskopie zeigte eine gut abgegrenzte Läsion mit einem unstrukturierten roten Bereich in der Mitte, der von einem weißen Erythematöser, nicht-ulzerierter Knoten im Bereich des Schulterblatts Erythematous non-ulcerated nodule of the scapular region Diagnosequiz

Erythematous non-ulcerated nodule of the scapular region

An otherwise healthy 57-year-old man presented with a sixmonth history of an asymptomatic, erythematous, non-ulcerated nodule in the left scapular region (Figure 1 ). Dermatoscopy revealed a well-demarcated lesion with a structureless red area at the center surrounded by a whitish collar. White lines arranged in a radial manner were also observed, more prominent at the periphery (Figure 2 ). Erythematous non-ulcerated nodule of the scapular region Case for Diagnosis

Schnell wachsende Plaque im Nacken eines gesunden Patienten: Diagnosequiz

Ein 45-jähriger Mann mit bekannter Psoriasis vulgaris wurde mit einer asymptomatischen Läsion auf der rechten Seite seines Nackens vorgestellt, die seit drei Monaten bestand. Er war bereits erfolglos mit Cloxacillin auf ein mögliches Erysipel behandelt worden, später außerdem aufgrund des Verdachts auf eine psoriatische Plaque mit topischen Kortikosteroiden. Bei der klinischen Untersuchung zeigte sich eine klar abgegrenzte, stark verhärtete, erythematöse Plaque mit schuppiger Oberfl äche auf der rechten Seite des Nackens (Abbildung 1 ). Die allgemeine physische Untersuchung war unauffällig. Schnell wachsende Plaque im Nacken eines gesunden Patienten Progressively growing plaque on the neck of a healthy patient Diagnosequiz

Progressively growing plaque on the neck of a healthy patient.

A 45-year-old man, with a past medical history of psoriasis, presented with an asymptomatic lesion on the right side of his neck, which had appeared three months earlier. He had been unsuccessfully treated with cloxacillin for possible erysipelas and later – on suspicion of a psoriasis plaque – with topical corticosteroids. Clinical examination revealed a sharply demarcated, highly indurated, erythematous plaque with a scaly surface on the right side of the neck (Figure 1 ). The general physical examination was unremarkable. Progressively growing plaque on the neck of a healthy patient Case for Diagnosis

Prolonged localized photosensitivity following allergic and photo-aggravated contact dermatitis from etofenamate

An otherwise healthy 35-year-old woman, with Fitzpatrick skin phototype II and without any previous history of abnormal reaction to sunlight, presented in September of 2011 with an acute, pruritic, erythematous, papulovesicular eruption on the dorsum of the right foot (Fig. 1a) following a 3-day application of Flogoprofen gel (Chiesi Labs, Barcelona, Spain) containing etofenamate and this in association with sun exposure. She had been using this gel because of a trauma, and although she mentioned that she had previously used a topical NSAID in other locations (because of trauma or muscular pain), she could not remember which topical NSAID she had applied. The lesion healed following a treatment with topical and oral corticosteroids, and she was advised not to use topical anti-inflammatory drugs anymore. In July 2012, after 1-hour sun exposure, the patient presented again with severe lesions with erythema, oedema, vesicles, bullae and erosions on the previously affected skin site and again in July 2013 (Fig. 1b and Fig. 1c), though this time to a lesser extent. The sandals she had worn on both occasions were different from those during the initial episode; hence, contamination of the shoes could be eliminated as the cause of the dermatitis. She further denied the use of oral or other topical treatment during both periods. In these three episodes, she only had lesions on the dorsum of the right foot, where the etofenamate gel had been applied, and not in other skin sites exposed to sunlight, so the possibility of a polymorphic light eruption could be excluded as the cause of these lesions. Photo testing, performed in 2012 on the skin of her lower back (using Xenon arc 16S, Solar Light Co., Philadelphia, PA, USA), showed a negative UVA response (i.e. with no erythema) with a dose of 10 J/cm and a UVB-MED of 24.66 mJ/cm [normal range 28 ± 4 mJ/cm, pathologic value < 19 mJ/cm, based on a recent multicentre study of the Spanish population carried out by members of the Spanish Group of Photobiology (data not published yet)]. Photo patch tests were performed with the baseline series of the Spanish Group of Photobiology (MartiTor, Barcelona, Spain) including etofenamate at 1% in a gel (prepared by the hospital pharmacy and containing water, isopropyl alcohol, ethanol and carbomer) being applied in duplicate to the skin of the upper back. After 2 days, one set was removed and irradiated with 5 J/cm UVA, and readings were done at day 1, 2 and 3 post-irradiation. Only the patch test to etofenamate was positive (i.e. a+ reaction), while the photo patch test showed photo aggravation (i.e. a+++ Photodermatology, Photoimmunology & Photomedicine