Enfermedad de Crohn metastásica tratada con ustekinumab / Metastatic Crohn Disease Treated With Ustekinumab

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Urticarial Lesions in a Pregnant Woman.

Dear Editor, Gestational pemphigoid (GP) is a rare autoimmune bullous dermatosis in pregnancy. GP usually occurs during the second or third month of pregnancy. It clinically manifests as the development of either early-onset urticarial lesions or late-onset subepidermal blisters that may linger for weeks or even months. Herein we report the case of a 45-year-old woman with the distinctive clinical onset of GP. A forty-five-year-old woman, gravida I, para 0, at 27 weeks gestation, was referred for evaluation to our Department with an extensive pruritic eruption that had developed over the previous 7 days. The lesions had first appeared on the proximal thighs and extended progressively to the abdomen. On physical examination, numerous round urticarial plaques of approximately 1 cm in diameter were noted on her abdomen, involving the periumbilical area. Her thighs and back were also affected (Figures 1 and 2). The palms and soles were spared. No mucosal involvement was seen. The patient medical history was unremarkable, and she denied use of any other medications or herbal remedies at the time the symptoms started or since. No other symptoms but pruritus were referred. Laboratory studies, including complete blood cell count, coagulation tests, and renal and hepatic function were all normal. A punch biopsy was taken from an urticarial plaque and stained with hematoxylin and eosin. Histological examination found spongiosis in combination with an intraepidermal eosinophilic infiltrate, without the development of blisters (Figure 3). Direct immunofluorescence of perilesional skin showed linear deposition of complement (C3) along the basement membrane zone (Figure 4). Serum antibody titers for BP180NC16a were detected by enzyme-linked immunosorbent assay (ELISA). We established a diagnosis of gestational pemphigoid. Our patient was treated with systemic glucocorticoids, no blisters developed, and lesions cleared 8 weeks after delivery. The newborn girl did not developed neonatal gestational pemphigoid. Gestational pemphigoid, originally misnamed herpes gestationis, is a rare autoimmune bullous dermatosis in pregnancy. Single cases have been also described in patients with molar pregnancies and trophoblastic tumors (1). Its etiology is based in the development of autoantibodies against the fetoplacental unit, triggering an autoimmune response against both skin and amnion hemidesmosomal proteins, mainly BP180, but also BP230 and type VII collagen. An association with HLA-DR3 and HLA-DR4 has been described (2). GP usually occurs during the second or third month of pregnancy, but it may appear at any time during pregnancy or puerperium. In the vast majority of cases, symptoms alleviate a few weeks before delivery, but they reemerge at the time of delivery. Recurrences are frequent in following pregnancies, with an earlier onset and more severe symptoms, and may occur during subsequent menstruations or hormonal contraceptive use (1). GP clinically consists of the development of either early-onset urticarial lesions or late-onset subepidermal blisters that mat linger for weeks or even months. They generally appear on the abdomen, specifically in the periumbilical area, with posterior widespread extension to proximal limbs. Facial and mucosal lesions are uncommon (1). Histopathological studies are necessary to establish the diagnosis. These findings vary depending on the stage and severity of the disease and include subepidermal blisters, papillary dermal edema, eosinophilic spongiosis, and a polymorphous perivascular inflammatory cell infiltrate with a predominance of eosinophils. Direct immunofluorescence of perilesional skin shows a linear deposition of C3 along the basement membrane zone in all cases. IgG deposits can also be seen (3). These deposits are located within the lamina lucida and localized to the proximal part of anchoring filaments of the epidermal fragment of salt-split skin (4). Moreover, immunoblot and ELISA of the NC16a domain of BP180 RP are highly sensitive diagnostic methods in GP (5). The aim of treatment is to alleviate the pruritus and prevent formation of new blisters. Topical corticosteroids and oral antihistamines may be used in mild cases. Systemic corticosteroids are the treatment of choice in moderate to severe cases. Other treatments that have been used are cyclophosphamide, dapsone, gold, methotrexate, and plasmapheresis (5).

Red nodule on the face with "spontaneous" regression.

Pseudolymphomatous folliculitis is a rare entity included among the cutaneous pseudolymphomas. A 32-year-old man, with an unremarkable medical history, presented with a two-month history of an asymptomatic solitary nodule on his left cheek. Histopathological examination demonstrated a dense nodular and diffuse dermal lymphocytic infiltrate with numerous histiocytes and dendritic cells that surrounded hypertrophic hair follicles. Pseudolymphomatous folliculitis commonly presents in the fourth decade of life, with no sex predominance, as an asymptomatic, rapidly growing and solitary red dome-shaped nodule on the face. It has a benign clinical course as the lesions usually resolve with surgical excision or regress spontaneously after incisional biopsy. Although there is no report of pseudolymphomatous folliculitis progressing into lymphoma in the literature, follow-up of these patients is recommended.

Red nodule on the face with "spontaneous" regression

Abstract Pseudolymphomatous folliculitis is a rare entity included among the cutaneous pseudolymphomas. A 32-year-old man, with an unremarkable medical history, presented with a two-month history of an asymptomatic solitary nodule on his left cheek. Histopathological examination demonstrated a dense nodular and diffuse dermal lymphocytic infiltrate with numerous histiocytes and dendritic cells that surrounded hypertrophic hair follicles. Pseudolymphomatous folliculitis commonly presents in the fourth decade of life, with no sex predominance, as an asymptomatic, rapidly growing and solitary red dome-shaped nodule on the face. It has a benign clinical course as the lesions usually resolve with surgical excision or regress spontaneously after incisional biopsy. Although there is no report of pseudolymphomatous folliculitis progressing into lymphoma in the literature, follow-up of these patients is recommended.

Diclofenac sodium 3% gel for darier's disease treatment.

BACKGROUND: Darier's disease (DD) is an autosomal dominant skin disorder which causative gene, ATP2A2, is located atchromosome 12q23-24. The lesions of DD are skin-coloured to brown, hyperkeratotic, greasy papules that coalesce into warty plaques commonly involving the seborrhoeic areas of the trunk and face, especially the scalp margins, temples, ears, and scalp. The most common complaint associated with the disease is itching, with exacerbations attributed to heat, sweating, sunlight, lithium, steroid therapy, stress, and menstruation OBJECTIVES: We report a patient with DD treated with topical diclofenac sodium 3%. METHODS: We report a 33-year-old patient with Darier's Disease. He was followed in our department since 2009, and we had tried to control several flares of lesions during follow-up, but oral isotretinoin was not tolerated because of adverse effects; and oral doxycycline showed lack of efficacy.At April 2014, patient presented with new lesions, involving anterior chest wall, abdomen, back and shoulders areas. We started with diclofenac sodium 3% in hyaluronic acid 2.5% once daily, only applied at abdomen and anterior chest wall. RESULTS: After six-month therapy, hyperkeratotic papules were flattened and less harshness of them was noticed, even some of them disappeared. CONCLUSIONS: We consider topical diclofenac therapy as a useful alternative treatment for DD patients, in which previous therapies have not shown efficacy. We did not observed topical adverse effects, neither systemic absorption symptoms, but werecognized further and larger studies are needed to asses the efficacy and safety of this treatment in DD.

Granuloma faciale treatment with tacrolimus.

We present a 40-year-old woman with a one-year history of a solitary and asymptomatic facial lesion. On physical examination a slightly infiltrated, smooth red to brown nodule was seen at the left malar region. A biopsy established the diagnosis of granuloma faciale. After two-months therapy with topical tacrolimus 0,1%, nodule was resolved.