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Dive into the research topics where Eduardo Fonseca is active.

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Featured researches published by Eduardo Fonseca.


Annals of Pharmacotherapy | 2004

Psoriasiform Eruption Induced by Infliximab

M.M. Verea; Jesús Del Pozo; M Teresa Yebra-Pimentel; Angeles Porta; Eduardo Fonseca

OBJECTIVE: To report a case of psoriasiform eruption induced by infliximab. CASE SUMMARY: A 46-year-old woman with enterocutaneous fistula secondary to Crohns disease developed pruriginous, erythematous, desquamative plaques on her elbows, knees, hands, and buttocks after receiving the second and third doses of intravenous infliximab. Histologic examination showed a lichenoid pattern. No new cutaneous lesions appeared after cessation of infliximab therapy. DISCUSSION: Several cutaneous reactions secondary to infliximab, a monoclonal antibody against tumor necrosis factor-alfa, have been described. Psoriasiform dermatitis has not been reported as a cutaneous reaction to infliximab, but there have been several previous reports of psoriasiform dermatitis secondary to other drugs. An objective causality assessment revealed that the adverse event was probable. CONCLUSIONS: This is the first report of a clinico-pathologic dissociated pattern of cutaneous reaction showing a histopathologic picture of lichenoid dermatitis resulting from infliximab treatment.


Journal of Cutaneous Pathology | 2009

Spitzoid melanoma in children: clinicopathological study and application of immunohistochemistry as an adjunct diagnostic tool

Sabela Paradela; Eduardo Fonseca; Salvador Pita; Sara M. Kantrow; Viktor N. Goncharuk; Hafeez Diwan; Victor G. Prieto

Introduction:  The term spitzoid melanoma (SM) is reserved for a rare group of tumors with striking resemblance to Spitz nevus, often developing in children diagnosed in retrospect after the development of metastases.


Lupus | 2008

Interface dermatitis in skin lesions of Kikuchi–Fujimoto’s disease: a histopathological marker of evolution into systemic lupus erythematosus?:

Sabela Paradela; J Lorenzo; W Martínez‐Gómez; T. Yebra-Pimentel; L Valbuena; Eduardo Fonseca

Kikuchi’s disease (KD) is a self-limiting histiocytic necrotizing lymphadenitis (HNL). Cutaneous manifestations are frequent and usually show histopathological findings similar to those observed in the involved lymph nodes. HNL with superposed histological features to KD has been described in patients with lupus erythematosus (LE), and a group of healthy patients previously reported as having HNL may evolve into LE after several months. Up to date, features to predict which HNL patients will have a self-limiting disease and which could develop LE have been not identified. In order to clarify the characteristics of skin lesions associated with KD, we report a case of HNL with evolution into systemic lupus erythematosus (SLE) and a review of previous reports of KD with cutaneous manifestations. A 17-year-old woman presented with a 4-month history of fever and generalised lymphadenopathy. A diagnosis of HNL was established based on a lymph node biopsy. One month later, she developed an erythematoedematous rash on her upper body, with histopathological findings of interface dermatitis. After 8 months, anti-nuclear antibodies (ANA) at titre of 1/320, anti-DNA-ds antibodies and marked decrease of complement levels were detected. During the following 2 years, she developed diagnostic criteria for SLE, with arthralgias, pleuritis, aseptic meningitis, haemolytic anaemia and lupus nephritis. To our knowledge, 27 cases of nodal and cutaneous KD have been reported, 9 of which later developed LE. In all these patients, the skin biopsy revealed interface dermatitis. Skin biopsy revealed a pattern of interface dermatitis in all reviewed KD cases, which evolved into LE. Even this histopathological finding was not previously considered significant; it might be a marker of evolution into LE.


Drug Safety | 2002

Indinavir-induced retinoid-like effects: incidence, clinical features and management.

J. García-Silva; Manuel Almagro; Carmen Peña-Penabad; Eduardo Fonseca

Since 1998, many cases of antiretroviral therapy-related paronychia of the toes or fingers and ingrown toenails have been reported. Most of them were related to indinavir. Other indinavir-induced mucocutaneous disorders resembling the adverse effects of systemic retinoid therapy have also been reported. Although there is some uncertainty in the literature regarding a cause-effect relationship, results of several epidemiological and in vitro studies, together with cumulated clinical experience leave no doubt that indinavir causes a retinoid-like effect and nail alterations. Indeed, indinavir is the only antiretroviral drug that produces these disorders, although ritonavir may enhance indinavir-induced retinoid-like effects through pharmacokinetic interactions leading to increased plasma indinavir concentrations.Approximately 30% of patients receiving indinavir show two or more retinoid-like manifestations and 4–9% develop paronychia. These adverse effects are not related to other epidemiological variables such as the patient’s sex, age or other risk factors or immune status. They seem to be exposure dependent and, therefore, largely dose-dependent.Chronic paronychia is considered generally to be caused by contact irritants and candidal infection. Nevertheless, indinavir is currently the most frequent cause of chronic or recurrent paronychia in HIV-infected patients. In addition, retinoid-like manifestations such as cutaneous xerosis and cheilitis are frequent mucocutaneous adverse effects related to indinavir.The exact mechanism of indinavir-induced retinoid-like effects is unclear. Hypotheses for pathogenesis include interference with retinoid metabolism by enhancing the retinoic acid signalling pathway, or by increasing retinoic acid synthesis, or by reducing cytochrome P450-mediated retinoic acid oxidative metabolism.Replacement of therapy by an antiretroviral regimen not containing indinavir, while retaining other protease inhibitors and lamivudine, resolves retinoid-like manifestations without recurrences.


Cancer | 2010

Prognostic Factors for Melanoma in Children and Adolescents: A Clinicopathologic, Single-Center Study of 137 Patients

Sabela Paradela; Eduardo Fonseca; Salvador Pita-Fernández; Sara M. Kantrow; Abdul H. Diwan; Cynthia Herzog; Victor G. Prieto

Cutaneous melanoma in childhood is rare; therefore, its prognostic factors and biologic behavior and the effectiveness of adjuvant diagnostic techniques in this group remain mostly unknown.


Journal of The European Academy of Dermatology and Venereology | 2008

Cutaneous lesions associated to multiple endocrine neoplasia syndrome type 1

A Vidal; Mj Iglesias; B Fernández; Eduardo Fonseca; F Cordido

Background  Multiple endocrine neoplasia type 1 (MEN1) is a genetic disease that predisposes to endocrine tumour development. Some cutaneous lesions (angiofibromas, collagenomas, melanosis guttaca, lipomas, melanomas, ‘cafe au lait macules’) have been associated to this syndrome. We compare the prevalence of cutaneous lesion in affected patients with their non‐carrier relatives.


Actas Dermo-Sifiliográficas (English Edition) | 2013

Spanish Evidence-Based Guidelines on the Treatment of Psoriasis With Biologic Agents, 2013. Part 1: On Efficacy and Choice of Treatment

Lluís Puig; J.M. Carrascosa; G. Carretero; P. de la Cueva; R.F. Lafuente-Urrez; Isabel Belinchón; M. Sánchez-Regaña; M. García-Bustinduy; Miquel Ribera; Mercè Alsina; Carlos Ferrándiz; Eduardo Fonseca; V. García-Patos; E. Herrera; J.L. López-Estebaranz; S.E. Marrón; J.C. Moreno; J. Notario; Raquel Rivera; C. Rodriguez-Cerdeira; A. Romero; R. Ruiz-Villaverde; Rosa Taberner; D. Vidal

Biologic therapy is a well-established strategy for managing moderate and severe psoriasis. Nevertheless, the high cost of such therapy, the relatively short span of clinical experience with biologics, and the abundance of literature now available on these agents have made evidence-based and consensus-based clinical guidelines necessary. The ideal goal of psoriasis treatment is to achieve complete or nearly complete clearing of lesions and to maintain it over time. Failing that ideal, the goal would be to reduce involvement to localized lesions that can be controlled with topical therapy. Although current evidence allows us to directly or indirectly compare the efficacy or risk of primary or secondary failure of available biologics based on objective outcomes, clinical trial findings cannot be directly translated to routine practice. As a result, the prescribing physician must tailor the treatment regimen to the individual patient. This update of the clinical practice guidelines issued by the Spanish Academy of Dermatology and Venereology (AEDV) on biologic therapy for psoriasis incorporates information from the most recent publications on this topic.


American Journal of Dermatopathology | 1990

Multiple self-healing indeterminate cell lesions of the skin in an adult

Félix Contreras; Eduardo Fonseca; Gamallo C; Burgos E

We report a case of multiple cutaneous indeterminate cell proliferative lesions in an adult without any other organ involvement. All lesions regressed spontaneously over 5 years without recurrence over a 4-year period of follow-up. The electron-microscopic and immunohistochemical features of the cellular infiltrate were those of the indeterminate cells. This case supports the hypothesis that indeterminate cell proliferative disorder is a wide spectrum of conditions with variegated clinicopathologic presentation and with different biological behavior.


International Journal of Dermatology | 2006

Lupus erythematosus tumidus: a series of 26 cases

Vanessa Vieira; Jesús Del Pozo; María Teresa Yebra-Pimentel; Walter Martínez; Eduardo Fonseca

Objective  To study 26 cases of lupus erythematosus tumidus (LET), a subset of chronic cutaneous lupus erythematosus (CCLE), referred to in the literature as a rare entity.


European Journal of Dermatology | 2008

Imiquimod in mycosis fungoides

M Covadonga Martínez-González; M Magdalena Verea-Hernando; M Teresa Yebra-Pimentel; Jesús Del Pozo; Marta Mazaira; Eduardo Fonseca

Imiquimod is a topically active imidazoquinoline immunomodulator agent. It works as an indirect antiviral and antitumoral and stimulates the production of INF-alpha and various other cytokines. We assayed topical imiquimod in treating early stages of mycosis fungoides. We applied imiquimod 5% cream in four patients with multi-treatment resistant plaques of MF (stages IA and IIB). We applied it on one patient in association with systemic INFalpha-2a. We observed a complete clinical clearance of the lesions in all four patients. In three cases we achieved a complete histopathological clearance and in one case a partial histopathological clearance. The patient treated with imiquimod and systemic INFalpha-2a showed the most spectacular improvement with a rapid total response. We ascribe this improvement to a synergic effect of imiquimod and systemic INFalpha-2a treatment. Before the introduction of imiquimod, this patient had been treated for 2 years with systemic INFalpha-2a alone, without any evidence of clinical response. Imiquimod could be an effective therapy for early-stage disease of CTCL, used alone or in combination with systemic immunomodulatory therapy.

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Dive into the Eduardo Fonseca's collaboration.

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Manuel Almagro

Complutense University of Madrid

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Walter Martínez

Complutense University of Madrid

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Carlos Ferrándiz

Autonomous University of Barcelona

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Félix Contreras

Hospital Universitario La Paz

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M.D. Mayan

University of A Coruña

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E. Daudén

Autonomous University of Madrid

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Lluís Puig

Autonomous University of Barcelona

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Arnald Alonso

Polytechnic University of Catalonia

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Sara Marsal

Autonomous University of Barcelona

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Benigno Acea

University of A Coruña

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