9 results on '"Lepreux S"'
Search Results
2. Imatinib mesylate in scleroderma-associated diffuse skin fibrosis: a phase II multicentre randomized double-blinded controlled trial.
- Author
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Prey, S., Ezzedine, K., Doussau, A., Grandoulier, A.-S., Barcat, D., Chatelus, E., Diot, E., Durant, C., Hachulla, E., de Korwin-Krokowski, J.-D., Kostrzewa, E., Quemeneur, T., Paul, C., Schaeverbeke, T., Seneschal, J., Solanilla, A., Sparsa, A., Bouchet, S., Lepreux, S., and Mahon, F.-X.
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IMATINIB ,SCLERODERMA (Disease) ,RANDOMIZED controlled trials ,ANTINEOPLASTIC agents ,SKIN diseases - Abstract
Background Imatinib mesylate is a potent inhibitor of platelet-derived growth factor and transforming growth factor-β signalling pathways which may play a role in systemic sclerosis (SSc)-associated skin changes. Objectives We aimed primarily at assessing the efficacy of imatinib mesylate in scleroderma skin fibrosis. Methods We performed a phase II double-blinded trial on patients with scleroderma with either morphoea involving > 20% of body surface area or SSc with extensive skin involvement: modified Rodnan Skin Score (mRSS) ≥ 20/51. Each patient was randomized to receive either imatinib mesylate 400 mg or placebo daily for a total of 6 months, and then was followed up 6 months after therapy discontinuation. Skin fibrosis was assessed by mRSS and measurement of the dermal thickness using skin biopsies performed at inclusion and at 6 months of treatment. In addition, quality of life (Dermatology Life Quality Index and modified Health Assessment Questionnaire for Scleroderma) was recorded at each visit, and pulmonary function before and after intervention. Results Twenty-eight patients were included in the study with a mean age of 48·9 years (range 30-71): 25 had a diagnosis of a SSc and three of diffuse cutaneous scleroderma. Demographic data, frequency of organ involvement of SSc and mRSS were comparable between groups. At 6 months, the proportion of variation of mRSS from inclusion was not statistically significantly different between the two groups (median +0·10 in imatinib group vs. −0·16 in placebo group, P = 0·098). Similarly, changes in dermal thickness, quality of life and diffusion capacity for carbon monoxide were not significantly different between groups. Conclusions This study failed to demonstrate the efficacy of imatinib 400 mg daily to improve skin fibrosis of diffuse scleroderma after 6 months of treatment based on validated outcome measurements. [ABSTRACT FROM AUTHOR]
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- 2012
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3. Cytokine imbalance with increased production of interferon-α in psoriasiform eruptions associated with antitumour necrosis factor-α treatments.
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Seneschal, J., Milpied, B., Vergier, B., Lepreux, S., Schaeverbeke, T., and Taïeb, A.
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PSORIASIS treatment ,CYTOKINES ,TUMOR necrosis factors ,PHARMACODYNAMICS ,LUPUS erythematosus ,BIOPSY ,INTERFERONS ,IMMUNOHISTOCHEMISTRY - Abstract
Background Psoriasiform eruptions occur in association with antitumour necrosis factor (TNF)-α treatments in autoinflammatory diseases. The major reported clinical presentation is palmoplantar pustulosis, sometimes accompanied with plaque-like psoriasis. In some reports, histological findings suggest psoriasis whereas others favour a lichenoid drug reaction. We present a case series with a comprehensive clinical, histopathological and immunohistochemical study. Objectives To investigate the mechanism involved in psoriasiform eruptions in patients receiving anti-TNF-α inhibitors. Methods Between July 2004 and May 2008, 13 patients with psoriasiform eruptions arising under anti-TNF-α treatment were enrolled in the study. Punch biopsy specimens of lesions were processed for standard and immunohistochemical analyses using antibodies against CD3, CD4, CD8, CD20, CD1a, KP1, CXCR3, CXCL9, Tia1 and MxA, which is specifically induced by type I interferons (IFNs). Additionally, we analysed biopsies from lesional skin of patients with cutaneous discoid lupus erythematosus, lichen planus and psoriasis. Control biopsies were taken from unaffected skin. Results All patients developed psoriasiform plaques on the body accompanied with palmoplantar keratoderma or pustulosis in three patients. Histological and immunohistochemical findings showed a psoriasiform pattern with focal lichenoid and spongiotic features. We detected strong production of the MxA protein in inflammatory cells, indicating involvement of type I IFNs, and the expression was higher than in control psoriasis samples. Expression of MxA was closely associated with the recruitment of CXCR3+ lymphocytes in the skin bearing markers of cytotoxic capacity. Conclusions Results support the hypothesis that psoriasiform eruptions are a new model of drug reaction characterized by an increased expression of type I IFNs induced by anti-TNF-α. [ABSTRACT FROM AUTHOR]
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- 2009
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4. Idiopathic facial aseptic granuloma: a multicentre prospective study of 30 cases.
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Boralevi, F., Léauté-Labrèze, C., Lepreux, S., Barbarot, S., Mazereeuw-Hautier, J., Eschard, C., and Taïeb, A.
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GRANULOMA ,ROSACEA ,CHILDREN ,ETIOLOGY of diseases ,FURUNCLE ,BARTONELLA infections ,PATHOLOGICAL physiology - Abstract
Background Idiopathic facial aseptic granuloma (IFAG) was recently described in a single-centre retrospective study as a skin condition that occurs specifically in childhood. Objectives To improve our epidemiological, clinical and pathological knowledge on IFAG, to search for an infectious aetiology, and to assess therapeutic recommendations. Methods Children presenting with one or several acquired nodules on the face, lasting for at least 1 month, with no evidence of any other recognizable clinical entity such as infantile acne, pilomatrixoma, furuncle, tumour or vascular malformation, were enrolled in a prospective multicentre study from June 2001 to June 2004, involving the main French paediatric dermatology outpatient units. We recorded clinical details about the nodule and its duration, ultrasound study pattern, cultures for bacteria and mycobacteria, and Bartonella henselae and Afipia felis antibody testing. Results Thirty children (17 boys and 13 girls, mean age 3·8 years) were enrolled. Ultrasound studies revealed a solid well-demarcated hypoechoic lesion without calcium deposit. Cultures for bacteria were negative in 70% of cases. Cultures for mycobacteria and cat scratch disease serologies were negative. Antibiotic therapy was ineffective; the lesion healed spontaneously with a mean duration of 11 months. Histological examination, performed in five cases, showed a chronic dermal lymphohistiocytic granuloma with numerous foreign body-type giant cells. Conclusions IFAG is characterized by a painless facial nodule, presenting as a single lesion localized on the cheek, with a prolonged course but spontaneous healing. Oral or local antibiotics are usually ineffective. Regarding the pathophysiology, our study rules out a primary infectious disease, and allows considering IFAG either as a granulomatous process appearing around an embryological residue or as a manifestation to include in the spectrum of granulomatous rosacea in childhood. [ABSTRACT FROM AUTHOR]
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- 2007
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5. Hereditary mucoepithelial dysplasia: clinical, ultrastructural and genetic study of eight patients and literature review.
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Boralevi, F., Haftek, M., Vabres, P., Lepreux, S., Goizet, C., Leaute-Labreze, C., and Taieb, A.
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DYSPLASIA ,CORNEA diseases ,INFLAMMATION ,BALDNESS ,ORAL mucosa ,GENETICS - Abstract
Hereditary mucoepithelial dysplasia is a dominantly inherited disease, mainly characterized by chronic mucosal lesions associated with keratitis, non-scarring alopecia, keratosis pilaris and perineal intertrigo. Since the original report by Witkop, this condition has been considered to be a disorder of desmosome/gap junction formation, but there has been no ex vivo investigation of these components using genetic and immunolabelling techniques. To perform light and immunoelectron microscopic studies, and partial genetic analysis on five patients in a family and three sporadic cases and to point out similarities of this rare disorder with chronic mucocutaneous candidiasis and other follicular keratosis syndromes, i.e. ichthyosis follicularis–alopecia–photophobia (IFAP), keratitis–ichthyosis–deafness (KID) and Siemens syndromes. Biopsies from the involved oral mucosa and armpit skin of patient 1 were prepared for standard histopathology, electron microscopy and immunocytochemistry. Microsatellite genotyping was performed in three affected family members. Direct sequencing after polymerase chain reaction amplification of the entire coding region was performed. A 14-year-old male had recurrent keratitis, widespread keratosis pilaris, perineal intertrigo, hypotrichosis and oral mucosal involvement. A similar phenotype was noted in four members of his family and in three sporadic cases. Histological examination of oral mucosa and skin samples showed a psoriasiform pattern, dyskeratotic features and cytoplasmic vacuoles. Expression of connexins (Cx), desmosomal, adherens junction and cytoskeleton proteins (Cx 26, 32 and 43, desmogleins 1 and 2, plakoglobin, desmoplakins I–II, plakophilin 1, β-catenin, E-cadherin, keratins, β-tubulin, vimentin and actin) was normal. Ultrastructural studies showed a reduced number of desmosomes. Dyskeratotic cells exhibited internalized gap junctions, long filamentous inclusions reactive with antikeratin antibodies, and bundles of perinuclear fibres resembling clear tonofilaments. Genetic analysis in the studied family excluded the desmosomal cadherins in chromosome 18q12 as candidate genes. A diagnosis of hereditary mucoepithelial dysplasia should be strongly suggested by the triad of non-scarring alopecia, well-demarcated erythema of oral mucosa and psoriasiform perineal rash, after exclusion of the clinically related follicular keratosis syndromes. Defective expression of cytoskeleton elements and/or a modification of mechanisms regulating junction-cytoskeleton assembly may be primarily responsible for impaired epithelial cohesion. [ABSTRACT FROM AUTHOR]
- Published
- 2005
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6. Melanocyte detachment after skin friction in non lesional skin of patients with generalized vitiligo.
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Gauthier, Y., Cario-Andre, M., Lepreux, S., Pain, C., and Taïeb, A.
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FRICTIONAL resistance (Hydrodynamics) ,MELANOCYTES ,VITILIGO - Abstract
Summary Background In vitiligo, melanocytes are gradually lost in depigmented macules of the skin. The disappearance of melanocytes has, however, not been clearly observed and consequently the aetiology of the disease (autoimmune, neural, cytotoxic) is still elusive. The starting point of vitiligo macules is frequently determined by local conditions such as wounds and excoriations, but may also follow minor traumas such as pressure or repeated friction. This prominent feature is often neglected. Objectives To clarify the biological consequences of repeated friction on the attachment and survival of melanocytes in non lesional vitiligo skin. Methods Light reproducible skin friction was performed for 4 min on the volar forearm of 18 patients with extensive vitiligo and five controls with normal healthy skin. Biopsies from the test area and control skin were taken at 1, 4, 24 and 48 h following friction. Serial sections were examined with standard light microscopy, transmission electron microscopy, histochemistry and immunohistochemistry (dihydroxyphenylalanine, HMB-45, E-cadherin and an early apoptosis marker, M30 cytoDEATH antibody). Results The observation of sections at 1 and 48 h after friction on vitiligo skin and at all time points in controls revealed no changes. In contrast, in vitiligo skin at 4 and 24 h after friction, several melanocytes had undergone detachment and were found in various suprabasal positions, including the stratum spinosum, granular layer, and within and outside the stratum corneum. Conclusions Detachment and transepidermal elimination of melanocytes following minor mechanical trauma in non lesional vitiligo skin is probably the cause of depigmentation occurring in the isomorphic response (Koebner phenomenon). We propose that transepidermal elimination of melanocytes in vitiligo should be regarded as a possible mechanism of chronic loss of pigment cells, perhaps previously damaged by another process. [ABSTRACT FROM AUTHOR]
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- 2003
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7. Severe linear form of granuloma annulare along Blaschko’s lines preceding the onset of a classical form of granuloma annulare in a child.
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Morice-Picard, F., Boralevi, F., Lepreux, S., Labrèze, C., Lacombe, D., and Taïeb, A.
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LETTERS to the editor ,GRANULOMA - Abstract
A letter to the editor is presented in response to the article concerning the severe linear form of granuloma annulare, along its classical form in a child.
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- 2007
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8. Psoriasis after cord blood stem cell transplantation.
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Hubiche, T., Leaute-Labreze, C., Lepreux, S., Perel, Y., and Taïeb, A.
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LETTERS to the editor - Abstract
A letter to the editor regarding a case study on psoriasis is presented.
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- 2007
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9. Lymphomatoid annular erythema: a new form of juvenile mycosis fungoides.
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Cogrel, O., Boralevi, F., Lepreux, S., Vergier, B., Merlio, J.P., Taieb, A., and Léautè-Labrèze, C.
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LETTERS to the editor ,ERYTHEMA - Abstract
Presents a letter to the editor focusing on lymphomatoid annular erythema.
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- 2005
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