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Stéphane Barete

Publications and source records attributed to Stéphane Barete.

6 recordsLinked to original sources
PubMed2004

Protein Z deficiency in antiphospholipid-negative Sneddon's syndrome.

BACKGROUND: Sneddon's syndrome is characterized by the association of ischemic cerebrovascular events and widespread livedo racemosa. The pathophysiology of Sneddon's syndrome remains elusive, but various prothrombotic abnormalities have been previously reported in this setting. Low levels of protein Z, a downregulator of coagulation, have been recently linked to an increased risk of arterial thrombosis. The purpose of this study was to investigate the levels of protein Z in a series of Sneddon's syndrome patients without circulating antiphospholipid antibodies in comparison with an age- and sex-matched control population. METHODS: Twenty-six patients and 78 healthy controls had determination of their protein Z blood levels by an enzyme-linked immunoassay test. Patients' thrombotic and vascular risk factors, including tobacco smoking, arterial hypertension, oral contraceptive agents, dyslipidemia, factor V Leiden, and factor II mutation were recorded. RESULTS: Protein Z plasma levels were significantly lower in patients (mean 1.47 mg/L) than in controls (mean 1.93 mg/L) (P=0.02). Prevalence of protein Z deficiency (level <1 mg/L) was significantly higher (P=0.001) among patients (31%) than among controls (3.8%). Factor V Leiden and heavy smoking were observed in 4 and 7 patients, respectively. CONCLUSIONS: Sneddon's syndrome could be viewed as the peculiar clinical expression of various and sometimes associated coagulation abnormalities. Low levels of protein Z may account, at least partly, for the thrombotic events observed in Sneddon's syndrome and shed a new light on its pathophysiology. Clinical implications for protein Z deficiency in this setting deserve further investigations.

Adult↗
PubMed2004

Antineutrophil cytoplasmic antibodies of IgA class in neutrophilic dermatoses with emphasis on erythema elevatum diutinum.

OBJECTIVE: To evaluate the prevalence of IgA and IgG antineutrophil cytoplasmic antibodies (ANCAs) in erythema elevatum diutinum in comparison with 2 other groups of neutrophilic dermatoses: Sweet syndrome and pyoderma gangrenosum. DESIGN: Detection of IgA and IgG ANCAs in the serum of patients with neutrophilic dermatoses and characterization of the previously known antigenic targets. SETTING: All serum was analyzed without knowledge of diagnosis in the Immunology Department, Pitié-Salpêtrière Hospital, Paris, France. PATIENTS: Ten patients with erythema elevatum diutinum, 10 with Sweet syndrome, 10 with pyoderma gangrenosum, and 10 healthy volunteers. MAIN OUTCOME MEASURES: IgA and IgG ANCAs were sought by indirect immunofluorescence with ethanol and formaldehyde-fixed human neutrophil preparations as the substrate. Enzyme-linked immunosorbent assays were further performed for antigen characterization. RESULTS: IgA ANCAs were observed in 60% and IgG ANCAs in 10 (33%) of the patients. All patients with erythema elevatum diutinum had IgA ANCAs. IgA fluorescence in formaldehyde-fixed neutrophils was restricted to those from patients with erythema elevatum diutinum. Enzyme-linked immunosorbent assays disclosed no single predominant target, and antigens remained largely undetermined in erythema elevatum diutinum. CONCLUSIONS: The ANCAs, particularly of IgA class, may prove to be a helpful paraclinical marker in erythema elevatum diutinum and an interesting perspective for understanding the pathophysiology of the disease. The nature of the unidentified targets and the pathogenicity of ANCAs, however, remain to be assessed.

Adolescent↗
PubMed2004

Additional conjunctival and penile pigmentation in Laugier-Hunziker syndrome: a report of two cases.

BACKGROUND: Laugier-Hunziker syndrome is a rare acquired hyperpigmentation of the oral mucosa and lips which is often associated with longitudinal melanonychia. We report two patients exhibiting the classical features of Laugier-Hunziker syndrome with additional and previously unreported conjunctival and penile pigmentation. PATIENTS AND METHODS: Two patients presented with a history of progressive acquired macular pigmentation of the oral mucosa, the lips, the ocular conjunctiva and the penis. Longitudinal melanonychia was found in one patient. Microscopic features (basal epithelial melanosis, moderate acanthosis and superficial pigmentary incontinence) and ultrastructural details (increased number of normal-appearing melanosomes inside basal keratinocytes and dermal melanophages) were characteristic of Laugier-Hunziker syndrome. CONCLUSIONS: These two observations illustrate the topographical variations of Laugier-Hunziker syndrome and highlight the need to expand the originally described features to include more widespread areas of hyperpigmentation.

Adult↗
PubMed2003

[Classification of dermatologic manifestations in lupus erythematosus].

Various dermatologic manifestations are observed in the different lupus subsets. Lupus lesions are characterized by a dermo-epidermal dermatitis. Other lesions, vascular or non vascular, are essentially present in association with systemic lupus erythematosus. Acute, subacute and chronic lupus erythematosus are distinguishable according to their clinical aspects, pathological features and evolution. Acute lesions are either localized to the midface or widespread. Subacute lesions may be annular or psoriasiform. Chronic lupus erythematosus includes localized or widespread discoid lupus, lupus tumidus, chilblain lupus and panniculitis. Therapy of cutaneous lupus is mainly based on antimalarials and avoidance of sun irradiation. In refractory cutaneous lupus, no universal guidelines are currently available. Except for acrosyndromes and urticaria-like lesions, vascular lesions may be due to vasculitis or thrombosis. An accurate diagnosis is absolutely necessary since therapy is different in thrombosis and vasculitis. Non vascular and non lupus lesions are numerous, some of them require special treatment such as dapsone for bullous lupus.

Acitretin↗
PubMed2002

[How to recognize scleroderma].

Systemic sclerosis is a multisystem disorder characterized by the presence of connective tissue sclerosis, vascular abnormalities concerning small-sized arteries and the microcirculation, and autoimmune changes. This disease is usually preceded by Raynaud's phenomenon. Cutaneous changes are useful for diagnosis. Sclerosis is initially proeminent on hands with frequently pitted scars. Telangiectases and calcium deposits are mainly observed in a good prognosis subset of the disease (CREST) characterized by the association of limited skin involvement and anti-centromere antibodies with possible late onset of pulmonary hypertension. The bad prognosis subset is associated with diffuse cutaneous sclerosis, pulmonary fibrosis, gastrointestinal disease, myocardial involvement and anti-topo-isomerase I antibodies. Histological skin changes are similar to those observed in morphea. In morphea, there is only localized sclerosis of the skin with highly variable aesthetic disability. The condition may be subdivided clinically into the following types: circumscribed plaques, linear morphea and frontoparietal lesions. The last two forms may be associated with atrophy of the underlying anatomic structures. Many other diseases may have a scleroderma-like appearance. In these diseases, nail folds abnormalities, visceral involvement and immunological changes are usually different from those observed in systemic scleroderma.

Diagnosis, Differential↗