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Biomedical subjects

O Chosidow

Publications and source records attributed to O Chosidow.

At least 91 records · Page 5Linked to original sources
PubMed1997

A peculiar form of amicrobial pustulosis of the folds associated with systemic lupus erythematosus and other auto-immune diseases.

Amicrobial pustulosis of the folds is a new entity which was initially described in association with systemic lupus erythematosus (SLE). We report four cases of this rare pustulosis occurring in the course of various auto-immune disorders. Dermatological features were similar in all patients. The primary lesions were small pustules which coalesced and formed erosive areas underlined with pustular lesions. They were localized in the folds. Three of the four patients had also isolated pustules on the scalp. Spongiform pustules were histologically present. A primary bacterial or fungal infection was ruled out by cultures on appropriate media. Serum calcium level was normal. Associated auto-immune diseases were: systemic lupus erythematosus, incomplete systemic lupus erythematosus, 'idiopathic' thrombocytopenic purpura and myasthenia gravis without thymoma (one of each). The relationship between this peculiar form of pustulosis and autoimmunity remains to be elucidated. The pustulosis did not respond to antibiotics but disappeared with systemic or topical corticosteroids.

Adolescent↗
PubMed1997

Inducible nitric oxide synthase and proinflammatory cytokine expression by human keratinocytes during acute urticaria.

BACKGROUND: IgE/allergen-dependent activation of skin mast cells is involved in acute urticaria and leads to their IL-4 release. Previously we have demonstrated in vitro the induction of the low-affinity receptor for IgE (CD23/Fc epsilon RII) in human keratinocytes (HK) upon stimulation with IL-4. In addition, we have observed that ligation of CD23 on keratinocytes induced type II nitric oxide synthase (iNOS), leading to the release of nitric oxide (NO) and proinflammatory cytokines (TNF-alpha, IL-6). According to these in vitro data, we explored whether keratinocytes could also express iNOS, TNF-alpha, IL-6, and CD23 in acute urticaria, an in vivo model in which activation of mast cells by IgE/allergen immune complexes is involved. MATERIALS AND METHODS: INOS, TNF-alpha, IL-6, and CD23 expression by keratinocytes was studied in acute urticaria (n = 11) in biopsies from lesional and autologous normal skin by immunohistochemistry, in situ hybridization, or RT-PCR. Nitrites and TNF-alpha synthesis were assayed in supernatants of cultured lesional keratinocytes. RESULTS: INOS mRNA expression was demonstrated with RT-PCR in 10 biopsies out of 11 sections of acute urticaria lesional skin. Immunohistochemistry showed that this iNOS positivity originated from keratinocytes located close to the dermoepidermal junction; TNF-alpha and IL-6 mRNA transcription was observed in all but one iNOS+ biopsy. Immunostaining and in situ hybridization with CD23-specific probes were strong in all but one iNOS+ skin biopsy. Noninflamed autologous skin was negative for iNOS (except for a weak positivity in one case), cytokines, and CD23. CONCLUSION: The colocalization of iNOS, proinflammatory cytokines, and CD23 within keratinocytes in acute urticaria demonstrates that these cells play an important role in the initiation and maintenance of the inflammatory reaction during this disease in humans through activation of the iNOS pathway by CD23 ligation with IgE/allergen immune complexes.

Acute Disease↗
PubMed1997

Acute hepatitis during hypersensitivity syndrome due to midecamycin.

We report here the first case of symptomatic acute hepatic injury due to midecamycin in a 58-year-old man. The clinical picture was compatible with a hypersensitivity syndrome with cutaneous, renal and hepatic involvement. Liver eosinophil polynuclear infiltrate, hypereosinophilia and acute interstitial nephritis were consistent with the hypothesis of an immunoallergic mechanism.

Acute Disease↗
PubMed1997

[Lichen].

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Adrenal Cortex Hormones↗
PubMed1997

[Degos disease].

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Atrophy↗
PubMed1996

Plasma and skin suction-blister-fluid pharmacokinetics and time course of the effects of oral mizolastine.

OBJECTIVE: To investigate plasma and skin suction-blister-fluid pharmacokinetics of oral mizolastine in order to determine whether the drug concentration in the fluid of suction-induced skin blisters could better predict the antihistamine activity than the plasma concentration. SETTING: Department of Internal Medicine, Université Paris 6. SUBJECTS: Ten healthy male volunteers. METHODS: The volunteers (mean age 26.8 years, mean weight 75.8 kg) received a single 10-mg oral dose of mizolastine at 1000 hours. The pharmacokinetic study included 11 plasma and 9 blister fluid samples and blister epidermal-roof specimens. Mizolastine was assayed by high-performance liquid chromatography (HPLC). Each volunteer also received nine intradermal injections of 5 micrograms histamine. Antihistamine activity was assessed as the post-treatment percentages of changes in the histamine-induced relative wheal and flare areas versus baseline. RESULTS: Mizolastine mean Cmax (SD) and median tmax were, respectively, 380 ng.ml-1 and 0.8 h in plasma, and 21.8 ng.ml-1 and 10 h in blister fluid. Mizolastine could not be quantified in the epidermis. The maximal histamine-induced relative flare inhibition was 72.5% and was attained at the median time of 3 h post-dosing and therefore was delayed by 2.2 h with respect to the plasma tmax. Mean relative wheal inhibition, although lower, showed the same time profile. A direct relationship could not be found between drug concentrations in blister fluid and antihistamine activity. Simulated concentrations in the peripheral compartment better explain the maximum inhibition effect on flare, observed 3 h post-dosing, with a flatter hysteresis loop obtained when plotting relative flare inhibition versus plasma or blister-fluid drug concentrations. CONCLUSION: The mizolastine concentrations in the skin suction-blister fluid were not predictive of the antihistamine activity.

Administration, Oral↗