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M C Lefebvre

Publications and source records attributed to M C Lefebvre.

8 recordsLinked to original sources
PubMed2001

The new topical ascomycin derivative SDZ ASM 981 does not induce skin atrophy when applied to normal skin for 4 weeks: a randomized, double-blind controlled study.

BACKGROUND: SDZ ASM 981 is a selective inhibitor of inflammatory cytokines released from T lymphocytes and mast cells, which has been developed for the treatment of inflammatory skin diseases. OBJECTIVES: In the present study, the atrophogenic potential of SDZ ASM 981 1% cream in humans was compared with that of medium and highly potent topical steroids, and vehicle. METHODS: Four different preparations, SDZ ASM 981 1% cream, the corresponding vehicle of SDZ ASM 981 1% cream, betamethasone-17-valerate 0.1% cream and triamcinolone acetonide 0.1% cream, were applied to the volar aspect of the forearms of 16 healthy volunteers, twice daily, 6 days a week, for 4 weeks. Skin thickness was evaluated by ultrasound examination, clinical signs of atrophy by stereomicroscopy, and epidermal thickness was assessed by histology. RESULTS: Both topical corticosteroids induced a significant reduction in skin thickness, as compared with SDZ ASM 981 1% cream and vehicle, which were shown to be equivalent. The difference in skin thickness (measured by ultrasound examination) between patients treated with SDZ ASM 981 1% cream and those receiving either of the two topical steroids was significant from day 8 onwards. Histological analysis performed at day 29 showed significant epidermal thinning with topical steroids compared with SDZ ASM 981 1% cream or the vehicle. Conclusion The lack of atrophogenic properties of SDZ ASM 981 1% cream in this short-term study demonstrates its potential as long-term treatment for inflammatory skin diseases, thus overcoming a major drawback of topical steroids. This may also be important for the treatment of children, and sensitive areas of skin, such as the face and skin-folds.

Administration, Topical↗
PubMed1991

[Pseudosurgical acute abdomen syndrome in primary pulmonary hypertension].

The case is reported of a 49-year-old chronic alcoholic woman, who presented with severe pulmonary arterial hypertension (PAH) mimicking as an acute abdomen. She was admitted with right-sided hypochondrial abdominal pain and hepatomegaly, with a moderate jaundice. On admission to intensive care unit, she had an arterial blood pressure of 110/70 mmHg, a heart rate of 100 b.min-1, and a respiratory rate of 36 c.min-1. An electrocardiogram showed sinus rhythm and right-sided heart failure. Whilst breathing 6 l.min-1 oxygen, her arterial blood gases were: PaO2 47 mmHg PaCO2 29 mmHg. Severe PAH was confirmed by measuring her mean pulmonary arterial pressure, which was 46 mmHg, whilst her pulmonary wedge pressure was 7 mmHg. Hepatic function was also altered: total bilirubin 41 mumol.l-1, alkaline phosphatase 145 UI.l-1 and gamma glutamyl transferase 1 340 UI.l-1. She developed arterial hypotension, which did not respond to increasing doses of isoproterenol. She died on the third day. Necropsy confirmed the diagnosis of primary PAH, with acute "cardiac liver".

Abdomen, Acute↗
PubMed1991

[TNF and sepsis].

Recent experiments have demonstrated that TNF plays an important role in the pathogenesis of septic shock. To confirm the involvement of TNF in human septic shock, serum TNF levels were measured in 10 adult patients admitted to the intensive care unit for sepsis with or without shock. Septic shock was corroborated by hemodynamic data (right catheterization, measurement of cardiac output by thermodilution). For TNF measurement, venous blood samples were withdrawn, as soon as possible after the onset of sepsis, into a pyrogen--free tube. Serum TNF levels were determined using a radioimmunoenzymatic assay (IRE Medgenix). During septic shock (n = 7), TNF levels were significantly higher (m = 354 +/- 131 pg/ml) than during sepsis without shock (n = 8; m = 145 +/- 35 pg/ml) (p less than 0.0005). TNF levels were also significantly higher in non-survivors (m = 392 +/- 111 pg/ml) than in survivors (m = 167 +/- 81 pg/ml) (p less than 0.0005). The value of 250 pg/ml seems to be critical: no patient without shock had TNF levels above 250 and all the patients who died early during the first 24 h) had TNF levels above 250. The TNF level is negatively correlated with the platelet count (r = -0.70; p less than 0.05). These data favor a pathophysiological for TNF in human sepsis and septic shock.

Adolescent↗
PubMed1989

[Nosocomial bronchopneumopathies].

Nosocomial bronchopulmonary infections are common and severe complications, particularly in intensive care units. The high incidence of pneumonia is related to multiple factors such as underlying disease, acute respiratory failure, nutritional disorders, depressed mental status and the frequent need tracheal intubation. The most frequent cause of respiratory tract infection is aspiration of oropharyngeal secretions. In hospitalized patients, there is usually an oropharyngeal colonization with Gram-negative bacteria. Prevention of nosocomial bronchopulmonary infections requires close attention to the patient's environment, proper techniques, handwashing and decontamination of respiratory equipment.

Bronchial Diseases↗
PubMedDate not supplied

[Hemodynamic and respiratory effects of enoximone in acute respiratory insufficiency of chronic obstructive bronchopneumopathy].

Hemodynamic effects and gas exchange were studied in twenty COPD patients undergoing mechanical ventilation before and 30 and 60 minutes after an intravenous administration of 1 mg/kg enoximone. Enoximone decreased significantly pulmonary arterial pressure and pulmonary vascular resistances without significantly decrease of systemic vascular resistances 60 minutes after a slight dose of 1 mg/kg. Right ventricular ejection fraction increased; O2 arterial pressure, CO2 arterial pressure, intrapulmonary shunt remained unchanged. We concluded that enoximone induced pulmonary vasodilation in patients with decompensated COPD and increased right ventricular function without deleterious effects in gas exchange.

Acute Disease↗