[Leg ulcers in patients with sickle-cell disease in Libreville (Gabon): clinical aspects and management]. / Ulcères de jambe chez le drépanocytaire à Libreville (Gabon) : aspects cliniques et prise en charge.

OBJECTIVES: To present the clinical aspects of leg ulcers among patients with sickle-cell disease, propose a protocol for treating them, and identify risk factors for their onset in our patients. PATIENTS AND METHODS: This 5-year retrospective descriptive study (2007-2012) includes six adolescents homozygous (SS) for this disease who had at least one leg ulcer during the study period. RESULTS: Our population was aged 16-20 years and comprised 4 young men and 2 young women. Signs at diagnosis included pallor (100%), jaundice (100%), splenomegaly (80%), and fever (70%). Painful crises most often involved a vaso-occlusive crisis (42%), followed by a splenic sequestration crisis (27%), a hemolytic crisis (18%), and erythroblastopenia (14%). CONCLUSION: Leg ulcers are a complication of sickle cell disease and cause esthetic, psychological, and economic problems. Prevention involves patient education to prevent the occurrence and recurrence of these ulcers.

Biochemical and immunologic characterization of a major IgE-inducing filarial antigen of Brugia malayi and implications for the pathogenesis of tropical pulmonary eosinophilia.

A major allergen of the human filarial parasite Brugia malayi has been identified by two-dimensional immunoblot analysis using a serum pool from patients with tropical pulmonary eosinophilia. The allergen is composed of two Ag with M(r) 23 and M(r) 25 and acidic isoelectric point (Bm23-25). Immunoblots using affinity-purified IgE antibodies to BM23-25 indicated that Bm23-25 is expressed mainly in the microfilarial stage. Digestion of the allergen with endoglycosidases indicates that it has N-linked oligosaccharide chains. Analysis of the reactivity of T cells derived from patients with lymphatic filariasis revealed that the Bm23-25 allergen was capable of stimulating T cell proliferation; Bm23-25 was also shown to induce IgE production in vitro from PBMC derived from patients with either TPE or other filarial symptoms. Bronchoalveolar lavage fluid of patients with TPE contained IgE antibodies that recognized Bm23-25 strongly, an observation suggesting that the microfilarial allergen might be involved in the pathogenesis of the TPE syndrome.

The development of cortisol metabolism in the perinatal period in the guinea-pig.

Cortisol metabolism appears to be active soon after birth in guinea-pigs. Indeed, plasma cortisol half-life measured in three day-old animals resembles that of adult guinea-pigs (48 min). The metabolic clearance rate (MCR) of plasma cortisol as measured by continuous infusions of 3H-cortisol in fetal and newborn guinea-pigs remained very low, increasing slowly and regularly during the perinatal period without abrupt change at birth. Whole cortisol MCR in fetus is presented as the resultant of the concomitant actions of three factors: transfer to the mother, fetal irreversible removal rate and placental metabolism. True fetal cortisol MCR could be dissociated from total cortisol MCR measured in fetus by comparing the ratios of other measured parameters in maternal and fetal plasmas. Until ten days post partum, cortisol MCR varied independently of body weight growth and reflected the maturation of catabolizing hepatic enzymes.