Activation of coagulation in chronic urticaria in relation to disease severity and activity.

BACKGROUND: The pathogenesis of chronic urticaria is incompletely understood. There is growing interest in the role of the coagulation cascade in chronic urticaria. We aimed to assess the possible activation of the coagulation cascade in chronic spontaneous urticaria (CSU) in relation to disease severity and activity. METHODS: This study was conducted on 30 patients with active CSU and 30 apparently healthy individuals as controls. Patients with acute urticaria, physical urticaria, or any form of urticaria other than spontaneous urticaria were excluded. Plasma levels of D-dimer and activated factor VII (FVIIa) were measured by ELISA at baseline for all recruited patients and controls. In addition, they were measured for CSU patients after complete disease remission. RESULTS: Plasma levels of D-dimer and FVIIa were significantly higher among patients with active CSU than among healthy controls. D-dimer levels were lowest among patients with grade 1 severity and highest among those with grade 4 severity. Factor VIIa levels did not differ significantly according to disease severity grades. After complete disease remission, there was a significant dramatic drop in levels of D-dimer and FVIIa among patients. CONCLUSION: We conclude that activation of the coagulation cascade occurs in CSU, and we demonstrate the novel finding that activated factor VII levels are significantly reduced after medical therapy, confirming the implication of the extrinsic pathway activation in CSU. Future controlled studies may investigate the role of anticoagulant therapy in refractory chronic urticaria.

Evaluation of angiotensin converting enzyme gene polymorphism and susceptibility to bronchial asthma among Egyptians.

BACKGROUND: Angiotensin converting enzyme (ACE) is expressed at high levels in the lungs and plays a role in the metabolism of the endogenous peptides involved in asthma pathogenesis. ACE gene polymorphisms have been reported to be linked to asthma. However, the results are conflicting, with no reported studies on Egyptian asthmatics. We aimed to assess ACE gene polymorphism among Egyptian asthmatics, and to determine its possible association with asthma severity. METHODS: This case-control study was conducted on 30 adult asthmatic patients, and 30 healthy controls with no history of asthma or atopy. Atopic status among asthmatics was determined by skin prick test (SPT). Lung functions were assessed by spirometry. Determination of ACE genotypes was performed for all subjects. Total serum IgE levels were measured by ELISA. RESULTS: The frequencies of the DD, ID and II genotypes were 46.7%, 40%, and 13.3%, respectively among the cases, and 33.3%, 40%, and 26.7%, respectively among the controls. No significant differences in ACE genotype distribution were observed between cases and controls (p=0.37). Genotype distribution did not differ according to age of onset or severity of asthma, total serum IgE levels, SPT positivity, or number of positive SPT reactions. Furthermore, ACE polymorphism was not statistically different between asthmatic patients without any associated atopic disease and those with an associated atopic disease. CONCLUSION: The results of our study indicate that ACE gene polymorphism is not significantly associated with bronchial asthma or with its severity among Egyptian adults.