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Production of 5‐lipoxygenase pathway metabolites by peripheral leucocytes in capillary leak syndrome (Clarkson disease)
Author(s) -
RONDEAU E.,
SRAER J.,
BENS M.,
DOLERIS L. MOULONGUET,
LACAVE R.,
SRAER J. D.
Publication year - 1987
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1987.tb01225.x
Subject(s) - arachidonic acid , vascular permeability , asymptomatic , leukotriene , peripheral , leukotriene b4 , lipoxygenase , chemistry , medicine , capillary action , immunology , in vitro , endogeny , peripheral blood , biochemistry , enzyme , inflammation , asthma , composite material , materials science
. Periodic systemic capillary leak syndrome (Clarkson disease) is characterized by unexplained attacks of a marked increase in capillary permeability. As leukotrienes, derived from arachidonic acid via the 5‐lipoxygenase pathway, enhance capillary permeability, we studied arachidonate metabolism in leucocytes of a patient with capillary leak syndrome. Leucocyte‐platelet suspensions, prepared from blood collected from the patient during asymptomatic periods ( n = 11) produced greater amounts of 5‐hydroxyeicosatetraenoic acid (5‐HETE) than control suspensions ( P < 0·05). Peripheral leucocytes, collected during attacks ( n = 3) and studied without addition of A23187 released LTB4 in vitro but not sulphidopeptides leukotrienes. This result was never observed with leucocytes from control subjects or from the patient out of a crisis. These results suggest that in the patient, peripheral leucocytes could be stimulated by an unknown, as yet to be determined, endogeneous factor to produce more 5‐HETE and LTB4. Whether LTB4 plays a pathogenic role in the capillary leakage remains to be determined.