Production of 5-lipoxygenase pathway metabolites by peripheral leucocytes in capillary leak syndrome (Clarkson disease).
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| Abstract |
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 less than 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, endogenous factor to produce more 5-HETE and LTB4. Whether LTB4 plays a pathogenic role in the capillary leakage remains to be determined.
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| Authors | E Rondeau, J Sraer, M Bens, L M Doleris, R Lacave, J D Sraer |
| Journal | European journal of clinical investigation (Eur J Clin Invest) Vol. 17 Issue 1 Pg. 53-7 (Feb 1987) ISSN: 0014-2972 [Print] England |
| PMID | 3032644 (Publication Type: Case Reports, Journal Article, Research Support, Non-U.S. Gov't) |
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