DECREASED PROSTACYCLIN-LIKE ACTIVITY IN HENOCH-SCHONBEIN PURPURA
Henoch-Schoniein purpura (HSP) is the most common type of childhood vasculitis. The skin lesions are the most obvious sign but visceral involvement carries a more serious prognosis. Increasing amounts of data are available regarding the possible role of prostacyclin (PGI2) in the pathogenesis of other vasculo-pathies, but no-one has previously investigated HSP. 17 HSP patients (mean age (SD) 5.7 (2.5) years) and 17 matched controls were studied. The ability of plasma (patient and control) to support PGI2 -like activity was tested. Human umbilical arteries were chopped into rings and incubated in buffer at 37° C. Aliquots of the supernatant were added to platelet rich plasma (PRP) and platelet aggregation measured (Malin's aggregometer). Repeated washings of the rings then depleted PGI. production. The rings were then incubated with test platelet poor plasma (PPP) at 37° C. PGI2 like activity was assessed as before and the results expressed as a percentage of the aggregation obtained by the same exhausted ring before addition of PPP. The results show that the ability of test PPP to support PGI2 like activity was reduced in 13/17 HSP patients. The difference between patients (21.3 (SD 20.5%) and controls (57.2 (SD 12.2%) was significant (p<0.001). Patients with renal and gastro-intestinal involvement (7.5 (SD 18.1%) were significantly different from those patients with only skin involvement (32.3 (SD 23.5%) (p<0.01). Plasma from six patients in which PGI^like activity was undetectable using the above method were further studied to detect PGI2 -inhibitory activity. Unexhausted umbilical rings were incubated at 37°C for 5mins. The baseline PGI2 like activity of the supernatant was compared with that produced after 5mins. incubation with test PPP (o patients, 6 controls). Less like activity was produced by the unexhausted rings when incubated with PPP from the HSP patients than with either control buffer or control PPP (both p<0.01). It seems likely that these abnormalities, having been demonstrated in yet another vasculitic syndrome, are secondary to endothelial damage. The disturbances, however, may well be of importance in extending the primary microvascular insult