Prostacyclin production by whole blood from children: impairment in the hemolytic uremic syndrome and excessive formation in chronic renal failure.
The capacity of leukocytes to produce prostacyclin (PGI2) from endogenous and from platelet-derived endoperoxides was tested in whole blood. During the acute phase of the hemolytic uremic syndrome (H.U.S.), the PGI2-production was lower than the controls, whereas the blood from children with chronic renal failure produced higher amounts. Production of PGI2 by blood from children 3/12 to 6 years after the acute phase of H.U.S. was normal, as was the case with blood from their parents. Furthermore, in two H.U.S.-patients studied serially, the decreased PGI2-production capacity normalized 2 1/2 months after the acute phase.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D011464:Epoprostenol / Q000096:biosynthesis*; D006463:Hemolytic-Uremic Syndrome / Q000097:blood*; D006801:Humans; D007223:Infant; D007676:Kidney Failure, Chronic / Q000097:blood*; D007962:Leukocytes / Q000378:metabolism*; D011453:Prostaglandins / Q000096:biosynthesis*; D013929:Thromboxane B2 / Q000096:biosynthesis
D011453:Prostaglandins; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol