1. Thromboxane A2 synthesis in pregnancy-induced hypertension
- Author
-
W Rocki, G. Mayo, Garret A. FitzGerald, Desmond J. Fitzgerald, and R Murray
- Subjects
Adult ,medicine.medical_specialty ,Adolescent ,Thromboxane ,Metabolite ,Pregnancy Complications, Cardiovascular ,Severity of Illness Index ,Excretion ,chemistry.chemical_compound ,Thromboxane A2 ,Pregnancy ,Internal medicine ,Medicine ,Humans ,Platelet ,Aspirin ,Creatinine ,business.industry ,Platelet Count ,General Medicine ,medicine.disease ,Platelet Activation ,Thromboxane B2 ,Blood pressure ,Endocrinology ,chemistry ,Evaluation Studies as Topic ,Pathophysiology of hypertension ,Hypertension ,Female ,business ,medicine.drug - Abstract
Urinary excretion of thromboxane B 2 metabolites as markers of thromboxane A 2 synthesis was measured in eight patients with moderate to severe pregnancy-induced hypertension and in six normotensive pregnant women at term. Excretion of both 2,3-dinor-TxB 2 (median 3919, range 683-16 680 pg/mg creatinine) and 11-dehydro-TxB 2 (median 10187, range 434-57 203 pg/mg creatinine) was significantly higher in the patients with pregnancy-induced hypertension than in the normotensive pregnant group (927[273-1343] and 774[500-2760] pg/mg creatinine, respectively). Thromboxane metabolite excretion correlated with mean arterial blood pressure, plasma lactate dehydrogenase, and platelet count which are indices of the severity of pregnancy-induced hypertension. Excretion of both metabolites fell rapidly post partum in parallel with resolution of clinical signs. Thus, increased thromboxane A 2 biosynthesis correlates with disease severity and may have a pathogenetic role in pregnancy-induced hypertension. These findings provide a rationale for the use of aspirin in the treatment as well as in the prevention of this disorder.
- Published
- 1990