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[Defects in the prostaglandin system. VI. Acquired plasma factor defect]
H Sinzinger1, P Fitscha, F Rauscha
1Atheroskleroseforschungsgruppe (ASF), Wien.
A 44 year-old male was admitted to hospital in October 1984 presenting with enzymatic and electrocardiographic signs of posterior wall myocardial infarction. At this time 2 separate examinations revealed normal plasma factor activity. At the 1 year follow-up (November 1985) plasma factor activity was still present. However, in February 1987 for the first time, the patient's plasma failed to enhance PGI2 synthesis from vascular tissue in vitro. 3 further follow-up examinations within the next 6 weeks again revealed an acquired absence of plasma factor activity of unknown cause. No deterioration in clinical condition occurred. All relatives tested showed normal plasma factor activity.
A 44 year-old male was admitted to hospital in October 1984 presenting with enzymatic and electrocardiographic signs of posterior wall myocardial infarction. At this time 2 separate examinations revealed normal plasma factor activity. At the 1 year follow-up (November 1985) plasma factor activity was still present. However, in February 1987 for the first time, the patient's plasma failed to enhance PGI2 synthesis from vascular tissue in vitro. 3 further follow-up examinations within the next 6 weeks again revealed an acquired absence of plasma factor activity of unknown cause. No deterioration in clinical condition occurred. All relatives tested showed normal plasma factor activity.