1445

ng/rni; range 1-5-14-1) than those with stable effort angina (2-27 [0-24] ng/ml; 1-5-4-6) and controls (1-56 [0 15] ng/ml; 0-5-3-6) (p < 0-0001). Lymphomonocyte preparations were isolated by Boyum’S7 method and kept at 37°C for 4 h in a CO2 incubator. Procoagulant activity was assayed by one-stage plasma recalcification time.8 All lymphomonocyte preparations from unstable angina patients showed high tissue-factor-like procoagulant activity after 4 h of incubation, whereas lymphomonocyte preparations from both controls and patients with stable effort angina produced only negligible amounts of procoagulant activity (p < 0-0001): Procoagulant activity (U per IOS monocytes)

Controls 14-25

(2-02)

Unstable

Stable

angina

angina

166-36

16-54

(22-30)

(3-10)

Neutrophil and lymphocyte preparations (98% pure) from bothunstable angina patients and controls did not develop much procoagulant activity within an 18 h incubation (data not shown). We conclude that monocytes from patients with unstable angina are activated and produce high procoagulant activity, which may be responsible for the increased thrombin formation in these patients. G. G. NERI SERNERI ROSANNA ABBATE GIAN FRANCO GENSINI ANNA MARIA GORI MONICA ATTANASIO FRANCESCA MARTINI

Medical Clinic I, University of Florence, 50134, Florence, Italy

of young women with metronidazole resistant organisms has reported in a smaller series from the Netherlands.’ Hospital notes and complete general practitioner records were available in 43 of our 60 patients whose primary isolate was metronidazole resistant. These were checked for previous metronidazole use and then compared with 43 age and sex matched controls whose H pylori isolate was metronidazole sensitive. Previous exposure to metronidazole was found in 26/43 (60%) of the cases compared with only 1 of 43 controls (p