Pregnancy in Henoch-Schönlein purpura.

A 22-year-old white woman with Henoch-Schönlein purpura was treated with frequent plasmapheresis for increased severity of the disease activity during pregnancy. Hypertension, azotemia, and placental dysfunction were not observed. A healthy infant was delivered by cesarean section, and evidence of vasculitis was not detected in the placenta.

Heparin-induced thrombocytopenia and recurrent thromboembolism in siblings.

Two brothers with heparin-induced thrombocytopenia and multiple arterial and venous thromboembolism affecting peripheral vessels are described. Heparin-dependent antiplatelet antibody was detected using platelet aggregometry in both patients. Although these observations may be coincidental, the possibility of familial occurrence of this adverse reaction to heparin cannot be excluded with certainty.

Treatment of uraemic bleeding with conjugated oestrogen.

A conjugated oestrogen preparation ('Premarin') was given to 6 uraemic patients with abnormal bleeding tendency in whom bleeding time was more than 30 min despite their being on chronic dialysis. In 4 patients the bleeding time became normal after 2 to 5 days of premarin therapy. In 1 of the 4 the prolonged bleeding time was repeatedly restored to normal (less than 7 min) after a single dose of premarin (25 mg). Bleeding time remained normal for 3 to 10 days after discontinuation of premarin. Bleeding time was significantly shortened (11 min) in the other 2 patients after 7 and 9 days of treatment. There was no consistent improvement in platelet aggregation nor increase in plasma factor-VIII-ristocetin cofactor activity during premarin therapy. 5 patients underwent surgery without abnormal bleeding. There were no side effects associated with premarin administration. Premarin treatment may be beneficial to uraemic patients with abnormal bleeding.

Procainamide-induced thrombocytopenia.

An 81-year-old female developed marked thrombocytopenia associated with numerous megakaryocytes in the bone marrow, but without anemia or leukopenia, after taking procainamide (3 g/day) for a period of 2 months. Despite continuation of this medication, treatment with prednisone led to rapid rise in platelet count, and withdrawal of steroid was followed by prompt recurrence of thrombocytopenia. The platelet counts returned to normal after discontinuation of procainamide, and readministration of this drug was followed by reappearance of thrombocytopenia. These observations indicate that exposure to procainamide can cause isolated thrombocytopenia, probably due to immune-mediated destruction of platelets, and that treatment with prednisone may be promptly beneficial in patients with procainamide-induced severe thrombocytopenia and bleeding.

Marrow neutrophil mass in patients with nonhematological tumor.

The state of granulocytopoiesis was assessed in 15 patients with metastatic carcinoma without infection, overt protein-calorie malnutrition, splenomegaly, or prior chemotherapy. Seven patients had decreased total marrow neutrophil mass, accompanied by proportional reduction in marrow proliferative and nonproliferative neutrophil pool, without increased numbers or proliferative capacity of marrow CFC or myeloid mitotic index. Four patients had decreased MGR assessed with hydrocortisone, but only one had reduced marrow nonproliferative neutrophil pool. Neither MGR nor blood neutrophil count correlates significantly with nonproliferative neutrophil pool or the number of band and segmented neutrophils in the bone marrow. The blood neutrophil count, however, correlates significantly with total marrow neutrophil mass (r = 0.69, p less than 0.01) and proliferative neutrophil pool (r = 0.68, p less than 0.01). These findings suggest that reduced marrow neutrophil mass is common in patients with metastatic carcinoma in the absence of overt protein-calorie malnutrition and that the reduced marrow neutrophil mass is most likely due to depressed granulocytopoiesis.