Pulmonary angiomatoid vascular changes in mitomycin C-associated hemolytic-uremic syndrome.

Angiomatoid vascular changes in lungs and pulmonary hemorrhage are described in a woman in whom mitomycin C-associated hemolytic-uremiclike syndrome developed. These changes represent part of the spectrum of vascular damage that may complicate mitomycin therapy. Patients receiving mitomycin C chemotherapy require careful monitoring for possible development of these complications.

Inflammatory fibrous histiocytoma: an important variant of malignant fibrous histiocytoma highly responsive to chemotherapy.

Inflammatory fibrous histiocytoma is a recently recognized variant of malignant fibrous histiocytoma. Patients managed with surgical excision or radiation therapy usually have had multiple recurrences, often with metastases. The disease is insidious but ultimately fatal. Four consecutive patients were treated with inflammatory fibrous histiocytoma with alkylating agents with or without anthracyclines and produced prolonged and sustained remissions. Inflammatory fibrous histiocytoma may be another highly chemotherapeutically responsive tumor that deserves active case identification for aggressive curative therapy.

Nonimmune interaction of leukocytes with platelets and megakaryocytes.

Platelet-leukocyte interaction was observed in an asymptomatic woman. After incubation in the patient's EDTA-plasma, autologous and allogeneic platelets adhered to the surfaces of neutrophils, monocytes, macrophages and, rarely, eosinophils. Monocytes, macrophages, and occasionally neutrophils phagocytosed platelets. Degranulation of peroxidase-positive lysosomes into the platelet-containing phagosome was demonstrated ultrastructurally. Bone marrow studies indicated that bands and earlier neutrophilic precursors did not participate in the reaction, and that neutrophils adhered to, and were rarely engulfed by megakaryocytes. Sequential exposure of the patient's EDTA-plasma to platelets and leukocytes indicated that a nondialyzable factor(s) was first absorbed by platelets which then interacted with leukocytes. The reaction proceeded best in the presence of EDTA at 21 degrees C, and was inhibited or dissociated by divalent cations or at 37 degrees C. Metabolic integrity of both platelets and leukocytes was also essential for the reaction since each was inhibited by formalin fixation and partially inhibited by the metabolic inhibitor 2-deoxyglucose. Formalin-treated platelets continued to absorb the plasma factor(s). The plasma and the cell fractions were inactivated by periodate and nonspecific protease. Treatment of the platelets with trypsin or the leukocytes with neuraminidase diminished the interaction by 50%. The reaction was also interfered with by concanavalin A. Immunofluorescent and immunoabsorption studies failed to identify an immune component of this interaction. These findings indicate that the plasma factor(s) and the cell surface receptors are nonimmune glycoconjugates and consequently differ from previously documented cases of platelet-leukocyte interaction.