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Of the first 14 patients with acute or chronic leukemia to undergo bone marrow transplantation at our hospital, 9 (64%), all good-risk, are still alive in remission at 18 to 42 months of follow-up (mean, 29 months) with their Karnofsky performance status between 80% and 100%. The conditioning regimen of fractionated-dose irradiation and high-dose chemotherapy eradicated their disease; only two patients relapsed after transplantation. Toxicity was acceptable. Acute graft-versus-host disease developed in six patients (43%) (grade I or II in four, grade IV in two) and progressed to chronic graft-versus-host disease in four. Viral pneumonitis developed in three patients (21%), but none had idiopathic interstitial pneumonitis. The mean hospital charge was $54,355. These preliminary results suggest that good-risk patients with acute or chronic leukemia can be treated with bone marrow transplantation in a university affiliated hospital with appropriate staff and support facilities and achieve results comparable to those in research institutions at a competitive cost.

We have previously demonstrated that lentil phytohemagglutinin (lentil-PHA) binds to human platelet membranes without causing either aggregation or the release reaction. When platelets are treated with thrombin, there is an increase in lentil-PHA binding suggesting the appearance of new receptor sites on the cell surface. We prepared a lentil-PHA-ferritin conjugate using affinity chromatography which was used to saturate cell surface receptor sites. Studies using this conjugate suggest that thrombin causes a complex change in the platelet surface involving a decrease in the number of lentil-PHA receptor sites on the external platelet surface with a marked increase in sites within the center of the canalicular system. These increased sites may result from fusion of granule membranes with the canalicular membranes during the secretion process. There is no obvious relationship between lentil-PHA receptor sites and intramembranous particles.

We have previously shown that the erythroagglutinating phytohemagglutinin (E-PHA) from Phaseolus vulgaris binds to the surface of intact human platelets and that adenylate cyclase activity in the particulate fraction of E-PHA-treated platelets is lower than in comparable controls. We now find that E-PHA induces release of [(14)C]serotonin from platelets. Release follows binding of E-PHA, and a haptenic inhibitor of E-PHA binding prevents induction of release. E-PHA does not produce platelet lysis and has little effect on [(14)C]serotonin uptake. Platelets possess approximately 300,000 receptor sites of E-PHA per cell, and we estimate that about 15% of these sites must be occupied by E-PHA to initiate the release reaction. Prior incubation of platelets with prostaglandin E(1), theophylline, or dibutyryl cyclic AMP prevents E-PHA-induced release, although these agents have little effect on E-PHA binding to platelets. Thrombin and E-PHA produce different rates and extents of serotonin release. Thrombin (1 U/ml) causes release of 75-85% of platelet [(14)C]-serotonin, with half-maximal release occurring less than 0.5 min after thrombin addition. E-PHA, however, induces release of only 30-60% of platelet serotonin at a 10-fold slower rate. In addition, utilizing electron microscopy, we have observed striking differences in the morphological changes that occur in platelets exposed to E-PHA as compared with thrombin. Thus, the platelet release reaction may be triggered in part by binding of E-PHA to the cell surface, but this reaction only partially resembles that produced by thrombin.

Inflammation of the cecum ("typhlitis") has been an unusual, but generally fatal complication of severe granulocytopenia and immunosuppression, occurring during the therapy of hematological malignancies. The diagnosis has usually been made only at autopsy, and early surgical intervention has often been withheld because of the patient's precarious hematological status. We report here a patient in whom the clinical diagnosis of typhlitis led to early operation, with intensive blood component support. The successful outcome suggests that such an approach might improve the usually grim prognosis in patients whose underlying malignancy offers a clear chance for remission.

Thrombocytopenia in patients with multiple myeloma is usually due to chemotherapy or marrow replacement with myeloma cells. Two patients with multiple myeloma who fulfilled criteria for the diagnosis of immune thrombocytopenic purpura are presented. The etiologic and therapeutic implications of this unusual association are discussed.

Less than 200 cases of malignant histiocytosis (histiocytic medullary reticulosis) have been reported in the literature. Five previously reported cases and the case reported in this article have been preceded by acute lymphocytic leukemia. All of these cases have had similar courses characterized by prompt response of the leukemia to chemotherapy followed in three to six months by the onset of rapidly fatal malignant histiocytosis. The leukemic lymphoblasts in the two cases studied for lymphocyte surface markers had T cell markers. No residual leukemia was identified at autopsy in four of the six cases.