Summary.A quantitative analysis of peripheral blood stem cell (PBSC) yield, measuring absolute numbers of CD34 þ cells × 10 6

Aims-To assess whether r-HuEPO (recombinant human erythropoietin) has any effect on thrombopoiesis in patients with chronic renal failure.Methods-This was a retrospective study of 78 patients with chronic renal failure undergoing either haemodialysis (n = 57) or intraperitoneal dialysis (n = 21). All patients had a full blood count (in EDTA) me before stling r-HuEPO and at monthly intervals thereafter up to six months. Variables studied were haematocrit, platelet count, mean platelet volume (MPV) and platelet distribution width (PDW). Other groups of control patients were also studiedpatients with chronic renal failure receiving dialysis but not r-HuEPO (n = 40) and a group of patients with normal renal function who were receiving aspirin (n = 30). Results-There was a significant increase in mean haematocrit (p < 0.01) and in mean platelet volume (p < 0-001) over the six month period, but no change in either total platelet count or platelet distribution width in the patients with chronic renal fiilure receiving r-HuEPO. In contrast, both the control groups showed no significant change in MPV. Conclusions-The results suggest that r-HuEPO affects thrombopoiesis and may be part of a group of humoral factors contributing to megakaryocyte development and maturation. Larger platelets are more reactive and may contribute to the increased risk of thrombosis associated with r-HuEPO. The dose of r-HuEPO began at 50 IU/kg twice weekly (by subcutaneous injection), increasing to 75 IU/kg twice weekly after two to three months if there was an insufficient rise in haematocrit and haemoglobin. It is the policy of the renal unit to give aspirin to all patients starting r-HuEPO. Twelve out of the 78 patients did not receive aspirin during the six month period of study as they had been given r-HuEPO before the establishment of this policy.All the patients had a full blood count (in EDTA) measured on a Coulter STKS (Coulter Electronics, Northwell Drive, Luton, Beds) at monthly intervals from baseline (before starting r-HuEPO) up to six months. As a result of organisational procedure both within the renal wards and the haematology laboratory, most of the samples would have been analysed within 4 hours of venepuncture, but we cannot exclude a few samples having been analysed at a later time.The variables studied were haematocrit, platelet count, mean platelet volume (MPV) and platelet distribution width (PDW).Changes in these variables were compared with baseline values and statistically analysed using Student's paired t test. A measure of the difference between the maximum value of a variable achieved over the six month period and baseline was calculated and used in the 159 on 7 May 2018 by guest. Protected by copyright.

Bone marrow necrosis is most frequently diagnosed at postmortem examination. Antemortem diagnosis is still uncommon. In a recent review of world literature, we have found 133 cases of bone marrow necrosis diagnosed during life. It has been observed during the course of a wide variety of diseases, most commonly in association with acute and chronic leukemia, carcinoma, malignant lymphoma, infections, and sickle cell disease. We report two intravitally diagnosed cases of bone marrow necrosis occurring in two patients with high-grade B-cell lymphoproliferative disease. These cases are unusual in that both patients had a triad of bone marrow necrosis, high-grade B-cell lymphoproliferative disease, and hypercalcemia. Despite chemotherapy, both cases ultimately proved fatal, with progressive involvement of the central nervous system.

Neurotoxicity in vincristine treatment has generally been considered a consequence of the cumulative dose of the drug, and liver dysfunction had been recognised as an indication to reduce the dosage. We demonstrate that neurotoxicity is also related to individual doses and that even when there is no other evidence of liver dysfunction, a raised level of serum alkaline phosphatase may predict severe neurotoxicity. Exposure to vincristine following IV injection of the drug was studied in 27 subjects by measuring the area under the vincristine plasma concentration time curve (AUC 0-infinity). A statistically significant relationship was found between the AUC0-infinity and the degree of neurotoxicity. The AUC0-infinity was related both to dose and to elevation of serum alkaline phosphatase, suggesting that elimination of the drug is impaired when serum alkaline phosphatase is raised. Among patients with elevated serum alkaline phosphatase, a small reduction in the dose of the drug resulted in lower vincristine plasma AUC0-infinity and less neurotoxicity.

Myelomatosis was diagnosed in a 64 year old man on the basis of a serum paraprotein band (type IgGA, 42g/1), plasma cell infiltration ofbone marrow, and multiple lytic lesions evident on skull x ray picture. Blood specimens taken into plain glass tubes showed bulky gelatinous clot formation with minimal clot retraction. Coagulation tests were significantly abnormal with an increase in thrombin time, prothrombin time, and reptilase time. The possibility that the paraprotein was interfering with fibrin production was investigated. The rate of fibrin monomer polymerisation (measured turbidometrically) was reduced in patient plasma compared with control plasma. Although purified fibrin monomer prepared from the patient's fibrinogen polymerised normally, the addition of purified paraprotein caused a dose dependent reduction in the rate of polymerisation. These results suggest that the paraprotein was impairing fibrin formation by inhibiting fibrin monomer polymerisation. After chemotherapy the paraprotein concentration decreased and the coagulation results returned to normal.