Summary:logous rescue following myeloablative therapy. 1 In this context, PBSC can be successfully mobilised with chemotherapy in combination with granulocyte colony-stimulatWe have carried out an analysis of 44 patients undergoing allogeneic PBSC transplants from fully HLAing factor (G-CSF) or with G-CSF alone. 2 Reports of the first allogeneic PBSC transplants (PBSCT) showed that matched related donors with particular emphasis on engraftment kinetics and the incidence and severity of PBSC could be safely mobilised from normal donors using G-CSF alone and could achieve trilineage engraftment in GVHD. The recipients had a median age of 37 years (range 5-56 years), 16 patients had standard-risk disthe recipients, without severe graft versus-host-disease (GVHD). 3,4 The feasibility of this approach has recently ease and 28 had poor-risk disease. GVHD prophylaxis was with cyclosporin A and methotrexate (n = 41), been confirmed in several reported series of patients undergoing allogeneic PBSCT. [5][6][7][8] In these reports large cyclosporin A alone (n = 2) or cyclosporin A and methylprednisolone (n = 1). Stem cells were mobilised using numbers of CD34 + cells were successfully collected from donors following administration of G-CSF and the data G-CSF, collecting a median of 5.75 × 10 6 CD34 + cells/kg recipient weight (range 0.94-35 × 10 6 CD34 + cells/kg).confirmed that blood stem cells resulted in long-term haemopoietic engraftment following transplantation. They Engraftment times to a neutrophil count Ͼ0.5 × 10 9 /l and platelets Ͼ20 × 10 9 /l were achieved at a median of also suggested that there may be advantages over allogeneic bone marrow transplantation (BMT) in terms of faster day +14 (range 10-25) and day + 14 (range 9-130) respectively. Patients receiving у4 × 10 6 CD34 + cells/kg haemopoietic engraftment, as is the case in autologous transplantation, 9 however, the number of CD34 + cells had significantly accelerated neutrophil and platelet engraftment and this number of CD34 + cells would required for optimal engraftment is still not certain. Allogeneic PBSCT have been performed in the United appear to be a prerequisite for maximum engraftment using PBSC. Acute GVHD occurred in 25 of 43 evaluKingdom (UK) since 1993. To obtain an overview of this activity we surveyed 20 BMT units in the UK and report an able patients although in only 12 was this clinically significant (grades II-IV). Chronic GVHD has occurred in analysis of 44 patients, from nine centres, where allogeneic transplantation using PBSC from related donors had been 17 out of 36 evaluable patients, there was no significant difference between the standard-and poor-risk groups undertaken between March 1993 and March 1996, specifically looking at engraftment kinetics and the incidence of in incidence of either acute or chronic GVHD. In conclusion, these results confirm the feasibility of using acute and chronic GVHD. PBSC for allogeneic transplantation without evidence for increased risk of either acute or chronic GVHD and provide further eviden...

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Non-caseating granuloma (NCG) remains a histopathological hallmark for sarcoidosis. Although the exact mechanism for NCG formation is unknown, the pathogenesis may involve a disordered antigen presentation in the monocyte/macrophage system, functional abnormalities in activated T-lymphocytes and uncontrolled cytokine production. Similar immunological dysfunction has been described in myelodysplastic syndrome (MDS). However, the association of NCG and MDS is rarely documented. We report a case of hypocellular MDS associated with generalized NCG. Despite treatment for both sarcoidosis and tuberculosis, the patient failed to respond. A clonal myeloid disorder which was initially suppressed by T-cell immunosurveillance evolved after treatment with anti-thymocyte globulin. Although the coexistence of sarcoidosis remains a possibility, the lack of supportive clinical evidence of sarcoidosis, the abnormal appearances of the bone marrow, together with the failure to improve on high-dose steroid favour the clonal myeloid disorder as the sole pathology.