Toxoplasmosis is a rare but often fatal complication that occurs after patients undergo allogeneic hematopoietic stem cell transplant. At our institution, toxoplasmosis was diagnosed in 8 of 301 patients who received stem cell transplants. Disseminated toxoplasmosis with a rapid fatal course was observed in 2 patients. Six patients had cerebral toxoplasmosis diagnosed on the basis of neurological signs and observation of the patients' mental confusion, seizures, and typical lesions (which were assessed by computed tomography, magnetic resonance imaging, or both). Seroconversion of antitoxoplasma immunoglobulin and a discovery of toxoplasma deoxyribonucleic acid in the cerebrospinal fluid (confirmed by use of polymerase chain reaction) were documented in all patients. Treatment consisted of clindamycin therapy (for 2 patients) and of pyrimethamine-clindamycin therapy, sulfadiazine therapy, or both (for 5 patients). Patients showed improvement after therapy, as assessed by clinical and radiological means. Three of 8 patients survive-1 without any residual neurological symptoms and 2 with minimal neurological symptoms.
In order to determine inpatient hospital mortality rates, causes of mortality and characteristics of inpatients at Kamuzu Central Hospital (KCH) in Lilongwe, Malawi, we conducted a prospective observational study of all patients admitted to KCH medical ward from 20 September 2008 to April 2, 2009. All admission diagnoses, HIV status and antiretroviral therapy (ART) use were recorded. Patients' vital status was determined at discharge. A descriptive analysis and two logistic regression models were used for the analysis. Of the 1895 enrolled patients, the overall hospital mortality rate was 14.6%, substantially higher among known HIV-infected patients (24.2% versus 10.8%, P = 0.0009) and men (17.1% versus 12%, P = 0.033). Patients with multiple diagnoses had significantly higher mortality (odds ratio [OR] 2.33; 95% confidence interval [CI] 1.47, 3.71). Most patients (62.3%) had unknown HIV status at admission. Among HIV-infected patients, ART use did not reduce hospital mortality or alter the spectrum of diseases. The majority of diagnoses were infectious (63.4%). The high inpatient mortality rate, especially among HIV-infected patients combined with the limited spectrum of diagnoses, emphasizes the need for improved inpatient management and diagnostic services. Expansion of HIV testing is warranted. Despite the rollout of ART, there remains a significant need for treatment of HIV-infected individuals.
Summary:We compared the outcomes in patients receiving unrelated peripheral blood stem cell transplants (PBSCT) with those receiving bone marrow transplants (BMT) in a matched pair analysis. Seventy-four patients with hematological malignancies with HLA-matched (77%) and mismatched (23%) donors were analyzed in this study. Thirty-four patients (45%) were considered as high risk patients. Sixty-eight patients received standard conditioning regimens with Bu/Cy or TBI/Cy. Six patients received an intensified conditioning regimen with the addition of etoposide, thiotepa or melphalan. GVHD prophylaxis consisted of prednisolone, cyclosporine and methotrexate. Groups were matched for patient, donor, transplant characteristics and HLA compatibility. Peripheral blood stem cell collection led to the collection of a higher number of CD34 + and CD3 + cells in comparison to bone marrow collection. Leukocyte engraftment in the PBSCT group occurred in 14 days (median; range 6-26 days) and in the BMT group in 19 days (range 9-29 days; P Ͻ 0.02). The time of platelet engraftment did not differ significantly. The incidence of grades II-lV acute GVHD in the group of HLA-identical patients was 35% in the PBSCT group and 25% in the BMT group (P Ͻ 0.33, log-rank). However, there was a significant difference (P Ͻ 0.05, logrank) in incidence and time to onset of acute GVHD II-IV comparing all patients, including the 17 mismatched transplants. Disease-free survival was 51% (19 patients) with a median of 352 days and 59% (21 patients) with a median of 760 days for PBSC and BMT transplants, respectively. In conclusion, our results indicate that allogeneic PBSCT led to significantly faster leukocyte engraftment but is associated with a higher incidence and more rapid onset of severe acute GVHD comparing all patients, including the 17 mismatched transplants. However, the incidence of severe acute GVHD in HLAidentical patients was not different between the PBSCT and BMT groups. Bone Marrow Transplantation (2001) 27, 27-33.
Summary:Hematopoietic stem cell transplantation (HSCT) is a treatment option for autoimmune diseases but can also cause clinical features similar to those of autoimmune diseases. In some of these cases the autoimmune-like condition is associated with autoimmune cytopenia, a complication that can be unresponsive to established treatment strategies and which may be fatal. The majority of cases reported on immune hemolytic anemia have been of alloimmune origin due to ABO red blood cell antigen incompatibilities between donor and recipient. We now report a patient with a lupus-like syndrome, presenting with severe thrombocytopenia and hemolytic anemia 9 months after HLA-mismatch, ABO compatible-related PBSCT who experienced no response to high-dose steroids, but who had a sustained response to repeated IvIG therapy. Bone Marrow Transplantation (2001) 27, 337-340. Keywords: autoimmune cytopenia; hematopoietic stem cell transplantation; lupus-like syndrome; alloimmunity; IvIG Hematopoietic stem cell transplantation (HSCT) can cause clinical symptoms characteristic of autoimmune diseases like myasthenia gravis, immune thyroiditis, as well as immune cytopenia. 1-11 Especially, autoimmune cytopenia is mostly refractory to standard therapeutic approaches. 2,3 We herein report a patient with a lupus-like syndrome associated with hemolytic anemia and severe thrombocytopenia after HSCT. Patient characteristicsNine months (day +277) after a mismatched related allogeneic stem cell transplant (PBSCT) for CML in first CP, a 38-year-old patient presented with weight gain, general GvHD prophylaxis consisted of cyclosporine (CYA) starting on day −3, prednisolone starting on day +7 after transplantation and MTX given as a short course on days +1, +3 and +6 at a dose of 15 mg/m 2 and twice at 10 mg/m 2 , respectively. Engraftment (leukocyte count Ͼ1000 × 10 9 /l, neutrophil count Ͼ0.5 × 10 9 /l) occurred on day +21 after PBSCT. He developed slight cutaneous GVHD grade I-II which responded promptly to increased immunosuppression with prednisolone (0.7 mg/kg bw × day) for 1 week, then tapered, and mycophenolate-mofetil (MMF) (2 g/day) for 3 months.CMV reactivation, as diagnosed by CMV-PCR, occurred 2 months after PBSCT (recipient CMV IgG positive, donor CMV IgG negative). This was successfully treated with ganciclovir, but the PCR became positive again shortly after cessation of therapy. He therefore received cidofovir as maintenance for 2 months.Immunosuppressive therapy on admission consisted of prednisolone 5 mg/day and CYA 150 mg/day given orally (blood level 284 ng/ml). Clinical findingsAs papular cutaneous lesions were the main clinical finding a viral infection was suspected, possibly herpes virus or VZV reactivation. CMV testing had been negative for the last 4 months. However, the CMV-PCR was positive at the time of admission. He was treated with foscarnet to avoid further myelosuppression in a graft which was already suboptimal. Testing for VZV and HSV was negative.Within a few days of admission the patient developed
Dose-dense induction with the S-HAM regimen was compared to standard double induction therapy in adult patients with newly diagnosed acute myeloid leukemia. Patients were centrally randomized (1:1) between S-HAM (2nd chemotherapy cycle starting on day 8 = “dose-dense”) and double induction with TAD-HAM or HAM(-HAM) (2nd cycle starting on day 21 = “standard”). 387 evaluable patients were randomly assigned to S-HAM (N = 203) and to standard double induction (N = 184). The primary endpoint overall response rate (ORR) consisting of complete remission (CR) and incomplete remission (CRi) was not significantly different (P = 0.202) between S-HAM (77%) and double induction (72%). The median overall survival was 35 months after S-HAM and 25 months after double induction (P = 0.323). Duration of critical leukopenia was significantly reduced after S-HAM (median 29 days) versus double induction (median 44 days)—P < 0.001. This translated into a significantly shortened duration of hospitalization after S-HAM (median 37 days) as compared to standard induction (median 49 days)—P < 0.001. In conclusion, dose-dense induction therapy with the S-HAM regimen shows favorable trends but no significant differences in ORR and OS compared to standard double induction. S-HAM significantly shortens critical leukopenia and the duration of hospitalization by 2 weeks.
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