BACKGROUND Patients with transfusion-dependent β-thalassemia need regular red-cell transfusions. Luspatercept, a recombinant fusion protein that binds to select transforming growth factor β superfamily ligands, may enhance erythroid maturation and reduce the transfusion burden (the total number of red-cell units transfused) in such patients. METHODS In this randomized, double-blind, phase 3 trial, we assigned, in a 2:1 ratio, adults with transfusion-dependent β-thalassemia to receive best supportive care plus luspatercept (at a dose of 1.00 to 1.25 mg per kilogram of body weight) or placebo for at least 48 weeks. The primary end point was the percentage of patients who had a reduction in the transfusion burden of at least 33% from baseline during weeks 13 through 24 plus a reduction of at least 2 red-cell units over this 12-week interval. Other efficacy end points included reductions in the transfusion burden during any 12-week interval and results of iron studies. RESULTS A total of 224 patients were assigned to the luspatercept group and 112 to the placebo group. Luspatercept or placebo was administered for a median of approximately 64 weeks in both groups. The percentage of patients who had a reduction in the transfusion burden of at least 33% from baseline during weeks 13 through 24 plus a reduction of at least 2 red-cell units over this 12-week interval was significantly greater in the luspatercept group than in the placebo group (21.4% vs. 4.5%, P<0.001). During any 12-week interval, the percentage of patients who had a reduction in transfusion burden of at least 33% was greater in the luspatercept group than in the placebo group (70.5% vs. 29.5%), as was the percentage of those who had a reduction of at least 50% (40.2% vs. 6.3%). The least-squares mean difference between the groups in serum ferritin levels at week 48 was −348 μg per liter (95% confidence interval, −517 to −179) in favor of luspatercept. Adverse events of transient bone pain, arthralgia, dizziness, hypertension, and hyperuricemia were more common with luspatercept than placebo. CONCLUSIONS The percentage of patients with transfusion-dependent β-thalassemia who had a reduction in transfusion burden was significantly greater in the luspatercept group than in the placebo group, and few adverse events led to the discontinuation of treatment. (Funded by Celgene and Acceleron Pharma; BELIEVE ClinicalTrials.gov number, NCT02604433; EudraCT number, 2015-003224-31.)

Since 1996, there have been several case reports of autochthonous visceral leishmaniasis in Thailand. Here we report a case in a 52-year-old Thai male from northern Thailand, who presented with subacute fever, huge splenomegaly and pancytopenia. Bone marrow aspiration revealed numerous amastigotes within macrophages. Isolation of Leishmania LSCM1 into culture and DNA sequence analysis (ribosomal RNA ITS-1 and large subunit of RNA polymerase II) revealed the parasites to be members of the Leishmania enriettii complex, and apparently identical to L. martiniquensis previously reported from the Caribbean island of Martinique. This is the first report of visceral leishmaniasis caused by L. martiniquensis from the region. Moreover, the majority of parasites previously identified as “L. siamensis” also appear to be L. martiniquensis.

BackgroundDengue infection patients are presented with acute febrile illness. Clinical presentations may mimic other infections. The serology for definite diagnosis is costly and inaccessible in many hospitals. We sought to identify the clinical features and hematologic parameters from a complete blood count (CBC) which distinguish dengue infection from other causes.MethodsThis was a retrospective single center study from Chiang Mai University Hospital. All patients who presented with acute fever between September 2013 and July 2015 were included. The diagnosis of dengue infection must be confirmed by serology. The control groups were patients who presented with acute febrile illness without localizing signs. Clinical data and CBC results were reviewed and compared. The Chi-square test was used to compare categorical variables. The CBC parameters were analyzed using the linear mixed model.ResultsOne hundred and fifty-four dengue and 146 control patients were included. Headache, nausea, loss of appetite and bleeding diathesis were significantly symptoms in dengue patients (p < 0.05). There was some diversity in the the CBC in the dengue patients compared to the control group. Moreover, this study also identified the day of fever which these parameters were statistically significant. The dengue group had higher hemoglobin and hematocrit from day 3 to day 10 (p < 0.001), lower white blood cell count from day 1 to day 10 (p < 0.001), lower platelet count from day 3 to day 10 (p < 0.001), higher monocyte on day 1–4 (p < 0.001), higher atypical lymphocyte percentage on day 5–9 (p < 0.001) and higher eosinophil percentage on day 9–10 (p = 0.001). Furthermore, the neutrophil to lymphocyte percentage ratio of dengue group was > 1 on the first 5 days then reversed on day 6 to Day 9 but in non-dengue group, the ratio was always > 1.ConclusionWe identified important clinical features and CBC parameters to differentiate dengue patients from other patients who had acute febrile illness from other causes. This identification could be done in local hospitals to give an accurate diagnosis, enabling further investigation to be tailored and treatment commenced earlier.

Studies in mice have shown that proinflammatory Th17 cells can cause acute graft-versus-host disease (aGVHD) related tissue damage; however, whether they play a role in human aGVHD remains unclear. In a prospective study, we measured the proportion of Th17 cells in the blood and skin of patients at the onset of aGVHD. We found no difference in the proportion or amount of IL-17 produced by T cells in the blood of patients with aGVHD (n = 20) compared with time-matched patients without GVHD (n = 14). Moreover, Th17 cells were not increased in the skin of patients with cutaneous aGVHD (n = 7) compared with healthy controls (n = 10). In contrast, we found significantly more interferon-γ-producing T cells in the skin of patients with aGVHD compared with controls. These data support the long-standing paradigm that tissue localized interferon-γ-producing cells are the perpetrators of aGVHD.