A new prognostic score comprising lactate dehydrogenase, albumin and neutrophil to lymphocyte ratio to predict sensitivity to first-line chemotherapy in patients with peripheral T-cell lymphomas.

No standard therapy for peripheral T-cell lymphomas (PTCLs) has been established, and treatment outcomes are poor. Upfront stem cell transplantation has been investigated in several studies, some of which have reported promising outcomes. However, some patients maintain long-term remission after chemotherapy alone. It is thus important to predict sensitivity to first-line chemotherapy to optimize treatment strategies. In the present study, we retrospectively analyzed time to treatment failure (TTF) of first-line chemotherapy in 59 patients with PTCLs. On multivariate analysis for TTF, elevated lactate dehydrogenase level, hypoalbuminemia, and high neutrophil-to-lymphocyte ratio were significant prognostic factors. Using these three factors, we also developed a new model that effectively distinguished patient outcomes. The TTF rate at 1 year from diagnosis was 71.4% in patients with score 0 (0 factor), 31.8% with score 1 (1 factor) and 4.5% with score 2 (2-3 factors) (P < 0.001). The prognostic power was superior to that of the Prognostic Index for PTCL-unspecified score. Patients with scores of 1 and 2 had poor TTF, and may be candidates for upfront stem cell transplantation if they respond to first-line chemotherapy. Further investigation in a larger cohort is warranted to determine the general applicability of this score.

Emergence of Dipstick Proteinuria Predicts Overt Nephropathy in Patients Following Stem Cell Transplantation.

BACKGROUND: Stem cell transplantation (SCT) places a heavy burden on the kidneys, often resulting in renal dysfunction or nephrotic syndrome. This study attempted to show that early-onset proteinuria predicts the development of overt nephropathy. METHODS: A total of 831 patients who received allogeneic SCT were surveyed. Excluding those with prior kidney disease and those lacking in an observation period ≥1 year after SCT, 251 patients were eligible for the study. Dipstick proteinuria ≥1+ within 1 year after SCT was defined as 'incident proteinuria', and subsequent persistence of an estimated glomerular filtration rate of <60 ml/min/1.73 m2 at 1 year or longer after SCT was defined as 'incident chronic kidney disease (CKD)'. Between-group differences were analyzed using the chi-square or Mann-Whitney U test. Factors associated with the incidence of CKD were investigated by multivariate Cox proportional regression analysis. Kidney-biopsied tissue was examined in all nephrotic syndrome patients. RESULTS: The mean duration of follow-up was 4 years. Thirty-four (13.5%) and 66 (26.3%) patients developed incident proteinuria and incident CKD, respectively. Nine (3.6%) patients developed nephrotic syndrome mainly due to membranous nephropathy. The incidence of CKD was significantly greater in patients with incident proteinuria than those without (61.8 vs. 20.7%, p < 0.0001), and incident dipstick proteinuria was a significant risk for incident CKD (hazard ratio 4.39, 95% CI 2.44-7.73, p < 0.0001). CONCLUSION: SCT patients who manifest dipstick proteinuria are predisposed to overt nephropathy. Routine monitoring of the urine dipstick test is strongly recommended, as it facilitates early nephrology care for post-SCT patients.

CD25 expression on residual leukemic blasts at the time of allogeneic hematopoietic stem cell transplant predicts relapse in patients with acute myeloid leukemia without complete remission.

Recent studies have shown that CD25 expression at the time of diagnosis of acute myeloid leukemia (AML) may be associated with an unfavorable outcome. We focus on patients with AML without complete remission (CR) and examine the clinical correlation between surface CD25 expression at the time of transplant and subsequent transplant outcomes. We observed a significant difference in overall survival (OS), disease-free survival (DFS) and cumulative incidence of relapse (CIR) between CD25 positive (+) (n = 22) and negative (-) groups (n = 44) (2-year OS; CD25 (+) group: 5% vs. CD25 (-) group: 40%, p < 0.0001, 2-year DFS; 5% vs. 29%, p < 0.0001, 2-year CIR; 77% vs. 52%, p = 0.03). Multivariate analysis showed that CD25 expression was an independent adverse factor for OS (p = 0.002) and relapse (p = 0.001). Patients with AML with residual CD25 positive blasts at the time of transplant may require additional therapy before or after transplant to improve survival.

Allogeneic hematopoietic stem cell transplant overcomes poor prognosis of acute myeloid leukemia with myelodysplasia-related changes.

Recent studies have shown that acute myeloid leukemia with myelodysplasia-related changes (AML-MRC) exhibits a worse clinical outcome than AML not otherwise specified (AML-NOS). However, transplant outcomes of patients with AML-MRC have not been reported compared to patients with AML-NOS. We analyzed transplant outcomes among 147 patients with AML-MRC or AML-NOS who underwent allogeneic hematopoietic stem cell transplant (allo-HSCT) in a single institution. There were no significant differences in the 2-year overall survival (OS), cumulative incidence of relapse (CIR), and non-relapse mortality (NRM) between the two groups (2-year OS: 48% vs. 59%; 2-year CIR: 37% vs. 35%; 2-year NRM: 19% vs. 13%). Subgroup analysis adjusting for age and disease status demonstrated the same results between the two groups. Furthermore, multivariate analysis showed that AML-MRC was not an independent prognostic factor for poor prognosis in the setting of allo-HSCT (p = 0.7). These results suggest that allo-HSCT may overcome the poor prognosis of AML-MRC.

Incidental detection of congenital Robertsonian translocation at diagnosis of Philadelphia chromosome-positive acute lymphocytic leukemia.

A man in his early forties who had undergone 3 years of unsuccessful treatment for infertility due to oligospermia and asthenospermia developed fever and bone pain in December 20XX. He was subsequently diagnosed with acute lymphocytic leukemia. Conventional cytogenetic analysis revealed Robertsonian translocation (RT) with der(13;14)(q10;q10) in addition to the Philadelphia (Ph) chromosome. Dasatinib and prednisolone induced complete remission (CR) with disappearance of the Ph chromosome. However, RT persisted despite achieving CR. We speculate that RT is possibly congenital in our present case and might also have been responsible for the aforementioned infertility. Hematologists should be aware of the possibility that congenital chromosomal disorders might be found incidentally through diagnostic chromosome analysis for leukemia.

Reduced expression of cytokeratin 4 and 13 is a valuable marker for histologic grading of esophageal squamous intraepithelial neoplasia.

Histologic evaluation of low-grade or high-grade intraepithelial neoplasia (LG-IN or HG-IN) of the esophagus is important for estimating the risk of progression to invasive carcinoma. Discrimination between LG-IN and HG-IN, or neoplasia and non-neoplastic lesion (NNL), however, is occasionally difficult. This study was designed to evaluate whether cytokeratin expression can be used for discrimination of these lesions. Esophageal Iodine-unstained lesions (n=154), less than 10 mm, were classified into HG-IN, LG-IN, and NNL. These lesions together with 154 foci of normal esophageal epithelium (NEE) were examined by immunohistochemistry for cytokeratins (CK4 and CK13), p53 overexpression, and the MIB-1 labeling index. The ratios of CK4- and CK13-positive staining were scored from 1 to 3. The CK4- and CK13-positive staining ratios were decreased in NNL (73% and 78%), LG-IN (55% and 69%), and HG-IN (33% and 48%), compared to NEE (91% and 95%). The differences between LG-IN and HG-IN, neoplasia and NNL, and among these three lesions and NEE were statistically significant (p < 0.005). The cytokeratin scores correlated with the MIB-1 labeling index (both: p < 0.0001), but not with p53 overexpression. CK4 and CK13 immunohistochemistry could be an objective method for evaluating the risk for progression to invasive carcinoma.