Iron deficiency anaemia (IDA) frequently occurs in haemodialysis
(HD) patients undergoing recombinant human erythropoietin (rHuEPO)
therapy and is commonly associated with rHuEPO hypo-responsiveness.
However, the conventional iron indices are inadequate to exhibit the status or
utilisation of iron during erythropoiesis. The aim of this study was to elucidate
the accuracy and usefulness of the reticulocyte haemoglobin (RET-He) test
for diagnosing IDA in HD patients undergoing rHuEPO therapy. Methods: In
this cross-sectional study, fifty-five blood samples of HD patients on rHuEPO
therapy were collected and analysed for haematological and biochemical
parameters. A receiver operating characteristics curve was also plotted for
sensitivity and specificity analysis. IDA detection rates by RET-He, soluble
transferrin receptor (sTfR) and serum ferritin were 63.64%, 3.64% and 0%,
respectively. RET-He level was significantly correlated with sTfR level, mean
cell volume, mean cell haemoglobin level and the transferrin receptor-ferritin
index. The sensitivity and specificity of RET-He in detecting IDA were 78.3%
and 92.0%, respectively, with an area under the curve of 0.864. IDA was more
frequently detected by RET-He than by ferritin or sTfR in HD patients
undergoing rHuEPO therapy. The RET-He level also showed higher sensitivity
and specificity for the iron status in these patients. Therefore, RET-He is a
useful biomarker for the detection of IDA in HD patients undergoing rHuEPO
therapy.
Chronic myeloid leukemia (CML) typically progresses from a chronic phase to an accelerated phase, and eventually to a blast crisis, often involving the bone marrow and peripheral blood, if left untreated. Central nervous system (CNS) involvement is an uncommon manifestation of CML, particularly as an isolated CNS relapse. Here, we present a rare case of CML in lymphoid blast crisis with an isolated CNS relapse. A 46-year-old female with underlying CML in lymphoid blast crisis, previously treated with chemotherapy and tyrosine kinase inhibitors, presented with visual disturbances. Imaging and cerebrospinal fluid analysis confirmed leukemic infiltration of the CNS without evidence of a systemic disease. Isolated CNS involvement is an atypical complication of CML and presents significant therapeutic challenges owing to the blood-brain barrier, which limits the efficacy of systemic therapies. Subsequently, the patient was treated with intrathecal chemotherapy targeting the CNS. Despite aggressive treatment, CNS relapse remains a major concern due to the limited penetration of standard therapies into the CNS. This case underscores the importance of early recognition of CNS symptoms in CML patients, particularly in those with blast crisis, and highlights the need for tailored therapeutic strategies to manage this rare and challenging manifestation.
Background: The association between dysregulated microRNAs (miRNAs) and acute myeloid leukemia (AML) is well known. However, our understanding of the regulatory role of miRNAs in the cytogenetically normal AML (CN-AML) subtype pathway is still poor. The current study integrated miRNA and mRNA profiles to explore novel miRNA-mRNA interactions that affect the regulatory patterns of de novo CN-AML. Methods: We utilized a multiplexed nanoString nCounter platform to profile both miRNAs and mRNAs using similar sets of patient samples (n = 24). Correlations were assessed, and an miRNA-mRNA network was constructed. The underlying biological functions of the mRNAs were predicted by gene enrichment. Finally, the interacting pairs were assessed using TargetScan and microT-CDS. We identified 637 significant negative correlations (false discovery rate <0.05). Results: Network analysis revealed a cluster of 12 miRNAs representing the majority of mRNA targets. Within the cluster, five miRNAs (miR-495-3p, miR-185-5p, let-7i-5p, miR-409-3p, and miR-127-3p) were posited to play a pivotal role in the regulation of CN-AML, as they are associated with the negative regulation of myeloid leukocyte differentiation, negative regulation of myeloid cell differentiation, and positive regulation of hematopoiesis. Conclusion: Three novel interactions in CN-AML were predicted as let-7i-5p:HOXA9, miR-495-3p:PIK3R1, and miR-495-3p:CDK6 may be responsible for regulating myeloid cell differentiation in CN-AML.