Iraqi Journal of Hematology

Hereditary spherocytosis (HS) is the most common inherited hemolytic anemia in populations of northern European descent, arising from mutations in genes encoding key erythrocyte membrane proteins, including ANK1, SPTB, SLC4A1, SPTA1, and EPB42. These genetic defects disrupt the vertical linkages between the red blood cell (RBC) plasma membrane and its underlying cytoskeleton, reducing RBC deformability and leading to characteristic spherocytosis, premature hemolysis, and accelerated splenic clearance. Inheritance is predominantly autosomal dominant, although autosomal recessive forms occur, particularly involving SPTA1 and EPB42. Clinically, HS manifests with anemia, jaundice, splenomegaly, and complications such as cholelithiasis. This study aimed to identify and characterize pathogenic variants in primary HS genes, establish genotype–phenotype correlations, and enhance diagnostic accuracy to guide personalized management within a defined cohort. Diagnostic advancements, notably the tests of next‑generation sequencing and the eosin‑5‑maleimide binding test, have improved the detection of genetic heterogeneity, yet regional underdiagnosis persists. A comprehensive understanding of the HS genetic spectrum is therefore critical not only for precise diagnosis and optimized patient care but also for informing the development of future gene‑targeted therapies, including CRISPR‑based approaches. Regional epidemiological investigations, including limited data from Iraq, suggest that HS remains underdiagnosed despite its significant clinical impact. A comprehensive understanding of the HS genetic spectrum is imperative for accurate diagnosis, optimized personalized management, and the eventual development of gene‑based therapeutic interventions.

BACKGROUND: Hemoglobin (Hb) Malay is a β‑globin variant associated with a β⁺⁺‑thalassemia phenotype, resulting from a point mutation at codon 19 of the β‑globin gene. Data on its prevalence and phenotypic characteristics remain fragmented.
AIMS: This study aimed to determine the prevalence of Hb Malay and describe its phenotypic spectrum across different regions.
METHODS: A systematic literature search was conducted using Medline (PubMed), CINAHL (EBSCOhost), and ScienceDirect. Relevant studies published from database inception to 2024 were screened according to predefined eligibility criteria. Meta‑analysis was performed using Review Manager (RevMan) version 5.4. Pooled prevalence estimates were calculated, and outcomes were reported with corresponding 95% confidence intervals.
RESULTS: Twenty‑two studies involving 19,956 participants were included. Due to substantial heterogeneity among studies (I2 = 86%, P < 0.001), a random‑effects model was applied. The overall pooled prevalence of Hb Malay was 3.53%. The highest prevalence was observed in Indonesia (12.18%), followed by Thailand (3.43%), Malaysia (3.02%), and Singapore (0.75%).
CONCLUSION: This study represents the first comprehensive meta‑analysis of Hb Malay prevalence and phenotypic characteristics over 30 years (1990–2024). Although Hb Malay is a relatively rare Hb variant largely confined to Southeast Asia, its clinical relevance is significant, particularly when coinherited with other β‑thalassemia mutations, which may modify disease severity and increase transfusion requirements. These findings provide valuable evidence to inform regional thalassemia screening strategies and support targeted genetic counselling programmes.

BACKGROUND: Infantile acute lymphoblastic leukemia (ALL) is associated with poor outcomes worldwide, particularly in low-resource settings. Despite advances in pediatric ALL therapy, survival rates for infants remain substantially lower than those observed in older children. Evaluating treatment outcomes over time may help identify factors associated with improved survival.
OBJECTIVES: To assess treatment outcomes and survival trends of infants with ALL treated at a single tertiary center in Iraq over three distinct treatment periods.
MATERIALS AND METHODS: This retrospective study included infants (<1 year old) diagnosed with ALL and treated at the Children’s Welfare Teaching Hospital in Baghdad between January 2000 and December 2016. Patients were treated using adapted UKALL-97, UKALL-2003, and UKALL-2011 protocols, with a small subset receiving an infant-specific protocol. Patients were grouped by treatment period (2000–2005, 2006–2011, and 2012–2016). Overall survival (OS) and event-free survival (EFS) were estimated using the Kaplan–Meier method and compared using the log-rank test.
RESULTS: Among 59 infants diagnosed with ALL, 11 (19%) refused treatment. Of the remaining 48 treated patients, 24 (50%) achieved complete remission, 4 (8%) were resistant to therapy, and 17 (35%) died during induction. Complete remission rates improved across treatment periods from 36% to 45% and 71%, respectively. Among responders, 6 (25%) relapsed, 10 died during subsequent therapy, and 5 were lost to follow-up. The 36-month OS and EFS for treated patients were 30.2% and 17%, respectively, with a nonsignificant trend toward improved EFS in the 2012–2016 cohort.
CONCLUSION: The outcomes of infantile ALL in this low-resource setting remain poor, characterized by high induction mortality and treatment abandonment. Although survival improved over time—particularly following the introduction of a steroid prephase and enhanced supportive care—overall prognosis remains unsatisfactory, underscoring the need for further therapeutic and supportive care improvements.

BACKGROUND: For children with serious hematologic, oncologic, and metabolic disorders, hematopoietic stem cell transplantation has significantly improved survival rates. Bone strength and fracture risk are indicated by bone mineral density (BMD), which quantifies the mineral content in bone tissue. Trabecular bone score (TBS) evaluates the microarchitecture and quality of bones.
OBJECTIVES: This study aimed to assess health‑related quality of life (HRQoL) in children who received bone marrow transplantation (BMT) for beta‑thalassemia major (β‑TM) in a single center Kurdistan Region of Iraq.
MATERIALS AND METHODS: This retrospective cross‑sectional study was carried out among 46 children previously diagnosed with β‑TM who were receiving chelation therapy. Children who had previously had BMT were followed retrospectively to evaluate their outcomes. The BMD and TBS were used to measure the bone strength and fracture risk in children.
RESULTS: The mean age of the children was 15.02 (Range: 7–18 year), who underwent BMT at a mean age of 6.83 years. Boys comprised 52.17% of participants. HRQoL scores (out of 100%) were: total HRQoL (71.0%), physical (69.2%), emotional (61.3%), social (82.1%), and school (73.4%). Most had acceptable HRQoL (89.13%), especially in social functioning (95.65%). No gender differences were found in HRQoL or BMD, but boys had higher TBS than girls (1.46 vs. 1.34; P = 0.0003). BMD and TBS were within normal ranges. BMD was significantly higher in patients followed 6–15 years versus 1–5 years (P = 0.000). No significant correlations were found between BMD or TBS and HRQoL domains.
CONCLUSIONS: Children with β‑TM who underwent BMT demonstrated overall good HRQoL and preserved bone health, with stable outcomes across follow‑up periods. Emotional functioning remained the most affected domain, underscoring the importance of ongoing psychosocial support alongside routine clinical care.

Abstract:
BACKGROUND: Chronic myeloid leukemia (CML) is driven by the BCR‑ABL1 oncogene (t(9;22)) and typically presents in a chronic phase (<10% of blasts). Immune dysfunction in CML includes impaired natural killer‑like T (NKT) cells, while NKT‑like cells increase with age. Interferon‑gamma (IFN‑γ), crucial for immunity, activates JAK‑STAT signaling, with dysregulation linked to disease.
OBJECTIVE: The study aimed to analyze the immunological parameters (NKT‑like cells, INF‑γ, and interleukin‑10 [IL‑10]) in CML patients.
MATERIALS AND METHODS: The study comprised 60 individuals: 20 with newly diagnosed CML and 40 who were undergoing treatment with TKIs. The present research, which took place from February to September 2025, utilized flow cytometry to measure NKT‑like cells. In addition, an enzyme‑linked immunosorbent assay was employed to measure the levels of key cytokines, including IFN‑γ and IL‑10, in patient samples.
RESULTS: Newly diagnosed CML patients showed depletion of NKT‑like cells and IFN‑γ but high levels of IL‑10. Controls had higher NKT‑like cells (57.5%) than untreated CML (26.1%), with partial recovery posttreatment (51.7%). IFN‑γ was elevated in controls (22.6 pg/ml), while IL‑10 dominated in untreated CML (49.6 pg/ml). Significant CML correlations revealed NKT‑like cells negatively associated with blast (r = −0.651) and BCR‑ABL levels (r = −0.547) while showing a positive correlation with IFN‑γ (r = 0.460). Conversely, IL‑10 positively correlated with (blasts: r = 0.380 and BCR‑ABL: r = 0.617) but negatively with NKT cells (r = −0.276).
CONCLUSION: The current study reveals profound immune dysregulation in CML, marked by decreased NKT‑like cells and IFN‑γ alongside elevated IL‑10, particularly in untreated patients. These findings support the known BCR‑ABL1‑mediated impairment of NKT function, highlighting key mechanisms of immune escape in CML pathogenesis.

Abstract:
BACKGROUND: Successful hematopoietic stem cell mobilization is essential for hematopoietic cell transplantation. However, mobilization failure remains a clinical challenge, particularly in settings with limited access to plerixafor. Understanding its predictors is crucial to improving transplant outcomes in Iraq.
OBJECTIVES: The aims of this study were to determine the incidence and predictors of stem cell mobilization failure in the Hematology and Transplant Center in Baghdad Medical City.
MATERIALS AND METHODS: This retrospective study was conducted at the HBMT Center, Baghdad Medical City, and included 395 adult and pediatric patients with various hematologic malignancies who underwent stem cell mobilization between January 2013 and December 2023. Clinical, disease, and treatment‑related factors were analyzed in relation to mobilization outcomes.
RESULTS: Mobilization failure occurred in 11.6% (46/395) of patients. Failure was significantly associated with bone marrow involvement and prior chemotherapy exposure, whereas diagnosis also influenced outcome – being most frequent among multiple myeloma patients. The mean age was 42.1 years, and the mean BMI was 27.4 kg/m2. Use of Plerixafor was rare during the study period.
CONCLUSION: Despite limited drug availability, the mobilization failure rate in our center was comparable to international data. Expanding access to c and optimizing mobilization protocols could enhance stem cell collection efficiency and reduce hospitalization days in Iraq.

BACKGROUND: Transferrin receptor 1, commonly referred to as cluster of differentiation 71 (CD71), is a crucial glycoprotein that mediates the cellular uptake of iron, avails as a substantial index of erythroid growth and iron metabolism, and typically exists in erythroid lineage cells within the bone marrow. We investigated the expression of CD71 in the peripheral blood of patients with transfusion‑dependent beta‑thalassemia major (βTM).
OBJECTIVES: This study examines the distinct role of CD71 in erythropoiesis, particularly in the context of βTM, and highlights its relevance in studying peripheral blood CD71 levels and their association with clinical and demographic criteria in Iraqi patients with βTM.
MATERIALS AND METHODS: This case–control study consisted of 60 βTM patients and 28 healthy controls (matched for age and sex), and they were evaluated. Samples of peripheral blood were examined by flow cytometry using anti‑CD71 and anti‑CD235a. Complete blood count, serum ferritin (SF), and liver function tests were assessed for all participants. Statistical associations with demographic, clinical, and laboratory parameters were examined.
RESULTS: The CD71 expression range was notably greater in patients (0.17%–18.20%) compared to controls (0.08%–0.19%), with a statistically significant difference (P = 0.0001). Thirty percent of patients exhibited <1% expression. Higher levels were found in splenectomized patients compared to splenomegaly patients, and in males compared to females. Positive correlations were identified with white blood cells, platelets, and liver transaminase enzymes. No correlations were found with hemoglobin, red blood cells, alkaline phosphatase, total serum bilirubin, or SF.
CONCLUSIONS: CD71 expression is a critical marker of ineffective erythropoiesis in βTM, affected by splenic status, gender, adherence to blood transfusion schedules, and correlates with various hematological and liver parameters. Incorporating CD71 into routine assessment may enhance the evaluation of disease activity and guide individualized prognosis and management in transfusion‑dependent thalassemia patients.

BACKGROUND: We have some serious complications during the treatment of hematological malignancies that adversely affect the outcome. Febrile neutropenia (FN) is one of the most common serious complications that carry a mortality rate of 10%–34%. Conventional microbiological cultures are still routinely investigated to identify the offending microorganisms causing this condition, then to treat according to the results of sensitivity testing. At the same time, factors affecting this outcome need to be explored to lower this high mortality rate.
OBJECTIVES: To evaluate the usefulness of blood culture (BC) in determining the antibacterial management plan in immunocompromised adult and pediatric patients being admitted with FN to Hiwa hospital in Sulaymaniyah.
MATERIALS AND METHODS: A descriptive retrospective study done at Hiwa Hospital in Sulaymaniyah, Kurdistan region of Iraq on 402 FN episodes admitted to the hospital over 18 months studied. Several variables were taken within the patients through their electronic records being reviewed thoroughly.
RESULTS: The positive cultures showed 6 (1.5%) sample fungal, 26 (6.5%) samples Gram‑positive bacteria, and 34 (8.5%) sample Gram‑negative bacteria. Age (odds ratio [OR] =1.027) (P ≤ 0.001, confidence interval [CI]:95%: 1.01–1.042), duration of neutropenia (OR = 1.020) (P ≤ 0.001, CI: 95%: 1.02–1.032), and hospital stay before BC (OR = 1.020) (P ≤ 0.001, CI: 95%: 0.010–0.035) were the predictors of death in patients.
CONCLUSIONS: The findings reveal that BC is still a useful intervention in the treatment of FN. Age, the duration of neutropenia, and length of stay in a hospital are the predictive factors of mortality.

BACKGROUND: Signal transducer and activator of transcription 3 (STAT3) is an essential transcription factor that functions through the Janus kinase/STAT signaling pathway, regulating cell proliferation, survival, tumorigenesis, immune surveillance, and inflammatory responses. Although dysregulated STAT3 activity has been implicated in numerous cancers, its specific contribution to non‑Hodgkin lymphoma (NHL) remains insufficiently defined.
OBJECTIVES: We evaluated STAT3 gene expression and two polymorphisms (rs72823022 T/C and rs744166 A/G) to determined their association with NHL susceptibility in an Iraqi population.
MATERIALS AND METHODS: This research follows a case–control study design. Hematological parameters, in addition to serum urea and creatinine levels, were assessed in lymphoma patients (n = 50) and healthy controls (n = 50). STAT3 mRNA expression was quantified by reverse transcription quantitative polymerase chain reaction (RT‑qPCR), and STAT3 polymorphisms were genotyped using polymerase chain reaction (PCR) followed by Sanger sequencing (ABI 3730XL platform).
RESULTS: STAT3 expression was upregulated in NHL patients compared to controls (mean fold change = 7.88). Some SNP genotypes showed potential protective effects, whereas others showed a trend toward increased susceptibility; however, these associations were not statistically significant.
CONCLUSION: STAT3 expression and its genetic variants may serve as potential biomarkers for the risk assessment and early detection of NHL, providing insights that could guide prognostic evaluation and therapeutic strategies.

BACKGROUND: Low platelet counts resulting from increased platelet breakdown and poor platelet generation are the hallmarks of immune thrombocytopenia (ITP), an autoimmune illness. Romiplostim increases platelet counts in the majority of patients and lowers bleeding risk in those with ITP.
OBJECTIVES: To evaluate the median dose of romiplostim required to maintain platelet counts ≥50 × 109/L and to assess platelet response rates among adult Iraqi patients with primary ITP.
MATERIALS AND METHODS: The cross‑sectional study looked at 200 patients’ ages ≥14 years who had primary ITP that failed 1st line treatment. They were treated at Baghdad Medical City from May 2022 to December 2023. Medical records were used to get the information. Romiplostim (Nplate®, Amgen Inc., Thousand Oaks, CA, USA) was injected subcutaneously once a week. The dose started at 1 µg/kg and was increased by 1 µg/kg each time to keep the platelet numbers between 50 and 200 × 109/L (maximum 10 µg/kg).
RESULTS: Among 200 patients (60% female), the median age was 38 years and the median treatment duration was 4 months. The median weekly dosage of romiplostim was 250 µg and the median baseline platelet count was 19 × 109/L, which significantly increased to 138 × 109/L after romiplostim therapy (P = 0.011). A total of 73.5% of patients achieved a platelet response ≥ 50 × 109/L. There was no significant difference in response between patients aged ≥ 60 years and those < 60 years (P = 0.25).
CONCLUSIONS: Romiplostim has a robust and persistent platelet response in adult patients with refractory ITP and good safety. Its effectiveness as a second‑line treatment was confirmed by its age‑neutral response.

BACKGROUND: Chronic lymphocytic leukemia (CLL) is the most common leukemia affecting the elderly. It is characterized by monoclonal B‑cell proliferation expressing CD5 and CD23. Interleukin‑8 (IL‑8) has been found to induce the proliferation of malignant cells and make them resistant to apoptosis. Thus, IL‑8 could be implicated in disease progression.
OBJECTIVE: The objective of the study was To determine the clinical significance of serum IL‑8 levels in CLL patients and to evaluate its potential as a biomarker for disease progression.
MATERIALS AND METHODS: A cross‑sectional study was conducted on 30 CLL patients and 30 normal individuals (control). Participants were recruited from October 2024 and continuing until August 2025 at The National Center of Hematology/Mustansiriyah University. Patients’ demographics were collected using a special form. Blood samples were collected and analyzed for IL‑8 levels using ELISA in addition to complete blood count.
RESULTS: The mean serum IL‑8 level for CLL patients was 28.83 ± 12.68 pg/mL, which is higher than that of the control group 10.20 ± 1.008 pg/mL, with no statistical significance (P = 0.1483). It was concluded that a statistically significant difference in IL‑8 levels existed across all stages of CLL (P = 0.0193). The highest median level was 16.28 pg/mL in Stage A, whereas the median levels in Stages B and C were 7.476 pg/mL and 7.608 pg/mL, respectively. The receiver operating characteristic curve showed that IL‑8 powerful in distinguishing between Stage A and C, with a sensitivity of 81.82%, and a specificity of 72.73% at a cutoff of 10.07 pg/mL. IL‑8 does not show a significant correlation with other variables.
CONCLUSION: As an autocrine growth and apoptosis resistance factor, higher level of IL‑8 among CLL patients may be related to the disease persistence, with higher levels among earlier stages of CLL in comparison to later stages, which may be related to immune system exhaustion. Thus, it could be useful in monitoring disease status.

BACKGROUND: Bloodstream infections (BSIs) cause significant morbidity and mortality in neutropenic patients with hematological malignancies, especially amid rising antimicrobial resistance. Updated local data are essential to guide empirical therapy.
OBJECTIVES: The aims of this study were to assessed the etiology, resistance patterns, clinical outcomes of BSIs, and the diagnostic performance of real‑time PCR (RT‑PCR) versus conventional blood culture.
MATERIALS AND METHODS: A prospective observational study was conducted at Azadi Teaching Hospital (September 2024–May 2025) on 109 neutropenic adults. Blood cultures and multiplex RT‑PCR were used to identify pathogens and resistance genes. Clinical features, antimicrobial susceptibility, and 30‑day outcomes were analyzed.
RESULTS: BSIs occurred in 24 patients (22%). Blood culture positivity was low (3.7%), while RT‑PCR detected pathogens in 20.2%, increasing diagnostic yield nearly sixfold. Gram‑negative bacteria predominated (70.8%), mainly Escherichia coli (37.5%), and Klebsiella pneumoniae (20.8%). ESBL production was universal, and 72.7% of Gram‑negative isolates were carbapenem‑resistant. Resistance genes included NDM (33.3%), VIM (8.3%), OXA‑48 (4.2%), and mecA (12.5%). MDR pathogens caused 54.2% of infections. Appropriate empirical therapy was achieved in 62.5%. Intensive care unit (ICU) admission occurred in 29.1% of BSI cases. Overall mortality was 10.1%, with BSI‑related mortality of 29.2%. Carbapenem‑resistant infections significantly increased mortality (57.1% vs. 11.1%). Predictors of death included carbapenem resistance, ICU admission, and neutropenia >7 days.
CONCLUSIONS: BSIs in neutropenic hematological patients are mostly caused by MDR Gram‑negative organisms with high carbapenem resistance. RT‑PCR substantially improves diagnostic sensitivity. Updated empirical therapy and stronger antimicrobial stewardship are urgently needed.

BACKGROUND: Iron deficiency anemia (IDA) represents a significant public health challenge worldwide, yet comprehensive epidemiological data from Saudi Arabia integrating clinical surveillance with population‑based evidence remain limited.
OBJECTIVES: This study aimed to quantify the clinical burden of IDA across demographic groups in Saudi Arabia using laboratory surveillance data, identify key risk factors through literature synthesis, analyze temporal trends from 1990 to 2024, and examine regional variations to inform Vision 2030 health priorities.
MATERIALS AND METHODS: We conducted a two‑stream study comprising: (1) a secondary analysis of laboratory‑based surveillance data from Al Borg Diagnostics Laboratories, including 420,956 individuals tested between January 2014 and February 2024 across all 13 administrative regions, and (2) a narrative review of 14 peer‑reviewed epidemiological studies supplemented with WHO Global Health Observatory and Global Burden of Disease Study 2021 data. Iron deficiency (ID) was defined as serum ferritin <30 ng/mL, while IDA was defined as hemoglobin below sex‑specific thresholds with concurrent ID. Descriptive statistics and Chi‑square tests were performed for laboratory data. Risk factors were extracted from multivariate analyses in reviewed studies.
RESULTS: Laboratory surveillance findings: Among 420,956 individuals seeking diagnostic services, IDA prevalence was 19.8%, with nonanemic ID affecting an additional 23.7%, yielding a combined ID prevalence of 43.5%. Women constituted 93% of all iron‑deficient cases. Significant regional variation was observed, ranging from 28% in Al‑Jouf to 42% in the Makkah region (P < 0.001). Among children <12 years tested (representing clinically suspected cases), 100% had anemia with 45% meeting IDA criteria, indicating extreme selection bias toward symptomatic presentations. Literature review findings: Population‑based studies documented IDA prevalence of 49% among infants aged 6–24 months in primary care settings and 40% among women of reproductive age in community‑based sampling. WHO national estimates indicated 43.7% prevalence in women of reproductive age and 45.5% in pregnant women. Key risk factors identified across studies included family history of IDA (adjusted odds ratio [OR] 2.91, 95% confidence interval [CI] 1.78–4.76), insufficient iron intake (OR 7.39, 95% CI 1.45–37.57), infrequent meat consumption (OR 1.54–7.70), and short birth intervals (OR 2.23, 95% CI 1.20–4.41). Global Burden of Disease 2021 data demonstrated a 44.5% decline in age‑standardized disability burden from dietary ID between 1990 and 2021.
CONCLUSIONS: IDA remains an important public health problem in Saudi Arabia, particularly affecting women of reproductive age and infants. The 93% female predominance in clinical samples

BACKGROUND: Idiopathic immune thrombocytopenia purpura is an autoimmune bleeding disorder that accounts for approximately one‑third of clinical hemorrhagic diseases. Pathophysiologically, it involves a complicated imbalance in the immune system.
OBJECTIVES: This study focuses on evaluating the levels of the immunomodulatory cytokines interleukin (IL)‑35, interleukin‑10, and transforming growth factor‑β (TGF)‑β in patients with refractory idiopathic immune thrombocytopenia undergoing treatment with romiplostim.
MATERIALS AND METHODS: A cross‑sectional study encompassed 78 individuals with idiopathic immune thrombocytopenia and conducted measurements of different immunomodulatory cytokines in response to different responses of idiopathic immune thrombocytopenia patients on romiplostim therapy. The research was carried out from May 1, 2025, to September 1, 2025, and it was conducted at the Haematology and Bone Marrow Transplant Centre, Medical City, Baghdad, Iraq.
RESULTS: More than half of them have responded to romiplostim 52 (66.7%) with a mean dose of 103.8 mcg. The study demonstrated a notable link between immunomodulatory cytokines (IL‑10, IL‑35, and TGF‑β) and platelet count; however, no significant difference was found between responders and nonresponders regarding these cytokines.
CONCLUSIONS: Romiplostim demonstrated effective management in Iraqi patients, and the Treg cells and their associated cytokines (IL‑35, IL‑10, and TGF‑β) may contribute to immune system dysregulation in adult patients with chronic idiopathic immune thrombocytopenia.

BACKGROUND: Beta‑thalassemia major (β‑TM) is a hereditary blood disorder requiring lifelong blood transfusions, which result in iron overload and progressive organ damage. Iron chelation therapy is therefore essential to reduce excess iron and its complications.
OBJECTIVES: This study aimed to evaluate the effect of different iron chelation therapies on the expression of iron‑regulatory genes and on biochemical markers related to iron metabolism and inflammation in patients with β‑TM.
MATERIALS AND METHODS: Thirty patients diagnosed with β‑TM and 20 healthy controls were enrolled and stratified according to iron chelation therapy, along with a healthy control group for comparison. Expression levels of Transferrin receptor‑2 (TFR2) and ferroportin (FPN) were evaluated by the polymerase chain reaction. Serum concentrations of interleukin‑6 (IL‑6), soluble TFR (sTFR), nontransferrin‑bound iron (NTBI), cortisol, thyroid stimulating hormone (TSH), and ferritin were determined using the standard biochemical methods.
RESULTS: The expression of the TFR2 gene and serum IL6 was statistically significant, whereas FPN gene showed no statistically change. The treatment elevated cortisol levels; however, the alteration was not statistically significant. sTFR, NTBI, TSH, and ferritin all showed that there was too much iron in the body, however, some comparisons did not show any big differences.
CONCLUSIONS: It can be concluded that iron chelation therapy, particularly deferasirox, is related to the extent of TFR2 gene expression and IL‑6 levels and changes in terms of iron metabolism and inflammation activity in β‑TM patients. TFR2 and IL‑6 showed significant alterations and may represent potential indicators of iron overload in β‑thalassemia major patients.

BACKGROUND: The accumulation of other abnormalities in both genetic and epigenetic pathways, in addition to the BCR‑ABL1 oncoprotein, affects the overall clinical consequences of chronic myeloid leukemia (CML), including treatment responsiveness.
OBJECTIVES: This study investigated the expression levels of fragile histidine triad (FHIT) gene among patients with CML and evaluated its association with the response of patients to imatinib mesylate treatment.
PATIENTS AND METHODS: Samples of blood were provided from sixty CML patients: Thirty responsive and thirty nonresponsive patients to imatinib mesylate treatment, as well as sixty healthy controls matched for age and sex were provided blood samples. The FHIT gene expression was estimated using reverse transcription quantitative polymerase chain reaction.
RESULTS: The results indicated that FHIT gene expression was significantly lower in CML patients than in the controls (P < 0.001). Compared to the responsive CML patients, the nonresponsive CML patients presented a significantly decreased level of FHIT gene expression (P < 0.001). A significant increase in FHIT gene expression was found at a cut‑off value of more than 0.0578 for distinguishing responsive from nonresponsive CML patients, as shown by receiver operating characteristic analysis, with 97% sensitivity and 72.4% specificity.
CONCLUSIONS: Reduced FHIT gene expression was associated with CML and with changes in hematopoietic patterns observed in the studied patients. Variations in FHIT expression were noted between responsive and nonresponsive patients, indicating a potential association with treatment response, suggesting that FHIT expression may have value as a complementary predictive biomarker for imatinib mesylate responsiveness, although further validation is required.

Chronic myeloid leukemia (CML) is a type of blood cancer caused by an abnormal chromosome which produces a gene that drives the uncontrolled growth of white blood cells. The objectives of the current article are to ascertain the role of precision medicine in CML, identify the potential challenges in low‑resource settings, and propose public health recommendations to overcome the identified challenges. The introduction of precision medicine has transformed care among patients with CML, where treatment is tailored to a specific molecular abnormality. Precision medicine ensures that the administered treatment‑tyrosine kinase inhibitors (TKIs) – functions as a targeted therapeutic modality and has remarkably improved survival rates, turning CML into a predominantly chronic condition. Acknowledging the high prevalence of CML and the role of precision medicine through TKIs in improving patient outcomes, there is an urgent need to implement targeted interventions to bridge the existing challenges in low‑resource settings so that the utility of precision medicine can be optimized. In conclusion, precision medicine has transformed CML care, but inequities in access to TKIs and diagnostics persist in low‑resource settings. By adapting precision strategies to local contexts, equitable outcomes can be accomplished, we can move closer to making treatment‑free remission a possibility for all patients, regardless of geography or availability of resources.

Pregnant women with sickle cell disease (SCD) have been acknowledged as a high‑risk pregnancy owing to the reported high incidences of complications, including death, both among the women and the fetus. The objectives of the current article are to identify various infections to which pregnant women with SCD are prone to acquire, enlist different challenges due to which pregnant women with SCD are at high risk to acquire infections, and propose infection prevention measures at different levels to reduce the overall burden. Pregnant women with SCD are at high risk of acquiring infections from multiple microorganisms. The high rates of infections among pregnant women with SCD are predominantly because of the presence of multiple barriers and challenges. Acknowledging the fetomaternal complications among pregnant women with SCD, high risks of acquiring infection, and the presence of multiple barriers, there is an urgent need to implement measures at different levels to mitigate the impact of these barriers. To conclude, pregnant women with SCD are prone to multiple risks, including acquiring a wide range of infections. The need of the hour is to adopt a multipronged approach to minimize the risk of acquisition of infections, thereby improving fetomaternal outcomes.