Iraqi Journal of Hematology

Immune thrombocytopenia (ITP) is an autoimmune disorder with increased risk of bleeding due to
a low number of platelets. The pathophysiology is complex and not fully understood, but platelet
autoantibodies and/or CD8+ T‑cells are responsible, via diverse mechanisms, for disrupting platelet
production and enhancing platelet destruction. The symptomatology of ITP seems to be more
complex than has traditionally been perceived as thrombocytopenia and bleeding as the disease
often has impact on the health‑related quality of life and daily functions. The management thus
requires a holistic approach and patient involvement at every stage. Corticosteroids still represent the
cornerstone of the first‑line treatment. Treatment with corticosteroid should not exceed 6–8 weeks.
Patients who fail to achieve remission with a short course of corticosteroids may require a second‑line
therapy. Most guidelines recommend starting with a thrombopoietin receptor agonist (TPO‑RA),
rituximab, or fostamatinib since these agents have been investigated in randomized trials and have
well‑characterized efficacy and safety profiles. Patient involvement to reach a shared decision
regarding choice of therapy is essential as these treatments have different modes of administration
and mechanisms of action. Less than 10% of adults ITP patients will fail to respond to and/or be
intolerant of multiple second‑line therapies and would thus require a third‑line therapeutic option.
Such patients may respond well to a combination of TPO‑RA and an immunomodulatory agent.
Splenectomy or a continuation with nontherapeutic agents that has different mechanism of action
may be an alternative approach.

Sickle cell anemia (SCA) is a genetic hemoglobinopathy marked by persistent hemolysis,
vaso‑occlusion, and many organ problems. Oxidative stress and inflammation are crucial in the
pathophysiology of SCA, contributing significantly to disease severity and development. High levels
of reactive oxygen species (ROS) and persistent inflammatory reactions worsen red cell sickling,
endothelial dysfunction, and vascular damage. The present research gives a thorough overview
of the processes that underpin inflammation and oxidative damage in SCA, emphasizing their
interconnectedness and clinical significance. Hemolysis‑induced ROS generation, redox imbalance,
and antioxidant depletion disrupt cellular homeostasis, while Pro‑inflammatory cytokines like
interleukin‑6 and tumor necrosis factor‑α promote immunological activation and leukocyte adherence.
Diagnostic approaches involving oxidative and inflammatory biomarkers are gaining clinical relevance
for disease monitoring and therapeutic guidance. Current therapeutic strategies focus on antioxidant
agents like Vitamin E and N‑acetylcysteine, disease‑modifying drugs such as hydroxyurea, and
lifestyle interventions to mitigate oxidative damage. Anti‑inflammatory drugs, statins, omega‑3 fatty
acids, and new biologics are all being investigated for their capacity to reduce chronic inflammation.
Advanced techniques, including genetic treatment approaches and stem cell‑based transplants,
show promise for therapeutic outcomes. Future research should emphasize personalized treatment
approaches, integrative antioxidant and anti‑inflammatory therapies, and the implementation of
large‑scale, long‑term clinical trials to establish efficacy and safety. Addressing these gaps is critical
for establishing focused, patient‑specific interventions that can greatly improve the quality of life and
clinical outcomes for people with SCA.

BACKGROUND: Chronic myeloid leukemia (CML) occurs when a pluripotent stem cell undergoes
malignant transformation and clonal myeloproliferation, leading to a striking overproduction of
immature granulocytes. It accounted for about 15% of all adult leukemias and can strike at any age
but rare in childhood. Many studies revealed a significant role of antiapoptotic B‑cell lymphoma‑2
oncogene (Bcl‑2) in disease progression.
OBJECTIVES: The aim of this study was to assess Bcl‑2 expression across CML phases and its
diagnostic value through immunohistochemistry compared to conventional morphology.
MATERIALS AND METHODS: A cross‑sectional retrospective study of Bcl‑2 expression in
histological sections of bone marrow trephine biopsies of randomly selected 60 patients diagnosed
with CML with age ranged between 14 and 81 years and presented with different clinical phases (30
with chronic phase, 15 with accelerated phase and other 15 with blastic transformation) which
stained immunohistochemically for BCL‑2 protein (Dakopatts Corporation) and evaluated by a
hemopathologist.
RESULTS: The expression of the antiapoptotic protein Bcl‑2 differs significantly with different clinical
phases of CML and increases with more advanced stages. Bcl‑2 oncoprotein expression increases
significantly with high bone marrow blast percentage.
CONCLUSIONS: Immunohistochemistry is a useful method for the detection of Bcl‑2 oncoprotein.
There is a relatively great relationship between Bcl‑2 oncoprotein expression with high bone marrow
blast count and advanced stages of the disease.

BACKGROUND: Aberrant expression of cluster of differentiation 7 (CD7) antigen has emerged as a
potential prognostic factor in adult de novo acute myeloid leukemia (AML) patients treated with the
3 + 7 regimen. Understanding the significance of CD7 expression in predicting remission achievement
and treatment outcomes is crucial for developing personalized therapeutic strategies in AML.
OBJECTIVES: The objectives of this study were to investigate the prognostic impact of CD7 antigen
expression on remission achievement and overall survival (OS) in adult de novo AML patients
receiving the 3 + 7 chemotherapy regimen.
MATERIALS AND METHODS: This study included 37 adult de novo AML patients treated with the
standard 3 + 7 induction regimen (3 days of daunorubicin plus 7 days of cytarabine). CD7 antigen
expression was evaluated using multicolor flow cytometry. Patients were categorized into CD7‑positive
and CD7‑negative groups. Clinical and laboratory parameters, including remission status at day 28
and OS duration, were collected and statistically analyzed to determine the association between
CD7 expression and treatment outcomes.
RESULTS: CD7 positivity was significantly associated with lower remission rates, with only 27.8%
of CD7‑positive patients achieving complete remission, compared to 68.4% of CD7‑negative
patients (P = 0.01). In addition, CD7‑positive patients had a significantly shorter mean OS of
2.6 months, whereas CD7‑negative patients had a mean survival of 4.6 months (P = 0.03).
CONCLUSION: CD7 antigen expression in de novo AML is significantly associated with reduced
remission rates and shorter survival, suggesting its potential role as a prognostic biomarker. Assessing
CD7 expression at diagnosis may help stratify patients and guide individualized therapeutic strategies
in AML.

BACKGROUND: Acute lymphoblastic leukemia is a diverse illness characterized by the development
of immature lymphoid cells. Programmed death‑ligand 1 (PDL‑1) is a protein 33-kDa glycoprotein
encoded by the CD274 gene on chromosome 9p24. It plays a crucial role in immune modulation
and serves as a checkpoint regulator.
OBJECTIVE: To evaluate the plasma level of PDL‑1 in pediatric patients with ALL and to correlate
the plasma level PDL‑1 with some hematological and clinical parameters.
MATERIALS AND METHODS: This study was conducted on 63 pediatric patients, <14 years
old (newly diagnosed) at the central teaching hospital of pediatrics, and 27 healthy children
were included in this study as a control group. Plasma PDL‑1 level measuring by enzyme‑linked
immunosorbent assay.
RESULTS: PDL‑1 was significantly higher in newly diagnosed patients with ALL 33.8 ng/ml for
B‑ALL and 43.5 ng/ml for T‑ALL than controls (31.6 ng/ml), with P = 0.024. A substantial positive
association was seen at the 0.05 level between PDL‑1 and total white blood cell (WBC) count, pallor,
and lymphadenopathy, whereas no significant correlation was found with other hematological and
clinical parameters.
CONCLUSIONS: Plasma level of PDL‑1 was significantly higher in newly diagnosed patients with
ALL than controls. Furthermore, there was significant positive correlation between PDL‑1 with total
WBC count, pallor, and lymphadenopathy, while there was no significant correlation with other
hematological and clinical parameters.

BACKGROUND: Limited availability of prevalence and clinical epidemiological data on adult primary
immune thrombocytopenia (pITP) and the inaccessibility of a gold standard test restricts the veracity
of the pITP representation in ASEAN countries, more so in Malaysia.
OBJECTIVE: This study aims to ascertain the incidence rate and the relationship between the
clinico-laboratory characteristics of adult pITP.
MATERIALS AND METHODS: A retrospective study involving a total of 141 adult patients diagnosed
with pITP at Hospital Pakar Universiti Sains Malaysia between 2000 and 2022. Incidence rates and
clinico-laboratory profiles were established based on findings collected from hospital databases.
RESULTS: The annual incidence rate of pITP was 1.2 per 100,000 person‑years (95% confidence
interval [CI]: 1.0–1.5). A higher incidence was observed in females compared to males (1.8 per
100,000 person‑years, 95% CI: 1.4–2.0 vs. 0.7 per 100,000 person‑years, 95% CI: 0.5–0.9), with
a male‑to‑female ratio of 1:2.5. The most presented symptoms in pITP patients were cutaneous
bleeding (53.2%), gingival bleeding (29.8%) and menorrhagia (19.1%) and they typically occurred in
pITP patients with a mean platelet count less than 50 × 109/L. The majority of the patients received
first‑line therapy (68.8%), whereas 17.7% received no treatment. First‑line therapy nonresponders
were given second‑line therapy (4.2%).
CONCLUSION: Our findings highlight the distinctive epidemiological patterns and clinical
presentations of pITP in the northeast region of Malaysia, particularly highlighting gender, race, and
age‑specific variations. Despite comprehensive treatment guidelines, diagnostic challenges remain.
Improved diagnostic tools are needed to enhance timely identification and effective management,
ultimately improving patient outcomes for pITP.

BACKGROUND: The noncoding RNAs with covalently closed loops, known as circular
RNAs (circRNAs), represent essential regulators of cancer biology. CircRNAs demonstrate stability
combined with regulatory properties that position them as biomarker candidates for the diagnosis of
hematologic malignancies such as acute myeloid leukemia (AML).
OBJECTIVE: The research investigates and compares the expression levels of hsa_circ_0001947
and hsa_circ_0009581 circRNAs in bone marrow (BM) and peripheral blood (PB) extracted from
AML patients to evaluate their biological function and clinical value in AML development.
MATERIALS AND METHODS: The study enrolled 73 AML patients who received their treatment at
Baghdad Teaching Hospital and the Hematology Center in the Medical City of Baghdad. The study
obtained PB from 50 patients while extracting BM aspirates from 23 patients. RNA extraction was
followed by cDNA synthesis. The assessment of circRNA expression through quantitative real‑time
polymerase chain reaction PCR (qRT‑PCR) utilized the U6 housekeeping gene as a normalization
factor.
RESULTS: Analysis of hsa_circ_0001947 expression showed lower expression in BM than PB.
The expression level of hsa_circ_0009581 in BM was significantly higher than that in PB samples,
which indicates how this circulatory RNA contributes to AML development in BM microenvironments.
CONCLUSION: The differential expression of circRNAs between BM and PB highlights their potential
involvement in AML biology. Specifically, hsa_circ_0009581 may serve as a promising molecular
target or biomarker for AML diagnosis and monitoring. These findings contribute to the growing
understanding of circRNA‑mediated gene regulation in leukemia

BACKGROUND: Beta‑thalassemia syndromes are inherited disorders marked by reduced beta‑globin
production, leading to excess free α‑globin chains that cause ineffective red blood cell production, anemia,
and oxidative stress. The heterozygous (trait) form causes mild anemia, while the homozygous form leads
to severe, transfusion‑dependent anemia. Genetic modifiers such as α‑globin mutations and hereditary
persistence of fetal hemoglobin (HPFH) can reduce disease severity by balancing globin chains. Alpha
hemoglobin (Hb) stabilizing protein (AHSP) plays a protective role by binding free α‑globin, preventing
its toxic effects. This chaperone function helps mitigate damage in conditions like β‑thalassemia.
OBJECTIVES: The aims of this study were to evaluate AHSP gene expression in patients with
beta‑thalassemia syndrome and correlate its expression with hematological parameters.
MATERIALS AND METHODS: Thirty‑five beta‑thalassemic pediatric patients’ leftover samples were
collected from thalassemia center in Baghdad/Iraq. The patients randomly selected regarding sex.
Twenty control leftover samples were collected from Al‑Kadhimiya pediatric hospital, who were age
and sex matched with the patient’s group. AHSP mRNA of 35 patients, patients with beta‑thalassemia
major (β‑TM) included 18 patients and 17 patients with beta‑thalassemia intermedia, and 20 normal
controls were measured using real‑time reverse transcription‑polymerase chain reaction (qRT‑PCR).
AHSP RNA of each sample was calculated by relative quantification using the equation of folding = 2−
ΔΔCT. ΔΔCT = ΔCT Treated − ΔCT Control.
RESULTS: There was a statistical difference found between the control and patients with
beta‑thalassemia syndrome regarding hematological parameters and AHSP gene expression and
a highly significant difference between β‑TM and intermedia regarding complete blood count finding,
duration of blood transfusion, and high‑performance liquid chromatography finding, while there was
no statistical difference regarding AHSP gene expression that was seen between those two groups.
CONCLUSION: The expression level of the AHSP gene was elevated in thalassemic individuals
compared to the healthy control, and it was higher in patients with the BI group than thalassemia
major group.

BACKGROUND: Chronic myeloid leukemia (CML) is driven by the BCR–ABL fusion gene, a
constitutively active tyrosine kinase that can be effectively targeted with tyrosine kinase inhibitors
(TKIs), particularly imatinib. Long-term real-world data on the effectiveness and safety of imatinib in
low-resource settings remain limited.
OBJECTIVES: The aims was to evaluate the ten-year clinical outcomes, treatment responses, and
tolerability of imatinib in CML patients in Iraqi Kurdistan.
MATERIALS AND METHODS: A retrospective cross‑sectional study involved 160 patients with
CML using recorded hospital data from three different hematology centers in Iraqi Kurdistan, from
2014 to 2024. Collected data included patients’ sociodemographic, clinical presentation, blood
parameters, blood film, bone marrow examination, response to therapy, and survival rate. Then,
they were analyzed and interpreted.
RESULTS: Most patients were females (51.25%), from Sulaimaniyah city (55%), aged 40–49 years
old (27%), diagnosed between 2020 and 2024 (43%), and presented with fatigue (50%). Blood
tests indicated low hemoglobin (<12 mg/dL) with extremely high leukocytes (44%), but normal
platelets (66%). The blood film and bone marrow biopsy were abnormal in most patients. Furthermore,
P210 expression was higher than P230 (98% vs. 2.0%). All patients received first‑line treatment (only
imatinib), 49 patients received a second line (mostly nilotinib), and only 7 patients received a third
line. Using imatinib for 1–3 years results in resistance development in (26%) of patients and leads
to discontinuation of the therapy. Despite several side effects of imatinib (especially anemia), the
survival rate was very high (87%).
CONCLUSION: Imatinib remains a highly effective frontline therapy for CML in resource-limited
settings, demonstrating durable responses and favorable long-term survival despite moderate rates
of resistance and side effects.

BACKGROUND: Janus kinase 2 (JAK2) mutation is a major genetic aberration in 95% of patients
with polycythemia vera (PV) and approximately 50% in those with essential thrombocythemia (ET).
Previous studies have reported inconsistent findings regarding the effects of JAK2 mutations in
myeloproliferative neoplasms (MPNs).
OBJECTIVES: This study investigated the influence of JAK2 mutations on the clinical characteristics
of MPNs in Saudi Arabia.
MATERIALS AND METHODS: This retrospective study analyzed the clinical profiles of 71 Saudi
patients diagnosed with JAK2‑positive MPNs (28 PV and 43 ET) between 2021 and 2024. Data were
collected from a laboratory database and stratified by disease subtype, gender, and risk category.
Statistical analyses were performed to identify the differences in clinical features and outcomes.
RESULTS: The mean age of the participants was 54 years, with no significant age difference between
the PV and ET groups. The PV group was mostly male, while the ET group was mostly female.
This study found that the rates of thrombosis, major hemorrhage, leukocytosis, polycythemia, and
thrombocytosis in PV and ET were consistent with previous research. However, the mean leukocyte
counts and proportion of patients with high‑risk scores were significantly higher in the PV group
than in the ET group. In addition, the mean platelet count with ET was significantly higher in female
patients; however, the proportion of male ET patients with high‑risk scores was higher.
CONCLUSIONS: The research findings are consistent with prior studies and shed further light on
the impact of JAK2 mutations on the clinical characteristics of MPNs.

BACKGROUND: Intermediate beta‑thalassemia has different clinical observations due to its
phenotypic differences, which may complicate how it has been managed. Understanding the
biochemical characteristics can assist in pharmacotherapeutic melee strategy.
OBJECTIVE: This study aims to establish a correlation between demographic variables and
biochemical indicators in intermediate thalassemia patients.
PATIENTS AND METHODS: This study used 200 beta-thalassemia intermedia patients’ information
by conducting a survey. In addition, blood levels of calcium, iron, magnesium, phosphorus, copper,
and zinc were measured. Age and gender, and their interactions with these biochemical markers
were investigated using multivariate regression analysis. Moreover, for grouping patients according
to their biochemical parameters, K‑means clustering was conducted.
RESULTS: The obtained data showed that gender provided the strongest effect on zinc levels based
on a P = 0.0014, thus establishing that males displayed lower mean zinc levels than females. The
zinc gender coefficient value (−17.691) proved that males experienced a substantial reduction in zinc
levels compared to females. The zinc model fit demonstrated an R‑squared value of 0.366, while its
adjusted R‑squared amounted to 0.220 with an F‑statistic probability of 0.048. These results indicated
suitable model compatibility compared to other markers. The patient samples were distributed into
three distinct clusters, which helped evaluate their biochemical compositions for determining risk
elements and required treatment methods. The intense chelation requirement exists for Cluster 1
because it has the highest iron content levels, even though Cluster 2 focuses on zinc supplementation
due to its lowest zinc concentration.
CONCLUSION: This study examined the biochemical characteristics of patients with intermediate
thalassemia, revealing significant disease heterogeneity and gender‑specific differences, particularly
lower zinc levels in males. Multivariate regression and cluster analyses identified distinct biochemical
patterns and patient subgroups, supporting the need for personalized, gender‑sensitive treatment
approaches. These insights suggest that individualized therapies tailored to each patient’s metabolic
profile can improve treatment outcomes and quality of life.

BACKGROUND: Chronic mature B‑cell lymphoproliferative disorders (B‑LPDs) are characterized
by the clonal proliferation of mature B‑lymphocytes in the peripheral blood (PB), bone marrow, and
lymphoid tissues. These disorders are classified based on morphology, flow cytometry (FC), biological
features, and genetics.
OBJECTIVES: This study aimed to characterize the demographic and clinical features of patients
and to analyze their immunophenotypic profiles.
MATERIALS AND METHODS: This retrospective study examined 182 cases of non‑CLL B‑LPDs
diagnosed over 2 years (April 2022–March 2024) at Baghdad Medical City Complex. Data included
patient demographics, clinical features, complete blood count (CBC) parameters, PB absolute
lymphocyte count (ALC), and immunophenotypic profiles. FC utilizing the BD FACSCanto™ II System
and immunophenotypic markers was assessed to establish diagnostic subtypes. Statistical analysis
was performed using SPSS version 25.
RESULTS: The most common subtypes included marginal zone lymphoma (MZL) (30.2%), mantle cell
lymphoma (MCL) (24.7%), and splenic MZL (13.7%). Age at diagnosis varied significantly among subtypes,
with a median of 61 years. Immunophenotypic analysis revealed distinct patterns, such as CD5 positivity
in MCL and atypical CLL, CD200 negativity differentiating MCL from other disorders, and CD10 positivity
in follicular lymphoma (FL). CBC parameters exhibited significant variability, with elevated ALC in atypical
CLL and distinct anemia and thrombocytopenia profiles in diffuse large B‑cell lymphoma subtypes.
CONCLUSION: This study highlights the diagnostic and clinical heterogeneity of non‑CLL B‑LPDs,
emphasizing the critical role of FC and immunophenotypic markers in subtype differentiation.
Age and hematological parameters displayed significant variability, reflecting biological diversity.
Immunophenotypic analysis revealed distinct patterns, such as CD5 positivity in MCL and atypical
CLL, CD200 negativity differentiating MCL from other disorders, and CD10 positivity in FL. These
findings provide insights into the diagnostic challenges and underscore the importance of tailored
approaches in resource‑limited settings.

BACKGROUND: The discovery of the Janus kinase 2 (JAK2) in 2005, along with calreticulin (CALR)
and myeloproliferative leukemia virus oncogene (MPL) gene mutations, significantly advanced our
understanding of primary myelofibrosis (PMF) and other myeloproliferative disorders (MPNs). These
mutations are now integral diagnostic markers in the World Health Organization classification of MPNs.
OBJECTIVES: The objective of this study was to assess the incidence of JAK2 mutation in Iraqi
patients with myelofibrosis (MF).
MATERIALS AND METHODS: Eighty patients with MF were enrolled in a cross‑sectional study at
the National Centre of Hematology, Al‑Mustansiriya University, and Hematology Centre in Baghdad
Medical City Complex, from February 2024 to November 2024. MPN Molecular Panel mutations
were analyzed, with demographic and clinical data collected. Data were presented as frequencies,
percentages, means, standard deviations, and ranges. Chi‑square (χ²) test were used for statistical
analysis.
RESULTS: Eighty patients, 52.5% were male and 47.5% female patients, with a median age of
57.6 years. 66.3% had (PMF), 22.5% had (postpolycythemia vera‑MF), and 11.3% had (postessential
thrombocythemia‑MF). Genetic analysis revealed that 75% had the JAK2V617F mutation, 10% had
CALR and MPL mutations, 1.2% had a JAK2 exon 12 mutation, and 3.8% were triple negative.
CONCLUSIONS: Mutations in MPN are key molecular markers for diagnosing myelofibrosis (MF), a
disease that mainly affects older adults. The JAK2V617F mutation was the most prevalent genetic
alteration observed. Fatigue was reported in 93.3% of JAK2, and 100% of CALR‑ and MPL‑mutated
patients. Weight loss occurred in 75%, 87.5%, and 50% of JAK2, CALR, and MPL, respectively.
Despite arising from distinct genes, these mutations share similar clinical, laboratory, and prognostic
outcomes

BACKGROUND: Protein C (PC), protein S (PS), and antithrombin levels dramatically reduced
in thalassemic patients, particularly those with splenectomies and few transfusions, indicating a
significant involvement in hypercoagulability. These findings question the cost‑effectiveness of
recommending prophylactic antithrombotic treatment for high‑risk thalassemic patients.
OBJECTIVES: The objectives of this study are to assess PC, PS, and antithrombin levels in
transfusion‑dependent β- thalassemic patients and determine their association with clinical,
biochemical, and hematological parameters.
MATERIALS AND METHODS: A study of 50 B‑thalassemia major patients under 18 years old who
received regular blood transfusions at the thalassemia center at Al Hadba Teaching Hospital in
Mosul from January to February 2025. Blood samples were taken for pack cell volume, antithrombin,
ferritin, serum alanine aminotransferase, serum aspartate aminotransferase, and viral hepatitis
screening. Enzyme‑linked immunosorbent assay was used to estimate PC, and free PS in plasma,
and radioimmunodiffusion was used to measure antithrombin. The data were analyzed using mean,
mean and standard deviation, percentages, Pearson’s correlation, and independent t‑test.
RESULTS: There was a significant reduction of PC, PS, and antithrombin in thalassemia patients
than the controls. Splenectomized thalassemic individuals show significant decreases in PC, PS,
and antithrombin levels.
CONCLUSION: Low amounts of PC and free PS in thalassemic individuals may be acquired early
in life. How much the imbalance between coagulation inhibitors and clotting factors contributes to
hypercoagulability in thalassemia is unknown.

BACKGROUND: Early and accurate diagnosis of early‑onset neonatal sepsis (EONS) is vital in
improving survival and outcome in affected neonates. To date, no single inflammatory biomarker
has demonstrated both high sensitivity and specificity for the diagnosis of EONS.
OBJECTIVES: The objective of this study was to explore the role of the red cell distribution
width‑to‑platelet ratio (RPR) and the platelet distribution width‑to‑platelet ratio (PPR) in the diagnosis
of EONS.
MATERIALS AND METHODS: A case–control study was conducted at a tertiary hospital in Baghdad,
Iraq, over 10 months. Cases included neonates with culture‑positive EONS, while healthy controls
were selected from the outpatient clinic in a ratio of case to control of 1:1. Sepsis screening was
performed for all neonates within 12–24 h of life and composed of complete blood count, C‑reactive
protein, and bacterial culture and sensitivity. The results of complete blood counts, along with PPR
and RPR values, were compared between cases and controls.
RESULTS: A total of 352 neonates (176 cases and 176 controls) were included. There was no
statistically significant difference in demographical characteristics between groups. The univariate
analysis revealed that RPR was higher in the case group than the control group, P = 0.02. In contrast,
PPR failed to show a statistically significant difference between cases and controls, P = 0.77. On the
receiver operating characteristic analysis, RPR had a sensitivity of 88.4% and specificity of 36.4%
for predicting sepsis. PPR had a sensitivity of 77.9% and specificity of 27.3% for predicting sepsis.
CONCLUSION: RPR and PPR exhibit high sensitivity, making them useful as initial screening tools
for EONS. However, their low specificity limits their reliability as standalone diagnostic markers.

BACKGROUND: Febrile neutropenia (FN) is a medical emergency commonly observed in patients
undergoing chemotherapy for hematological malignancies, and without timely administration of
broad‑spectrum antibiotics, infections can quickly worsen within the first few hours of fever onset.
Due to the immunosuppressed state of these patients, FN demands immediate evaluation and
management to prevent severe complications, including severe illness and death.
OBJECTIVES: The study aimed to evaluate the perspectives and approaches of Iraqi hematologists
in treating neutropenic fever in patients with hematological diseases.
MATERIALS AND METHODS: This study is an observational cross‑sectional study that included
patients with FN while undergoing chemotherapy for various acute and chronic hematological
malignancies. The study population was drawn from hematology wards in different centers in Baghdad
and Al‑Nasiriya, where cases of FN were routinely managed.
RESULTS: The study enrolled 100 patients with FN, with a mean age of 41.53 years (±9.3 years).
Among them, 21% had acute lymphoblastic leukemia (ALL), and 26% had acute myeloid
leukemia (AML). Regarding empiric antibiotic therapy, 56% of patients were treated with combination
antibiotics, while 44% received monotherapy. Infections were most commonly identified in the
gastrointestinal tract (34%) and skin (23%), with less frequent involvement of the lungs. In 20% of
cases, the infection source remained unidentified despite the presence of bloodstream infections.
Cultures of the blood were positive in 25% of patients, while 75% had negative results. No significant
association was found between neutrophil count and blood culture positivity or between blood culture
results and different underlying hematological diagnoses.
CONCLUSION: Severe neutropenia was closely linked to a higher risk of infection, particularly
in patients with AML and ALL. The decision to use mono or combination antibiotic therapy varied
based on hematologists’ preferences and drug availability. Gastrointestinal and skin infections were
the most frequently documented infection sites. These findings underscore the need for improved
infection prevention strategies in this vulnerable population.

BACKGROUND: Tyrosine kinase inhibitors (TKIs) have significantly improved the prognosis of
chronic myeloid leukemia (CML). However, resistance or intolerance to first‑ and second‑generation
TKIs remains a clinical challenge.
OBJECTIVE: The objective of this study was to evaluate the safety and efficacy of bosutinib in CML
patients following failure of previous TKIs (imatinib and/or nilotinib).
MATERIALS AND METHODS: In this prospective cohort study, 35 CML patients in chronic or
accelerated phase were treated with bosutinib at the Basrah Center of Hematology between August
2021 and January 2024. Patients were followed for 1 year and evaluated for hematologic and
molecular responses, as well as treatment‑related adverse events (AEs).
RESULTS: The majority were female (60%), with a mean age of 45.6 years. Bosutinib was primarily
indicated for molecular response failure (60%). Complete hematologic response was achieved in 74%
of patients, and major molecular response was observed in 40.7% at 12 months. The most common
AEs were gastrointestinal (e.g., diarrhea in 80% and nausea in 51%). Most AEs were Grade 1–11.
Severe hematologic toxicities were rare.
CONCLUSION: Bosutinib demonstrated a favorable safety and efficacy profile in CML patients with
prior TKI failure. It remains a viable treatment option in resource‑constrained settings where mutation
analysis may be unavailable.

BACKGROUND: Acute myeloid leukemia (AML) is a clonal malignancy affecting hemopoietic
immature cells, characterized by uncontrolled proliferation and impaired differentiation of these cells,
causing their accumulation in the marrow and ultimately marrow failure. Cluster of differentiation 56 or
CD56 antigen is typically found on the majority of healthy natural killer cells, some cytotoxic T‑cells, and
a number of CD4+ T‑cells. However, in around 20%–40% of AML patients, it is aberrantly expressed.
OBJECTIVES: The aims of this study were to determine the frequency of abnormal CD56 expression
in adult de novo AML blasts and evaluate its correlation with complete blood count (CBC), blast
percentages, AML subtypes, extramedullary disease, and induction therapy response.
MATERIALS AND METHODS: Thirty adult cases (>15 years) with de novo AML were consequently
selected in the period from August 1, 2023, to January 30, 2024. On average, their age was
38.97 years old. Cytomorphology, with the use of flow cytometry in suspected instances, was used
to diagnose all AML patients in accordance with the World Health Organization criteria for AML. At
the first diagnosis, the blast cell percentage was determined by counting the cells on the peripheral
blood (PB) and bone marrow (BM)‑stained films, and the CBC was performed using a 5‑part automated
analyzer. Using an eight‑color (BD FACSCanto II USA), aberrant CD56 expression was examined.
Extramedullary manifestations were determined at the time of diagnosis and determine its correlation
with CD56 expression. Three weeks after the completion of the first chemotherapy cycle, the patients
were re‑assessed for the accomplishment of complete remission.
RESULTS: Expression of CD56 was observed on blast cells in 26.7% of AML patients. Patients with
AML exhibiting positive CD56 expression were older compared to those with negative expression.
Furthermore, CD56 expression was more prevalent in males, with the male: female ratio of 7:1.
Nevertheless, no statistically significant correlations were identified between either of the aberrant
expressions and age or sex. CD56 expression was significantly higher in blasts of AML subtypes with
monocytic differentiation. The total white blood cell (WBC) count and the percentage of PB and/or BM
blast cells in AML patients exhibiting positive expression were significantly higher compared to those
without such expression. Significant correlations were observed between aberrant CD56 expression
and extramedullary manifestations and with the nonresponsiveness to the induction therapy.
CONCLUSION: There is evidence of aberrant CD56 expression in around a quarter percent of
all instances of AML. It was discovered that neither the age nor the gender of the patient had a
significant correlation with this expression. It was shown that monocytic AML subtypes had a higher
expression of CD56. It was shown that individuals with AML who had aberrant CD56 expression
had considerably higher overall WBC, as well as greater percentages of blast cells in both the PB
and BM. There was a substantial association between the abnormal expression of CD56 and the
extramedullary symptoms, as well as the nonresponsiveness to the induction treatment.

BACKGROUND: Multiple myeloma (MM) is a plasma cell disorder characterized by the infiltration
of clonal plasma cells in the bone marrow and the detection of a monoclonal immunoglobulin in
serum and/or urine. Renal failure, anemia, hypercalcemia, and the presence of bone lesions are
the hallmarks of the disease.
OBJECTIVES: The study aimed to evaluate the clinical, hematological, radiological, and
immunophenotypic features of MM patients and to identify prognostic factors influencing survival
outcomes.
MATERIALS AND METHODS: This cohort study included 77 newly diagnosed, untreated MM patients.
Their clinical presentation, laboratory data, imaging results, and the expression of flow cytometry
markers were analyzed in correlation with the 1‑year overall survival (OS).
RESULTS: The mean age was 59.29 ± 12.1 years, bone pain was the most common symptom (81.8%),
and anemia was observed in 87% of patients. Radiologically, lytic lesions were present in 70.1% of
cases, with 33.8% having pathological fractures. Flow cytometry revealed universal expression of
CD319 (100%) and high expression of CD56 (98.7%). CD117 positivity was significantly associated
with shorter OS (P = 0.029), and CD28 showed a tendency toward poorer prognosis (P = 0.054).
Other markers, such as CD44 and CD49e, did not show significant prognostic associations.
CONCLUSIONS: MM may manifest at an earlier age in specific populations. The most significant
features were anemia, bone lesions, and renal dysfunction. Lower hemoglobin levels, higher blood urea
and serum creatinine, along with a lower glomerular filtration rate, hyperuricemia, and hypoalbuminemia,
contribute to poorer outcomes, as the expression of CD117 has an inverse prognostic outcome.

Abstract:
BACKGROUND: Chronic myeloid leukemia (CML) is a malignant blood disorder characterized by
BCR‑ABL1 transcript production, which results in constitutive tyrosine kinase activity. The use of
tyrosine kinase inhibitors (TKIs), notably imatinib, has greatly improved patient outcomes. However,
treatment resistance, intolerance, and adherence remain significant concerns.
OBJECTIVES: This study aimed to assess the hematological and molecular responses of patients
with CML in Iraqi Kurdistan treated with first‑line imatinib while also identifying factors related to
resistance, intolerance, and adherence.
MATERIALS AND METHODS: This retrospective descriptive study included 161 CML patients
diagnosed since 2010 across three major hematology/oncology centers in Duhok, Erbil, and
Sulaymaniyah. Data were collected from patient records, including demographics, clinical
presentation, laboratory findings, BCR‑ABL1 transcript levels, comorbidities, treatment regimens,
and follow‑up response at 3, 6, 12, and 15 months. Data analyses were carried out using SPSS
version 26, with significance set at P < 0.05.
RESULTS: Of 161 patients, 140 (86.9%; 95% confidence interval [CI]: 81.1–91.3) achieved complete
hematological response at 3 months. At 15 months, 93 patients (57.8%; 95% CI: 49.7–65.6) attained
optimal molecular response, including 40 (24.8%) with major molecular response, 37 (23.0%) with
deep molecular response, and 16 (9.9%) with complete molecular response. Resistance occurred in
46 patients (28.6%), significantly associated with delayed diagnosis (P = 0.021). Imatinib intolerance
was observed in 13 (8.1%), poor adherence in 7 (4.3%), and T315I mutation in 3 (1.9%).
CONCLUSION: While imatinib remains an effective first‑line treatment, resistance and adherence
issues necessitate early molecular monitoring and consideration of second‑generation TKIs. Future
research should focus on genetic profiling, treatment modifications, and socioeconomic interventions
to enhance CML management in Iraqi Kurdistan.