Radiologic Evaluation of Paranasal Sinuses in Sickle Cell Anemia and Thalassemia: Case–Control Study

ABSTRACT

Background

Sickle cell disease and thalassemia are inherited hematological disorders that are common worldwide. These patients suffer from chronic hemolytic anemia, which can result in bone marrow dysfunction and, in rare cases, extramedullary hematopoiesis. These pathophysiological changes can predispose patients to sinus complications or misdiagnosis in imaging studies.

Objective

Evaluate the maxillary sinus abnormalities in patients with β‐thalassemia, sickle cell anemia, and sickle cell–beta thalassemia.

Methods

A multicenter, case–control study was conducted, including 212 participants, categorized into four groups: control (n = 100), sickle cell anemia (n = 51), β‐thalassemia (n = 15), and sickle cell‐beta thalassemia (n = 46). Demographic information, laboratory parameters (mean hemoglobin levels and hemoglobin electrophoresis), history of hydroxyurea use, and blood transfusion were recorded. Computed tomography was used to assess sinus wall thickness, extramedullary hematopoiesis, and related sinonasal abnormalities.

Results

Significant maxillary sinus wall thickening across all disease groups was found, with the β‐thalassemia exhibiting the most pronounced changes (p < 0.001). A negative correlation was observed between hemoglobin levels and sinus wall thickness in sickle cell anemia. Extramedullary hematopoiesis in the paranasal sinuses, although rare, was identified in five patients with β‐thalassemia. Obstruction of the ostiomeatal complex was observed in 14.3% of the β‐thalassemia, 13.7% of sickle cell anemia, and 6.5% of sickle cell–beta thalassemia.

Conclusion

Our findings reveal significant maxillary sinus wall thickening in β‐thalassemia, sickle cell anemia, and sickle cell–beta thalassemia. Recognizing these structural changes is important for radiologists and otolaryngologists, as they may resemble other pathologies and lead to diagnostic challenges if not carefully interpreted.

Level of Evidence

4.

This study assessed CT findings in patients with β‐thalassemia, sickle cell anemia, and sickle cell–β‐thalassemia. Significant sinus wall thickening and rare cases of paranasal sinus extramedullary hematopoiesis were observed. These findings may resemble other pathologies and present diagnostic challenges.

1. Introduction

Sickle cell disease (SCD) and β‐thalassemia (β‐Thal) are inherited hemoglobinopathies with significant global health concern [1]. According to the World Health Organization (WHO), over 300,000 infants are born annually worldwide¹and are most prevalent among the African, Mediterranean, Middle Eastern, and Indian populations [1]. In Saudi Arabia, the prevalence of SCD and β‐Thal is among the highest in the Middle East, at 4.5% and 0.05%, respectively [2].

SCD results from a mutation in the beta‐globin gene that leads to the production of hemoglobin S (HbS) [3, 4]. The most common and severe form is the homozygous inheritance of HbS (HbSS), also known as sickle cell anemia (SCA) [5]. Under hypoxic conditions, HbS undergoes polymerization, resulting in the distortion of red blood cells into a sickle shape [3, 4]. This distortion causes complications, such as vaso‐occlusion, hemolysis, and organ damage [3, 4]. In contrast, β‐Thal is caused by impaired synthesis of beta‐globin chains, leading to chronic anemia and complications such as skeletal deformities and iron overload [4]. β‐Thal mutations are classified as β⁰, which result in a complete absence of β‐globin chain synthesis and are typically associated with the severe phenotype, β‐Thal major; or as β⁺, where partial β‐globin production is preserved, often seen in intermedia or minor forms [4]. Clinically, β‐Thal is further categorized into transfusion‐dependent thalassemia (TDT) and nontransfusion‐dependent thalassemia (NTDT), based on disease severity [6]. Sickle cell‐beta thalassemia (Hb S/β‐Thal) combines features of both conditions, with clinical severity varying depending on the specific β‐Thal mutations and Hemoglobin A levels [7]. Hb S/β‐Thal is typically divided into two subtypes: Hb S/β⁰‐Thalassemia and Hb S/β⁺‐Thalassemia [7]. Hb S/β⁰‐Thalassemia causes symptoms similar to SCA due to a lack of hemoglobin A production [7].

Under these conditions, chronic anemia and ineffective erythropoiesis can result in compensatory bone marrow hypertrophy and extramedullary hematopoiesis (EMH) [3, 4, 8]. EMH is defined as the formation of hematopoietic tissue outside the bone marrow, frequently involving the spleen, liver, lymph nodes, and rarely the paranasal sinuses [3, 9, 10]. Changes in the paranasal sinuses, including marrow hypertrophy, reduced pneumatization, and sinus obliteration, are documented in β‐Thal patients and occasionally observed in SCA (HbSS) [4, 11, 12, 13]. However, studies assessing paranasal sinus abnormalities in patients with β‐Thal, SCA, and Hb S/β‐Thal are limited. Furthermore, the frequency and features of EMH in the paranasal sinuses remain unknown.

This study aims to assess maxillary sinus abnormalities in patients with β‐Thal, SCA, and Hb S/β‐Thal in comparison to a control group. To the best of our knowledge, this is the first study to examine maxillary sinus changes in patients with Hb S/β‐Thal. Additionally, we evaluated the prevalence of EMH in the maxillary sinuses across study groups.

2. Materials and Methods

2.1. Study Population

This multicentric case–control study included 212 participants recruited from the electronic medical records of Qatif Central Hospital and Hereditary Blood Diseases Center in Al‐Ahsa, Saudi Arabia.

Inclusion criteria:

1. Diagnosed with SCA (HbSS), β‐Thal, or Hb S/β‐Thal using electrophoresis and following up with hematology department.

2. Availability of multiplanar reconstructed computed tomography (CT) scans with a slice thickness of 2 mm (paranasal sinuses, head, facial bones, and temporal bones).

Exclusion criteria:

1. Absence of relevant CT scans.

2. Age ≤ 10 years.

3. History of craniofacial trauma, head and neck surgery, or radiation therapy.

4. Diseases other than SCA (HbSS), β‐Thal, or Hb S/β‐Thal.

The control group comprised healthy individuals with no history of hematological or sinonasal pathology, selected randomly from those undergoing CT scans for other nonsinonasal‐related pathologies.

2.2. Demographic and Clinical Data Collection

Demographic information (age and sex), laboratory parameters (mean hemoglobin levels and hemoglobin electrophoresis), history of hydroxyurea use or blood transfusion, and frequency were recorded. The mean hemoglobin levels were obtained within approximately 6 months of the corresponding CT scan. According to our hospital policy, all patients diagnosed with transfusion‐dependent β‐Thal are managed under a regular transfusion protocol. This protocol involves blood transfusions every 2–4 weeks to maintain pretransfusion hemoglobin levels between 9 and 10 g/dL.

CT scans of the paranasal sinuses, facial bones, and temporal bones were performed using a 64‐multidetector CT scanner (Siemens SOMATOM, Germany). Helical scanning was performed in the axial direction; 2 mm slices were reconstructed in the axial, coronal, and sagittal planes using both bone and soft tissue algorithms. Scanning voltages of 120 kV for adults and 80 kV for pediatric patients are adequate to delineate the bony structures of the ENT region.

2.3. CT Imaging and Measurements

CT scans were evaluated for:

1. EMH lesions with details of lesion location. An EMH was defined as a soft tissue mass with variable enhancement within the paranasal sinuses without bony erosion or intracranial or intraorbital extension.

2. Maxillary sinus wall thickness was measured at the mid‐portion of the maxillary antrum, with full visualization of the pterygoid plates as a reference landmark.

3. The maximum thicknesses of the anterior, posterior, medial, and lateral sinus walls were recorded in millimeters.

4. Hounsfield Unit (HU) values of the maxillary sinus.

5. Patency of the ostiomeatal complex (OMC) and associated sinus findings, such as mucosal thickening, sinus opacification, or other sinus pathologies.

Two consultant radiologists independently reviewed scans, and discrepancies between radiologists were resolved by consensus.

2.4. Statistical Analysis

Statistical analyses were performed using R v4.3. Group differences in maxillary sinus measurements were analyzed using Welch's analysis of variance, which is suitable for unequal variances and sample sizes, with effect sizes quantified using the eta‐squared test. Pairwise post hoc comparisons were conducted using the Games‐Howell test, with Holm's method used to adjust the p values. Nonnormally distributed variables were log‐transformed when required.

Linear regression was used to assess the associations between the average left and right sinus measurements and predictors, such as age, sex, history of blood transfusion, and hydroxyurea usage. All hypothesis tests were two‐sided, with a significance level of 5%.

3. Results

3.1. Study Population Characteristics

The study included 212 participants, categorized into four groups: control (n = 100), SCA (n = 51), β‐Thal (n = 15), and Hb S/β‐Thal group (n = 46). The sex distribution was similar across the groups (p = 0.813), with women representing 54.7% and men 45.3% of the total population. Participants' ages varied significantly among the groups (p = 0.001), primarily due to the younger age of the β‐Thal group compared to others. Hemoglobin levels were not significantly different between disease groups (p = 0.620), with the highest levels in the Hb S/β‐Thal group (9.29 ± 1.54 g/dL) and the lowest in the SCA group (9.03 ± 1.29 g/dL). All β‐Thal participants were transfusion‐dependent β‐Thal patients on a chronic blood transfusion protocol, whereas 50% of the SCA and Hb S/β‐Thal groups required frequent transfusions and had received over 10 units of red blood cells or blood exchange in their lifetime (p = 0.002) (Table 1).

TABLE 1.

Descriptive statistics for the study population.

	All	Control	SCA	β‐thal	Hb S/β‐Thal	p overall
	N = 212	N = 100	N = 51	N = 15	N = 46
Age	39.1 (15.0)	41.2 (14.0)	38.2 (13.8)	25.1 (10.7)	40.3 (17.3)	0.001
Gender						0.813
Women	116 (54.7%)	54 (54.0%)	27 (52.9%)	10 (66.7%)	25 (54.3%)
Men	96 (45.3%)	46 (46.0%)	24 (47.1%)	5 (33.3%)	21 (45.7%)
Hgb level (g/dL)	9.15 (1.33)	NA	9.03 (1.29)	9.10 (0.61)	9.29 (1.54)	0.620
Blood transfusion						0.002
No	48 (42.9%)	100 (100%)	25 (49.0%)	0 (0.00%)	23 (50.0%)
Yes	64 (57.1%)	0 (0%)	26 (51.0%)	15 (100%)	23 (50.0%)

Abbreviations: β‐thal, β‐thalassemia; Hb S/β‐Thal, sickle cell‐beta thalassemia; SCA, sickle cell anemia. Bold numbers indicate statistically significant p‐values (p < 0.05).

3.2. Bone Thickness Measurements

Significant differences were observed in the maxillary sinus bone wall thickness across the groups (p < 0.001), with the lateral wall being the thickest. Bilaterally, the β‐Thal group exhibited the highest thickness in all walls, which was significantly greater than the Control, SCA, and Hb S/β‐Thal groups (p < 0.05). The disease groups exhibited significantly lower HU of the maxillary sinus walls than the controls (Table 2). No statistically significant correlation was found between patient age and sinus wall thickness on either side (p > 0.05). Furthermore, neither blood transfusion, hydroxyurea therapy, nor patient sex demonstrated a significant association with sinus wall measurements (p > 0.05).

TABLE 2.

Maxillary sinus wall measurements across group.

	Control	SCA	β‐Thal	Hb S/β‐Thal	p
	N = 100	N = 51	N = 10	N = 46
Right
Anterior bone thickness of maxillary sinus (mm)	1.28 (0.52)	2.35 (1.93)	2.92 (2.39)	2.12 (0.76)	< 0.001
Posterior bone thickness of maxillary sinus (mm)	1.11 (0.68)	1.96 (1.97)	3.68 (2.12)	1.58 (0.69)	< 0.001
Lateral bone thickness of maxillary sinus (mm)	3.77 (1.74)	6.01 (3.52)	12.7 (7.80)	6.30 (3.37)	< 0.001
Medial bone thickness of maxillary sinus (mm)	1.03 (1.00)	1.57 (0.80)	2.41 (0.73)	1.47 (0.41)	< 0.001
Left
Anterior bone thickness of maxillary sinus (mm)	1.24 (0.62)	2.65 (2.35)	5.45 (9.42)	2.06 (0.67)	< 0.001
Posterior bone thickness of maxillary sinus (mm)	1.15 (0.68)	2.62 (2.93)	3.14 (1.72)	1.49 (0.56)	< 0.001
Lateral bone thickness of maxillary sinus (mm)	4.02 (4.13)	5.98 (3.98)	13.7 (6.42)	6.34 (3.19)	< 0.001
Medial bone thickness of maxillary sinus (mm)	1.09 (1.14)	1.50 (0.50)	2.37 (1.03)	1.41 (0.44)	< 0.001
The Hounsfield unit (HU)	723 (348)	327 (328)	131 (66.5)	310 (211)	< 0.001

Abbreviations: β‐thal, β‐thalassemia; Hb S/β‐Thal, sickle cell‐beta thalassemia; SCA, sickle cell anemia. Bold numbers indicate statistically significant p‐values (p < 0.05).

3.3. EMH

Five out of 15 β‐Thal patients demonstrated evidence of EMH, all of whom had bilateral involvement. The mean age was 25.8 years (range: 10–39 years), and the mean hemoglobin level was 9.3 g/dL. All the patients received regular blood transfusion regimens. None of the patients underwent a biopsy or surgical treatment (Figure 1).

FIGURE 1.

Noncontrast CT paranasal sinuses in a patient with transfusion‐dependent β‐Thal (A) coronal cuts and (B) axial cuts: Showing an expansile lytic lesion involving the maxillary sinus walls, without periosteal reaction, cortical destruction, or invasion to the adjacent structures. These findings are consistent with extramedullary hematopoiesis within the maxillary sinus.

3.4. Hemoglobin and Bone Thickness Correlations

A significant negative correlation was observed between hemoglobin levels and sinus wall thickness for both the left (r = −0.25, p = 0.01) and right sides (r = −0.21, p = 0.03). In the SCA group, the negative correlation was stronger and statistically significant for the left side (r = −0.30, p = 0.008) and approached significance on the right side (r = −0.26, p = 0.072). In contrast, no significant correlations were identified in the β‐Thal or Hb S/β‐Thal groups (p > 0.05).

3.5. Ostiomeatal Complex Obliteration and Sinonasal Findings

OMC obliteration rates were significantly associated with the disease groups (p = 0.001). The highest obstruction rate was observed in the β‐Thal group (14.3%), followed closely by the SCA group (13.7%), while the Hb S/β‐Thal group exhibited the lowest rate (6.5%). Maxillary sinus findings differ significantly across diagnostic groups (p = 0.001), with SCA, β‐Thal, and Hb S/β‐Thal groups exhibiting varying degrees of mucosal thickening, retention cysts, and sinus opacification (Figure 2).

FIGURE 2.

Distribution of maxillary sinus findings across different diseased groups.

4. Discussion

Craniofacial and skeletal changes in β‐Thal and SCD, primarily resulting from chronic hemolytic anemia and compensatory bone marrow hyperplasia, are well‐documented [14]. In β‐Thal, these changes are marked, manifesting as frontal bossing, prominent malar eminences, nasal bridge depression, maxillary hypertrophy, and slant eyes [14]. Extensive bone marrow expansion can cause mechanical interruption of bone formation, leading to cortical bone thinning, rarefaction of the cancellous bone, and loss of bone density [4, 15, 16]. Bone marrow expansion also occurs in SCD. However, associated skeletal changes are generally less pronounced [4, 17]. According to Licciardello et al. cephalometric analysis showed that patients with SCD exhibited moderate craniofacial abnormalities compared to healthy controls [17]. Furthermore, these abnormalities were less severe in Hb S/β‐Thal patients compared to SCA patients [17].

Studies of β‐Thal major have documented marked anatomical changes in the paranasal sinuses, including increased bone thickness, particularly in the posterior and lateral walls of the maxillary sinuses, as well as a reduction in sinus volume and pneumatization in patients with β‐Thal [12, 13, 18]. Similar results were observed in the present study. These findings, attributed to bone marrow hyperplasia, may result in sinus obliteration, potentially leading to nasal obstruction or chronic rhinosinusitis (CRS) [11, 13, 18]. Di Mauro et al. reported that β‐Thal patients have a 2.87 times higher risk of developing sinusitis compared to controls [18]. Additionally, Ahmed et al. reported that children with thalassemia have a significantly higher risk of nasal obstruction, possibly because of the smaller posterior choanae and reduced nasal cavity size [13]. The OMC is the primary drainage pathway for the frontal, maxillary, and anterior ethmoid sinuses [19]. Anatomical variations such as concha bullosa, septal deviation, Haller cells, and abnormalities of the uncinate process can narrow the OMC, increasing the risk of impaired sinus drainage [19, 20]. In hemoglobinopathies like β‐Thal, bony hypertrophy secondary to marrow expansion may contribute to the narrowing of the sinonasal passages by reducing internal sinus dimensions and thickening the walls, potentially predisposing patients to sinonasal disease [12, 13, 18]. A retrospective analysis of pediatric patients with β‐Thal and SCA demonstrated an increased risk of CRS compared to healthy controls [11]. However, Martino et al. suggested that the anatomical changes in β‐Thal patients may complicate CT interpretation rather than directly cause CRS [11]. The present study did not directly assess the diagnostic impact of these anatomical changes, and further research is needed to determine whether they act as confounding factors or contribute directly to CRS risk. Our data reveal a complex relationship between anatomical changes and radiographic evidence of sinonasal pathology. Although patients with β‐Thal exhibited the most pronounced maxillary sinus wall thickening and a 14.3% prevalence of OMC obstruction, they paradoxically demonstrated fewer radiologic signs of active sinonasal pathology, such as mucosal thickening, retention cysts, or sinus opacification. In contrast, the Hb S/β‐Thal group, despite having the lowest frequency of OMC obstruction (6.5%), showed a higher prevalence of such radiological findings. These findings underscore the complexity of sinonasal disease pathophysiology, suggesting that while anatomical narrowing of the OMC is a recognized risk factor, it may not uniformly result in clinically or radiographically evident pathology [21, 22]. It is increasingly acknowledged that mucosal inflammation may play a more dominant role in certain populations, even in the absence of overt structural obstruction [21, 22]. Therefore, a multifactorial approach that considers both anatomical and inflammatory contributors is essential when evaluating sinonasal pathology in patients with hemoglobinopathies.

Skeletal manifestations of SCD are relatively infrequent in the maxillofacial region; the orbital wall, mandible, and skull base are the most commonly affected sites [3, 23]. These osseous abnormalities can present acutely as vaso‐occlusive crises or osteomyelitis, or chronically as bone marrow hyperplasia and osteoporosis [3, 24]. Studies utilizing CT scan to investigate paranasal sinus alterations in SCA remain notably limited. Martino et al. conducted a retrospective analysis of 90 pediatric patients postallogeneic bone marrow transplantation (59 with β‐Thal major and 31 with SCA). They found significant bony changes in the maxillary sinuses of β‐Thal patients, whereas the sinuses were normal in both SCA patients and controls [11]. Although maxillary sinuses in SCA patients show fewer structural abnormalities, ischemic injuries can potentially lead to arrested sinus pneumatization, particularly in the sphenoid sinus [25]. Our study revealed significant maxillary wall thickening in individuals with SCA compared to patients with Hb S/β‐Thal and the control group. Additionally, a negative correlation between hemoglobin levels and maxillary wall thickness was found only in the SCA group, unlike the other groups. Conversely, Ragab et al. identified a significant negative correlation between hemoglobin levels and posterior maxillary wall thickness in patients with β‐Thal [13]. The observed differences could be attributed to the differences in sample sizes, treatment regimens, and targeted hemoglobin levels. The mean hemoglobin level was higher in our β‐Thal patients compared to Ragab et al. (9.10 vs. 6.61 g/dL, respectively). Our study is the first to investigate the maxillary sinus wall thickness in patients with Hb S/β‐Thal, revealing a significantly greater thickness compared to the control group.

EMH is a known compensatory mechanism to ineffective erythropoiesis in chronic hemolytic anemias. However, paranasal sinus involvement is rare [3, 9, 10]. The maxillary sinuses are the most frequently affected, followed by the sphenoid and ethmoid sinuses [3, 10]. Clark et al. identified 15 cases of sinonasal EMH in the literature, with nasal obstruction, headache, and epistaxis as the common presenting symptoms [10]. Despite this rarity, we observed five cases of paranasal sinus EMH within β‐Thal patients. Radiologically, sinonasal EMH appears as a homogeneously enhancing soft tissue mass on CT and MR, with attenuation or signal intensity similar to that of the red marrow [3, 26]. These masses may mimic inflammatory or neoplastic conditions but lack radiological evidence of bony erosion or intracranial extension, differentiating them from more aggressive pathologies [8]. EMH can sometimes be challenging to interpret on imaging modalities. Yet, the presence of lesions at multiple anatomical sites may provide a diagnostic clue, especially in patients with established risk factors [27]. Although biopsy is often required for the definitive diagnosis of nonspecific soft tissue masses, the highly vascular nature of EMH lesions necessitates careful consideration of the potential risk of hemorrhagic complications when planning such procedures [27]. Of the 15 cases reviewed by Clark et al., 12 required biopsies for diagnostic confirmation. We acknowledge that histological examination remains the definitive method for diagnosing EMH; however, in our patients, biopsy was not performed because the imaging findings were considered sufficiently characteristic, and there was reasonable clinical familiarity with this entity at our institution. This conservative approach was adopted, as surgical procedures in patients with SCA and β‐Thal are associated with increased perioperative risks [28, 29]. Moreover, as noted earlier, tissue biopsy or surgical resection in cases of suspected EMH carries a significant risk of bleeding [27]. Therefore, in asymptomatic patients where clinical history and radiologic features are highly suggestive of EMH with no evidence of aggressive or invasive behavior, close radiological and clinical follow‐up may be considered a reasonable alternative to biopsy, with the decision individualized based on the overall clinical context. Regarding management, EMH is observed more frequently in transfusion‐independent patients, as the bone marrow attempts to compensate for inadequate erythropoiesis [9]. Furthermore, effective blood transfusion therapy can prevent the progression of irreversible bone pathology in children with β‐Thal [18]. Currently, no standardized therapeutic guidelines exist for managing paranasal sinus EMH; however, based on findings from case reports, conservative management, including blood transfusion or exchange transfusion to normalize hematocrit levels and suppress hematopoietic foci, is often recommended, but evidence is limited to small case series [10]. Alternative approaches, such as low‐dose radiation therapy, have been reported for spinal EMH but lack validation for sinonasal involvement [30].

Radiologists and otorhinolaryngologists should be aware of anatomical changes in paranasal sinuses of patients with SCA, β‐Thal, or Hb S/β‐Thal, such as sinus wall thickening, reduced pneumatization, and rare EMH, which may mimic neoplastic or inflammatory conditions [11, 13, 18, 27]. These findings can complicate CT interpretation and clinical management, necessitating a multidisciplinary approach involving hematologists to optimize diagnosis and treatment.

Our multicenter case–control study contributes to the existing literature by addressing several limitations observed in previous research on paranasal sinus abnormalities in hemoglobinopathies. Prior investigations were largely restricted to pediatric populations, often consisting of isolated case reports or small‐scale studies [11, 12, 13, 18]. Furthermore, many lacked data on understudied subgroups, such as SCA or Hb S/β‐Thal. However, our study also has some limitations. First, the reliance on CT imaging without comprehensive ENT examinations limits our ability to correlate radiographic findings with clinical symptoms, potentially underestimating the prevalence of sinonasal disease. Second, the nonage‐matched control group may introduce bias, as age‐related changes in sinus anatomy could confound comparisons. Third, the relatively small sample size for the β‐Thal group, as well as the limited number of pediatric patients, may affect the generalizability of findings. In addition, our analysis was restricted to the maxillary sinuses; a broader evaluation of all paranasal sinuses with clinical examination would provide further insights and should be considered in future studies. Finally, although most scans were performed for neurological indications rather than sinus complaints, the specific clinical indication for each scan was not systematically recorded, which could introduce a selection bias.

In conclusion, our findings reveal significant maxillary sinus wall thickening in β‐Thal, SCA, and Hb S/β‐Thal, with the most pronounced changes observed in patients with β‐Thal. Knowledge of these structural changes, including EMH, is important for radiologists and otorhinolaryngologists, as they may mimic other pathologies and potentially lead to diagnostic challenges if not correctly identified.

Ethics Statement

Ethical approval was obtained for this study. The study was conducted in accordance with the institutional guidelines. Ethical approval was obtained from the Institutional Review Board of the Qatif Health Network, Eastern Province, Saudi Arabia.

Conflicts of Interest

The authors declare no conflicts of interest.

Alharbi M. A., AlDarwish A., Alamier R. M., et al., “Radiologic Evaluation of Paranasal Sinuses in Sickle Cell Anemia and Thalassemia: Case–Control Study,” Laryngoscope Investigative Otolaryngology 10, no. 5 (2025): e70268, 10.1002/lio2.70268.

Data Availability Statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.