Extramedullary hematopoiesis of the paranasal sinuses in sickle cell disease

Collins, William O.; Younis, Ramzi T.; Garcia, Maria Alice Amorim

doi:10.1016/j.otohns.2004.07.007

Cited by 21 publications

(17 citation statements)

References 4 publications

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“…However, it is possible that children with SCD have other anatomic abnormalities, such as those affecting their craniofacial structure particularly due to extramedullary hematopoiesis, 30 and/or functional factors that may increase upper airway collapsibility, 31 thereby increasing their risk for SDB or OSAS. Thus, additional studies are warranted to elucidate such potential contributors in this population.…”

Section: Acknowledgmentsmentioning

confidence: 99%

Upper Airway Lymphoid Tissue Size in Children With Sickle Cell Disease

Strauss

Sin

Marcus

et al. 2012

Chest

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Sleep-disordered breathing (SDB), a condition associated with abnormalities in respiratory gas exchange during sleep (particularly intermittent oxyhemoglobin desaturation), has been implicated as a possible risk factor for deleterious cerebrovascular complications in children with sickle cell disease (SCD). [1][2][3] Although the prevalence of SDB in these children has not been well established, estimates range from 5% to 79% 4-10 and are far greater than the prevalence of 1% to 4% in children without SCD. 11 In addition, the pathophysiology of SDB in these children is not well understood. Possible mechanisms include hypoven tilation due to chronic lung disease, 12,13 obstructive sleep apnea syndrome (OSAS) 6 (a disorder characterized by recurrent events of partial or complete Background: The prevalence of obstructive sleep apnea syndrome (OSAS) is higher in children with sickle cell disease (SCD) as compared with the general pediatric population. It has been speculated that overgrowth of the adenoid and tonsils is an important contributor. Methods: The current study used MRI to evaluate such an association. We studied 36 subjects with SCD (aged 6.9 Ϯ 4.3 years) and 36 control subjects (aged 6.6 Ϯ 3.4 years). Results: Compared with control subjects, children with SCD had a signifi cantly smaller upper airway (2.8 Ϯ 1.2 cm 3 vs 3.7 Ϯ 1.6 cm 3 , P , .01), and signifi cantly larger adenoid (8.4 Ϯ 4.1 cm 3 vs 6.0 Ϯ 2.2 cm 3 , P , .01), tonsils (7.0 Ϯ 4.3 cm 3 vs 5.1 Ϯ 1.9 cm 3 , P , .01), retropharyngeal nodes

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Section: Acknowledgmentsmentioning

confidence: 99%

Upper Airway Lymphoid Tissue Size in Children With Sickle Cell Disease

Strauss

Sin

Marcus

et al. 2012

Chest

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“…It acts as a vital part of the patient's functioning hematopoietic tissue. Extramedullary haematopoiesis in the paranasal sinuses has been documented in just a few handfuls of cases [14]. Extramedullary haematopoiesis should be considered in the differential diagnosis of any paranasal sinus mass presenting in a patient with known chronic anaemia.…”

Section: Rhinological Problemsmentioning

confidence: 99%

Otorhinolaryngological manifestations of sickle cell disease

Abou-Elhamd

2012

International Journal of Pediatric Otorhinolaryngology

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“…7 These facts are related to: (1) an adenotonsilar hypertrophy in these children related to compensatory lymphoid tissue hyperplasia due to functional asplenia and chronic infections 8 ; (2) chronic hemolysis that increases extramedulary hematopoiesis and can alter the bone facial structure. 9 During sleep, children with SCD have transient periods of hypoxemia (accompanied by hypercapnia and acidosis) that causes sickling of the erythrocytes. This causes acute vaso-occlusion events (the major cause of admissions in these children) and chronic microvasculature alterations posing a major risk factor for cardiac events and cerebral ischemic events (silent or symptomatic).…”

Section: Introductionmentioning

confidence: 99%