Expert review of hematology · 2025
Vasculopathy among children and adolescents with sickle cell disease: the crosstalk with annexin A1, vitamin D, and myocardial iron overload.
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ElAlfy Mohsen Saleh, Ismail Eman Abdel Rahman, Makkeyah Sara Mostafa, Samir Ahmed, Salama Dina Husseiny, Salah Eldin Nanis Mohammed, ElMaghraby Dina Mohamed Fathy, Gad Nada Ayman, Ali Marwa Fath Ahmed, Ebeid Fatma Soliman Elsayed
Аннотация
BACKGROUND: Annexin A1 plays an important role in myocardial defense against ischemia-reperfusion injury. We aimed to evaluate the role of annexin A1 as a potential marker of vasculopathy in children and adolescents with sickle cell disease (SCD) and its relation to myocardial iron content (MIC) and vitamin D status.
RESEARCH DESIGN AND METHODS: Forty-one patients with SCD were compared with 40 age- and sex-matched healthy controls, and underwent assessment of serum annexin A1, vitamin D, Doppler echocardiography and cardiac magnetic resonance (CMR).
RESULTS: Six (14.6%) SCD patients had cardiac disease, five (12.2%) had abnormal MIC (≥1.16) and 10 (24.4%) had pulmonary hypertension risk. Annexin A1 levels were significantly lower among patients with SCD compared with healthy controls (p < 0.001). SCD patients with pulmonary hypertension risk, evidence of diastolic dysfunction, and nephropathy as well as those with serum ferritin ≥ 2500 µg/L and vitamin D deficiency had lower Annexin A1 levels than those without. Serum annexin A1 levels were negatively correlated to urinary albumin creatinine ratio (UACR) and Tei index while positively correlated to vitamin D among SCD patients.
CONCLUSIONS: Annexin A1 could be a promising marker of vasculopathy and may provide a biochemical explanation for vitamin D deficiency in SCD.
RESEARCH DESIGN AND METHODS: Forty-one patients with SCD were compared with 40 age- and sex-matched healthy controls, and underwent assessment of serum annexin A1, vitamin D, Doppler echocardiography and cardiac magnetic resonance (CMR).
RESULTS: Six (14.6%) SCD patients had cardiac disease, five (12.2%) had abnormal MIC (≥1.16) and 10 (24.4%) had pulmonary hypertension risk. Annexin A1 levels were significantly lower among patients with SCD compared with healthy controls (p < 0.001). SCD patients with pulmonary hypertension risk, evidence of diastolic dysfunction, and nephropathy as well as those with serum ferritin ≥ 2500 µg/L and vitamin D deficiency had lower Annexin A1 levels than those without. Serum annexin A1 levels were negatively correlated to urinary albumin creatinine ratio (UACR) and Tei index while positively correlated to vitamin D among SCD patients.
CONCLUSIONS: Annexin A1 could be a promising marker of vasculopathy and may provide a biochemical explanation for vitamin D deficiency in SCD.