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Analysis of CD177 neutrophil expression in β‐thalassemia patients
Author(s) -
MONTASER LAILA MAHMOUD,
ELRASHIDI FARIDA HUSSEIN,
ESSA ENAS SAID,
AZAB SAMAR MOSTAFA
Publication year - 2011
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1600-0463.2011.02755.x
Subject(s) - thalassemia , medicine , erythropoiesis , beta thalassemia , immunology , ineffective erythropoiesis , transferrin , immunoassay , gastroenterology , endocrinology , anemia , antibody
Montaser LM, El‐Rashidi FH, Essa ES, Azab SM. Analysis of CD177 neutrophil expression in β‐thalassemia patients. APMIS 2011; 119: 674–80. Ineffective erythropoiesis plays a well established role in the pathophysiology of disease expression in β‐thalassemia major and intermedia. CD177 expression was investigated in different clinical conditions. The study aimed to analyze neutrophil expression of CD177 in β‐thalassemia patients and its correlation with serum soluble transferrin receptor (s‐TfR) concentration as a marker for the extent of erythropoiesis and hence disease severity in these patients. Flow cytometric analysis of neutrophil CD177 expression and enzyme immunoassay measurement of serum s‐TfR concentration were assessed in 45 β‐thalassemia patients of whom 36 had β‐thalassemia major and nine had β‐thalassemia intermedia. They were also assessed in 21 age‐ and gender‐matched control children. Neutrophil mean fluorescence intensity ratio (MFIR) of CD177 expression was significantly higher in patients than in controls (p < 0.001). There was highly significant increase in serum s‐TfR concentration in β‐thalassemia patients than in controls (p < 0.001). There was a highly significant positive correlation between MFIR of CD177 expression and serum s‐TfR concentration in β‐thalassemia patients (r = 0.59, p < 0.001). Elevated CD177 expression is not only a specific feature of polycythemia rubra vera (PV) but may be also an indicator of increased erythropoietic activity in thalassemia syndromes.

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