Paroxysmal Nocturnal Haemoglobinuria Masquerading as Malaria: A Case Report

Dambal, Archana; Nimbal, Naren; Kalsad, Shanmukh T; Pramod, K; Madhavaranga, M P

doi:10.7860/jcdr/2015/13465.6329

Cited by 2 publications

(2 citation statements)

References 7 publications

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“…Somatic mutation in PIG-A gene causes a deficiency of glycosylphosphatidylinositol (GPI), a glycolipid that anchors these proteins onto the cell membrane. Lack of GPI causes loss of CD55 and CD59, leading to excessive destruction of red cells in PNH [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Expression of CD55, CD59, and CD35 on red blood cells of β-thalassaemia patients

Kurtoǧllu

Koçtekin

Kurtoğlu³

et al. 2017

cejoi

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Aim of the studyβ-thalassaemia (β-Thal) is considered a severe, progressive haemolytic anaemia, which needs regular blood transfusions for life expectancy. Complement-mediated erythrocyte destruction can cause both intravascular and extravascular haemolysis. Complement regulatory proteins protect cells from such effects of the complement system. We aimed to perform quantitative analysis of membrane-bound complement regulators, CD55 (decay accelerating factor – DAF), CD35 (complement receptor type 1 – CR1), and CD59 (membrane attack complex inhibitory factor – MACIF) on peripheral red blood cells by flow cytometry.Material and methodsThe present study was carried out on 47 β-thalassemia major (β-TM) patients, 20 β-thalassaemia intermedia (β-TI) patients, and 17 healthy volunteers as control subjects.ResultsCD55 levels of β-TM patients (58.64 ±17.06%) were significantly decreased compared to β-TI patients (83.34 ±13.82%) and healthy controls (88.57 ±11.69%) (p < 0.01). CD59 levels of β-TM patients were not significantly different than β-TI patients and controls, but CD35 levels were significantly lower in the β-TM patients (3.56 ±4.87%) and β-TI patients (12.48 ±9.19%) than in the control group (39.98 ±15.01%) (p < 0.01).ConclusionsLow levels of CD55 and CD35 in thalassaemia major patients indicates a role for them in the aetiopathogenesis of haemolysis in this disease, and also this defect in a complement system may be responsible for the chronic complications seen in these patients.

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Section: Discussionmentioning

confidence: 99%

Expression of CD55, CD59, and CD35 on red blood cells of β-thalassaemia patients

Kurtoǧllu

Koçtekin

Kurtoğlu³

et al. 2017

cejoi

View full text Add to dashboard Cite

show abstract

“…Somatic mutation in phosphatidylinositol glycan class A (PIG-A) gene causes a deficiency of glycosylphosphatidylinositol (GPI), a glycolipid that anchors these proteins onto the cell membrane. Lack of GPI causes loss of CD55 and CD59, leading to excessive destruction of red cells in PNH [22]. This could explain why in our study the CD55 and CD59 expression on the RBCs of β-thalassemia major patients was diminished to below that of the healthy controls, with a statistical significance.…”

Section: Discussionmentioning

confidence: 46%

Role of Complement Regulatory Proteins (CD55, CD59, and CD35) on Red Blood Cells of <i>β</i>-Thalassaemia Patients

Mahmoud¹,

Nasef²,

Eldewi³

et al. 2021

OJBD

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Background: β-thalassaemia (β-Thal) is an inherited chronic haemolytic anaemia resulting from absent or low level of synthesis of β-globin chains of haemoglobin A in erythropoietic cells. The complement system is an important part of innate immune response that may be implicated in red blood cell (RBC) lysis. Mammalian cells are provided with surface bound complement regulatory proteins (MCRPs) that regulate the activation of complement cascade, thus protecting them from uncontrolled complement-mediated lysis. Objective is to evaluate the role of complement regulatory proteins (CD55, CD59, and CD35) on red blood cells, and to explain the pathogenesis of anaemia in β-thalassemia major. Methods: This case-control study enrolled 74 β thalassemia major patients who were compared with 40 age and sex matched controls. We performed expression of CD55, CD59, and CD35 on RBCs using flow cytometry. Results: CD55 levels of β-thalassemia major patients (79.78% ± 18.54%) were significantly decreased compared to healthy controls (99.45% ± 0.59%) (P < 0.001). CD59 levels of β-thalassemia major patients (97.76% ± 1.72%) were significantly lower than in the controls (99.75% ± 0.36%) (P < 0.001), also CD35 levels were significantly lower in the β-thalassemia major patients (4.30% ± 4.66%) than in the control group (19.40% ± 10.90%) (P < 0.001). Conclusion: β-thalassemia major patients suffer from increased haemolysis and a consequent increase in their demand for blood transfusion. Complement-mediated haemolysis was shown in our study by decreased expression of CD55, CD59, and CD35 in β-thalassemia major patients. This allows complement deposition on RBCs and enhances or accelerates their lysis.

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Paroxysmal Nocturnal Haemoglobinuria Masquerading as Malaria: A Case Report

Cited by 2 publications

References 7 publications

Expression of CD55, CD59, and CD35 on red blood cells of β-thalassaemia patients

Expression of CD55, CD59, and CD35 on red blood cells of β-thalassaemia patients

Role of Complement Regulatory Proteins (CD55, CD59, and CD35) on Red Blood Cells of <i>β</i>-Thalassaemia Patients

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Paroxysmal Nocturnal Haemoglobinuria Masquerading as Malaria: A Case Report

Cited by 2 publications

References 7 publications

Expression of CD55, CD59, and CD35 on red blood cells of β-thalassaemia patients

Expression of CD55, CD59, and CD35 on red blood cells of β-thalassaemia patients

Role of Complement Regulatory Proteins (CD55, CD59, and CD35) on Red Blood Cells of &lt;i&gt;β&lt;/i&gt;-Thalassaemia Patients

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Role of Complement Regulatory Proteins (CD55, CD59, and CD35) on Red Blood Cells of <i>β</i>-Thalassaemia Patients