Aspirin-Induced Acute Haemolytic Anaemia in Glucose-6-Phosphate Dehydrogenase-Def icient Children with Systemic Arthritis

1989 ◽  
Vol 81 (4) ◽  
pp. 208-209 ◽  
Author(s):  
Tullio Meloni ◽  
Gavino Forteleoni ◽  
Augusto Ogana ◽  
Vannina Franca
Keyword(s):  
Haemolytic Anaemia ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Systemic Arthritis

scholarly journals Glucose 6-phosphate dehydrogenase Palermo R257M: a novel variant associated with chronic non-spherocytic haemolytic anaemia

2010 ◽  
Vol 149 (2) ◽  
pp. 296-297 ◽  
Author(s):  
Paolo Rigano ◽  
Carmelo Fabiano ◽  
Fannj Pojero ◽  
Marcello Niceta ◽  
Alice Pecoraro ◽  
...  
Keyword(s):  
Haemolytic Anaemia ◽  
Novel Variant ◽  
Glucose 6 Phosphate Dehydrogenase

Glucose-6-phosphate dehydrogenase deficiency

2020 ◽  
pp. 5472-5479
Author(s):  
Lucio Luzzatto
Keyword(s):  
Haemolytic Anaemia ◽  
Viral Infections ◽  
Selective Advantage ◽  
Screening Tests ◽  
Lumbar Pain ◽  
Dark Urine ◽  
Direct Demonstration ◽  
Life Saving ◽  
High Doses ◽  
Glucose 6 Phosphate Dehydrogenase

Deficiency of the enzyme glucose-6-phosphate dehydrogenase (G6PD) in red blood cells is an inherited abnormality due to mutations of the G6PD gene on the X chromosome that renders the cells vulnerable to oxidative damage. The condition is widespread in many populations living in or originating from tropical and subtropical areas of the world because it confers a selective advantage against Plasmodium falciparum malaria. Clinical features—G6PD deficiency is mostly an asymptomatic trait, but it predisposes to acute haemolytic anaemia in response to exogenous triggers, including (1) ingestion of fava beans—favism; (2) certain bacterial and viral infections; and (3) some drugs—notably some antimalarials (e.g. primaquine), some antibiotics (e.g. sulphanilamide, dapsone, nitrofurantoin), and even aspirin in high doses. Other manifestations include (1) severe neonatal jaundice; and (2) chronic nonspherocytic haemolytic anaemia—the latter is only seen with rare specific genetic variants. The acute haemolytic attack typically starts with malaise, weakness, and abdominal or lumbar pain, followed by the development of jaundice and passage of dark urine (haemoglobinuria). Most episodes resolve spontaneously. Diagnosis relies on the direct demonstration of decreased activity of G6PD in red cells: a variety of screening tests are available, with (ideally) subsequent confirmation by quantitative assay. Prevention is by avoiding exposure to triggering factors of previously screened subjects. Prompt blood transfusion is indicated in severe acute haemolytic anaemia and may be life-saving.

Red blood cells

2016 ◽  
Author(s):  
Shaun R. McCann
Keyword(s):  
Bone Marrow ◽  
Blood Loss ◽  
Red Blood Cells ◽  
Haemolytic Anaemia ◽  
Blood Cells ◽  
G6pd Deficiency ◽  
Paroxysmal Nocturnal Haemoglobinuria ◽  
Globin Chains ◽  
Glucose 6 Phosphate Dehydrogenase

Red blood cells, erythrocytes, are unique in that they do not contain a nucleus. This fact facilitates the study of their metabolism. Erythrocytes contain the protein pigment haemoglobin, which is in solution in the cells and consists of globin chains and iron. In this chapter, the development of the understanding of erythrocytes is linked to the blood conditions haemolytic anaemia and paroxysmal nocturnal haemoglobinuria. Premature destruction of erythrocytes, in the absence of blood loss, is termed haemolysis. If the bone marrow is unable to compensate adequately, then anaemia ensues and the condition is called haemolytic anaemia. The underlying defect is a deficiency in the activity of the enzyme glucose-6-phosphate dehydrogenase, termed G6PD deficiency.

A novel single-base mutation in the glucose 6-phosphate dehydrogenase gene is associated with chronic non-spherocytic haemolytic anaemia

1994 ◽  
Vol 94 (5) ◽  
pp. 560-562 ◽  
Author(s):  
Stefonia Filosa ◽  
Wangwie Cai ◽  
Renzo Galanello ◽  
Antonio Cao ◽  
Domenico De Mattia ◽  
...  
Keyword(s):  
Haemolytic Anaemia ◽  
Single Base ◽  
Dehydrogenase Gene ◽  
Glucose 6 Phosphate Dehydrogenase
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