Cause Of Hemolytic Anemia Research Articles

Anémie hémolytique immunoallergique due à l'ambroxol

Introduction Drug-induced immune hemolytic anemia is a rare cause of hemolytic anemia. Case record A 68-year-old male patient developed an acute intravascular hemolysis with acute renal failure. Common causes of hemolysis were ruled out and the patient rapidly improved. An immune mechanism was confirmed by the positivity of the direct antiglobulin test with anti-IgA in the presence of ambroxol only, one of the drug the patient had received during 6 days before hospitalization. Discussion To our knowledge, this is the first report of ambroxol-induced immune hemolytic anemia. This case also underlined that the direct antiglobulin test should also be performed with anti-IgA to ruled out any false negative.

Anemia secundaria a déficit de piruvato cinasa en sucesivas gestaciones

Pyruvate kinase deficiency is a rare cause of hemolytic anemia. During pregnancy, severe cases have traditionally been treated with prophylactic blood transfusions to maintain the hemoglobin concentration above arbitrary thresholds of 7-8 g/dL. Case report A case of hemolytic anemia due to pyruvate kinase deficiency was discovered during the first pregnancy of a 32-year-old woman. The anemia was treated with blood transfusions. In a second pregnancy, the patient required a greater number of transfusions to keep the hemoglobin concentration above 7 g/dL. Both newborns were healthy and had adequate birth weight for gestational age. Conclusions This kind of anemia is rare and sometimes occurs in special situations such as pregnancy, infection, or stress.

Anästhesie bei Patienten mit Glukose-6-Phosphat-Dehydrogenase-Mangel

Glucose-6-phosphate dehydrogenase (G6PD) deficiency, a frequent congenital human enzyme defect, is the most frequent cause of hemolytic anemia triggered by drugs or infectious diseases. Drugs which induce acute hemolysis in patients with G6PD deficiency are often used in anesthesia and perioperative pain therapy. Considering the fact that patients from geographic regions with a high prevalence of the disease are often treated in European hospitals, special attention should be paid to this problem. We report a case of a 30-year-old female patient with favism and review the disease and anesthesia-related implications.

Infantile pyknocytosis: a cause of haemolytic anaemia of the newborn

This study defined the incidence, clinical and haematological characteristics of infantile pyknocytosis in a monocentric retrospective study of 149 blood samples referred for unexplained neonatal haemolytic anaemia. Pyknocytosis was diagnosed in 14 patients (9.4%). All patients had neonatal jaundice and severe anaemia (mean nadir haemoglobin: 6.8 g/dl) at a mean age of 21 d. The percentage of pyknocytes was 4-23%. Packed red blood cell transfusions were needed in 11 of 14 patients. Haemoglobin levels reached normal values within a mean time of 4 months. Infantile pyknocytosis is an unusual cause of neonatal haemolytic anaemia, which requires careful examination of blood smears.

A child with recurrent episodes of dark urine: answer

Glucose-6-phosphate dehydrogenase (G6PD) screening and Heinz body preparation are both negative, and the haptoglobin level is decreased at 2.2 mg/dl (normal range: 27–139 mg/dl). C3 and C4 complement levels are normal, and the antinuclear antibody titer, anti-streptolysin O titer and Coombs tests are all negative. The paucity of intact red blood cells and the presence of pigment casts in the urinary sediment in this dark reddish-brown urine suggest the presence of hemoglobin or myoglobin. The moderate anemia, elevated reticulocyte count, and decreased haptoglobin are consistent with intravascular hemolysis. There are autoimmune causes of hemolytic anemia and G6PD deficiency can cause hemolytic anemia, but the Coombs test and G6PD preparation are normal. The fact that more than one hematopoietic cell line is abnormal suggests a clonal disorder. The history of mild leukopenia, thrombocytopenia, and hemolysis is consistent with paroxysmal nocturnal hemoglobinuria. The presence of a cell population lacking decay-accelerating factor (DAF) on the cell membrane determined by flow cytometric analysis with anti-DAF fluorescent antibody confirms the diagnosis.

Current concepts in feline haemobartonellosis

HAEMOBARTONELLA felis is an important cause of haemolytic anaemia in cats. Over the past five years significant advances in the understanding of this organism have been made, which have led...

Hemolysis and Methemoglobinemia Secondary to Rasburicase Administration

To report a case of hemolytic anemia and methemoglobinemia developing after rasburicase administration to a patient with glucose-6-phosphate dehydrogenase (G6PD) deficiency. A 50-year-old African American man was hospitalized with new onset seizure, diabetic ketoacidosis, respiratory failure, and acute renal failure. Serum uric acid concentrations were elevated, and the patient was treated with one dose of intravenous rasburicase 22.5 mg for acute renal failure secondary to hyperuricemia. Routine arterial blood gas analyses performed after rasburicase was administered revealed elevated methemoglobin concentrations, which peaked at 14.7%. Hemolytic anemia developed as evidenced by a fall in blood hemoglobin from 14.8 to 5.3 g/dL. The patient made a full recovery following aggressive fluid therapy, blood transfusions, and respiratory support. G6PD deficiency was subsequently confirmed. The Naranjo probability scale indicated that rasburicase was a probable cause of hemolytic anemia and methemoglobinemia. Rasburicase is contraindicated in patients with G6PD deficiency as it may cause hemolytic anemia and methemoglobinemia. As of September 26, 2005, simultaneous occurrence of hemolytic anemia and methemoglobinemia has not been reported in patients receiving rasburicase. As of September 26, 2005, screening for G6PD deficiency should be performed whenever possible prior to chemotherapy administration in patients at risk of developing tumor lysis syndrome.

Paroxysmal Nocturnal Hemoglobinuria

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare hemolytic disorder of acquired origin and is clinically manifested by chronic hemolysis, thromboses in various sites, and bone marrow failure. The disease is so rare that the delay in the diagnosis is not uncommon and this bears a tremendous impact on patient management. We present this case to draw attention to this uncommon cause of hemolytic anemia, which should be considered in any patient, of any age, who has signs of chronic hemolysis.

Ｃ型肝炎患者におけるリバビリン誘導性貧血及び酸化ストレスに対するエイコサペンタエン酸の効果

A major side effect of ribavirin (RBV) is a hemolytic anemia. One of the causes of hemolytic anemia is considered to be oxidative stress to erythrocytes. Recently, a beneficial effect of eicosapentaenoic acid (EPA) for ribavirin-induced anemia has been reported. This study evaluated effects of EPA for ribavirin-induced anemia and thioredoxin (TRX) as an indicator of oxidative stress in chronic hepatitis C patients within 8 weeks. Nighteen of 41 patients who had received interferon/ribavirin therapy were treated with EPA (1800 mg/day) (EPA group). EPA therapy significantly prevented progression of anemia (P<0.01). Moreover, serum TRX levels were significantly decreased in EPA group at 4 weeks (P<0.01). Reduction of oxidative stress by EPA might play an important role for preventing ribavirin-induced anemia.

Xerocitosis congénita

Hereditary xerocytosis is a genetic disease inherited as an autosomal dominant trait and is a rare cause of hemolytic anemia. It is caused by abnormal erythrocyte membrane permeability: monovalent cation pump activity is increased and the Na/K pump cannot compensate for the K lost. As a consequence, xerocytes dehydrate, becoming rigid and sensitive to metabolic stress and oxidation. Morbility depends on the severity of the hemolytic anemia. Periodic episodes of jaundice are common during mild infections; most patients remain asymptomatic but experience mild-to-moderate hemolytic anemia, which is generally well compensated. The diagnostic clues are a markedly increased flow through the Na/K pump with a decrease in total intracellular cation content and subsequent red cell dehydration. Treatment is based on monitoring for eventual complications and careful observation during infections, which may worsen the anemia. Splenectomy is not useful and for some authors may even be contraindicated. The prognosis is generally very good. We report the case of a patient with episodes of hemolytic anemia during intercurrent infections and positive diagnostic tests for hereditary xerocytosis.

A pilot study of eicosapentaenoic acid therapy for ribavirin-related anemia in patients with chronic hepatitis C

One of the major side effects of ribavirin/interferon alpha combination therapy for chronic hepatitis C is hemolytic anemia. One of the causes of hemolytic anemia is considered to be decreasing deformability of erythrocytes resulting from the accumulation of phosphorylated ribavirin in erythrocytes. The administration of eicosapentaenoic acid (EPA), which has a wide variety of pharmacological actions, increases the deformability of erythrocytes. We conducted an uncontrolled pilot study of EPA therapy for patients with ribavirin-related anemia. Six patients with chronic hepatitis C, who had developed anemia while receiving combination therapy, were treated with an oral ethyl ester of EPA (1800 mg/day) for two months. The hemoglobin level of all six patients increased following EPA therapy. The mean hemoglobin level significantly increased from 10.8 g/dl to 11.4 g/dl one month after therapy was initiated (P<0.05), and this level was obtained again one month later (11.5 g/dl). None of the patients developed an adverse reaction. These findings suggest that EPA has a beneficial effect in patients with ribavirin-related anemia. Further study is required to confirm our results.

Iron and iron proteins found in the genetic disease, hereditary spherocytosis

Hereditary spherocytosis (HS) is a disorder of the red blood cell (RBC) membrane, characterized by abnormally fragile and spherical RBCs. It is the predominant cause of haemolytic anaemia in people of northern European descent. Owing to the increased rate of RBC synthesis that is characteristic of the condition, it may result in an increase in absorption of iron from the diet by the affected individual. Ultimately, pathological iron overload may develop. Fortunately, the condition responds well to surgical removal of the spleen (splenectomy). In this project, iron studies were performed on a set of spleen tissue samples obtained following routine splenectomy for HS. Cell architecture and level of deposition of haemosiderin, the distinctive form of iron found in iron-loaded tissues, were assessed. The tissue iron content was determined by AAS and ICP (mean value=2276±507 μg g−1 dry tissue, values reported for normal spleens range from 972±60 to 1345±190 μg g−1). Ion exchange chromatography was employed to separate the protein content of the tissue into four chromatographic bands, notionally transferrin, ferritin, haemprotein and haemosiderin, and these proteins quantified. Mössbauer spectroscopy identified the iron as Fe(III), predominantly in ferrihydrite (5Fe2O3·9H2O) and haem environments within the tissue. Typical spectral parameters, recorded at 300 K, were: isomer shift and quadrupole splitting of 0.36 and 0.62 mm s−1, respectively, (ferrihydrite) and 0.14 and 1.97 mm s−1 (haem). The results indicate a condition corresponding to mild iron overload.

Anemia hemolítica secundaria a regurgitación periprotésica

Rev Esp Cardiol 2002;55(9):987 987 A 73-year-old woman was admitted for severe anemia 2 months after mitral and aortic cardiac valve replacement with Saint Jude mechanical prostheses. The differential blood count showed macrocytic anemia (hemoglobin 7.1 g/dL; MCV 111 fl; corrected reticulocyte count, 3.5%). The blood smear revealed marked anisopoikilocytosis, intense polychromasia, and abundant schistocytes (Figure 1, arrows). Total bilirubin was 1.76 mg/dL (indirect bilirubin, 1.36 mg/dL). LDH was markedly increased (5259 U/L) and haptoglobin reduced (6.0 mg/dL; normal, 100-300 mg/dL), which was compatible with intravascular hemolysis. The serum was brownish colored secondary to hemoglobinemia and the presence of methemalbuminemia, a product of erythrocyte fragmentation, which originates a characteristic color (Figure 2 A). The urine had a similar color (Figure 2 B). Transesophageal echocardiography revealed severe mitral periprosthetic regurgitation (Figure 3), as well as moderate aortic periprosthetic regurgitation. Conservative treatment was attempted, but the patient required a large number of transfusions (more than 2 units of packed red blood cells per week), so surgical repair was decided on. Mitral and aortic cardiac valve replacement was performed with Carpentier-Edwards biological prostheses, with good results. The most frequent causes of hemolytic anemia in patients undergoing valve replacement are mechanical trauma by disks to red blood cells and periprosthetic regurgitation. The treatment is generally medical, but surgical repair is required for periprosthetic regurgitation.

The immune haemolytic anaemias: a century of exciting progress in understanding.

The immune haemolytic anaemias: a century of exciting progress in understanding.

Deficiencies of glycolytic enzymes as a possible cause of hemolytic anemia

The critical minimum values of Na,K-ATPase and glycolytic enzyme activities at which the erythrocyte viability is lost were calculated using the mathematical model of the erythrocyte, which included all reactions of glycolysis, adenylate metabolism, ionic balance, and osmotic regulation of erythrocyte volume. The criterion for cell death was an increase in its volume to the level at which it is sequestrated from the circulation or is lysed. In hemolytic anemia associated with hexokinase or pyruvate kinase deficiency, activities of these enzymes measured in patient erythrocytes appeared to be close to the calculated critical values. By contrast, in hemolytic anemia associated with phosphofructokinase, glucosephosphate isomerase, triosephosphate isomerase, or phosphoglycerate kinase deficiency, activities of these enzymes measured in patient erythrocytes were significantly greater than the calculated critical values. In this case, if the deficient enzyme were stable, i.e. its activity in the cell were low, but constant in time, the deficiency observed would not account for the erythrocyte destruction observed and the development of hemolytic anemia. It was shown, however, that in phosphofructokinase, glucosephosphate isomerase, triosephosphate isomerase, or phosphoglycerate kinase deficiency, hemolytic anemia can arise because of the instability of these enzymes in time.

The molecular basis of disorders of the red cell membrane.

Haemolytic anaemia denotes a state in which there is an increased rate of red cell destruction. It can be classified on the basis of whether the defect is intrinsic to...

Disorders of the red cell membrane

Summary Red cell membrane defects are a common cause of haemolytic anaemia—hereditary spherocytosis (HS) alone affects between 1 in 2500 and 1 in 5000 individuals and are due to defects in either the quality or quantity of the proteins of the cytoskeleton. They present a heterogeneous clinical picture varying from severe transfusion-dependent anaemia to an incidental finding in completely well individuals. In this review, the author will concentrate on two conditions: HS and elliptocytosis.

Congenital Erythrocyte Enzyme Deficiencies

Congenital hemolytic anemias resulting from PK, PFK, and G6PD enzyme deficiencies have been reported in domestic animals. Dogs with PFK deficiency may have episodes of intravascular hemolysis with hemoglobinuria in addition to a persistent compensated hemolytic anemia. Patients with mild G6PD deficiency are not anemic but may show increased susceptibility to oxidant-induced erythrocyte injury. Persistent methemoglobinemia has been reported in dogs and cats with methemoglobin reductase enzyme deficiency. Affected animals have cyanotic-appearing mucous membranes but show no or only mild clinical signs attributable to hypoxemia. Enzyme assays are usually done after acquired causes of hemolytic anemia and methemoglobinemia have been ruled out.

HEMOLYTIC DISORDERS ASSOCIATED WITH CANCER

Three principal environmental causes of hemolytic anemia in malignancy have been identified: (1) hemolysis mediated by auto-antibodies to red cells; (2) hemolysis due to microangiopathic disorders; and (3) chemotherapy-induced red cell destruction. These three environmental stressors occur rarely in cancer patients, and they form the subject of this review.

Hemolytic anemia and cancer

One of the most fundamental tenets of medical diagnosis is that when presented with a complex problem, the clinician attempts to make a single, unifying diagnosis. In approaching the problem of hemolytic anemia in the patient with cancer, it is often difficult to adhere to this tenet. The underlying diagnosis is cancer, which frequently causes hypoproductive anemias through chronic inflammation or infiltration of the bone marrow. Cancers can also cause hyperproductive anemias from blood loss and hemolytic anemias. The problem for the clinician then, is to examine the anemia in the cancer patient with the starting premise that the patient may have one, two or even three causes of anemia. Against this background, the problem of hemolytic anemia in the patient with cancer is reviewed. The causes of hemolytic anemia are divided into microangiopathic hemolytic anemia, enzymopathies, hemoglobinopathies, hemophagocytic syndrome, immune, chemotherapy-induced and hypersplenism. Each of these major mechanisms is defined and discussed in terms of pathophysiology, clinical factors and therapy.