Case Of Severe Hemolytic Anemia Research Articles

Acute Hemolytic Anemia Caused by G6PD Deficiency in Children in Mayotte: A Frequent and Severe Complication.

Severe hemolytic anemia is a rare complication of glucose-6-phosphate dehydrogenase (G6PD) deficiency. It occurs with the Mediterranean (Med) variant corresponding to a class 2 deficiency according to the World Health Organization (WHO) classification, and it correlates with a severe deficiency in G6PD activity. In Mayotte, the majority of patients have the African (A-) variant as a WHO class 3 deficiency. Yet we have observed numerous cases of severe hemolytic anemia defined by a hemoglobin level of <6 g/dL. In this study, we aimed to describe the epidemiological, clinical, and biological features as well as the treatment modalities of children presenting with a severe hemolytic crisis secondary to G6PD deficiency in Mayotte. The secondary objective was to study the disease genotype when this information was available. Between April 2013 and September 2020, 73 children presented with severe anemia because of G6PD deficiency in Mayotte. The median hemoglobin level during the hemolytic crises was 3.9 g/dL. All of the patients underwent a transfusion and hospitalization. Twenty patients had a disease genotype: 11 had the African mutation and 9 had the Med mutation. Although they are among the most common triggers of G6PD acute hemolytic anemia, drugs were found to not be present and fava bean ingestion was found in only 1 child. One of the specific triggers was traditional medicine, including Acalypha indica . Severe hemolytic crisis in children because of G6PD deficiency is a frequent occurrence in Mayotte. The patients had severe disease symptoms, but the severity did not correlate with the genotype: the African (A-) variant and the Med variant resulted in the same level of disease severity.

Severe hemolytic anemia and acute renal failure after mitral valve repair associated with non-endothelialization of artificial chordae tendinae: case report

BackgroundMechanical hemolytic anemia and acute renal failure are rare complications of mitral valve repair.Case presentationWe report a unique case of severe hemolytic anemia and severe acute renal failure after mitral valve repair using artificial chordae tendinae. Conservative therapy including plasmapheresis and blood transfusion was not effective. The major cause of the mechanical hemolysis was mild mitral regurgitation originating from the centre of the valve and striking the annuloplasty ring. The hemolytic anemia resolved gradually after the replacement of mitral valve. The new artificial chordae tendinae was found to be completely non-endothelialized in the surgery. Non-endothelialization of artificial chordae tendinae may also play a role in the genesis of mechanical anemia.ConclusionsThe major cause of the mechanical hemolysis was mild mitral regurgitation originating from the centre of the valve and striking the annuloplasty ring. Non-endothelialization of foreign materials might be another mechanism of hemolysis after mitral repair.

Intravascular hemolysis and methemoglobinemia from high dose vitamin C

Background: Vitamin C is often used by complementary and alternative medicine practitioners for its antioxidant properties. We describe a case of severe hemolytic anemia and methemoglobinemia paradoxically resulting from an oxidative stress of high dose vitamin C in a patient with previously undiagnosed glucose-6-phosphate dehydrogenase (G6PD) deficiency. Case Presentation: A 47-year-old man presented with severe hemolytic anemia and methemoglobinemia days after receiving 395 g of intravenous (IV) vitamin C at an alternative medicine practice. He was managed conservatively with transfusions and his hemolysis subsided after several days. His G6PD level, measured months after his presentation, was deficient at 0.4 units/g. Conclusion: While vitamin C is often considered an antioxidant, its utilization in tissues produces its oxidized form (dehydroascorbic acid) which depletes intra-erythrocyte stores of glutathione. Patients with G6PD deficiency have reduced abilities to restore intracellular glutathione, placing them at risk for oxidative stress, and subsequent hemolysis that can be life threatening.

A Severe Episode of Hemolytic Anemia After Amoxicillin Exposure in A G6PD Deficient Patient.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzyme deficiency worldwide, with genetic variants resulting in a range of phenotypes that vary from asymptomatic to severe hemolysis. We report a case of severe hemolytic anemia in a G6PD deficient patient whose only known exposure was amoxicillin two weeks prior to his episode of severe hemolysis, for which he presented to our hospital. An extensive infectious and hematologic workup resulted negative with the exception of a positive G6PD deficiency result. Although rare, we suggest that the patient’s severe hemolytic anemia is possibly related to amoxicillin exposure.

Discoid lupus erythematosus: First clue to autoimmune haemolytic anaemia in a child

Introduction Discoid lupus erythematosus (DLE) is uncommon in the first decade of life. It has been described as part of systemic lupus erythematosus (SLE) or in isolation in adults. We report a case of severe haemolytic anaemia with discoid lesions that gave a clue to diagnosis and management.

Impella induced massive hemolysis: reemphasizing echocardiographic guidance for correct placement.

The Impella LP 2.5 (Abiomed, Danvers, MA) has been a tool of use for high risk coronary procedures and for cardiogenic shock. As with any invasive or intracardiac device, improper placement can result in disastrous complications. Hemolytic anemia secondary to Impella implantation is one of the documented complications. However, cases of severe hemolytic anemia are rare in the literature. Proven imaging modalities like ultrasound need to be used to guide proper placement. We present a case of device induced severe hemolysis due to Impella insertion and the need to use ultrasound guidance to avoid such an unnecessary complication.

A Case of Severe Hemolytic Anemia and Acute Renal Failure Caused by Rfp

A Case of Severe Hemolytic Anemia and Acute Renal Failure Caused by Rfp

Severe non-valve-related hemolytic anemia following aortic root replacement

Aortic interposition grafting combined with aortic root replacement (conduit) is widely performed to manage thoracic aortic aneurysms. Intravascular hemolysis without clinical significance is occasionally observed as a complication after prosthetic valve replacement. Symptomatic lysis of red blood cells (RBCs) is rare and primarily attributed to mechanical damage as result of high shear stress, turbulent flow, and physical interaction. We report a case of severe hemolytic anemia shortly after mechanical conduit implantation. The RBC damage was not related to the valve prosthesis and resolved completely after replacement of a section of the kinked Dacron tube graft to correct a fold.

Mycoplasma pneumoniae associated with severe autoimmune hemolytic anemia: case report and literature review

We report a case of severe hemolytic anemia following Mycoplasma pneumoniae infection in a 29-year-old male patient who was treated with azithromycin. Direct Coombs' test was strongly positive and the cold agglutinin titer was high, with anti-I specificity. Antimycoplasma antibody titer by complement fixation was high 1:10,240. The patient was discharged after 12 days of hospitalization in good health. He remains clinically well with no recurrence of jaundice.

A case of severe hemolytic anemia induced mitral valve replacement after 20 years

A case of severe hemolytic anemia induced mitral valve replacement after 20 years

Comment on: Severe hemolytic anemia and fatal hepatic failure associated with nimesulide

I read with interest the paper about a case of severe hemolytic anemia and fatal hepatic failure associated with prolonged nimesulide use [ [1] Betrosian AP, Flevari K, Andrianakis I, Boudouri I, Douzinas EE. Severe hemolytic anemia and fatal hepatic failure associated with nimesulide. Dig Liver Dis; 2008, doi:10.1016/j.dld.2008.06.013. Google Scholar ], considering that apparently only one case of this association has previously published [ [2] Rodrigo L. de Francisco R. Pérez-Pariente J.M. Cadahia V. Tojo R. Rodriguez M. et al. Nimesulide-induced severe hemolytic anemia and acute liver failure leading to liver transplantation. Scand J Gastroenterol. 2002; 37: 1341-1343 Crossref PubMed Scopus (31) Google Scholar ]. In fact, spontaneous reports of adverse drug events are helpful warning signals of rare toxicities.

Hemolytic anemia after atrioventricular septal defect repair without synthetic material

We report a rare case of severe hemolytic anemia following repair of a congenital heart defect without the use of prosthetic material. A review of the literature, diagnosis, and management are described. Although this is an unusual complication following congenital heart surgery, a high index of suspicion must be maintained and a possible mechanical cause should be sought and corrected.

Introduction to discussion of Heinz body anemias—Unstable hemoglobinopathies

During the past 18 years, numerous cases of “congenital Heinz body anemia” have been reported. It is now clear that unstable, thermolabile hemoglobins are present in most or all such cases. Unstable hemoglobins Zurich. H. Koln, Hasharon and L Ferrara have been reported in more than one family. Most of the unstable hemoglobins may be attributed to point mutations in the genetic code, such as a change from guanine to adenine. Nearly 30 such unstable hemoglobinopathies have been characterized from the standpoint of the molecular pathology—that is, the change in structure of the globin chains of hemoglobin. The manner by which these molecular changes cause instability of the hemoglobin molecule seems to be variable, but very likely the effect in most is to loosen the bond between heme and globin, followed by formation of mixed disulfides and denaturation and precipitation of globin. Erythrocytes that contain unstable hemoglobins may exhibit accelerated glucose consumption, low glutathione concentration, decreased glutathione stability, and low concentrations of adenosine triphosphate. The rate of methemoglobin formation and of in vitro autohemolysis may be increased. Oxygen dissociation is abnormal in some of these disorders. The inheritance of these disorders is commonly autosomal dominant. Hemolysis may be mild to severe; it may occur only after sulfonamide ingestion or may not be demonstrable at all. Splenectomy has been beneficial in a few cases of severe hemolytic anemia due to unstable hemoglobinopathy.

Acute hemolytic anemia in childhood with unusual cardiac manifestation

Summary A case of severe hemolytic anemia with icterus of the Lederer type is reported, characterized by the following: 1. Sudden onset with high fever, jaundice, leucocytosis, and severe anemia. 2. Evidence of rapid and enormous blood destruction. 3. Hemoglobinuria. 4. Mechanical interference of renal function. 5. The presence of apical systolic and aortic diastolic hemic murmurs added unusually interesting features to this case. 6. Prompt and permanent recovery following a single transfusion. 7. The causative agent is unknown.