Sickle cell anemia

Sickle cell disease (SCD) can pose serious maternal and fetal risk in pregnancy. Transfusion, both during and outside of pregnancy, can improve patient morbidity and mortality but carries risk of alloimmunization, complicating future management.

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Continued part 1, part 2 of ebook "Transfusion management of the obstetrical patient: A clinical casebook" provide readers with content about: importance of getting a sample for ABO type early in a resuscitation; risks of giving uncrossmatched red cells; management of thrombotic microangiopathies in pregnancy; hyperhemolysis syndrome in a pregnant woman with sickle cell anemia; fetal and neonatal alloimmune thrombocytopenia; warm autoantibodies during pregnancy;...

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Global standards require that spirometry should be performed by trained and experienced personnel, who would be able to assess the correct performance of tests by patients and assure good quality of the result.

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Understanding the genetics underlying the heritable subphenotypes of sickle cell anemia, specific to each population, would be prognostically useful and could inform personalized therapeutics.

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Preclinical studies have evaluated haptoglobin (Hp) polymers from pooled human plasma as a therapeutic protein to attenuate toxic effects of cell-free hemoglobin (Hb). Proof of concept studies have demonstrated efficacy of Hp in hemolysis associated with transfusion and sickle cell anemia.

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Children with sickle cell anemia (SCA) are highly susceptible to stroke and other manifestations of pediatric cerebral vasculopathy. Detailed evaluations in sub-Saharan Africa are limited.

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In resource-poor settings, transfused children often experience recurrence of severe anemia (SA) following discharge from hospital. This study determined the factors associated with recurrent severe anemia (RSA) among previously transfused Ugandan children aged less than 5 years.

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Sickle cell anemia is a serious genetic health problem dominated in Tharu community of western Nepal. Molecular methods like PCR and RFLP are the best method to identify Sickle c ell anemia trait. Molecular analysis needed many steps and expensive chemicals and Kits. The aim of this research was to develop a simple and cheapest method to process from whole blood sample for the polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) without the use of expensive reagents and Kits.

8p nguathienthan1 27-11-2019 26 0   Download

Accelerated oxidative damage is one of the hallmarks in both sickle cell disease (SCD) and thalassemia major (TM). A decreased antioxidant level is found in both diseases. Our study was carried out to evaluate the variation in serum levels of Selenium and Vitamin E among a group of transfusion dependant Egyptian SCD and TM patients, further more to correlate these levels with iron overload status or transfusion requirements.

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Uncovering Recurrent Submicroscopic Rearrangements As a Cause of Disease For five decades since Fred Sanger's (1) seminal discovery that proteins have a specific structure, since Linus Pauling's (2) discovery that hemoglobin from patients with sickle cell anemia is molecularly distinct, and since Watson and Crick's (3) elucidation of the chemical basis of heredity, the molecular basis of disease has been addressed in the context of how mutations affect the structure, function, or regulation of a gene or its protein product.

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Tham khảo sách 'diseases and disorders: personality disorders', y tế - sức khoẻ, y học thường thức phục vụ nhu cầu học tập, nghiên cứu và làm việc hiệu quả

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Only one randomized trial, the Multicenter Study of Hydroxyurea for Sickle Cell Anemia (MSH Study), tested the efficacy of hydroxyurea in adults with sickle cell anemia, with six additional analyses either based on this trial or on followup studies. The significant hematological effects of hydroxyurea after 2 years (as compared to the placebo arm) included a small mean increase of 0.6 g/dl in total hemoglobin and a moderate absolute increase in fetal hemoglobin of 3.2 percent.

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Sickle cell disease is a genetic disorder that decreases life expectancy by 25 to 30 years and affects approximately 80,000 Americans. Individuals are diagnosed with sickle cell disease if they have one of several genotypes that result in at least half of their hemoglobin being hemoglobin S (Hb S). Sickle cell anemia refers specifically to the condition associated with homozygosity for the Hb S mutation (Hb SS). Several other hemoglobin mutations, when occurring with an Hb S mutation, cause a similar but often milder disease than sickle cell anemia.

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Tuyển tập các báo cáo nghiên cứu về hóa học được đăng trên tạp chí sinh học đề tài : Hydroxyurea and sickle cell anemia: effect on quality of life

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Balogun et al. Journal of Orthopaedic Surgery and Research 2010, 5:2 http://www.josr-online.com/content/5/1/2 RESEARCH ARTICLE Open Access Spectrum of musculo-skeletal disorders in sickle cell disease in Lagos, Nigeria Rufai A Balogun†, Dike C Obalum*†, Suleiman O Giwa†, Thomas O Adekoya-Cole†, Chidiebere N Ogo†, George O Enweluzo† Abstract Background: Sickle cell anemia (SCA) is a common genetic disease in Nigeria. Past studies from West Africa focused on isolated aspects of its medical and surgical presentations.

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Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Salmonella pyomyositis complicating sickle cell anemia: a case report...

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Clinical Manifestations of Sickle Cell Trait Sickle cell trait is usually asymptomatic. Anemia and painful crises are exceedingly rare. An uncommon but highly distinctive symptom is painless hematuria often occurring in adolescent males, probably due to papillary necrosis. Isosthenuria is a more common manifestation of the same process. Sloughing of papillae with urethral obstruction has been reported, as have isolated cases of massive sickling or sudden death due to exposure to high altitudes or extremes of exercise and dehydration.

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Clinical Manifestations of Sickle Cell Anemia Most patients with sickling syndromes suffer from hemolytic anemia, with hematocrits from 15–30%, and significant reticulocytosis. Anemia was once thought to exert protective effects against vasoocclusion by reducing blood viscosity. However, natural history and drug therapy trials suggest that an increase in the hematocrit and feedback inhibition of reticulocytosis might be beneficial, even at the expense of increased blood viscosity. The role of adhesive reticulocytes in vasoocclusion might account for these paradoxical effects.

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Classes There are five major classes of hemoglobinopathies (Table 99-1). Structural hemoglobinopathies occur when mutations alter the amino acid sequence of a globin chain, altering the physiologic properties of the variant hemoglobins and producing the characteristic clinical abnormalities. The most clinically relevant variant hemoglobins polymerize abnormally, as in sickle cell anemia, or exhibit altered solubility or oxygen-binding affinity. Thalassemia syndromes arise from mutations that impair production or translation of globin mRNA, leading to deficient globin chain biosynthesis.

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Hemolytic disorders that cause excessive heme production may be either inherited or acquired. Inherited disorders include spherocytosis, sickle cell anemia, thalassemia, and deficiency of red cell enzymes such as pyruvate kinase and glucose-6-phosphate dehydrogenase. In these conditions, the serum bilirubin rarely exceeds 86 µmol/L (5 mg/dL). Higher levels may occur when there is coexistent renal or hepatocellular dysfunction or in acute hemolysis such as a sickle cell crisis.

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