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Anemia (Hemolytic)
Published in Charles Theisler, Adjuvant Medical Care, 2023
Red blood cells carry oxygen for every cell (except cartilage and the cornea) throughout the entire body. Hemolytic anemia is a condition in which red blood cells are prematurely destroyed and removed from the bloodstream before their normal lifespan is over. When destruction of red blood cells outpaces the bone marrow’s production of these cells, hemolytic anemia occurs. Like other anemias, hemolytic anemia can cause pallor, fatigue, dizziness, and low blood pressure. Yellowing of the skin and whites of the eyes (jaundice), dark urine, shortness of breath, and a rapid heart rate or an enlarged spleen may also occur.1
Carrier Screening For Inherited Genetic Conditions
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
Whitney Bender, Lorraine Dugoff
Alpha-thalassemia results from a gene deletion of two or more copies of the four alpha-globin genes on chromosome 16. It is common among individuals of Southeast Asian, African, West Indian, and Mediterranean ancestry. Deletion of two genes, alpha-thalassemia trait, causes a mild hemolytic anemia. The deletions may occur on the same chromosome (cis aa/-) or on two different chromosomes (trans a-/a-). Individuals of Southeast Asian descent are more likely to carry the cis configuration compared to their African counterparts. Individuals with alpha-thalassemia trait are at increased risk for having a child with a more severe form of alpha-thalassemia. Hemoglobin H disease is caused by the deletion of three alpha-globin genes. Affected individuals have mild to moderate hemolytic anemia. Alpha-thalassemia major (Hb Bart disease) results from the absence of functional alpha-globin genes. Fetal hydrops and intrauterine fetal demise is the expected outcome in these cases due to the inability to produce functional HbF. Hemoglobin Bart disease does not usually occur in fetuses of alpha-thalassemia carriers of African origin, since individuals of African descent usually have the trans-configuration genotype. See Chap. 14 in Maternal-Fetal Medicine Evidence Based Guidelines.
Hyperkinetic Movement Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Morales-Briceno Hugo, Victor S.C. Fung, Annu Aggarwal, Philip Thompson
First decade (∼40%): Hepatic—jaundice, cirrhosis, acute (fulminant) liver failure.Hemolytic anemia.
Distinct lipid profile in haemolytic anaemia-related gallstones compared with the general gallstone
Published in Annals of Medicine, 2023
Ziqi Wan, Xiaoyin Bai, Chengqing He, Yueyi Zhang, Ying Wang, Kaini Shen, Li Meizi, Qiang Wang, Wu Dongsheng, Yunlu Feng, Aiming Yang
Electronic medical records were retrospectively reviewed to collect patients’ baseline information, data regarding laboratory tests and clinical courses. The baseline information included age, sex, height, weight, blood pressure, history of hypertension or diabetes mellitus (DM) and length of hospital stay. The laboratory tests included complete blood counts (haemoglobin, platelets, neutrophils and reticulocyte percentage), liver biochemistry tests (total bilirubin, direct bilirubin, alanine transaminase (ALT), aspartate aminotransferase (AST), lactic dehydrogenase (LDH) and γ-glutamyl transferase (GGT)), kidney function tests (creatine (SCR), uric acid (UA) and urea (BUN)), fasting blood glucose and serum lipids. We extracted values obtained from the last two tests before any treatment related to anaemia (for the case group) or gallstones (for the control group), and presented the mean value. The clinical courses generally included features of haematolytic anaemia (onset, causes, treatments and complications) and characteristics of gallstones (onset, symptoms, ultrasound results, acute diseases, treatments and complications). Symptoms related to haemolytic anaemia included fatigue, weakness, shortness of breath, jaundice, dark urine and splenomegaly. Symptoms of acute gallstone diseases included abdominal pain, fever and jaundice. Data were censored on December 2022.
Effect of deletions in the α-globin gene on the phenotype severity of β-thalassemia
Published in Hemoglobin, 2022
Dipankar Saha, Prosanto Kr. Chowdhury, Amrita Panja, Debashis Pal, Kaustav Nayek, Gispati Chakraborty, Prashant Sharma, Reena Das, Surupa Basu, Raghunath Chatterjee, Anupam Basu
Subjects of both sexes, with primary symptoms of hemolytic anemia, were screened. Those found positive for a β hemoglobinopathy (homozygous/compound heterozygous states) by high performance liquid chromatography (HPLC); the VARIANT II™ system (Bio-Rad Laboratories, Hercules, CA, USA) was used. Accordingly, 270 thalassemia subjects were recruited for the present study. A total of 89 normal subjects, diagnosed as normal by the HPLC method, were included in this study as controls. All the subjects were from West Bengal and the surrounding states of Eastern India. The subjects were further classified based on their phenotype status. Approval for this study was given by the clinical ethics committee, The University of Burdwan, Burdwan, India. Written informed consent was obtained from each subject before the enrollment in this study.
Screening tools for hereditary hemolytic anemia: new concepts and strategies
Published in Expert Review of Hematology, 2021
Elisa Fermo, Cristina Vercellati, Paola Bianchi
Hereditary hemolytic anemias may also be caused by deficiencies of enzymes of the erythrocyte metabolism, that is composed by three main pathways: glycolysis, the main source of metabolic energy in the erythrocytes, pentose phosphate pathway, and nucleotide metabolism. G6PD deficiency is the most widespread erythroenzymopathy, and is usually associated with acute hemolysis caused by oxidative stress, with the exception of the class-I variants, that result in chronic hemolytic anemia. Pyruvate kinase (PK) deficiency is the most frequent enzymopathy affecting glycolysis, followed by glucose ephosphate isomerase (GPI), whereas pyrimidine 5′-nucleotidase (P5′N) and adenylate kinase (AK) deficiency involve the nucleotide metabolism. Some enzymes, such as triose phosphate isomerase (TPI), phosphoglycerate kinase (PGK) and phosphofructokinase (PFK), are not confined to the red cells but also expressed in other tissues; in such cases, hemolytic anemia may be accompanied to non-hematological symptoms such as myopathy, neuromuscular impairment and mental retardation [5–7].