DOCSLIB.ORG

The Control of Methemoglobinemia with Methylene Blue

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Control of Methemoglobinemia with Methylene Blue THE CONTROL OF METHEMOGLOBINEMIA WITH METHYLENE BLUE William B. Wendel J Clin Invest. 1939;18(2):179-185. https://doi.org/10.1172/JCI101033. Research Article Find the latest version: https://jci.me/101033/pdf THE CONTROL OF METHEMOGLOBINEMIA WITH METHYLENE BLUE"12 By WILLIAM B. WENDEL (From the Department of Internal Medicine, Washington University School of Medicine, St. Louis; and the Department of Chemistry, University of Tennessee, College of Medicine, Memphis) (Received for publication October 13, 1938) The cyanosis seen in a high percentage of pa- the concentration of methemoglobin from levels tients receiving sulfanilamide and related drugs as high as 25 to 40 per cent of the total pigment has been attributed variously to methemoglo- to less than 4 per cent in 30 to 40 minutes. binemia (1, 2), sulfhemoglobinemia (1), an un- In one case of sulfhemoglobinemia methylene usual degree of unsaturation of the venous blood blue was without effect upon the abnormal (3), and to the presence of aniline black (4) and pigment. other colored derivatives of sulfanilamide (5) ANIMAL OBSERVATIONS in the red blood corpuscles. Marshall and Walzl Since, in our experience, sulfanilamide does not (4) and Chesley (6) consider methemoglobin to produce methemoglobin in dogs, rabbits, rats, and be of no importance except perhaps in an occa- mice, nitrite was used to produce experimental sional patient. methemoglobinemia. Figure 1 illustrates the The present paper summarizes the results of course of blood pigment changes in seven control determinations of methemoglobin in the blood of dogs which received intravenous injections of 30 more than one hundred patients who were receiv- mgm. of sodium nitrite per kilogram of body ing sulfanilamide and showing cyanosis. Methe- weight. Following injection of nitrite, methemo- moglobin was found, at least in traces, in over 90 globin 8 rapidly accumulates and after 60 to 100 per cent of these. In thirty-five cases the blood minutes reaches a maximum concentration corre- contained methemoglobin to the extent of 15 per sponding to a loss of 60 to 70 per cent of the cent or more of the total pigment. In one in- normal oxygen capacity. It then progressively stance 40 per cent of the total blood pigment was decreases, due to reconversion to hemoglobin, and in the form of methemoglobin after 8 to 9 hours has entirely disappeared. The Animal experiments are described which con- average maximum rate of regeneration of hemo- firm and extend the observations of Williams and globin from methemoglobin (indicated in Figure Challis (7), Steele and Spink (8), and Hauschild 1 by a broken line) in these seven animals was (9) that methylene blue hastens disappearance of 0.03 volumes per cent per minute. This is essen- methemoglobin from the blood. Clinical applica- tially the same rate as observed when blood con- tion of these experiments to patients showing taining methemoglobin from these animals is in- cyanosis from sulfanilamide has shown that intra- cubated at body temperature in zitro, and may be venous injection of 0.1 to 0.2 cc. of one per cent looked upon as the rate at which the enzyme methylene blue per kilogram body weight reduces systems in the erythrocytes are able to reduce methemoglobin (10). 1 A preliminary report of this work was given before the Middle Section of the American Laryngological, 8 Methemoglobin concentration is expressed in this Rhinological, and Otological Society, St. Louis, January paper in two ways, as per cent of the total pigment and 26, 1938, and the American Society of Biological Chem- as volumes per cent, one volume per cent of methemo- ists, Baltimore, March 30, 1938 (J. Biol. Chem., 1938, globin being that concentration which results from loss 123, cxxiv), and was contained in a letter to the Editor of one volume per cent oxygen capacity. of the J. A. M. A., 1937, 109, 1216. In most experiments methemoglobin was determined 2This work was supported at both schools by grants by a spectroscopic method which will appear in a forth- from the Upjohn Company, Kalamazoo, Michigan. The coming number of the J. Lab. and Clin. Med. Occa- Upjohn Company has supplied the writer with 10 cc. sionally, methemoglobin was determined also by differ- ampoules of methylene blue which were used in the ence between total pigment and oxygen capacity. The clinical studies. two methods usually gave identical results. 179 180 WILLIAM B. WENDEL atD z -J 0x 0;0 Li IN- Lhi 200 300 MINUTES AFTER NITRITE INJECTION FIG. 1. AccumuLMAoN AND DISAPPEARANCE OF METHEMOGLO}IN IN THE BLOOD OF DOGS FOLLOWING THE INTRAVENOUS INJECTION OF SODIUm NimTE (30 MGM. PER KILOGRAM OF BODY WEIGHT) Having determined the physiological rate of obtained with a number of dogs, shows that in- hemoglobin regeneration from methemoglobin jection of 2 mgm. of methylene blue (in the form various substances were tested for possible accel- of a one per cent aqueous solution) per kilogram erating action upon this process. Sodium formal- of body weight increases the rate of disappearance dehyde sulfoxylate, which reduces methemoglobin of methemoglobin 'from the blood four or five- in aqueous solution, was found to be without ef- fold. Table I summarizes the results of a series fect in trvo. Sodium formaldehyde sulfoxylate, of similar experiments in which the effect of vari- however, reduces methylene blue and since re- ous quantities of wnethylene blue upon the rate of duced (leuco) methylene blue converts methe- disappearance of methemoglobin from the blood moglobin to hemoglobin very rapidly, it seemed was determined. A measurable effect is evident possible that simultaneous injection of these two even with the smallest amount of dye injected, substances might accelerate conversion of methe- namely, 0.1 mgm. per kilogram of body weight. moglobin to hemoglobin. A cycle between sul- Oxygen capacity figures in Table I indicate that foxylate in the plasma and methemoglobin in the the methemoglobin which disappears rapidly fol- red cells mediated by methylene blue was pictured. lowing injection of methylene blue is converted When tested it was found that simultaneous intra- to functionally active hemoglobin. The duration venous injection of methylene blue and sulfoxy- of the anti-methemoglobin action of 5 mgm. of late caused methemoglobin to disappear from the methylene blue per kilogram in dogs is at most blood very rapidly. Control experiments, how- about 2 hours. ever, showed that methylene blue alone was equally Methylene blue accelerates the disappearance of effective. Figure 2, which illustrates the results methemoglobin also from the blood of rabbits. METHEMOGLOBINEMIA AND METHYLENE BLUE 181 Methylene blue is effective as an anti-methemo- DOG 22 globin agent also when given by mouth. As com- HbO2, INITIAL, 16.4 VOL.X N AFTER 95 MIN. 6.3 VOL L.X pared with intravenous injection the response to o t 155 15.4 administration by mouth is slow, and more of the 10- 2 MG. MB./KG. dye is required. Observations to date indicate that SLOPE 0.2 VOL- /MIN. accumulation of methemoglobin can be prevented in adults by oral administration of 0.5 to 1.0 gram i-j of methylene blue per day even when the patient is receiving large doses of sulfanilamide. z Before methylene blue was injected into pa- 0 -i tients receiving sulfanilamide, compatibility of 0 these two substances was tested in dogs and rab- Lai s bits. Several times as much methylene blue was Lai injected into experimental animals as is required in humans. Also the dye was injected at a time when the animals were severely toxic from large MB doses of sulfanilamide (1 gram per kilogram per I I No increase in was evident follow- 0 100 200 300 day). toxicity MINUTES AFTER NITRITE I NJECTION ing intravenous injection of the dye. In order to elicit cumulative effects of administra- FIG. 2. EmFCr OF INTRAVENOUS INJECTION OF [ETHY- possible LENE BLUE, 2 MGM. PER KILOGRLAM OF BODY WEIG:ET ON tion of the combination of drugs one dog was RATE OF CONVERSION OF METHEMOGLOBIN TO HEMO*GLOBIN given 0.6 gram sulfanilamide per kilogram per IN THE DoG day and 0.27 gram of methylene blue per day HbO, means oxygen capacity. MB over arrovv mdi- by mouth for 4 weeks. No outward evidence of cates injection of methylene blue. toxicity or abnormal blood rhanges was observed. Preliminary experiments with Dr. Anna Dula- CLINICAL APPLICATION ney of the University of Tennessee Medical In collaboration with Dr. Alexis F. Harn tmann School on mice injected with highly virulent of Washington University Medical School, where strains of beta hemolytic streptococci indicate that the writer began and completed an importanit part of this work, these observations receivedI first TABLE I clinical application in the summer of 1937. Since Effect of various amounts of methykne blue on rate of these early observations many others have been conversion of methemoglobin to hemoglobin in dogs made with the cooperation of physicians c n the staff of the University of Tennessee Mledical Amount of Rate of OXYen capacity Dog methylene disappear- School. In summary, intravenous injection of number blue ance of After After icted methemoglobin Before 0.1 to 0.2 cc. per kilogram of body weighit of a nitrite i methlee bluet Mm. per otumes per cent soluma otusm solume one per cent aqueous solution of methylene blue kilegram per minute per cent per cet per cent converts in the course of about 45 minutes all of 14 10 0.77 17.3 (50 minutes) 14 10 0.33t 12.8 4.4 13.2 (30 minutes) in the ocytes 21 10 0.31t the methemoglobin circulating erythr 16 5 0.19 functionally active hemoglobin, even when 18 5 0.25 17.7 7.3 17.0 (65 minutes) into 17 2 0.23 the concentration representss initi- 22 2 0.20 16.4 6.3 15.4 (60 minutes) methemoglobin 19 1 0.076 12.7 5.5 10.6 (95 minutes) as much as 25 to 40 per cent of the totsal pig- 20 1 0.14 ally 6 0.5 0.12 ment.
Load more

Recommended publications
  • Fetal and Embryonic Haemoglobins P
    Review Article J Med Genet: first published as 10.1136/jmg.10.1.50 on 1 March 1973. Downloaded from Journal of Medical Genetics (1973). 10, 50. Fetal and Embryonic Haemoglobins P. A. LORKIN MRC Abnormal Haemoglobin Unit, University Department of Biochemistry, Cambridge Haemoglobin has been the subject of intensive form a nearly spherical molecule with extensive research for many years and is one of the most areas of contact between unlike chains; the two thoroughly understood of all protein molecules. main types of contact are denoted alp, and alg2 The amino-acid sequences of haemoglobins from The tetramer exhibits cooperative behaviour or many species of animals have been determined haem-haem interaction. As each haem combines (tabulated by Dayhoff, 1969) and the molecular with oxygen the affinity of successive haems in- structures of horse and human haemoglobins have creases. The oxygen affinity curve of the tetramer been determined in great detail by x-ray crystallo- is sigmoidal and may be represented approximately graphy (Perutz et al, 1968a and b; Perutz 1969). A by the Hill equation:* mechanism of action of haemoglobin has been pro- = kpo2n posed (Perutz, 1970a and b and 1972). The y haemoglobins of higher organisms share a common +kpo2n tetrameric structure built up of two pairs of unlike Oxygen affinity data are usually presented in copyright. chains; the a chains containing 141 amino-acid terms of P102, the partial pressure of oxygen re- residues and the non-a chains containing generally quired to attain half saturation with oxygen, and of 145 or 146 amino acids. In man, five types of n, the exponent of the Hill equation.
    [Show full text]
  • Your Baby Has Hemoglobin E Or Hemoglobin O Trait for Parents
    NEW HAMPSHIRE NEWBORN SCREENING PROGRAM Your Baby Has Hemoglobin E or Hemoglobin O Trait For Parents All infants born in New Hampshire are screened for a panel of conditions at birth. A small amount of blood was collected from your baby’s heel and sent to the laboratory for testing. One of the tests looked at the hemoglobin in your baby’s blood. Your baby’s test found that your baby has either hemoglobin E trait or hemoglobin O trait. The newborn screen- ing test cannot tell the difference between hemoglobin E and hemoglobin O so we do not know which one your baby has. Both hemoglobin E trait and hemoglobin O trait are common and do not cause health problems. Hemoglobin E trait and hemoglobin O trait will never develop to disease. What is hemoglobin? Hemoglobin is the part of the blood that carries oxygen to all parts of the body. There are different types of hemoglobin. The type of hemoglobin we have is determined from genes that we inherit from our parents. Genes are the instructions for how our body develops and functions. We have two copies of each gene; one copy is inherited from our mother in the egg and one copy is inherited from our father in the sperm. What are hemoglobin E trait and hemoglobin O trait? The normal, and most common, type of hemoglobin is called hemoglobin A. Hemoglobin E trait is when a baby inherited one gene for hemoglobin A from one parent and one gene for hemoglobin E from the other parent.
    [Show full text]
  • Alpha Thalassemia Trait
    Alpha Thalassemia Trait Alpha Thalassemia Trait Produced by St. Jude Children’s Research Hospital, Departments of Hematology, Patient Education, 1 and Biomedical Communications. Funds were provided by St. Jude Children’s Research Hospital, ALSAC, and a grant from the Plough Foundation. This document is not intended to replace counseling by a trained health care professional or genetic counselor. Our aim is to promote active participation in your care and treatment by providing information and education. Questions about individual health concerns or specific treatment options should be discussed with your doctor. For general information on sickle cell disease and other blood disorders, please visit our Web site at www.stjude.org/sicklecell. Copyright © 2009 St. Jude Children’s Research Hospital Alpha thalassemia trait All red blood cells contain hemoglobin (HEE muh glow bin), which carries oxygen from your lungs to all parts of your body. Alpha thalassemia (thal uh SEE mee uh) trait is a condition that affects the amount of hemo- globin in the red blood cells. • Adult hemoglobin (hemoglobin A) is made of alpha and beta globins. • Normally, people have 4 genes for alpha globin with 2 genes on each chromosome (aa/aa). People with alpha thalassemia trait only have 2 genes for alpha globin, so their bodies make slightly less hemoglobin than normal. This trait was passed on from their parents, like hair color or eye color. A trait is different from a disease 2 Alpha thalassemia trait is not a disease. Normally, a trait will not make you sick. Parents who have alpha thalassemia trait can pass it on to their children.
    [Show full text]
  • Fact Sheettrait Result: Screening Program Blood Spot Screen Result Notification
    Family Minnesota Newborn Fact SheetTRAIT Result: Screening program Blood Spot Screen Result Notification FAC - Hemoglobin C Trait What was found on the newborn screen? How do you know if your baby actually has The newborn screen that was collected at birth hemoglobin C trait? found that your baby has fetal hemoglobin (F), adult A simple blood test called a hemoglobin electrophoresis hemoglobin (A), and abnormal hemoglobin (C). can tell if your baby has hemoglobin C trait. This test will likely be performed when your baby is between nine and What does this mean? twelve months of age. Talk with your baby’s doctor about This means your baby likely has hemoglobin C trait (AC). plans for testing and any questions you have about it. The fetal hemoglobin goes away as babies get older. Why is it important to know? What is hemoglobin C trait? When a baby has hemoglobin C trait, we know that Hemoglobin C trait is not a disease and can never at least one parent has it too. Trait is passed on from become a disease. Hemoglobin C trait does not cause parent to child like other genes for eye color and height. health problems. You may have hemoglobin C trait and If only one parent has trait, it is not a problem. However, not know it. People with hemoglobin C trait will always if one parent has hemoglobin C trait and the other has have it; you cannot grow out of it. hemoglobin C trait or sickle cell (S) trait, each pregnancy can result in the child having sickle cell disease.
    [Show full text]
  • Hemoglobin C Trait What Does This Mean for My Baby, Me and My Family?
    My Baby Has Hemoglobin C Trait What does this mean for my baby, me and my family? Your baby's newborn screening test showed tell them their chance to have a baby with a that he or she has hemoglobin C trait (this is hemoglobin disease. also referred to as being a “hemoglobin C carrier”). Babies who have hemoglobin C trait What does having a baby with hemoglobin are no more likely to get sick than any other C trait mean for me, my partner and for baby. They do not need any special medical future pregnancies? treatment. Hemoglobin C trait will not change Since your baby has hemoglobin C trait, this into a disease later on. means that either you or your partner or both of you have hemoglobin C trait. In almost all What causes hemoglobin C trait? cases, ONLY ONE OF YOU will have Hemoglobin C trait happens when the part of hemoglobin C trait. the red blood cell that carries oxygen throughout the body is changed. This part that Most people do not know that they have is changed is called hemoglobin. Hemoglobin hemoglobin C trait. Now that your baby is is important because it picks up oxygen in the known to have hemoglobin C trait, both you lungs and carries it to the other parts of the and your partner have the option of being body. tested. Testing involves a blood test. People usually have one type of hemoglobin. IF ONLY ONE OF YOU HAS HEMOGLOBIN This is called hemoglobin A. Babies with C TRAIT, in every pregnancy there is a: hemoglobin C trait have a second type of • 1 in 2 (50%) chance to have a baby with hemoglobin called hemoglobin C, as well as only the usual hemoglobin A.
    [Show full text]
  • Increasing Fetal Hemoglobin As a Possible Key for Improvement of Hypoxia and Saving Last Breath in COVID-19 Patient: “Postulating a Hypothesis” Muhamed A
    Abdelzaher et al. The Egyptian Journal of Bronchology (2021) 15:33 The Egyptian Journal https://doi.org/10.1186/s43168-021-00078-7 of Bronchology COMMENTARY Open Access Increasing fetal hemoglobin as a possible key for improvement of hypoxia and saving last breath in COVID-19 patient: “postulating a hypothesis” Muhamed A. Abdelzaher1, Ashraf E. S. Ibrahim2 and Essamedin M. Negm3* Abstract Background: COVID-19 patients normally experience mild cold-like symptoms that progress from the early viral response phase through the lung phase to the hyper-inflammation phase. Acute respiratory distress syndrome (ARDS) characterizes the most critical stage of the illness with progressive respiratory failure. Hypoxemia is the most dangerous and challenging problem. We suggest an inductive study approach to postulate a hypothesis and synthesis of supporting evidence as a trial to resolve hypoxia in patients with COVID-19 by increasing the volume of fetal hemoglobin which has a high affinity for oxygen using methods for hypothesis related research evidence synthesis. Conclusion: We recommend involving umbilical cord fetal blood transfusion or the use of hydroxyl urea as a clinical trial on COVID-19 patients and also for all other types of ARDS to determine its efficacy in correction of hypoxemia, controlling progression of the disease, and increasing survival rate. Keywords: COVID-19, Hypoxia, Fetal hemoglobin, Fetal blood, Hydroxyurea Background Mortality are as high as 46% in critically ill patients re- In December 2019, a sudden public health incident (the quiring intensive care unit admission and oxygen ther- corona virus disease [COVID-19] epidemic) occurred in apy [4], suggesting an urgent need to try therapeutic Wuhan, China [1].
    [Show full text]
  • Arizona Hemoglobin Bart's Fact Sheet for Health Care Providers
    Arizona Hemoglobin Bart’s Fact Sheet for Health Care Providers Hemoglobin Barts Your patient has been found on the Arizona Newborn Genetic Screen to have a hemoglobin electrophoresis pattern consistent with "FA Bart’s". The acronym stands for the hemoglobin species present in the baby's blood in descending order of prevalence. The F designates fetal hemoglobin (a2 y2), A denotes hemoglobin A (a2ß2) and Bart’s represents hemoglobin Bart's, a tetramer of y-globin molecules (y4). Hemoglobin Barts (y4) appears in the newborn when one or more of the 4 human a-globin genes are missing. The relative over abundance of y-globin molecules leads to y4 production and the diagnosis of Hemoglobin Barts. Alpha thalassemia is caused by deletions of the alpha globin genes on chromosome 16. Normal individuals have 4 copies of the gene with 2 on each chromosome. It is possible to lose 1 to 4 of these genes. The presence of hemoglobin Bart’s on newborn screen usually suggests that the infant is missing at least 1 alpha gene. The silent carrier: One deleted Alpha Gene Neonates and children with three functional alpha genes have a complete or nearly completely silent phenotype. The red cell indices are normal and remain so for life. When only one a gene is non- functional, the hemoglobin Barts percentage is usually 1-2% in the newborn, and is not detectable when the fetal hemoglobin synthesis stops at 6 months of age. As the newborn matures, the red cells can rarely exhibit a reduced MCV, MCH, but will show normal HBA2 and F levels if the hemoglobin electrophoresis is repeated.
    [Show full text]
  • Hemoglobin E Trait: What You Need to Know
    Hemoglobin E Trait: What You Need to Know... Hemoglobin E trait is common and can occur in any race What is a gene? or ethnicity. It is most common in individuals of Southeast Genes are the instructions Asian descent. You may have heard of sickle cell trait in our DNA that tell our before, while not exactly the same, sickle cell trait and bodies how to function. For example, genes hemoglobin E trait are similar. determine eye color, hair What is hemoglobin E trait? color, and height. We inherit half our genes from Hemoglobin E trait (AE) is an inherited condition which affects the hemoglobin in your red blood cells. our mother and half from our father. • Hemoglobin is a protein in red blood cells. The job of hemoglobin is to carry oxygen through the body. How do you • Each person inherits two hemoglobin genes – one from each parent. A normal gene will make normal hemoglobin (A). A specific change know if you in the hemoglobin gene will make hemoglobin E (E). have hemoglobin E trait (AE)? » Red blood cells with normal hemoglobin (A) are doughnut A simple blood test called a hemoglobin shaped; electrophoresis can tell your hemoglobin type. Talk with your healthcare provider if you have more » Red blood cells with hemoglobin E (E) are smaller than normal. questions about hemoglobin trait or if you want to • People with hemoglobin E trait have both normal hemoglobin (A) be tested. and hemoglobin E (E) in their red blood cells. Chance with each pregnancy It is important to know if you have Hemoglobin Hemoglobin hemoglobin E trait.
    [Show full text]
  • Fact Sheet: Hemoglobin E Trait
    hemoglobin E trait. trait. E hemoglobin region. It is possible for a person of any nationality to have have to nationality any of person a for possible is It region. came from Africa, India, the Middle East, or the Mediterranean Mediterranean the or East, Middle the India, Africa, from came Hematology came from Asia. It can also be found in people whose ancestors ancestors whose people in found be also can It Asia. from came Hemoglobin E trait is very common in people whose ancestors ancestors whose people in common very is trait E Hemoglobin Who can have hemoglobin E trait? E hemoglobin have can Who hemoglobin. People with hemoglobin E trait usually do not have enough enough have not do usually trait E hemoglobin with People Trait E in their red blood cells. Hemoglobin E is not normal. normal. not is E Hemoglobin cells. blood red their in E People with hemoglobin E trait have hemoglobin A and hemoglobin hemoglobin and A hemoglobin have trait E hemoglobin with People Hemoglobin E E Hemoglobin A. hemoglobin type, (1) one only have the lungs to all parts of your body. People with normal hemoglobin hemoglobin normal with People body. your of parts all to lungs the Your red blood cells contain hemoglobin, which carries oxygen from from oxygen carries which hemoglobin, contain cells blood red Your FACT SHEET SHEET FACT Hemoglobin E trait is a condition that affects the red blood cells. blood red the affects that condition a is trait E Hemoglobin What is hemoglobin E trait? E hemoglobin is What BMC–05/19 (BK76000) BMC–05/19 What if one (1) parent has hemoglobin E trait and the other parent has beta thalassemia trait? If one (1) parent has hemoglobin E trait Hemoglobin E Beta Thalassemia and the other parent has beta Trait Trait thalassemia trait, there is a 25 percent (1 (AE) (Aβ) in 4) chance with each pregnancy of having a child with hemoglobin E/beta thalassemia disease.
    [Show full text]
  • Alpha Thalassemia Trait; Alpha Gene Number, 2) Or
    Inheritance Pattern for For more information Alpha Tha lassemia Contact your local SCDAA organization or other Alpha health agency at: When each parent is a "silent" carrier of alpha Thalassemia thalassemia ( + / ) Trait their baby + may have + Or contact the SCDAA National Office at the address and telephone number below. / (normal alpha gene number, 4) or Stay connected with Get Connected the first patient powered registry + + + / + (alpha thalassemia trait; alpha gene number, 2) or Register at www.getconnectedscd.com + + / + (silent carrier of alpha thalassemia; Sickle Cell Disease alpha gene number, 3) Association of America, Inc. 3700 Kopper Street, Suite 570 Baltimore, MD 21227 Note: Alpha genes are inherited in pairs, one pair ( ) from each parent. A person with normal alpha genes has four ( / ). www.sicklecelldisease.org Alpha thalassemia may result in a total of 3, 2, 1 or 0 alpha genes. There are two common types of alpha thalassemia: alpha-plus ( +) and alpha-zero( o ) ©2018 Sickle Cell Disease Association of America, Inc.; All YOUR QUESTIONS In + thalassemia, one of the 2 genes is removed (deleted) -; rights reserved. No portion of this material can be published and in o thalassemia, both a genes are deleted - -. In this without the owner’s express written consent. example we have shown alpha-plus ( +) thalassemia. ANSWERED I want to learn more... ALPHA THAL TRAIT- WHAT DOES THAT HOW DOES A PERSON GET ALPHA THAL NOW, WHAT IS ALPHA THALASSEMIA? REALLY MEAN? TRAIT? The usual hemoglobin in our red blood cells is hemoglobin Alpha thal trait is a mild form of alpha thalasemia. In alpha A person gets or inherits alpha thal trait the same way he got A.
    [Show full text]
  • The Free Alpha-Hemoglobin: a Promising Biomarker for Β-Thalassemia
    r Biomar ula ke c rs le o & M D f i a o g l Journal of Molecular Biomarkers n a o n Abdullah, et al., J Mol Biomark Diagn 2014, 5:5 r s i u s o J DOI: 10.4172/2155-9929.1000197 ISSN: 2155-9929 & Diagnosis Review Article Open Access The Free Alpha-Hemoglobin: A Promising Biomarker for β-Thalassemia Uday YH Abdullah1, Ahmed GF Al-Attraqchi1, Hishamshah M Ibrahim2, Zilfalil Bin Alwi3, Atif A Baig1, Iekhsan Othman4, Noraesah B Mahmud2, Rosline B Hassan3, Nor Hedayah A Bakar1 and Alawiyah B A Abd Rahman5 1University Sultan Zainal Abidin (UniSZA), Faculty of Medicine and Health Sciences, Kuala Terengganu, Malaysia 2Hospital Kuala Lumpur (HKL), Kuala Lumpur, Malaysia 3Univesiti Sains Malaysia (USM), School of Medical Science, Kelantan, Malaysia 4Monash University, Selangor, Malaysia 5Hospital Sultana Nor Zahirah (HSNZ), Kuala Terengganu, Malaysia *Corresponding author: Uday Younis Hussein Abdullah, University Sultan Zainal Abidin (UniSZA), Kampus Kota, Jalan Sultan Mahmud 20400, Kuala Terengganu, Malaysia, Tel: 609-625607; Fax: 60-6275771/5772; E-mail: [email protected] Rec date: Aug 28, 2014; Acc date: Sep 27, 2014; Pub date: Sep 29, 2014 Copyright: © 2014 Abdullah UYH, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract The purpose is to review the current knowledge and methods of determination of the free alpha hemoglobin with emphasis on its potential implications in patients with beta-thalassemia (β-thal).The severity of β-thal correlates with the extent of imbalance between α- and non-α-globin chains and the amount of the free alpha hemoglobin (free α- Hb) pool in the erythrocytes.
    [Show full text]
  • Hemoglobin E
    Hemoglobin E Hemoglobin E trait is an inherited blood trait. It is Hemoglobin E Trait more often found in people with Southeast Asian When you have one working copy of the beta ancestry (e.g., Cambodian, Thai, Laotian, globin gene and one copy making hemoglobin Vietnamese, Burmese, Malaysian, and Hmong) or E you have hemoglobin E trait. Your body is Asian Indian ancestry, but it can be found in people still able to make plenty of the common with ancestry from any part of the world. To hemoglobin, hemoglobin A, but also makes a understand this condition, it helps to know more less common type of hemoglobin, called about how your blood is made. hemoglobin E. This is not a disease and does not affect your health. This trait can cause the Hemoglobin red blood cells to be slightly smaller than usual. Your blood contains millions of red blood cells. Sometimes, this is mistaken for low iron levels Each of your red blood cells has hemoglobin, which (iron-deficiency anemia). However, taking an gives blood its red color and carries oxygen iron supplement does not change the size of throughout your body. Hemoglobin is made by the red blood cells. combining a “heme” portion (iron) and a “globin” portion (protein). The iron comes from the food you Hemoglobin E trait does not change into a eat and your body makes the globins. blood disease. The importance of identifying hemoglobin E trait is that it helps find couples There are different kinds of hemoglobin that the whose children may be born with a related body can make.
    [Show full text]