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Metformin Thalassemia

The Potential Hepatoprotective Effect Of Metformin In Patients With Beta Thalassemia Major

The Potential Hepatoprotective Effect Of Metformin In Patients With Beta Thalassemia Major

You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. The Potential Hepatoprotective Effect of Metformin in Patients With Beta Thalassemia Major The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details. ClinicalTrials.gov Identifier: NCT02984475 Information provided by (Responsible Party): Mona Sobhy Abd El-Mon'em Gaber, Cairo University Top of Page Study Description Study Design Arms and Interventions Outcome Measures Eligibility Criteria Contacts and Locations More Information Beta Thalassemia is a major public health problem in Mediterranean countries.In Egypt, it is considered as the most common chronic hemolytic anemia.one of the major complications in this inherited disorder is iron overload which lead to oxidative stress and tissue damage. Regarding toxic effect of iron overload on liver, hepatomegaly is one of the most findings that resulting from hemosiderosis, extra medullary hematopoiesis, transmitted hepatitis B and C and cirrhosis. A lot of studies have been carried out recently to study the beneficial role of metformin in non-diabetic patients of different disorders as non-alcoholic fatty liver disease (NAFLD).Among several studies, it's demonstrated that metformin significantly improved insulin resistance, aminotransferase levels and liver morphology. The role of metformin in these studies is mainly thought to be antioxidant and anti-inflammatory effects. However, the role of Metformin on hepatic function in diff Continue reading >>

Uthealth | Clinical Trials

Uthealth | Clinical Trials

Confirmed diagnosis of sickle cell anemia or non-transfusion dependent thalassemia Age greater than or equal to 12 and less than or equal to 40 years of age. If on hydroxyurea, fetal hemoglobin less than 20% at maximum tolerated dose Creatinine less than or equal to 1.4mg/dL and estimated glomerular filtration rate greater than 45 ml/min/1.73 m2 Liver function tests less than or equal to 3 times upper limits of normal Simple or chronic red blood cell transfusion therapy in the last 3 months OR a HbA level >5% in SCA patients Refusal to use medically effective birth control if female and sexually active. If on hydroxyurea, not at stable maximum tolerated dose for a minimum of 4 months (temporary exclusion). Subjects who are currently taking Hydroxyurea as part of standard of care and have sickle cell anemia. Metfomin will be taken daily. The metformin dose will be increased during two time points per subject if protocol dose escalation criteria is met. Questionnaires will be completed to assess the impact quality of life Subjects who are not taking Hydroxyurea as part of standard of care and have non-transfusion dependent thalassemia or sickle cell anemia. Metfomin will be taken daily. The metformin dose will be increased during two time points per subject if protocol dose escalation criteria is met. Continue reading >>

Fighting Sickle Cell Disease Using A Type 2 Diabetes Medication

Fighting Sickle Cell Disease Using A Type 2 Diabetes Medication

Dr. Vivien Sheehan, assistant professor of pediatrics at Baylor and Texas Childrens Cancer and Hematology Centers Sickle cell disease and the blood disorder beta thalassemia affect more than 180,000 Americans and millions more worldwide. Both diseases can be made milder or even cured by increasing fetal hemoglobin (HbF) levels, but current treatment to ramp up HbF is limited in its effectiveness. Researchers at Baylor College of Medicine and Texas Childrens Cancer and Hematology Centers have discovered a gene, FOXO3, involved in controlling fetal hemoglobin production and were able to target the gene and turn on fetal hemoglobin levels in patient samples in the lab using the diabetes drug metformin. This offers promising new treatments the first new drug treatment for sickle cell disease in 30 years and the first ever for beta thalassemia. It was a major breakthrough to show that a common drug already in use for type 2 diabetes could be a treatment for sickle cell disease by inducing fetal hemoglobin, a type of hemoglobin that doesnt become sickle shaped but is usually turned off in infancy, said Dr. Vivien Sheehan , assistant professor of pediatrics at Baylor and Texas Childrens Cancer and Hematology Centers and lead investigator of the research. This is an exciting example of collaborative, bench-to-bedside research that has now resulted in a clinical trial that is already enrolling patients. Sheehan launched this research as a clinical fellow at Baylor College of Medicine in 2011 with the goal of identifying new drug targets to help sickle cell patients make more fetal hemoglobin. The only widely used drug to treat sickle cell disease, hydroxyurea, targets fetal hemoglobin by slowing red blood cells from maturing, but does not make enough HbF to help up to half of s Continue reading >>

Scientists Re-activate Defective Gene Linked To Sickle Cell Disease

Scientists Re-activate Defective Gene Linked To Sickle Cell Disease

Scientists re-activate defective gene linked to sickle cell disease Published on January 12, 2017 by Life Science Daily News Desk Researchers from Baylor College of Medicine and the Texas Childrens Cancer and Hematology Centers recently discovered a new application for type 2 diabetes medication in the treatment of sickle cell disease. The collaborative team identified the gene responsible for fetal hemoglobin production, and demonstrated a means by which the gene can be turned on using the diabetes drug metformin, thereby improving or sometimes curing conditions such as sickle cell disease and beta thalassemia. It was a major breakthrough to show that a common drug already in use for type 2 diabetes could be a treatment for sickle cell disease by inducing fetal hemoglobin, a type of hemoglobin that doesnt become sickle shaped but is usually turned off in infancy, lead study investigator Vivien Sheehan, assistant professor of pediatrics at Baylor and Texas Childrens, said. This is an exciting example of collaborative, bench-to-bedside research that has now resulted in a clinical trial that is already enrolling patients. Sheehan and her colleagues have been searching for new drug targets for sickle cell disease since 2011. A clinical trial examining the effectiveness of metformin in the treatment of sickle cell and related conditions is currently underway. Patients who make this much fetal hemoglobin would, in theory, be cured of sickle cell disease, and act like a sickle cell trait patient clinically, Sheehan said. Metformin may also be an effective therapy for beta thalassemia patients, as it can help them make more hemoglobin by adding HbF, without slowing the production of red cells like hydroxyurea. Continue reading >>

The Icet-a Recommendations For The Diagnosis And Management Of Disturbances Of Glucose Homeostasis In Thalassemia Major Patients

The Icet-a Recommendations For The Diagnosis And Management Of Disturbances Of Glucose Homeostasis In Thalassemia Major Patients

The ICET-A Recommendations for the Diagnosis and Management of Disturbances of Glucose Homeostasis in Thalassemia Major Patients 5Division of Pediatric and Adolescent Endocrinology, Paedi Center for Specialized Pediatrics, St. Georges University Medical School at the University of Nicosia, Cyprus 6Department of Pediatrics, Endocrinology Unit, Alexandria University Childrens Hospital, Egypt, and Child Health Department, Sultan Qaboos University Hospital, Muscat, Oman 10Department of Hematology, College of Medicine and Health Sciences Sultan Qaboos University Oman, Sultanate of Oman & Visiting Scholar, Stellenbosch Institute for Advanced Study (STIAS), Wallenberg Research Centre at Stellenbosch University, Stellenbosch 7600, South Africa 1Adolescent Outpatient Clinic, Quisisana Hospital, Ferrara, Italy 2Department of Pediatrics, Division of Endocrinology, Alexandria University Childrens Hospital, Alexandria, Egypt 3Department of Pediatrics, Ain Shams University, Cairo, Egypt 4Pediatric Endocrine Unit, Department of Child Health, Sultan Qaboos University Hospital, Al-Khoud, Sultanate of Oman 5Division of Pediatric and Adolescent Endocrinology, Paedi Center for Specialized Pediatrics, St. Georges University Medical School at the University of Nicosia, Cyprus 6Department of Pediatrics, Endocrinology Unit, Alexandria University Childrens Hospital, Egypt, and Child Health Department, Sultan Qaboos University Hospital, Muscat, Oman 7Paediatric Endocrinologist,Screening and Functional Endocrine Diagnostics SBALDB. Professor Ivan Mitev, Medical University Sofia, Bulgaria 8Department of Pediatrics, NYU School of Medicine, New York, USA 9Medical Advisor, Thalassemia International Federation (TIF), Nicosia, Cyprus 10Department of Hematology, College of Medicine and Health Sciences Continue reading >>

Clinical Trials - Thalassemia.org The Cooleys Anemia Foundation Site

Clinical Trials - Thalassemia.org The Cooleys Anemia Foundation Site

Thalassemia.org the Cooleys Anemia Foundation site Thalassemia Clinical Trials Which Are Currently Recruiting U.S. Patients The Cooleys Anemia Foundation provides links to clinical trials for informational purposes only. The Foundation is not endorsing any one trial over others. The clinical studies listed here are currently enrolling new thalassemia patients in the United States. The links below provide information from the clinicaltrials.gov website about the requirements for participating in these studies (Eligibility). They also provide information about where the trials are taking place (Locations). If you have questions about any of the trials listed below, please contact the CAF Patient Outreach Director, Sandy Gilbert, at 212-279-8090 (extension 207) for more information. You are also encouraged to speak to your doctor about any clinical trials which might be of interest to you. The Cooleys Anemia Foundation (CAF) provides these links for informational purposes only, and is not endorsing any one trial over the others. Please note that there are additional studies taking place in other countries which are not listed here. I.Clinical Trials of Gene Therapy in Beta-Thalassemia Major -Thalassemia Major With Autologous CD34+ Hematopoietic Progenitor Cells Transduced With TNS9.3.55 a Lentiviral Vector Encoding the Normal Human -Globin Gene (This trial is currently suspended in order to secure funding to treat the next cohort of participants. Patients with questions concerning this trial should contact Dr. Farid Boulad at [email protected] .) II. Clinical Trials of Gene Editing in Transfusion-Dependent Beta Thalassemia A Study to Assess the Safety, Tolerability, and Efficacy of ST-400 for Treatment of Transfusion-Dependent Beta-thalassemia (TDT) A Study to Determine t Continue reading >>

Clinical Trials

Clinical Trials

SEG101, Sickle cell disease, crizanlizumab, pediatric, pharmacokinetic, P-selectin Bolus supplementation, Pilot randomised controlled trial, Vitamin D Hydroxyurea, Community health worker (CHW), Text messages, Medication adherence hydrops fetalis, birth defect, fetal anomaly, whole exome sequencing Beta thalassemia, Beta-thalassemia, Thalassemia major, Cooley's anemia, ZFN mediated genome editing, zinc finger nuclease Children's Hospital Medical Center, Cincinnati shared decision making, parent-provider communication, hydroxyurea, sickle cell disease bone marrow cellularity, bone marrow transplant Sickle cell disease, Allo-immunization, Blood transfusion Health Care Transition, Adolescent, Young Adult A Study to Determine the Efficacy and Safety of Luspatercept in Adults With Non Transfusion Dependent Beta ()-Thalassemia ()-Thalassemia, Beta-Thalassemia, Phase 2, Luspatercept, ACE-536, Safety, Efficacy, Placebo, Red Blood Cell Transfusions, Erythrocyte transfusion, Hb increase, NTDT Virtual reality, Pain, Nonpharmacological The First Affiliated Hospital, Guangzhou University of Traditional Chinese Medicine Thalassemia, Pregnancy, Globin expression, Colla corii asini Non-Myeloablative Conditioning Regimen With Haploidentical T-Cell-Depleted Peripheral Blood Transplant for Patients With Severe Sickle Cell Disease Sickle Cell Disease, Sickle Cell Disorders, Hemoglobinopathies, Thalassemia, Anemia, Sickle Cell, Haploidentical Transplant, Nonmyeloablative Conditioning, CD4+ T cell, CD4+ T cell-depleted Hematopoietic Cell Transplant, Mixed Chimerism mHealth, Medication adherence, Barriers to adherence Sickle Cell Disease, Hematopoietic stem cell transplantation, Haploidentical stem cell transplantation, Post-transplant Cytoxan Gene therapy, lentivirus vector, BCL11A, Fetal H Continue reading >>

Sickle Cell Anemia Patients May Benefit From Diabetes Drug Metformin, Study Suggests

Sickle Cell Anemia Patients May Benefit From Diabetes Drug Metformin, Study Suggests

Metformin, a common drug for Type 2 diabetes, could be used to turn onfetal hemoglobin levels in sickle cell anemia patients, according to a study by researchers at Baylor College of Medicine and Texas Childrens Cancer and Hematology Centers . The studys lead investigator called the finding a major breakthrough in treating the disease. Sickle cell patients adult hemoglobin causes their red blood cells to become sickle-shaped and get stuck inside the blood vessels, leading to pain and other complications. Fetal hemoglobin, a type of hemoglobin present in newborns, does not cause red blood cells to become sickle-shaped, but its production stops at about6 months old. The only drug thats widely used to treat sickle cell anemia is hydroxyurea. It slows red blood cells maturation in an attempt to keep fetal hemoglobin levelshigh. But the amount of fetal hemoglobin produced using the drug is not sufficient, and the treatment does not workfor about half of sickle cell patients. It also is not effective in treating beta thalassemia, a blood disorder in which insufficient amounts of hemoglobin are produced. In an attempt to identify new drugs that can increase fetal hemoglobin levels,lead investigator Vivien Sheehan , MD, PhD, and her colleagues analyzed genetic difference between people with sickle cell anemia and healthy controls. They found that people with sickle cell had mutations in the FOXO3 gene, which resulted in them producing less fetal hemoglobin. To confirm the finding, the researchers stopped the FOXO3 genes expressionin cells taken from human bone marrow and grown in a lab. They saw that blocking the gene made the cells produce less fetal hemoglobin. In a reverse experiment, increasing expression of the gene increased fetal hemoglobin production. The researchers t Continue reading >>

Use Of Metformin As A Fetal Hemoglobin Inducer In Patients With Hemoglobinopathies

Use Of Metformin As A Fetal Hemoglobin Inducer In Patients With Hemoglobinopathies

Use of Metformin as a Fetal Hemoglobin Inducer in Patients With Hemoglobinopathies Fetal Hemoglobin Induction Treatment Metformin The purpose of this study is to determine whether metformin is effective in the treatment for sickle cell anemia (SCA) and non-transfusion dependent thalassemia (NTDT). This is a dose escalation, pilot study for subjects with sickle cell anemia (SCA) disease and non-transfusion dependent thalassemia (NTDT) to determine if metformin has a beneficial effect on the treatment and quality of life of SCA and NTDT patients. Change in Fetal Hemoglobin (HbF) Percentage (SCA) or Change in Total Hemoglobin (Hb) (NTDT) Metfomin will be taken daily. The metformin dose will be increased during two time points per subject if protocol dose escalation criteria is met. Questionnaires will be completed to assess the impact quality of life 1. Confirmed diagnosis of sickle cell anemia or non-transfusion dependent thalassemia 2. Age greater than or equal to 12 and less than or equal to 40 years of age. 3. If on hydroxyurea, fetal hemoglobin less than 20% at maximum tolerated dose 4. Creatinine less than or equal to 1.4mg/dL and estimated glomerular filtration rate 5. Liver function tests less than or equal to 3 times upper limits of normal 2. Simple or chronic red blood cell transfusion therapy in the last 3 months OR a HbA 4. Refusal to use medically effective birth control if female and sexually active. 5. If on hydroxyurea, not at stable maximum tolerated dose for a minimum of 4 months 7. Liver function tests greater than 3x upper limits of normal The University of Texas Health Science Center at Houston Subjects who are currently taking Hydroxyurea as part of standard of care and have sickle cell anemia. Subjects who are not taking Hydroxyurea as part of stand Continue reading >>

Vitamin B12 Deficiency: A Chronic Complication Of Metformin Therapy That Can Cause Irreversible Neuronal Damage

Vitamin B12 Deficiency: A Chronic Complication Of Metformin Therapy That Can Cause Irreversible Neuronal Damage

Vitamin B12 deficiency: A chronic complication of metformin therapy that can cause irreversible neuronal damage Expert recommends annual monitoring or injections of vitamin B12 for long-term metformin users. Please provide your email address to receive an email when new articles are posted on this topic. Receive an email when new articles are posted on this topic. Vitamin B12 levels, often depleted due to metformin-induced malabsorption, should be monitored on a yearly basis in patients with diabetes receiving long-term metformin therapy, Editorial Board member David S.H. Bell, MD, suggested in a case report published in the A more cost-effective alternative method to avoid vitamin B12 deficiency may be an annual vitamin B12 injection to provide more than the annual vitamin B12 requirements for patients on chronic metformin therapy, said Bell, of Southside Endocrinology and clinical professor of medicine at the University of Alabama School of Medicine, Birmingham. Vitamin B12 malabsorption is a chronic complication of metformin therapy and can present with irreversible neuronal damage. Many people are unaware of metformin-induced malabsorption of vitamin B12 and that is a potential problem, he told His recommendation comes after a case report of a 69-year-old white man with well-controlled type 2 diabetes (HbA1c, 6%) for six years. The patient developed numbness in the feet, but did not report the symptom to his physician. Several months later, a routine complete blood count showed a hematocrit drop from 34% to 24% despite no change in mean corpuscular volume. The patient also had a very low vitamin B12 level and was started on vitamin B12 therapy. After vitamin B12 therapy, the patients hematocrit level returned to 24% but the numbness persisted. On physical examinati Continue reading >>

Article Medicale Tunisie, Article Medicale

Article Medicale Tunisie, Article Medicale

Si vous avez oubli votre mot de passe : cliquez ici Y.M., a 25-year-old thalassemic Tunisian patient, born from consanguineous heterozygous beta thalassemia parents. There was no evidence of family history of diabetes. The primary symptom of the disease was pallor and yellow colour. Homozygous beta-thalassemia had been diagnosed since the age of 12 months. The patient had to be started on regular periodic red cell transfusions since the age of 24 months. Chelation therapy was started by deferoxamine mesylate since the age of 4. He presented an impaired puberty secondary to hypogonadotrophic hypogonadism with Tanner stage III testis development and pubic hair at the age of 19. The basal serumtestosterone, luteinizing and FSH hormones were respectively [2.1 nmol/l (normal, 10.4-41.6nmol/l); 1.1 mIU/ml (normal, 1- 8mIU/ ml) and 1.2 mIU/ ml (normal,0.6-12mIU/ ml)]. Magnetic Resonance Imaging showed a reduction of pituitary signal intensity in T2-weighted images. Long-term compliance with deferoxamine therapy was poor with high hepatic iron levels: 14.1mg/g liver dry weight at the age of 21; (range accepted as optimal, 3-7mg/g liver dry weight). The mean serum ferritin and alanine transaminase values were respectively [2248ng/ml (normal, 6.9-323ng/ml) and 21IU/l (normal, 0-37IU/l)]. At the age of 23, he developed diabetes mellitus with a fasting glucose value of 1.28g/l confirmed by a repeat value 1.38g/l one month later. Insulin and peptide C blood levels were respectively 26 pmol/l (normal, 13 - 161 pmol/l) and 1.56 g/l (normal, 0. 8 - 4. 2 g/l)]. Physical examination revealed height: 162cm (-1.5SD), BMI of 20.4kg/m2 and blood pressure of 120/60mmHg. Serological results were negative for B and C hepatitis. Total cholesterol, low-density lipoprotein cholesterol, triglyceri Continue reading >>

Metformin Side Effects - Pros And Cons Of Continuing?

Metformin Side Effects - Pros And Cons Of Continuing?

Metformin side effects - pros and cons of continuing? I was assuming the ER would mean a steadier dose but not affect numbers, but what you say makes sense. I've been struggling to get my daytime numbers down under 100 which is where I had been mostly keeping them. You give me hope - ! A problem with metformin is that it causes macrocytosis. As far as I can tell macrocytosis is not a problem in itself, the question is why metformin causes it. One obvious reason is the apparent decrease in B-12 that is observed with metformin. However, it appears to have a liver toxicity that goes beyond poor B-12 absorption. Of course, its benefit appears to be its slowing the liver's conversion of glycogen to glucose. Which is a form of liver toxicity and may be create macrocytosis as a side-effect. Metformin is not innocuous, it creates problems. The attached article from the AAFP describes macrocytosis and you can see that metformin is one of the problems. If you wonder if metformin is affecting you in this way look at your CBC results. Your MCV may be elevated or you MCH may be elevated. Also, metformin may make you more sensitive to the affects of alcohol on your liver. In other words, an acceptable amount of alcohol - 2 drinks a day -- may combine with metformin to push your MCV above the normal range. A problem with metformin is that it causes macrocytosis. As far as I can tell macrocytosis is not a problem in itself, the question is why metformin causes it. I have thalassemia (beta, minor) so I have the opposite, microcytosis. Any idea what metformin might be doing to me? I don't see any differences in my labs since I've been taking metformin. The universe is made of stories, not atoms. Muriel Rukeyser I have thalassemia (beta, minor) so I have the opposite, microcytosis. Any i Continue reading >>

Diabetes In Thalassaemia

Diabetes In Thalassaemia

WHO calls for the publication of all the resultsof clinical trials - Read More Dr Maria Barnard, Lead Consultant in Diabetes The Whittington Hospital NHS Trust London Honorary Senior Lecturer, University College London Medical School Diabetes mellitus is a major global health challenge. In 2007, around 246 million people worldwide were living with diabetes and that number is predicted to increase to 380 million by 2025. In the UK, the number of people with diabetes could reach three million by 2010. Already each day in the UK, 10 million is spent on treating diabetes and diabetic complications, including heart disease, stroke, blindness, kidney disease and amputations. People with diabetes may also develop severely abnormal blood glucose (sugar) levels, requiring urgent medical attention. All this means that people with diabetes have a reduced life expectancy. Worldwide, every ten seconds, a person dies from diabetes-related causes. Diabetes is diagnosed by detecting an increased glucose level on a blood sample. If this does not give a definite answer, an oral glucose tolerance test (OGTT) is done, when blood glucose is measured before and2 hours after having a glucose drink. In some people, the blood glucose level is not high enough to diagnose diabetes, but is not low enough to be classified normal. This impaired glucose tolerance or pre-diabetic syndrome can be a precursor to developing diabetes. Affects 5-10% of people with diabetes and is most commonly diagnosed in childhood. It is caused by autoimmune destruction of the -cells, when antibodies are made that directly attack these insulin-producing cells. People are born with a genetic tendency to develop type 1 diabetes, which is then triggered possibly by exposure to a viral infection. This affects 9095% of peopl Continue reading >>

Higher Prevalence Of Metformin-induced Vitamin B12 Deficiency In Sulfonylurea Combination Compared With Insulin Combination In Patients With Type 2 Diabetes: A Cross-sectional Study

Higher Prevalence Of Metformin-induced Vitamin B12 Deficiency In Sulfonylurea Combination Compared With Insulin Combination In Patients With Type 2 Diabetes: A Cross-sectional Study

Click through the PLOS taxonomy to find articles in your field. For more information about PLOS Subject Areas, click here . Higher Prevalence of Metformin-Induced Vitamin B12 Deficiency in Sulfonylurea Combination Compared with Insulin Combination in Patients with Type 2 Diabetes: A Cross-Sectional Study Affiliation Division of Endocrinology and Metabolism, Department of Internal Medicine, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea Affiliation Division of Endocrinology and Metabolism, Department of Internal Medicine, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea Affiliation Division of Endocrinology and Metabolism, Department of Internal Medicine, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea Affiliation Division of Endocrinology and Metabolism, Department of Internal Medicine, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea Affiliation Division of Endocrinology and Metabolism, Department of Internal Medicine, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea Affiliation Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, South Carolina, United States of America Continue reading >>

Thalassemias - Blood Disorders - Merck Manuals Consumer Version

Thalassemias - Blood Disorders - Merck Manuals Consumer Version

All thalassemias have similar symptoms, but they vary in severity. In alpha-thalassemia minor and beta-thalassemia minor, people have mild anemia with no symptoms. In alpha-thalassemia major, people have moderate or severe symptoms of anemia, including fatigue, shortness of breath, paleness, and an enlarged spleen , which leads to a feeling of fullness and abdominal discomfort. In beta-thalassemia major (sometimes called Cooley anemia), people have severe symptoms of anemia, such as fatigue, weakness, and shortness of breath, and they may also have jaundice , causing yellowing of the skin and whites of the eyes, skin ulcers, and gallstones . People may also have an enlarged spleen. Overactive bone marrow may cause some bones, especially those in the head and face, to thicken and enlarge. The long bones in the arms and legs may weaken and fracture easily. Children who have beta-thalassemia major may grow more slowly and reach puberty later than they normally would. Because iron absorption may be increased and frequent blood transfusions (providing even more iron) are needed, excessive iron may accumulate and be deposited in the heart muscle, eventually causing iron overload disease and heart failure and early death. Blood tests are done for diagnosis of thalassemia. Doctors measure blood counts and examine a sample of blood under a microscope. Characteristic abnormalities of the red blood cells can be seen. Hemoglobin electrophoresis , another blood test, is also done. In electrophoresis, an electrical current is used to separate the different types of hemoglobin and thus detect abnormal hemoglobin. Testing a drop of blood by electrophoresis is helpful but may be inconclusive, especially for alpha-thalassemia. Therefore, the diagnosis is usually based on special hemoglo Continue reading >>

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