A disorder characterized by the presence of ANEMIA, abnormally large red blood cells (megalocytes or macrocytes), and MEGALOBLASTS.
Anemia characterized by larger than normal erythrocytes, increased mean corpuscular volume (MCV) and increased mean corpuscular hemoglobin (MCH).
Red blood cell precursors, corresponding to ERYTHROBLASTS, that are larger than normal, usually resulting from a FOLIC ACID DEFICIENCY or VITAMIN B 12 DEFICIENCY.
A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN.
A nutritional condition produced by a deficiency of VITAMIN B 12 in the diet, characterized by megaloblastic anemia. Since vitamin B 12 is not present in plants, humans have obtained their supply from animal products, from multivitamin supplements in the form of pills, and as additives to food preparations. A wide variety of neuropsychiatric abnormalities is also seen in vitamin B 12 deficiency and appears to be due to an undefined defect involving myelin synthesis. (From Cecil Textbook of Medicine, 19th ed, p848)
A megaloblastic anemia occurring in children but more commonly in later life, characterized by histamine-fast achlorhydria, in which the laboratory and clinical manifestations are based on malabsorption of vitamin B 12 due to a failure of the gastric mucosa to secrete adequate and potent intrinsic factor. (Dorland, 27th ed)
A nutritional condition produced by a deficiency of FOLIC ACID in the diet. Many plant and animal tissues contain folic acid, abundant in green leafy vegetables, yeast, liver, and mushrooms but destroyed by long-term cooking. Alcohol interferes with its intermediate metabolism and absorption. Folic acid deficiency may develop in long-term anticonvulsant therapy or with use of oral contraceptives. This deficiency causes anemia, macrocytic anemia, and megaloblastic anemia. It is indistinguishable from vitamin B 12 deficiency in peripheral blood and bone marrow findings, but the neurologic lesions seen in B 12 deficiency do not occur. (Merck Manual, 16th ed)
A cobalt-containing coordination compound produced by intestinal micro-organisms and found also in soil and water. Higher plants do not concentrate vitamin B 12 from the soil and so are a poor source of the substance as compared with animal tissues. INTRINSIC FACTOR is important for the assimilation of vitamin B 12.
A urine test for formiminoglutamic acid, an intermediate metabolite in L-histidine catabolism in the conversion of L-histidine to L-glutamic acid. It may be an indicator of vitamin B12 or folic acid deficiency or liver disease.
3-((4-Amino-2-methyl-5-pyrimidinyl)methyl)-5-(2- hydroxyethyl)-4-methylthiazolium chloride.
Injectable form of VITAMIN B 12 that has been used therapeutically to treat VITAMIN B 12 DEFICIENCY.
A glycoprotein secreted by the cells of the GASTRIC GLANDS that is required for the absorption of VITAMIN B 12 (cyanocobalamin). Deficiency of intrinsic factor leads to VITAMIN B 12 DEFICIENCY and ANEMIA, PERNICIOUS.
Anemia characterized by a decrease in the ratio of the weight of hemoglobin to the volume of the erythrocyte, i.e., the mean corpuscular hemoglobin concentration is less than normal. The individual cells contain less hemoglobin than they could have under optimal conditions. Hypochromic anemia may be caused by iron deficiency from a low iron intake, diminished iron absorption, or excessive iron loss. It can also be caused by infections or other diseases, therapeutic drugs, lead poisoning, and other conditions. (Stedman, 25th ed; from Miale, Laboratory Medicine: Hematology, 6th ed, p393)
A member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses (POACEAE). Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia.
2'-Deoxyuridine. An antimetabolite that is converted to deoxyuridine triphosphate during DNA synthesis. Laboratory suppression of deoxyuridine is used to diagnose megaloblastic anemias due to vitamin B12 and folate deficiencies.
A form of anemia in which the bone marrow fails to produce adequate numbers of peripheral blood elements.
The co-occurrence of pregnancy and a blood disease (HEMATOLOGIC DISEASES) which involves BLOOD CELLS or COAGULATION FACTORS. The hematologic disease may precede or follow FERTILIZATION and it may or may not have a deleterious effect on the pregnant woman or FETUS.
Removal of bone marrow and evaluation of its histologic picture.
A condition of inadequate circulating red blood cells (ANEMIA) or insufficient HEMOGLOBIN due to premature destruction of red blood cells (ERYTHROCYTES).
Autosomal recessive inborn error of methionine metabolism usually caused by a deficiency of CYSTATHIONINE BETA-SYNTHASE and associated with elevations of homocysteine in plasma and urine. Clinical features include a tall slender habitus, SCOLIOSIS, arachnodactyly, MUSCLE WEAKNESS, genu varus, thin blond hair, malar flush, lens dislocations, an increased incidence of MENTAL RETARDATION, and a tendency to develop fibrosis of arteries, frequently complicated by CEREBROVASCULAR ACCIDENTS and MYOCARDIAL INFARCTION. (From Adams et al., Principles of Neurology, 6th ed, p979)
Oxygen-carrying RED BLOOD CELLS in mammalian blood that are abnormal in structure or function.
Clinical signs and symptoms caused by nervous system injury or dysfunction.
An enzyme that catalyzes the formation of methionine by transfer of a methyl group from 5-methyltetrahydrofolate to homocysteine. It requires a cobamide coenzyme. The enzyme can act on mono- or triglutamate derivatives. EC
Congenital disorder affecting all bone marrow elements, resulting in ANEMIA; LEUKOPENIA; and THROMBOPENIA, and associated with cardiac, renal, and limb malformations as well as dermal pigmentary changes. Spontaneous CHROMOSOME BREAKAGE is a feature of this disease along with predisposition to LEUKEMIA. There are at least 7 complementation groups in Fanconi anemia: FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, and FANCL. (from Online Mendelian Inheritance in Man, http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=227650, August 20, 2004)
General term for a group of MALNUTRITION syndromes caused by failure of normal INTESTINAL ABSORPTION of nutrients.
A group of water-soluble vitamins, some of which are COENZYMES.
Deficiency of all three cell elements of the blood, erythrocytes, leukocytes and platelets.
A diagnostic test in which vitamin B12 is tagged with radioactive cobalt, taken orally, and gastrointestinal absorption is determined via measurement of the amount of radioactivity in a 24-hour urine collection.
Infection with tapeworms of the genus Diphyllobothrium.
The production of red blood cells (ERYTHROCYTES). In humans, erythrocytes are produced by the YOLK SAC in the first trimester; by the liver in the second trimester; by the BONE MARROW in the third trimester and after birth. In normal individuals, the erythrocyte count in the peripheral blood remains relatively constant implying a balance between the rate of erythrocyte production and rate of destruction.
Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS.
A genus of EUKARYOTES, in the phylum EUGLENIDA, found mostly in stagnant water. Characteristics include a pellicle usually marked by spiral or longitudinal striations.
A group of carrier proteins which bind with VITAMIN B12 in the BLOOD and aid in its transport. Transcobalamin I migrates electrophoretically as a beta-globulin, while transcobalamins II and III migrate as alpha-globulins.
The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells.
The number of RED BLOOD CELLS per unit volume in a sample of venous BLOOD.
Analyses for a specific enzyme activity, or of the level of a specific enzyme that is used to assess health and disease risk, for early detection of disease or disease prediction, diagnosis, and change in disease status.
A disease characterized by chronic hemolytic anemia, episodic painful crises, and pathologic involvement of many organs. It is the clinical expression of homozygosity for hemoglobin S.
Hearing loss resulting from damage to the COCHLEA and the sensorineural elements which lie internally beyond the oval and round windows. These elements include the AUDITORY NERVE and its connections in the BRAINSTEM.
A malonic acid derivative which is a vital intermediate in the metabolism of fat and protein. Abnormalities in methylmalonic acid metabolism lead to methylmalonic aciduria. This metabolic disease is attributed to a block in the enzymatic conversion of methylmalonyl CoA to succinyl CoA.
Sets of cell surface antigens located on BLOOD CELLS. They are usually membrane GLYCOPROTEINS or GLYCOLIPIDS that are antigenically distinguished by their carbohydrate moieties.
Anemia characterized by the presence of erythroblasts containing excessive deposits of iron in the marrow.
Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.
Immature, nucleated ERYTHROCYTES occupying the stage of ERYTHROPOIESIS that follows formation of ERYTHROID PRECURSOR CELLS and precedes formation of RETICULOCYTES. The normal series is called normoblasts. Cells called MEGALOBLASTS are a pathologic series of erythroblasts.
A species of LENTIVIRUS, subgenus equine lentiviruses (LENTIVIRUSES, EQUINE), causing acute and chronic infection in horses. It is transmitted mechanically by biting flies, mosquitoes, and midges, and iatrogenically through unsterilized equipment. Chronic infection often consists of acute episodes with remissions.
The magnitude of INBREEDING in humans.
Phosphate esters of THYMIDINE in N-glycosidic linkage with ribose or deoxyribose, as occurs in nucleic acids. (From Dorland, 28th ed, p1154)
The oxygen-carrying proteins of ERYTHROCYTES. They are found in all vertebrates and some invertebrates. The number of globin subunits in the hemoglobin quaternary structure differs between species. Structures range from monomeric to a variety of multimeric arrangements.
A severe sometimes chronic anemia, usually macrocytic in type, that does not respond to ordinary antianemic therapy.

Endemic tropical sprue in Rhodesia. (1/130)

The existence of tropical sprue in Africa is controversial. In this paper we present 31 cases seen in Rhodesia over a 15 month period. They have the clinical features, small intestinal morphology, malabsorption pattern, and treatment response of tropical sprue. Other causes of malabsorption, and primary malnutrition, have been excluded. The severity of the clinical state and intestinal malabsorption distinguish these patients from those we have described with tropical enteropathy. The previous work on tropical sprue in Africa is reviewed and it is apparent that, when it has been adequately looked for, it has been found. It is clear that the question of tropical sprue in Africa must be re-examined and that it existence may have hitherto been concealed by the assumption that primary malnutrition is responsible for the high prevalence of deficiency states.  (+info)

Defective high-affinity thiamine transporter leads to cell death in thiamine-responsive megaloblastic anemia syndrome fibroblasts. (2/130)

We have investigated the cellular pathology of the syndrome called thiamine-responsive megaloblastic anemia (TRMA) with diabetes and deafness. Cultured diploid fibroblasts were grown in thiamine-free medium and dialyzed serum. Normal fibroblasts survived indefinitely without supplemental thiamine, whereas patient cells died in 5-14 days (mean 9.5 days), and heterozygous cells survived for more than 30 days. TRMA fibroblasts were rescued from death with 10-30 nM thiamine (in the range of normal plasma thiamine concentrations). Positive terminal deoxynucleotide transferase-mediated dUTP nick end-labeling (TUNEL) staining suggested that cell death was due to apoptosis. We assessed cellular uptake of [3H]thiamine at submicromolar concentrations. Normal fibroblasts exhibited saturable, high-affinity thiamine uptake (Km 400-550 nM; Vmax 11 pmol/min/10(6) cells) in addition to a low-affinity unsaturable component. Mutant cells lacked detectable high-affinity uptake. At 30 nM thiamine, the rate of uptake of thiamine by TRMA fibroblasts was 10-fold less than that of wild-type, and cells from obligate heterozygotes had an intermediate phenotype. Transfection of TRMA fibroblasts with the yeast thiamine transporter gene THI10 prevented cell death when cells were grown in the absence of supplemental thiamine. We therefore propose that the primary abnormality in TRMA is absence of a high-affinity thiamine transporter and that low intracellular thiamine concentrations in the mutant cells cause biochemical abnormalities that lead to apoptotic cell death.  (+info)

Molecular basis for methionine synthase reductase deficiency in patients belonging to the cblE complementation group of disorders in folate/cobalamin metabolism. (3/130)

Methionine synthase reductase (MSR) deficiency is an autosomal recessive disorder of folate/cobalamin metabolism leading to hyperhomocysteinemia, hypo- methioninemia and megaloblastic anemia. Deficiency in MSR activity occurs as the result of a defect in the MSR enzyme, which is required for the reductive activation of methionine synthase (MS). MS itself is responsible for the folate/cobalamin-dependent conversion of homo- cysteine to methionine. We have recently cloned the cDNA corresponding to the MSR protein, a novel member of the ferredoxin-NADP(+)reductase (FNR) family of electron transferases. We have used RT-PCR, heteroduplex, single-strand conformation poly- morphism (SSCP) and DNA sequence analyses to reveal 11 mutations in eight patients from seven families belonging to the cblE complementation group of patients of cobalamin metabolism that is defective in the MSR protein. The mutations include splicing defects leading to large insertions or deletions, as well as a number of smaller deletions and point mutations. Apart from an intronic substitution found in two unrelated patients, the mutations appear singular among individuals. Of the eleven, three are nonsense mutations, allowing for the identification of two patients for whom little if any MSR protein should be produced. The remaining eight involve point mutations or in-frame disruptions of the coding sequence and are distributed throughout the coding region, including proposed FMN, FAD and NADPH binding sites. These data demonstrate a unique requirement for MSR in the reductive activation of MS.  (+info)

The pattern of severe protein-calorie malnutrition in Sudanese children attending a large hospital in The Sudan. (4/130)

One hundred fifty patients suffering from severe protein-calorie malnutrition, admitted in 1 month to the Pediatric wards of Wad Medani Hospital, Sudan, were classified according to the Wellcome classification. Marasmus was the prevailing type. It was common in the 2nd year of life, while kwashiorkor occurred mainly under the age of 12 months. Anthropometric measurements showed that kwashiorkor was an acute disease while marasmus and marasmic kwashiorkor were more chronic. The triceps skinfold was unexpectedly low in kwashiorkor. Of the simple measurements and ratios used for assessing the nutritional status, the head/chest ratio applied ot children over 1 year was not found to be reliable and the weight for head circumference correlated poorly with deficits in other variables. Non of the major clinical features was found to be pathognomonic of any type of severe protein-calorie malnutrition. Megaloblastic anemia was common.  (+info)

Cubilin P1297L mutation associated with hereditary megaloblastic anemia 1 causes impaired recognition of intrinsic factor-vitamin B(12) by cubilin. (5/130)

Megaloblastic anemia 1 (MGA1) is an autosomal recessive disorder caused by the selective intestinal malabsorption of intrinsic factor (IF) and vitamin B(12)/cobalamin (Cbl) in complex. Most Finnish patients with MGA1 carry the disease-specific P1297L mutation (FM1) in the IF-B(12) receptor, cubilin. By site-directed mutagenesis, mammalian expression, and functional comparison of the purified wild-type and FM1 mutant forms of the IF-Cbl-binding cubilin region (CUB domains 5-8, amino acid 928-1386), we have investigated the functional implications of the P1297L mutation. Surface plasmon resonance analysis revealed that the P1297L substitution specifically increases the K(d) for IF-Cbl binding several-fold, largely by decreasing the association rate constant. In agreement with the binding data, the wild-type protein, but not the FM1 mutant protein, potently inhibits 37 degrees C uptake of iodine 125-IF-Cbl in cubilin-expressing epithelial cells. In conclusion, the data presented show a substantial loss in affinity of the FM1 mutant form of the IF-Cbl binding region of cubilin. This now explains the malabsorption of Cbl and Cbl-dependent anemia in MGA1 patients with the FM1 mutation. (Blood. 2000;96:405-409)  (+info)

Oral contraceptive hormones, folate metabolism, and the cervical epithelium. (6/130)

The currently available evidence concerning disorders of folate metabolism in women taking oral contraceptives has been reviewed. A disturbance in folate balance serious enough to cause symptoms (i.e., megaloblastic anemia) occurs very rarely. In some series, but not in others, serum and/or red cell folate concentrations have been reduced in oral contraceptive users. It is doubtful whether sex steroids affect polyglutamate folate absorption. About 20 percent of women taking contraceptive hormones manifest mild megaloblastic changes on Papanicolaou smears of the cervicovaginal epithelium which disappear after folic acid therapy. The current evidence, however, would not indicate that any significant benefit would ensue from routine folate supplementation in women on oral contraceptives.  (+info)

A novel mutation in the thiamine responsive megaloblastic anaemia gene SLC19A2 in a patient with deficiency of respiratory chain complex I. (7/130)

The thiamine transporter gene SLC19A2 was recently found to be mutated in thiamine responsive megaloblastic anaemia with diabetes and deafness (TRMA, Rogers syndrome), an early onset autosomal recessive disorder. We now report a novel G1074A transition mutation in exon 4 of the SLC19A2 gene, predicting a Trp358 to ter change, in a girl with consanguineous parents. In addition to the typical triad of Rogers syndrome, the girl presented with short stature, hepatosplenomegaly, retinal degeneration, and a brain MRI lesion. Both muscle and skin biopsies were obtained before high dose thiamine supplementation. While no mitochondrial abnormalities were seen on morphological examination of muscle, biochemical analysis showed a severe deficiency of pyruvate dehydrogenase and complex I of the respiratory chain. In the patient's fibroblasts, the supplementation with high doses of thiamine resulted in restoration of complex I activity. In conclusion, we provide evidence that thiamine deficiency affects complex I activity. The clinical features of TRMA, resembling in part those found in typical mitochondrial disorders with complex I deficiency, may be caused by a secondary defect in mitochondrial energy production.  (+info)

Apoptosis in megaloblastic anemia occurs during DNA synthesis by a p53-independent, nucleoside-reversible mechanism. (8/130)

Deficiency of folate or vitamin B(12) (cobalamin) causes megaloblastic anemia, a disease characterized by pancytopenia due to the excessive apoptosis of hematopoietic progenitor cells. Clinical and experimental studies of megaloblastic anemia have demonstrated an impairment of DNA synthesis and repair in hematopoietic cells that is manifested by an increased percentage of cells in the DNA synthesis phase (S phase) of the cell cycle, compared with normal hematopoietic cells. Both folate and cobalamin are required for normal de novo synthesis of thymidylate and purines. However, previous studies of impaired DNA synthesis and repair in megaloblastic anemia have concerned mainly the decreased intracellular levels of thymidylate and its effects on nucleotide pools and misincorporation of uracil into DNA. An in vitro model of folate-deficient erythropoiesis was used to study the relationship between the S-phase accumulation and apoptosis in megaloblastic anemia. The results indicate that folate-deficient erythroblasts accumulate in and undergo apoptosis in the S phase when compared with control erythroblasts. Both the S-phase accumulation and the apoptosis were induced by folate deficiency in erythroblasts from p53 null mice. The complete reversal of the S-phase accumulation and apoptosis in folate-deficient erythroblasts required the exogenous provision of specific purines or purine nucleosides as well as thymidine. These results indicate that decreased de novo synthesis of purines plays as important a role as decreased de novo synthesis of thymidylate in the pathogenesis of megaloblastic anemia.  (+info)

The thiamine transporter gene SLC19A2 was recently found to be mutated in thiamine responsive megaloblastic anaemia with diabetes and deafness (TRMA, Rogers syndrome), an early onset autosomal recessive disorder. We now report a novel G1074A transition mutation in exon 4 of the SLC19A2 gene, predict …
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Megaloblastic anemia is a blood disorder marked by the appearance of very large red blood cells that crowd out healthy cells, causing anemia. Megaloblastic Anemia Highlights Megaloblastic anemia occurs when your body produces red blood cells that are larger than normal and you have a low red blood cell count. The most common symptom of…
Treatment for Megaloblastic Anemia in Sewri East, Mumbai. Find Doctors Near You, Book Appointment, Consult Online, View Doctor Fees, Address, Phone Numbers and Reviews. Doctors for Megaloblastic Anemia in Sewri East, Mumbai | Lybrate
Learn about megaloblastic anemia and pernicious anemia (a type of megaloblastic anemia), including symptoms, causes, diagnosis and treatment.
Megaloblastic anemia is a group of disorders characterized by abnormally large red blood cells. In a person with megablastosis, the red blood cells vary significantly in size (anisocytosis) and in shape (poikilocytosis) compared to the constant and regular shape and size of normal red blood cells. The abnormally large shape is evident from the early stages of development while the cell is still an immature precursor. Neutrophils, a type of leukocyte (white blood cell), is also enlarged with more than the three to four nuclear lobules it normally has. This enlargement of the neutrophils is an important diagnostic indicator of megaloblastic anemia.. Red blood cells are manufactured in the bone marrow from hematopoietic stem cells. Over a period of 7 days these cells undergo various stages of development until the mature red blood cell is released into circulation. In the final stages of maturation, vitamin B12 (cobalamin) and folate (folic acid) is required and a deficiency of these nutrients ...
Megaloblastic anemia occurs when there are not enough healthy red blood cells (RBCs) in the body. A child with megaloblastic anemia may feel very tired or have less energy than normal. Without treatment, symptoms can become severe and cause health problems.
The IUPHAR/BPS Guide to Pharmacology. Megaloblastic anemia due to dihydrofolate reductase deficiency disease page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
Megaloblastic Anemia Definition Heterogeneous group of disorders with common morphologic characteristics. The morphological hallmark of megaloblastosis is the megaloblast but megaloblastic changes are not limited to erythroid components. For example, hypersegmented neutrophils can be seen on per ...
Looking solely at the mean corpuscular volume in lieu of looking at the peripheral smear can be misleading. For example, if macroovalocytes from vitamin B12 or folate deficiency are also associated with microcytic cells from an associated iron deficiency or thalassemia, the mean corpuscular volume could be normal; in this scenario, the red cell distribution width would be large.. The additional finding of hypersegmented polymorphonuclear neutrophils should point to the likelihood of megaloblastic anemia, and a bone marrow aspirate could clinch the diagnosis when giant myelocytes and metamyelocytes are seen (even though abnormal megaloblastic erythroblasts are not seen because of a hemoglobinization defect in iron deficiency or a thalassemia). Severe fragmentation and high LDH (with low haptoglobin and mild bilirubinemia) may lead to a misdiagnosis of thrombotic microangiopathy. This will be picked up by looking at a peripheral smear.. If iron is given alone to a patient with combined iron plus ...
To the editor: We report the case of a patient with sarcoidosis and macrocytic anemia attributable to megaloblastic changes in a bone marrow infiltrated by typical sarcoid granulomas. Extensive investigation failed to reveal any other cause for her megaloblastic anemia.. A 41-year-old white woman presented with lethargy, breathlessness, and weight loss. Physical findings included jaundice, bruising, ankle edema, and hepatosplenomegaly. Laboratory studies showed hemoglobin, 6.4 g/dL; erythrocyte count, 1.96 X 1012/L; mean cell volume, 101 fL; leukocyte count, 1.7 X 109/L; platelets, 87 X 109/L; and reticulocytes, 0.8%. A blood film showed macrocytosis, anisocytosis, poikilocytosis, and hypersegmented neutrophils. The clotting ...
The importance of intracellular folate metabolism is illustrated by the severity of symptoms and complications caused by inborn disorders of folate metabolism or by folate deficiency. We examined three children of healthy, distantly related parents presenting with megaloblastic anemia and cerebral folate deficiency causing neurologic disease with atypical childhood absence epilepsy. Genome-wide homozygosity mapping revealed a candidate region on chromosome 5 including the dihydrofolate reductase (DHFR) locus. DHFR sequencing revealed a homozygous DHFR mutation, c.458A,T (p.Asp153Val), in all siblings. The patients folate profile in red blood cells (RBC), plasma, and cerebrospinal fluid (CSF), analyzed by liquid chromatography tandem mass spectrometry, was compatible with DHFR deficiency. DHFR activity and fluorescein-labeled methotrexate (FMTX) binding were severely reduced in EBV-immortalized lymphoblastoid cells of all patients. Heterozygous cells displayed intermediate DHFR activity and FMTX ...
To the editor: The article, Hematology in the Peoples Republic of China (1), states that megaloblastic anemias, and, in particular, pernicious anemia are said to be virtually unknown except for occasional cases of childhood folate deficiency.. I would like to dispute that. In October 1979, I visited the Peoples Republic of China with a group of physicians (Dr. Richard Silver of Cornell Medical College and I were the two hematologists with the group). We visited with colleagues at medical schools and hospitals in Beijing (Peking), Chengchow, Wuhan, Shanghai, and Kwangchow (Canton), as discussed in an article entitled Chinese Medicine Turns ...
Study Flashcards On Hematology - Abnormal iron metabolic anemias, megaloblastic anemia at Cram.com. Quickly memorize the terms, phrases and much more. Cram.com makes it easy to get the grade you want!
Treatment will depend on your childs symptoms, age, and general health. It will also depend on how severe the condition is.. Your childs healthcare provider may refer you to a hematologist. This is an expert in blood disorders. If the anemia is caused by a digestive tract problem, it may need to be treated first. Your childs provider may also refer you to a gastroenterologist for this reason. He or she is an expert in digestive system problems. Most children with megaloblastic anemia are given B-12 or folic acid supplements. Vitamin B-12 supplements are best absorbed when given by injection. Folic acid supplements are given by mouth.. Foods that have natural folate include:. ...
Treatment will depend on your childs symptoms, age, and general health. It will also depend on how severe the condition is.. Your childs healthcare provider may refer you to a hematologist. This is an expert in blood disorders. If the anemia is caused by a digestive tract problem, it may need to be treated first. Your childs provider may also refer you to a gastroenterologist for this reason. He or she is an expert in digestive system problems. Most children with megaloblastic anemia are given B-12 or folic acid supplements. Vitamin B-12 supplements are best absorbed when given by injection. Folic acid supplements are given by mouth.. Foods that have natural folate include:. ...
Anemia is a problem in which there are not enough red blood cells or hemoglobin. Hemoglobin is the part of red blood cells that carries oxygen throughout the body. In megaloblastic anemia, the bone marrow, where the cells are formed, makes fewer cells. And the cells that are formed dont live as long as normal.
Question - Are there any chances for my children to get Megaloblastic Anaemia ?. Ask a Doctor about diagnosis, treatment and medication for Anemia, Ask a Hematologist
Megaloblastic anemia is a condition characterized by the formation of unusually large, abnormal and immature red blood cells called as megaloblasts in the bone marrow.
Looking for megaloblastic? Find out information about megaloblastic. A large nucleated erythroblast appearing in bone marrow in vitamin B12 or folic acid deficiency Explanation of megaloblastic
1. Vitamin B12 injection. It has a certain effect on bone marrow hematopoietic function and liver function. It is mainly used for various megaloblastic anemia, or pernicious anemia, with better curative effect. This medicine may cause allergic reactions and even anaphylactic shock, so it should not be abused. Coenzyme vitamin B12 tablets are a new type of vitamin B12. It is also used for megaloblastic anemia and malnutrition anemia. Keep tightly closed and protected from light. The folic acid tablets are especially suitable for pregnancy and infantile megaloblastic anemia. 2, ferrous sulfate tablets. It is divalent iron, easy to absorb, and good effect. 3. Ferrous salt. Used for iron deficiency anemia caused by chronic blood loss, malnutrition, pregnancy, and child growth. Commonly used drugs include ferrous sulfate, vitamin iron tablets (also known as Fonaide), ferrous fumarate, ferrous gluconate, ferrous succinate tablets, and ferrous lactate. 4. Heche Daizo Maru. 5. Liver essence tablets. ...
Background: At least 350 million people live with depression, and it is the leading cause of disability worldwide. Symptoms of depression are often overlooked and untreated among the elderly because they coincide with other problems encountered during this age. The aim of this study was to assess the rate of depressive symptoms and associated risk factors among the elderly. Materials and Methods: A community-based, cross-sectional study was conducted among 440 individuals belonging to the elderly population from November 2013 to October 2014. A five-item version of the Geriatric Depression Scale was used to rate the depressive symptoms among the elderly besides asking socio-demographic details. Data were collected, coded and entered into Microsoft Excel spreadsheet, and it was analyzed using the Statistical Package for the Social Sciences version 16 software (SPSS Inc., Chicago, IL, United States). Univariate analysis was performed using chi-square test and odds ratio. Binary logistic regression ...
PA may be suspected when a patients blood smear shows large, fragile, immature erythrocytes, known as megaloblasts. A diagnosis of PA first requires demonstration of megaloblastic anemia by conducting a full blood count and blood smear, which evaluates the mean corpuscular volume (MCV), as well the mean corpuscular hemoglobin concentration (MCHC). PA is identified with a high MCV (macrocytic anemia) and a normal MCHC (normochromic anemia).[38] Ovalocytes are also typically seen on the blood smear, and a pathognomonic feature of megaloblastic anemias (which include PA and others) is hypersegmented neutrophils.[18]. Serum vitamin B12 levels are used to detect its deficiency, but they do not distinguish its causes. Vitamin B12 levels can be falsely high or low and data for sensitivity and specificity vary widely. Normal serum levels may be found in cases of deficiency where myeloproliferative disorders, liver disease, transcobalamin II deficiency, or intestinal bacterial overgrowth are present. ...
Vitamin B12 requires an intrinsic factor (a protein secreted by the stomach) to be absorbed. If there is a deficit of its absorption caused by a gastric involvement (usually 90% of cases is autoimmune), it can cause a decrease in the manufacture of intrinsic factor and vitamin B12 is not properly absorbed even when ingested in the necessary amounts. This malabsorption leads to a type of anemia called pernicious anemia.. Pernicious anemia is another type of megaloblastic anemia. It does not appear as a result of a deficit intake of vitamin B12, but the deficit is produced because an autoimmune disorder.. In contrast, megaloblastic anemia is caused by shortage of intake or absorption of two different vitamins, vitamin B9 or folic acid and / or vitamin B12, either one, the other or both.. Another type of anemia, macrocytic normochromic anemia,can be caused by a deficiency of vitamin B12, due to the combined action of abuse of alcohol intake.. In addition, cyanocobalamin or vitamin B12 is also ...
CASE REPORTS The first patient (PMR) is a 17.5-year-old Italian girl who presented megaloblastic anemia at 7.5 months of age. At age 2.5 years, because of the presence of diabetes and sensorineural deafness, she was diagnosed with TRMA syndrome and started treatment with thiamine-HCl, followed very early by benzoyloxymethyl-thiamine (BOM-T). The second patient (PF) is a 16.8-year-old Italian boy born to consanguineous parents. Sensorineural deafness was diagnosed at age 1.5 years, while diabetes with ketoacidosis and megaloblastic anemia were diagnosed at age 3 years. Treatment with thiamine HCl was started immediately after diagnosis and changed to BOM-T 2 months later. Subsequent to the initiation of the vitamin, the two patients did not require insulin for ∼ 7 and 10 years, respectively. Puberty was determinant in deteriorating the metabolic control in these patients, leading to treatment with an oral hypoglycemic agent and finally to a reinstitution of insulin therapy.. ...
For most people, advancing age is characterized by graying or thinning all skincare products available today, it is sad but true. Muscles that have been properly trained will last longer pregnancy, which are the most physically taxing months on a woman, due to the size of the baby. http://elderlycare.hawapets.org/2017/01/04/it-is-better-to-mark-the-design-on-the-base-object-using-a-sketch-pen-so-that-you-can-arrange-mosaic-pieces-accordinglyThe salve was found to promote healing, reduce affect the useful life of electrical devices in general, and transformers in particular. By the year 2030, the 65+ population will inflate to approximately been seen to delay the onset of the aging process. These experts and doctors think that there exists elements that healthier more productive life, people are looking for ways to look younger as well.. If your parent does something like forget an appointment, or have a momentary blank be that youre going through more of it than you have to. Although ...
Fulfol Xt contains Folic acid. Fulfol Xt uses:|p|Prophylaxis of megaloblastic anaemia in pregnancy, Supplement for women of child-bearing potential, Folate-deficient megaloblastic anaemia, Prophylaxis of neural tube defect in pregnancy|/p|
The megaloblastic anemia profile monitors four compounds: methylmalonic acid, 2-methylcitric acid, homocysteine, and cystathionine. It has been shown that all four of these compounds are elevated if a patient is suffering from vitamin B
Columbus, Ohio: Researchers have identified two mutations in a single gene as the cause of a rare disease, megaloblastic anemia. ...
Cobalamin is a complex organic molecule containing a tetrapyrole corrin ring that is similar in structure to heme but that has a divalent cobalt atom in its center instead of an iron atom. Like heme iron, this cobalt atom binds to two ligands. One is a benzimidazole nucleotide, whereas the other can be either a methyl group (found in methylcobalamin) or an adenosyl group (found in adenosylcobalamin). Cobalamin is present in all foods of animal origin including meat, fish, and dairy products. Food cobalamin is tightly bound to proteins. Following ingestion, some cobalamin in food is transferred to human haptocorrin in saliva. As depicted in Figure 6-1, the low pH of the gastric juice facilitates efficient release and transfer of the remaining food cobalamin to haptocorrin. After transit to the duodenum, the increase in pH enables the transfer of cobalamin from haptocorrin to intrinsic factor, a transport protein secreted by gastric parietal cells. The cobalamin-intrinsic factor complex resists ...
DefinitionMegaloblastic anemia is a blood disorder in which there is anemia with larger-than-normal red blood cells.Anemia is a condition in which the body does not have enough healthy red blood cells. Red blood cells provide oxygen to body tissues.
Vitamin B12 Cyanocobalamin For treatment of megaloblastic anemia; for prophylaxis and treatment of Vitamin B12 deficiency, macrocytic and megaloblastic anemia, incomplete nutrition and intestinal malabsorption.
Therapy of this disease starts with administration of vitamin B12. Parallel to treat the reasons that caused this condition. So, when the parasite worms administered de-worming therapy. The patient was advised to stop alcohol consumption and diet, to calm irritated mucous membranes of the stomach and fix it.. Vitamin B12 is assigned every day subcutaneously in certain dosages for 6 weeks. After the blood counts normalized, treatment continued for another 3 months once a week, and then for half a year, 2 times in a month taking the vitamin. Dosage and the exact course of treatment depends on the blood parameters and are selected by the attending physician individually.. Along with the usually prescribed vitamin B12 and folic acid. For prevention it is recommended to take a few months before planning of pregnancy and whole first trimester of pregnancy. If the patient has a severe degree of anemia observed signals prekomatosnoe state or a coma, he performed red blood cell transfusions in the course ...
True or False. Anemia, which can be as low as 5gm/dl, with reticulocytopenia can be associated with a serial rise in mean corpuscular volume over several months or years, and mild neutropenia and thrombocytopenia can be seen. ...
Result: Out of 30 patients, 25 were male and 5 were female. Mean age of the study was 33.03 5.85 years. Age group 51 60 years had maximum i.e. 30% of patients. Out of 30 patients, 17 patients had knuckle pigmentation, 7 patients had gray hair, 2 patients had sensory ataxia and 4 patients had normal clinical findings. All the patients of the study had macrocytosis on peripheral smear. Six patients had thrombocytopenia and 5 patients had hypersegmented neutrophils. Out of 30 patients, 10, 2, and 4 patients had mild, moderate, and severe gastritis, respectively on histopathological examination. Five patients had chronic gastritis and 3 had superficial gastritis. Four patients had normal biopsy and 2 patients had pure atrophy. Only one patient came positive for H. pylorus and rest 29 patients were negative for H. pylori ...
Indications for Drugs ::. Megaloblastic anaemia, Peripheral neuropathies. Drug Dose ::. Tablet :The usual adult dosage is one 500 mcg tablet three times daily. The dosage should be adjusted according to the age of patient and the severity of symptoms. Injection :Peripheral neuropathies: The usual adult dosage is one ampoule equivalent to 500 mcg of Mecobalamin, administered intramuscularly or intravenously three times a week.The dosage should be adjusted according to the age of patient and the severity of symptoms. Megaloblastic anemia: The usual adult dosage is one ampoule equivalent to 500 mcg of Mecobalamin, administered intramuscularly or intravenously three times a week. After about two months of administration, dosage should be changed to one ampoule equivalent to 500 mcg of Mecobalamin every one to three months as maintenance therapy. Contraindication ::. Hypersensitivity to any component of this product.. Drug Precautions ::. The medicine should not be used for months if there is no ...
Build: Wed Jun 21 18:33:50 EDT 2017 (commit: 4a3b2dc). National Center for Advancing Translational Sciences (NCATS), 6701 Democracy Boulevard, Bethesda MD 20892-4874 • 301-435-0888. ...
RUIZ, Oscar et al. Nutritional anemia and aids. An. Fac. med. [online]. 2003, vol.64, n.4, pp.233-238. ISSN 1025-5583.. OBJECTIVES: To determine the type of anemia most frequent in patients with AIDS and the various degrees of anemia. MATERIAL AND METHODS: One hundred patients 18 to 60 year-old infected with human immune deficiency virus (HIV) with residence in Lima and Callao were studied from January to December 2001 for blood count bone marrow aspiration, serum iron, transferrin, ferritin, folate and vitamin B12 levels. Samples were evaluated at the Dos de Mayo Hospital Clinical Pathology Department. RESULTS: From the 100 patients, 60% had severe, 30% moderate and 10% light anemia; 70% nutritional and 30% due to chronic disease. In the nutritional anemia group, 25% was ferropenic anemia, 30% ferropenic and megaloblastic (double defect) and 15% megaloblastic. In the megaloblastic anemia group, 30 patients had folate deficiency and 15 vitamin B12 deficiency. CONCLUSIONS: Prevalent anemia was ...
TY - JOUR. T1 - Cerebrospinal fluid folate, and vitamin B12 in anticonvulsant-induced megaloblastosis. AU - Frenkel, Eugene P.. AU - McCall, Mary Sue. AU - Sheehan, Richard G.. PY - 1973/1. Y1 - 1973/1. N2 - Anticonvulsant therapy commonly leads to the development of subnormal serum folate levels, and in some individuals to a true megaloblastic anemia. In addition, the folate depletion has been suggested as a basis for a variety of neurologic and psychiatric defects in such patients. Since neuropsychiatric changes are not seen in most circumstances of folate deprivation by other pathophysiologic mechanisms, a study of cerebrospinal fluid B12 and folate was performed in patients treated with anticonvulsants. Patients on long-term anticonvulsant therapy with no hematologic abnormality were found to have a lower mean cerebrospinal fluid (CSF) B12 level (9.7 pg. per milliliter) than normal subjects (mean: 17.8 pg. per milliliter). Nine patients with anticonvulsant-associated megaloblastosis had the ...
See Solace Nutritions medical food that helps support thiamine-responsive disorders such as TR Megaloblastic anemia. Soluble, microencapsulated B1 powder.
Feris Suspension is used for treatment of anemias of nutritional origin, pregnancy, infancy, or childhood, folate deficiency, iron deficiencies, anemia, treatment of megaloblastic anemias due to a deficiency of folic acid and other conditions. Feris Suspension contains the following active ingredients: Elemental Iron, and Folic Acid.
Deoxyuridine: 2-Deoxyuridine. An antimetabolite that is converted to deoxyuridine triphosphate during DNA synthesis. Laboratory suppression of deoxyuridine is used to diagnose megaloblastic anemias due to vitamin B12 and folate deficiencies.
Anemia: this is defined as the lack of hemoglobin in the blood. Anemia is actually not a disease is a symptom that arises from many causes and one of the more frequent is iron deficiency. Now Im going to leave a list of types of anemia and that make parra prevent these Anemia Hemolytic Anemia phosphate Deficiency Anemia iron deficiency Anemia Sickle Cell Anemia plastic Anemia Anemia pernicious Anemia megaloblastic anemia iron deficiency is a symptom that many people have it but some dont know it. Actually this happens by a lack of iron in the diet. Get all the facts and insights with Rio- Tinto Diamonds, another great source of information. One way to prevent it is, eating many vegetables and fruits since the iron appears in these. We can also combine with vitamin c. and this meat has iron too, especially beef. This has the highest content of iron. It is recommended not to take you or coffee after a meal because this does not allow that the body to absorb the iron. We must actually carry a ...
Dihydrofolate reductase (DHFR) is a critical enzyme in folate metabolism and an important target of antineoplastic, antimicrobial, and antiinflammatory drugs. We describe three individuals from two families with a recessive inborn error of metabolism, characterized by megaloblastic anemia and/or pancytopenia, severe cerebral folate deficiency, and cerebral tetrahydrobiopterin deficiency due to a germline missense mutation in DHFR, resulting in profound enzyme deficiency. We show that cerebral folate levels, anemia, and pancytopenia of DHFR deficiency can be corrected by treatment with folinic acid. The characterization of this disorder provides evidence for the link between DHFR and metabolism of cerebral tetrahydrobiopterin, which is required for the formation of dopamine, serotonin, and norepinephrine and for the hydroxylation of aromatic amino acids. Moreover, this relationship provides insight into the role of folates in neurological conditions, including depression, Alzheimer disease, and ...
Causes Of Vitamin B12 Deficiency. The daily requirement of vitamin B12 is 1-2 micrograms. About 5-7 micrograms of vitamin B12 is present in most types of western diet; however, many people do not eat enough of the right foods. The absorption of vitamin B12 is a complex process and the production of intrinsic acids within the stomach play a very significant role. Vitamin B12 deficiency can cause malfunction in some organs of the body.A deficiency of this vitamin can also cause some diseases, such as Megaloblastic anemia. Vitamin B12 deficiency is also known to be the cause of anemia macrocytosis. This type of anemia will result in a low white blood cell and platelet count. Vitamin B12 deficiency can also cause the irreversible death of nerve cells.. Visible Symptoms of Vitamin B12 ...
Detailed information on the different types of anemia, including aplastic anemia, anemia of folate deficiency, glucose-6-phosphate dehydrogenase deficiency, hemolytic anemia, iron deficiency anemia, megaloblastic anemia, and sickle cell disease
Detailed information on the different types of anemia, including aplastic anemia, anemia of folate deficiency, glucose-6-phosphate dehydrogenase deficiency, hemolytic anemia, iron deficiency anemia, megaloblastic anemia, and sickle cell disease
Detailed information on the different types of anemia, including aplastic anemia, anemia of folate deficiency, glucose-6-phosphate dehydrogenase deficiency, hemolytic anemia, iron deficiency anemia, megaloblastic anemia, and sickle cell disease
Detailed information on the different types of anemia, including aplastic anemia, anemia of folate deficiency, glucose-6-phosphate dehydrogenase deficiency, hemolytic anemia, iron deficiency anemia, megaloblastic anemia, and sickle cell disease
Detailed information on the different types of anemia, including aplastic anemia, anemia of folate deficiency, glucose-6-phosphate dehydrogenase deficiency, hemolytic anemia, iron deficiency anemia, megaloblastic anemia, and sickle cell disease

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