An illness’s definition.Causes of the disease B12-deficiency anemia (B12DA) is a condition in which the body does not have enough vitamin B12 to make red blood cells and hemoglobin.
Synonyms:Birmer, megaloblastic, and pernicious anemia is Addison’s anemia.
All blood cells (erythrocytes, leukocytes, and platelets) and cells of the gastrointestinal tract are made by vitamin B12, which also ensures that the nervous system’s cells function normally.
As a result, when vitamin B12 deficiency causes anemia, the level of platelets and leukocytes in the blood test drops, indicating damage to the gastrointestinal and nervous systems.
Also see:Unusual symptoms of colon cancer that people ignore for years Prevalence B12DA affects both children and adults, and it occurs in 1500 people per 1 million people.However, the majority of affected individuals are older than 60.The prevalence is higher in women than in men:There is a 10:7 ratio.
B12 deficiency anemia is brought on by insufficient vitamin intake, a disruption in the vitamin’s absorption, transport, metabolism (metabolism), or an increase in its consumption.Let’s examine each reason in greater detail.
1.inadequate supplyOnly animal foods contain vitamin B12.B12DA develops after two to four years if food contains little or no vitamin B12, as in vegetarianism or veganism.Due to a vitamin deficiency in the mother, a deficiency can occur in infants when breast milk contains less B12.
2.The following factors have been shown to interfere with food B12 release:
damage to the stomach’s parietal cells or their loss.In the form of protein, food contains vitamin B12.The stomach’s protein-digesting enzymes and hydrochloric acid influence the release of B12 from food.The stomach’s parietal cells produce hydrochloric acid.The destruction or loss of parietal cells as a result of one or more of the following could be the causes of the violation of its production:
Surgical treatment for stomach problems:in gastric cancer, for example, total or partial resection.
The stomach is chronically inflamed with atrophic gastritis.Counting immune system gastritis, in which the safe framework erroneously perceives the parietal cells of the stomach as unfamiliar and annihilates them with the assistance of explicit antibodies.
The parietal cells of the mucous membrane are damaged and displaced by stomach cancer or polyposis.
enzyme deficiency in the pancreas.Vitamin B12 is shielded from stomach acidity by binding to the salivary protein haptocorrin after being released from dietary proteins.Pancreatic enzymes influence the release of B12 in the duodenum.Pancreatic insufficiency, chronic pancreatitis, or Zollinger-Ellison syndrome (a pancreatic tumor) can all result in enzyme deficiency.
3.Vitamin absorption problems in the small intestine.Possible explanations:
Deficit in the intrinsic factor of Castle.B12 binds to the intrinsic factor of Castle, a stomach parietal cell-produced protein, following the vitamin’s release from salivary proteins.The vitamin can only be absorbed in the small intestine through this connection.Castle’s intrinsic factor deficiency causes:
A hereditary condition known as congenital deficiency of intrinsic factor Castle is characterized by a defect in the gene that makes this factor.
loss of stomach parietal cells.
Bowel Conditions Acquired and Congenital:
A rare hereditary condition known as Imerslund-Gresbeck Syndrome is brought on by a problem with the cube receptor in the ileum.This receptor is used to get vitamin B12.
Gluten intolerance that causes damage to the small intestine’s lining is known as celiac disease.
Chronic inflammatory bowel disease is Crohn’s disease.
lymphomas and other small intestine tumors
The ileum is resected.
Consistent use of particular drugs:aminosalicylic acid, metformin, colchicine, neomycin, biguanides, cimetidine, oral contraceptives, and others are proton pump inhibitors.
4.transportation violation.Vitamin B12 binds to the transporter protein transcobalamin II in the bloodstream after being absorbed in the intestine.It delivers the vitamin to the cells that need it.A disruption in the transport of vitamin B12 and its deficiency are caused by a defect in the transporter protein that occurs at birth or by antibodies that are produced against it.
5.infringement on metabolismVitamin B12 enters cells through the blood and participates in intricate biochemical processes like DNA synthesis, cell division and maturation, fatty acid metabolism, and homocysteine metabolism.B12DA can develop as a result of deficiencies in the enzymes that support these processes, which can be acquired or congenital.
6.consumption of more vitamin B12It may be brought on by:
Conditions that go along with more consumption:Thyrotoxicosis, multiple pregnancies, and oncohematological conditions (such as multiple myeloma and myeloproliferative disorders)
Consumption of the vitamin competitively:by bacteria, such as in blind loop syndrome and diverticulosis;parasites, including whipworm and diphyllobothriasis.
B12 deficiency anemia symptoms may begin in the first few months or years of life in children with intrinsic factor deficiency, transport protein deficiency, intracellular metabolism disorders, and other congenital conditions.Symptoms typically appear in adults and children over seven years old when dietary deficiencies or malabsorption occur.
There are three types of B12DA manifestations:
symptoms that are associated with anemia of the hemoglobin;
gastrointestinal tract damage symptoms, such as gastroenterological syndrome;
neuropsychic syndrome—symptoms of damage to the nervous system.
Each of these categories of symptoms can be present on its own or in combination.
Skin pallor, sometimes with an anicteric tint, is seen with B12DA, as with any other type of anemia.With little physical effort, may experience general weakness, fatigue, drowsiness, and shortness of breath.
Dizziness, palpitations, tinnitus, and flashing “flies” in front of the eyes are all possible symptoms.The decline in memory, performance, and performance at school or university is the focus of attention.There is a possibility of growth and development disorders in children who have an anemic syndrome.
Inflammation of the tongue, accompanied by discomfort and pain, is one symptom of damage to the gastrointestinal tract in patients with B12DA.At the same time, areas of inflammation, cracks, and ulcerations, smoothed papillae (Gunther’s glossitis), and a bright red tongue are present.There may be pain in the lips and gums as well as sores in the corners of the mouth.
Possibly diarrhea, a feeling of heaviness in the abdomen, a decrease in appetite and, as a result, weight loss.A doctor can palpate the abdomen or use ultrasound to look at the organs in the abdomen to detect a slight increase in the liver and spleen.
Funicular myelosis is the name given to the condition in which the nervous system is damaged by B12DA.It affects peripheral nerves as well as the posterior and lateral columns of the spinal cord.Men are more affected.Numbness, paresthesias (a crawling sensation), leg weakness, and impaired gait are symptoms of this condition.These complaints from the hands are less common, and it can be hard to make precise movements.
Mental disorders range from irritability to severe dementia and psychosis, and sometimes hearing, smell, and vision are affected.There may be neurological manifestations like involuntary defecation and urinary incontinence.In young children, muscle weakness, trembling, and involuntary muscle contractions are signs of damage to the nervous system.Psychomotor development may be slowed down, and skills may be lost.
How B12 deficiency anemia develops Vitamin B12 enters the body through animal foods:milk, cheese, eggs, and meat productsFrom the association with food proteins, the nutrient is delivered first affected by cooking, and afterward hydrochloric corrosive and gastric juice chemicals.
The intrinsic factor Castle, which is produced by the stomach’s parietal cells, is combined with vitamin B12 in the duodenum.Vitamin B12 enters the cells of the ileum’s mucous membrane thanks to the Castle factor.The blood then transports it to consumer cells, primarily the liver and bone marrow, where it binds to the transport protein transcobalamin II.
Vitamin B12 is broken down into two coenzymes in the cell:methyl and adenosylcobalamin, respectively.Coenzymes are substances that enzymes require to function.
The coenzyme for the enzyme methionine synthase, which transforms homocysteine into methionine, is methylcobalamin.Homocysteine builds up in the body and the pyrimidine bases that are needed to make DNA do not form if this process fails.DNA synthesis and cell division are disrupted as a result.Cells that divide quickly, like hematopoietic cells in the bone marrow, which make blood, and gastrointestinal epithelial cells, are particularly sensitive to this change.As a result, changes in the blood test such as atrophy of the mucous membranes, leukopenia (a decrease in the number of leukocytes), and thrombocytopenia (a decrease in the number of platelets) appear.
Adenosylcobalamin, the second coenzyme, is necessary for the metabolism of myelin, the substance that makes up the sheath of nerve fibers. It is involved in the metabolism of fatty acids.Lack of vitamin B12 causes incorrect fatty acid metabolism that results in the accumulation of methylmalonic and propionic acids, both of which are harmful to the nervous system.In the spinal cord’s posterior and lateral columns, myelin synthesis is impaired.As a consequence of this, there is a clinic for nervous system damage.
Classification of B12-deficiency anemia and its stages of development Classification of V12DA for its causes of development:
Forms inherited (congenital).Described as occurring in children with vitamin B12 metabolism and transport impairments.
The presence of antibodies to the stomach’s parietal cells or the Castle factor is the primary autoimmune cause of vitamin B12 deficiency in the primary form.The progression of conditions like autoimmune thyroiditis, vitiligo, and type 1 diabetes mellitus is frequently complicated by the primary form of B12DA.
A strict vegan diet causes the secondary form to develop.
Transformative phases B12YES:
Beginning – inactive lack.The serum vitamin level is lower, but the number of erythrocytes and hemoglobin levels remain unaffected.At this stage, clinical manifestations may not be observed.In the laboratory, it is possible to observe a change in the parameters of erythrocytes:an increase in the average amount of hemoglobin in an erythrocyte (MCH parameter) and the average volume of an erythrocyte (MCV parameter in a blood test).
stage of the clinical signs and symptoms.It is accompanied by damage to the nervous system, anemia-like symptoms, and a drop in hemoglobin levels.
The seriousness of V12DA:
Moderate: a hemoglobin level between 90 and 70 g/l. Mild: a hemoglobin level below 90 g/l. Moderate:
Complications of B12 deficiency anemia Growth and developmental delay in children are possible as a result of a decrease in hemoglobin with B12DA. Severe – hemoglobin level below 70 g / l.
Heart disease.Anemia can exacerbate concomitant cardiovascular pathology, such as heart failure, in elderly patients.
Appetite reduction and gastrointestinal manifestations may lead to weight loss.
When deep leukopenia (low leukocyte count) develops, infectious complications may develop.In most cases, there is no significant decrease in platelets, and there are no complications of hemorrhage.
Thrombosis and atherosclerosisVitamin B12 deficiency can lead to an increase in homocysteine levels, which can lead to atherosclerosis and blood clot formation.Collecting in the body, homocysteine harms the internal mass of the supply routes, which prompts cracks of the internal covering of the vessels – the endothelium.Calcium and cholesterol settle at the site of damage, forming an atherosclerotic plaque that causes the vessel lumen to narrow and occasionally become clogged.The risk of thrombosis or vessel rupture is presented by this.
Thrombotic microangiopathy, a disease characterized by inflammation of the vascular wall and damage to small vessels that leads to the formation of blood clots in their lumen, is another severe complication of B12DA that is described.As a result, organ and tissue ischemia may occur.
Spasticity (excessive muscle tone and involuntary movements) and paraplegia (complete paralysis of both arms or legs) can result from brain and spinal cord damage that does not receive treatment.The anemic syndrome and neurological manifestations quickly subside when B12DA treatment begins.However, spinal cord injury may be irreversible in severe vitamin B12 deficiency.
For the diagnosis of B12 deficiency anemia to be accurate, a hematologist’s examination is necessary.You will need to see a gastroenterologist in order to get answers to questions and find solutions to issues related to how the gastrointestinal tract works.To evaluate neurological manifestations, a neurologist may require an examination.
Examination of the patient During the examination, the doctor may pay attention to pale skin, a slight yellowing, an increase in heart rate, and an expansion of the heart’s boundaries.Examining the oral cavity, particularly the tongue, is essential.A nervous system specialist can survey muscle tone and the presence of neurotic reflexes.
The evaluation of a clinical blood test is one of the most crucial stages of diagnosis in the laboratory.The study demonstrates:
anemia due to a decrease in hemoglobin
macrocytosis is the presence of a large number of red blood cells (macrocytes) that are abnormally large in the blood.
hyperchromic refers to the intense staining of red blood cells brought on by an increase in the blood’s hemoglobin content;
the number of platelets and leukocytes might go down.
A blood smear, in which a morphologist can observe the pathological forms of red blood cells, is required.
ovalocytes (oval-molded erythrocytes) and degenerative structures;
an expansion in the distinction in the size of erythrocytes (boundary RDW);
specific pathological inclusions like Cabot rings and Jolly bodies;
in severe cases, megaloblasts and megalocytes.
Neutrophils can also take on pathological forms, such as:
neutrophils with five or more segments of nuclear hypersegmentation;
neutrophilic leukocytes in their infancy are metamyelocytes.
Reticulocytes, or young forms of erythrocytes, generally decrease in number.Reticulocyte indices can provide additional useful information if a laboratory opportunity exists:The proportion of immature reticulocytes rises, as do the average reticulocyte volume and hemoglobin content.
A biochemical blood test reveals:
diminished levels of the B12 vitamin;
A sign of early erythrocyte destruction (hemolysis) in the blood and the breakdown of erythrocyte precursors in the bone marrow is elevated indirect bilirubin and lactate dehydrogenase.
iron and ferritin levels are typical.
Folic acid levels must be checked because B12 deficiency and folic acid deficiency have similar clinical findings but different treatments.Serum holotranscobalamin (active vitamin B12) levels should be checked if B12DA is suspected but folic acid and vitamin B12 levels are normal.There is a decrease in its content when there is a B12 deficiency.It is possible to observe an increase in the serum homocysteine and methylmalonic acid levels.
Persistent proteinuria, or the presence of protein in the urine, can be detected in general urine analysis.The levels of homocysteine and methylmalonic acid can rise in some cases.
The following are additional lab tests that may assist in determining the cause of a vitamin B12 deficiency:
the study of antibodies in blood serum to the internal factor of Castle (IgG) and stomach parietal cells;
an examination of the gastric juice to determine the internal factor of Castle and the antibodies to this factor (IgA, which are produced by the stomach’s parietal cells);
The Schilling test measures the intestinal absorption of vitamin B12 and the activity of internal factor Castle;
tests for malabsorption, or poor nutrient absorption.
Since amniocytes (fetal membrane cells) produce the transcobalamin II transport protein, it is possible to diagnose a genetically determined deficiency during pregnancy.
Instrumental diagnostics An elevated liver and spleen can be detected by ultrasound examination of the abdominal organs.
All newly diagnosed B12DA patients are shown to undergo endoscopic studies, fibro gastro duodenoscopy (FGDS) and colonoscopy, in order to detect conditions of the gastrointestinal tract that can prevent vitamin B12 from being absorbed.A decrease in gastric secretion and chronic atrophic gastritis and duodenitis can be detected with FGDS.A biopsy of the gastric mucosa and subsequent histological examination are required in the presence of pathological changes.
Differential Diagnosis The following diseases of the blood system are considered in the differential diagnosis of B12-deficiency anemia, particularly when there is a decrease in leukocytes and platelets:
A group of hematological disorders known as myelodysplastic syndromes occurs when the bone marrow does not produce enough of one or more types of blood cells:red blood cells, platelets, and white blood cells.
Anemia known as aplastic anemia is caused by a decrease in the number of hematopoietic stem cells, which results in an insufficient production of red blood cells.
A morphological examination of the bone marrow and a puncture may be required to clarify the diagnosis.Within the sight of B12DA, an expert morphologist portrays in the bone marrow the trademark changes in stem begetter cells:
hyperplasia, or growth, of the erythroid germ, which are the stem cells that are used to make erythrocytes;
megaloblastic hematopoiesis, in which pathological mitoses, large cells with granular nuclei, and Jolly bodies are formed;
violation of myeloid cell and platelet precursor maturation:Multinucleated megakaryocytes, giant metamyelocytes, neutrophil hypersegmentation, and treatment of B12 deficiency anemia Dietary changes and intramuscular vitamin B12 administration are used to treat anemia caused by inadequate food vitamin intake.Consuming animal products is necessary for a vitamin B12-rich diet.Bread, fruits, and vegetables lack vitamin B12.
Diet modification won’t work for other reasons.In all instances, standard protocols are followed when administering a vitamin B12 supplement.The patient’s age and the presence of neurological symptoms may influence the dosage.
Outpatient care is usually used for treatment.Extreme weakness (hemoglobin level under 70 g/l) and old age can act as a sign of hospitalization.
It is strongly discouraged to begin treatment with vitamin B12 or multivitamin complexes if B12DA is suspected without laboratory confirmation. This is due to the fact that the introduction of B12 causes the rapid disappearance of morphological cell abnormalities, making it difficult to make a correct diagnosis.In B12 deficiency, misuse of folic acid can exacerbate neurological symptoms.
As a result, it is critical to begin treatment only after the diagnosis has been confirmed by laboratory testing.
Saturation is the first stage of therapy.It involves intramuscular administration of cyanocobalamin in a therapeutic dose for four to six weeks.Sublingual forms of vitamin B12 might work in some cases.After the first three to five injections of the medication, improvements can be seen.
A reticular crisis, or an increase in the blood level of reticulocytes by two to three times compared to the baseline on days four through seven following the beginning of therapy, is the first laboratory sign that the treatment is working.After one to two months, hemoglobin levels return to normal, whereas peripheral neuropathy progresses more slowly.
Due to the active division of progenitor cells in the bone marrow, it is possible to add folic acid and iron deficiency to cyanocobalamin therapy. Therefore, seven to ten days after starting vitamin B12 therapy, it is necessary to prescribe folic acid and, in conjunction with a decrease in ferritin levels, iron preparations.
The second stage is therapy for fixing:The amount of vitamin B12 taken remains the same, but it is taken less often.
The third stage is upkeep treatment.It lasts a lifetime.Severe anemia characterized by hypoxia and circulatory failure calls for erythrocyte suspension transfusion.With the improvement of neutropenia (decline in the quantity of neutrophils) and the expansion of irresistible confusions, anti-infection treatment might be required.
Also see:You can heal yourself – Predictable indicators of cancer in your bodyPrevention The prognosis for B12DA is favorable, regardless of the patient’s age, with prompt diagnosis, effective treatment, and proper follow-up after recovery.In elderly patients, concomitant cardiovascular diseases and damage to the nervous system (funicular myelosis) may worsen prognosis.
Avoidance of B12DA is diminished with the remedy of the eating regimen.Preventing the disease is limited to taking vitamin B12 on a regular basis throughout one’s entire life if the disease cannot be eradicated (such as when a portion of the stomach is removed or if the internal factor of Castle is insufficient).Every three to four months, you should have your blood tested.Annual EGD is recommended for patients with atrophic gastritis because they are more likely to develop gastric neoplasms.
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