Anemia diarrhea. Anemia Symptoms: A Comprehensive Guide to Understanding and Identifying Various Types
What are the common symptoms of anemia. How do different types of anemia manifest unique symptoms. What causes anemia and how is it diagnosed. How can anemia be treated and prevented.
Understanding Anemia: Causes, Types, and General Symptoms
Anemia is a condition characterized by a lack of healthy red blood cells to carry adequate oxygen to the body’s tissues. It can occur due to various reasons, including iron deficiency, vitamin B12 deficiency, chronic diseases, and inherited disorders. The severity of anemia can range from mild to severe, with symptoms varying accordingly.
Common symptoms shared by most types of anemia include:
- Fatigue and weakness
- Dizziness, especially when standing up
- Shortness of breath
- Headaches
- Cold hands and feet
- Pale skin, particularly in the gums and nail beds
- Chest pain
- Irregular heartbeat (arrhythmia)
The intensity of these symptoms often correlates with the severity of the anemia. Mild cases may present no noticeable symptoms, while severe anemia can significantly impact daily life.
Iron Deficiency Anemia: Symptoms and Causes
Iron deficiency anemia is one of the most common types of anemia. It occurs when the body doesn’t have enough iron to produce hemoglobin, the protein in red blood cells that carries oxygen.
Unique symptoms of iron deficiency anemia include:
- Unusual cravings for non-food items (pica), such as ice or dirt
- Brittle nails
- Swollen or sore tongue
- Cracks at the corners of the mouth
- Increased susceptibility to infections
Can iron deficiency anemia be prevented? Yes, in many cases. Consuming a diet rich in iron-containing foods, such as lean meats, leafy greens, and fortified cereals, can help prevent this type of anemia. For those at risk, iron supplements may be recommended under medical supervision.
Vitamin B12 Deficiency: Pernicious Anemia and Its Symptoms
Pernicious anemia is a type of vitamin B12 deficiency anemia. It occurs when the body can’t absorb enough vitamin B12 from food, often due to a lack of intrinsic factor, a protein produced by the stomach.
Distinctive symptoms of pernicious anemia include:
- Nerve damage
- Confusion and memory problems
- Depression
- Nausea and heartburn
- Weight loss
- Smooth, red tongue
How is pernicious anemia treated? Treatment typically involves lifelong vitamin B12 injections or high-dose oral supplements. In some cases, nasal or sublingual forms of B12 may be used. Regular monitoring is essential to ensure adequate B12 levels are maintained.
Sickle Cell Anemia: A Genetic Blood Disorder
Sickle cell anemia is an inherited disorder where red blood cells are abnormally shaped, resembling a crescent or sickle. This shape can cause the cells to stick together, blocking blood flow and leading to various complications.
Characteristic symptoms of sickle cell anemia include:
- Sudden, severe pain (sickle cell crisis)
- Swelling in hands and feet
- Frequent infections
- Vision problems
- Delayed growth in children
- Jaundice (yellowing of the skin and eyes)
Is there a cure for sickle cell anemia? While there’s no widely available cure, treatments can help manage symptoms and prevent complications. These may include pain management, blood transfusions, and medications to reduce the frequency of pain crises and prevent infections.
Aplastic Anemia: When the Bone Marrow Fails
Aplastic anemia is a rare but serious condition where the bone marrow fails to produce enough blood cells. This can lead to a deficiency in all types of blood cells: red blood cells, white blood cells, and platelets.
Specific symptoms of aplastic anemia may include:
- Frequent or prolonged infections
- Unexplained bruising
- Nosebleeds and bleeding gums
- Skin rashes
- Nausea
- Fever
How is aplastic anemia diagnosed? Diagnosis typically involves blood tests and a bone marrow biopsy. These tests can reveal the deficiency in blood cell production and help rule out other conditions with similar symptoms.
Hemolytic Anemia: When Red Blood Cells Break Down Too Quickly
Hemolytic anemia occurs when red blood cells are destroyed faster than they can be replaced. This can be due to inherited conditions or acquired factors such as autoimmune disorders, infections, or certain medications.
Distinctive symptoms of hemolytic anemia include:
- Jaundice
- Dark urine
- Leg ulcers
- Abdominal pain
- Enlarged spleen
What causes hemolytic anemia? The causes can be broadly categorized into inherited and acquired factors. Inherited causes include conditions like sickle cell disease and thalassemia. Acquired causes can range from autoimmune disorders to certain medications and infections.
Folic Acid Deficiency Anemia: The Importance of B Vitamins
Folic acid, also known as folate, is a B vitamin crucial for the production of healthy red blood cells. A deficiency in folic acid can lead to a specific type of anemia with its own set of symptoms.
Unique symptoms of folic acid deficiency anemia include:
- Irritability
- Diarrhea
- Smooth tongue
- Difficulty concentrating
- Gray hair
How can folic acid deficiency be prevented? Consuming a diet rich in folate-containing foods such as leafy green vegetables, citrus fruits, beans, and fortified grains can help prevent this type of anemia. In some cases, particularly for pregnant women, folic acid supplements may be recommended.
Diagnosing and Treating Anemia: A Multifaceted Approach
Diagnosing anemia typically begins with a complete blood count (CBC) test, which measures various components of your blood, including red blood cells, white blood cells, and hemoglobin. If anemia is detected, further tests may be conducted to determine the underlying cause.
Treatment for anemia varies depending on the type and underlying cause. Some common approaches include:
- Iron supplements for iron deficiency anemia
- Vitamin B12 injections or supplements for pernicious anemia
- Folic acid supplements for folate deficiency
- Blood transfusions for severe cases or certain types of anemia
- Medications to stimulate blood cell production
- Treatment of underlying conditions causing anemia
Can lifestyle changes help manage anemia? In many cases, yes. A balanced diet rich in iron, vitamin B12, and folate can help prevent and manage certain types of anemia. Regular exercise, stress management, and avoiding tobacco use can also support overall blood health.
The Role of Diet in Anemia Prevention and Management
A nutrient-rich diet plays a crucial role in preventing and managing many types of anemia. Here are some key nutrients and their food sources:
- Iron: Lean red meat, poultry, fish, beans, lentils, tofu, fortified cereals
- Vitamin B12: Meat, fish, eggs, dairy products, fortified plant-based milk
- Folate: Leafy green vegetables, citrus fruits, beans, peas, fortified grains
- Vitamin C: Citrus fruits, berries, bell peppers, tomatoes (aids iron absorption)
Is a vegetarian or vegan diet compatible with anemia prevention? With careful planning, yes. Plant-based diets can provide adequate iron and other nutrients necessary for preventing anemia. However, vitamin B12 supplementation may be necessary for those following a strict vegan diet.
Anemia in Special Populations: Pregnancy, Elderly, and Chronic Diseases
Certain groups are at higher risk of developing anemia and may require special consideration:
- Pregnant women: Higher iron needs to support fetal development
- Elderly: Increased risk due to chronic diseases and poor nutrient absorption
- Chronic disease patients: Conditions like kidney disease, cancer, and inflammatory bowel disease can increase anemia risk
How does anemia affect pregnancy outcomes? Severe anemia during pregnancy can increase the risk of premature birth, low birth weight, and maternal mortality. Regular prenatal care, including blood tests and appropriate supplementation, is crucial for managing anemia in pregnancy.
The Link Between Anemia and Other Health Conditions
Anemia can be both a cause and a consequence of other health issues. Some conditions closely associated with anemia include:
- Chronic kidney disease
- Inflammatory bowel diseases (Crohn’s disease, ulcerative colitis)
- Certain types of cancer
- Rheumatoid arthritis
- HIV/AIDS
How does chronic kidney disease lead to anemia? Chronic kidney disease can reduce the production of erythropoietin, a hormone that stimulates red blood cell production. This can result in anemia, which is a common complication in advanced kidney disease.
Anemia in Children: Unique Considerations and Impacts
Anemia in children can have significant impacts on growth, development, and cognitive function. Common causes of anemia in children include:
- Iron deficiency (often due to rapid growth or inadequate diet)
- Lead poisoning
- Inherited disorders (e.g., sickle cell disease, thalassemia)
- Chronic diseases
How does anemia affect a child’s development? Severe or chronic anemia can lead to delayed physical growth, impaired cognitive development, and reduced academic performance. Early detection and treatment are crucial to mitigate these potential long-term effects.
Emerging Treatments and Research in Anemia Management
The field of anemia treatment is continually evolving. Some promising areas of research include:
- Gene therapy for inherited anemias like sickle cell disease
- New iron formulations with improved absorption and fewer side effects
- Novel erythropoiesis-stimulating agents
- Targeted therapies for specific types of anemia
What is the potential of gene therapy in treating sickle cell anemia? Recent clinical trials have shown promising results in using gene therapy to produce healthy hemoglobin in patients with sickle cell disease. While still in experimental stages, this approach could potentially offer a cure for this inherited form of anemia.
Living with Anemia: Coping Strategies and Quality of Life
Managing anemia often involves more than just medical treatment. Strategies for coping with anemia and improving quality of life include:
- Energy conservation techniques
- Stress management and relaxation methods
- Regular, moderate exercise as tolerated
- Adequate sleep and rest
- Joining support groups or seeking counseling
How can individuals with chronic anemia maintain a fulfilling lifestyle? While challenging, many people with chronic anemia lead active and fulfilling lives. Key strategies include adhering to treatment plans, maintaining open communication with healthcare providers, and making appropriate lifestyle adjustments to manage energy levels.
The Global Burden of Anemia: Public Health Perspectives
Anemia remains a significant global health issue, particularly in developing countries. Factors contributing to the global burden of anemia include:
- Malnutrition
- Parasitic infections
- Limited access to healthcare
- Lack of awareness about proper nutrition
What initiatives are in place to combat anemia globally? Various international organizations, including the World Health Organization, have implemented programs aimed at reducing anemia worldwide. These include iron fortification of staple foods, distribution of iron supplements, and efforts to control parasitic infections that can cause anemia.
In conclusion, anemia is a complex condition with various causes and manifestations. Understanding its symptoms, causes, and treatment options is crucial for early detection and effective management. Whether dealing with iron deficiency anemia, pernicious anemia, or rarer forms like sickle cell anemia, proper diagnosis and tailored treatment can significantly improve quality of life. As research continues to advance, new therapies and management strategies offer hope for better outcomes for those affected by anemia.
A Guide to Anemia Symptoms
There are many different types of anemia with many different causes. A handful of symptoms are shared by nearly all types of anemia, whether you have iron deficiency anemia or Fanconi anemia.
And each type of anemia shares a basic end effect: Your body does not have enough oxygen-bearing red blood cells for its needs.
How severe or frequent your symptoms are relates to how severe your anemia is. People who have mild anemia, from a mild iron deficiency, for instance, may not have any symptoms at all, while people with severe anemia can have much more noticeable and longer lasting symptoms.
Anemia symptoms include:
- Fatigue. This is by far the most common anemia symptom. You may feel very tired or weak and unable to summon the energy for most daily activities.
- Dizziness. Dizziness is most likely to occur when you stand up from a sitting or resting position.
- Shortness of breath
- Headaches
- Cold skin, especially the hands and feet
- Paleness. Your gums and the base of your nails may be especially pale.
- Chest pain. Without enough oxygen-rich red blood cells, your heart has to work much harder to keep your body supplied with the nutrients it requires. You may feel pain and tightness in your chest when your heart muscle is not getting the oxygen it needs.
- Arrhythmia. Also known as dysrhythmia or an abnormal heart rhythm, an uneven or altered rate or pattern of heartbeats can also result from your heart working harder to circulate blood.
If the condition is severe enough, these symptoms are found to some degree in every type of anemia.
Differentiating Anemia Symptoms
There are many different types of anemia, some with symptoms that set them apart:
- Aplastic anemia. Nausea and skin rashes are known signs of this type of anemia, which occurs when the bone marrow stops making enough red blood cells.
- Fanconi anemia. This is a rare inherited disorder that prevents your bone marrow from making all three needed types of blood cells and results in delayed development in a multitude of areas, from learning abilities to physical growth.
- Folic acid deficiency anemia. Not having enough folic acid — one of the B vitamins, also known as folate — in your diet may lead to this type of anemia. Symptoms unique to this anemia include irritability, diarrhea, and a smooth tongue.
- Hemolytic anemia. Jaundice, leg ulcers, and abdominal pain are hallmarks of this type of anemia, in which red blood cells are prematurely destroyed within the body. The excess hemoglobin released by this destructive process causes many of the symptoms.
- Iron deficiency anemia. This type of anemia is due to a lack of iron in your diet or chronic blood loss. Iron deficiency anemia can be identified through symptoms that include unusual cravings (such as ice or dirt), brittle nails, a swollen or sore tongue, tiny cracks on the sides of your mouth, and frequent infections.
- Pernicious anemia. This type of anemia is caused by a lack of vitamin B12. Not having enough vitamin B12, or being unable to absorb it, can lead to symptoms such as nerve damage, confusion, dementia, memory loss, depression, nausea, heartburn, weight loss, and a smooth, beefy red tongue.
- Sickle cell anemia. Sudden pain throughout the body is a hallmark of this type of anemia, which occurs because the body makes red blood cells shaped like sickles (or a “C” shape) instead of smooth disc shapes. These abnormally shaped cells can clump together, blocking blood flow in many organs and causing painful sickle cell crises. Swelling in the hands and feet and damage to the spleen are also symptoms of this type of anemia.
Symptoms of anemia cover a wide range, depending on the cause of the anemia and the severity of the condition. However, there are a few symptoms, especially tiredness, that occur with all types of anemia. If you suspect you have anemia, talk to your doctor about your options.
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Iron, anaemia, and inflammatory bowel diseases
1. Oldenburg B , Koningsberger JC, Berge Henegouwen GP, et al. Iron and inflammatory bowel disease. Aliment Pharmacol Ther 2001;15:429–38. [PubMed] [Google Scholar]
2. Gasche C . Anemia in IBD: the overlooked villain. Inflamm Bowel Dis 2000;6:142–50. [PubMed] [Google Scholar]
3. Macdougall IC. Quality of life and anemia: the nephrology experience. Semin Oncol 1998;25 (suppl 7) :39–42. [PubMed] [Google Scholar]
4. Vatner SF. Effects of hemorrhage on regional blood flow distribution in dogs and primates. J Clin Invest 1974;54:225–35. [PMC free article] [PubMed] [Google Scholar]
5. Daneryd P , Svanberg E, Korner U, et al. Protection of metabolic and exercise capacity in unselected weight-losing cancer patients following treatment with recombinant erythropoietin: a randomized prospective study. Cancer Res 1998;58:5374–9. [PubMed] [Google Scholar]
6. Ludwig H , Strasser K. Symptomatology of anemia. Semin Oncol 2001;28 (suppl 8) :7–14. [PubMed] [Google Scholar]
7. Pickett JL, Theberge DC, Brown WS, et al. Normalizing hematocrit in dialysis patients improves brain function. Am J Kidney Dis 1999;33:1122–30. [PubMed] [Google Scholar]
8. Bruner AB, Joffe A, Duggan AK, et al. Randomised study of cognitive effects of iron supplementation in non-anaemic iron-deficient adolescent girls. Lancet 1996;348:992–6. [PubMed] [Google Scholar]
9. Mitchell A , Guyatt G, Singer J, et al. Quality of life in patients with inflammatory bowel disease. J Clin Gastroenterol 1988;10:306–10. [PubMed] [Google Scholar]
10. Demetri GD, Kris M, Wade J, et al. Quality-of-life benefit in chemotherapy patients treated with epoetin alfa is independent of disease response or tumor type: results from a prospective community oncology study. Procrit Study Group. J Clin Oncol 1998;16:3412–25. [PubMed] [Google Scholar]
11. Crawford J , Cella D, Cleeland CS, et al. Relationship between changes in hemoglobin level and quality of life during chemotherapy in anemic cancer patients receiving epoetin alfa therapy. Cancer 2002;95:888–95. [PubMed] [Google Scholar]
12. Gasche C , Dejaco C, Waldhoer T, et al. Intravenous iron and erythropoietin for anemia associated with Crohn disease. A randomized, controlled trial. Ann Intern Med 1997;126:782–7. [PubMed] [Google Scholar]
13. Leitgeb C , Pecherstorfer M, Fritz E, et al. Quality of life in chronic anemia of cancer during treatment with recombinant human erythropoietin. Cancer 1994;73:2535–42. [PubMed] [Google Scholar]
14. Curt GA. Impact of fatigue on quality of life in oncology patients. Semin Hematol 2000;37 (suppl 6) :14–17. [PubMed] [Google Scholar]
15. Monsen ER, Hallberg L, Layrisse M, et al. Estimation of available dietary iron. Am J Clin Nutr 1978;31:134–41. [PubMed] [Google Scholar]
16. Parkkila S , Niemela O, Britton RS, et al. Molecular aspects of iron absorption and HFE expression. Gastroenterology 2001;121:1489–96. [PubMed] [Google Scholar]
17. Mishkin S . Dairy sensitivity, lactose malabsorption, and elimination diets in inflammatory bowel disease. Am J Clin Nutr 1997;65:564–7. [PubMed] [Google Scholar]
18. Ballegaard M , Bjergstrom A, Brondum S, et al. Self-reported food intolerance in chronic inflammatory bowel disease. Scand J Gastroenterol 1997;32:569–71. [PubMed] [Google Scholar]
19. Lomer MC, Kodjabashia K, Hutchinson C, et al. Intake of dietary iron is low in patients with Crohn’s disease: a case-control study. Br J Nutr 2004;91:141–8. [PubMed] [Google Scholar]
20. Child JA, Brozovic B, Dyer NH, et al. The diagnosis of iron deficiency in patients with Crohn’s disease. Gut 1973;14:642–8. [PMC free article] [PubMed] [Google Scholar]
21. Bartels U , Pedersen NS, Jarnum S. Iron absorption and serum ferritin in chronic inflammatory bowel disease. Scand J Gastroenterol 1978;13:649–56. [PubMed] [Google Scholar]
22. Cavill I . Erythropoiesis and iron. Best Pract Res Clin Haematol 2002;15:399–409. [PubMed] [Google Scholar]
23. Seligman PA, Kovar J, Gelfand EW. Lymphocyte proliferation is controlled by both iron availability and regulation of iron uptake pathways. Pathobiology 1992;60:19–26. [PubMed] [Google Scholar]
24. de Sousa M . Immune cell functions in iron overload. Clin Exp Immunol 1989;75:1–6. [PMC free article] [PubMed] [Google Scholar]
25. Brock JH. Iron in infection, immunity, inflammation and neoplasia. In: Brock JH, Halliday JW, Pippard MJ, et al, eds. Iron metabolism in health and disease. Philadelphia: WB Saunders Co Ltd, 1994:353–91.
26. Weiss G . Iron acquisition by the reticuloendothelial system. In: Templeton D, ed. Molecular and cellular iron transport. New York: Marcel Decker Inc, 2002:468–87.
27. Forbes JR, Gros P. Divalent-metal transport by NRAMP proteins at the interface of host-pathogen interactions. Trends Microbiol 2001;9:397–403. [PubMed] [Google Scholar]
28. Blackwell JM, Searle S, Goswami T, et al. Understanding the multiple functions of Nramp1. Microbes Infect 2000;2:317–21. [PubMed] [Google Scholar]
29. Weiss G , Fuchs D, Hausen A, et al. Iron modulates interferon-gamma effects in the human myelomonocytic cell line THP-1. Exp Hematol 1992;20:605–10. [PubMed] [Google Scholar]
30. Recalcati S , Pometta R, Levi S, et al. Response of monocyte iron regulatory protein activity to inflammation: abnormal behavior in genetic hemochromatosis. Blood 1998;91:2565–72. [PubMed] [Google Scholar]
31. Oexle H , Kaser A, Most J, et al. Pathways for the regulation of interferon-gamma-inducible genes by iron in human monocytic cells. J Leukoc Biol 2003;74:287–94. [PubMed] [Google Scholar]
32. Mencacci A , Cenci E, Boelaert JR, et al. Iron overload alters innate and T helper cell responses to Candida albicans in mice. J Infect Dis 1997;175:1467–76. [PubMed] [Google Scholar]
33. Weiss G , Werner-Felmayer G, Werner ER, et al. Iron regulates nitric oxide synthase activity by controlling nuclear transcription. J Exp Med 1994;180:969–76. [PMC free article] [PubMed] [Google Scholar]
34. Melillo G , Taylor LS, Brooks A, et al. Functional requirement of the hypoxia-responsive element in the activation of the inducible nitric oxide synthase promoter by the iron chelator desferrioxamine. J Biol Chem 1997;272:12236–43. [PubMed] [Google Scholar]
35. MacMicking J , Xie QW, Nathan C. Nitric oxide and macrophage function. Annu Rev Immunol 1997;15:323–50. [PubMed] [Google Scholar]
36. Bogdan C . Nitric oxide and the immune response. Nat Immunol 2001;2:907–16. [PubMed] [Google Scholar]
37. Fritsche G , Larcher C, Schennach H, et al. Regulatory interactions between iron and nitric oxide metabolism for immune defense against Plasmodium falciparum infection. J Infect Dis 2001;183:1388–94. [PubMed] [Google Scholar]
38. Gordeuk V , Thuma P, Brittenham G, et al. Effect of iron chelation therapy on recovery from deep coma in children with cerebral malaria. N Engl J Med 1992;327:1473–7. [PubMed] [Google Scholar]
39. Gomes MS, Boelaert JR, Appelberg R. Role of iron in experimental Mycobacterium avium infection. J Clin Virol 2001;20:117–22. [PubMed] [Google Scholar]
40. Gordeuk VR, McLaren CE, MacPhail AP, et al. Associations of iron overload in Africa with hepatocellular carcinoma and tuberculosis: Strachan’s 1929 thesis revisited. Blood 1996;87:3470–6. [PubMed] [Google Scholar]
41. Jason J , Archibald LK, Nwanyanwu OC, et al. The effects of iron deficiency on lymphocyte cytokine production and activation: preservation of hepatic iron but not at all cost. Clin Exp Immunol 2001;126:466–73. [PMC free article] [PubMed] [Google Scholar]
42. Weiss G . Pathogenesis and treatment of anaemia of chronic disease. Blood Rev 2002;16:87–96. [PubMed] [Google Scholar]
43. Moura E , Verheul AF, Marx JJ. A functional defect in hereditary haemochromatosis monocytes and monocyte-derived macrophages. Eur J Clin Invest 1998;28:164–73. [PubMed] [Google Scholar]
44. Ludwiczek S , Aigner E, Theurl I, et al. Cytokine-mediated regulation of iron transport in human monocytic cells. Blood 2003;101:4148–54. [PubMed] [Google Scholar]
45. Yang F , Liu XB, Quinones M, et al. Regulation of reticuloendothelial iron transporter MTP1 (Slc11a3) by inflammation. J Biol Chem 2002;277:39786–91. [PubMed] [Google Scholar]
46. Graziadei I , Gaggl S, Kaserbacher R, et al. The acute-phase protein alpha 1-antitrypsin inhibits growth and proliferation of human early erythroid progenitor cells (burst-forming units-erythroid) and of human erythroleukemic cells (K562) in vitro by interfering with transferrin iron uptake. Blood 1994;83:260–8. [PubMed] [Google Scholar]
47. Ganz T . Hepcidin, a key regulator of iron metabolism and mediator of anemia of inflammation. Blood 2003;102:783–8. [PubMed] [Google Scholar]
48. Means RTJ, Krantz SB. Progress in understanding the pathogenesis of the anemia of chronic disease. Blood 1992;80:1639–47. [PubMed] [Google Scholar]
49. Wang CQ, Udupa KB, Lipschitz DA. Interferon-gamma exerts its negative regulatory effect primarily on the earliest stages of murine erythroid progenitor cell development. J Cell Physiol 1995;162:134–8. [PubMed] [Google Scholar]
50. Fuchs D , Hausen A, Reibnegger G, et al. Immune activation and the anaemia associated with chronic inflammatory disorders. Eur J Haematol 1991;46:65–70. [PubMed] [Google Scholar]
51. Maciejewski JP, Selleri C, Sato T, et al. Nitric oxide suppression of human hematopoiesis in vitro. Contribution to inhibitory action of interferon-gamma and tumor necrosis factor-alpha. J Clin Invest 1995;96:1085–92. [PMC free article] [PubMed] [Google Scholar]
52. Rafferty SP, Domachowske JB, Malech HL. Inhibition of hemoglobin expression by heterologous production of nitric oxide synthase in the K562 erythroleukemic cell line. Blood 1996;88:1070–8. [PubMed] [Google Scholar]
53. Cazzola M , Ponchio L, de Benedetti F, et al. Defective iron supply for erythropoiesis and adequate endogenous erythropoietin production in the anemia associated with systemic-onset juvenile chronic arthritis. Blood 1996;87:4824–30. [PubMed] [Google Scholar]
54. Gasche C , Reinisch W, Lochs H, et al. Anemia in Crohn’s disease. Importance of inadequate erythropoietin production and iron deficiency. Dig Dis Sci 1994;39:1930–4. [PubMed] [Google Scholar]
55. Gasche C , Dejaco C, Reinisch W, et al. Sequential treatment of anemia in ulcerative colitis with intravenous iron and erythropoietin. Digestion 1999;60:262–7. [PubMed] [Google Scholar]
56. Faquin WC, Schneider TJ, Goldberg MA. Effect of inflammatory cytokines on hypoxia-induced erythropoietin production. Blood 1992;79:1987–94. [PubMed] [Google Scholar]
57. Means RTJ, Krantz SB. Inhibition of human erythroid colony-forming units by gamma interferon can be corrected by recombinant human erythropoietin. Blood 1991;78:2564–7. [PubMed] [Google Scholar]
58. Moldawer LL, Marano MA, Wei H, et al. Cachectin/tumor necrosis factor-alpha alters red blood cell kinetics and induces anemia in vivo. FASEB J 1989;3:1637–43. [PubMed] [Google Scholar]
59. Fillet G , Beguin Y, Baldelli L. Model of reticuloendothelial iron metabolism in humans: abnormal behavior in idiopathic hemochromatosis and in inflammation. Blood 1989;74:844–51. [PubMed] [Google Scholar]
60. Kraus J , Schneider R. Pernicious anemia caused by Crohn’s disease of the stomach. Am J Gastroenterol 1979;71:202–5. [PubMed] [Google Scholar]
61. Laidlaw ST, Reilly JT. Antilymphocyte globulin for mesalazine-associated aplastic anaemia. Lancet 1994;343:981–2. [PubMed] [Google Scholar]
62. Anttila PM, Valimaki M, Pentikainen PJ. Pure-red-cell aplasia associated with sulphasalazine but not 5-aminosalicylic acid. Lancet 1985;2:1006. [PubMed] [Google Scholar]
63. van Hees PA, van Elferen LW, van Rossum JM, et al. Hemolysis during salicylazosulfapyridine therapy. Am J Gastroenterol 1978;70:501–5. [PubMed] [Google Scholar]
64. Bernstein CN, Artinian L, Anton PA, et al. Low-dose 6-mercaptopurine in inflammatory bowel disease is associated with minimal hematologic toxicity. Dig Dis Sci 1994;39:1638–41. [PubMed] [Google Scholar]
65. Black AJ, McLeod HL, Capell HA, et al. Thiopurine methyltransferase genotype predicts therapy-limiting severe toxicity from azathioprine. Ann Intern Med 1998;129:716–18. [PubMed] [Google Scholar]
66. Colombel JF, Ferrari N, Debuysere H, et al. Genotypic analysis of thiopurine S-methyltransferase in patients with Crohn’s disease and severe myelosuppression during azathioprine therapy. Gastroenterology 2000;118:1025–30. [PubMed] [Google Scholar]
67. Gearry RB, Barclay ML, Burt MJ, et al. Thiopurine S-methyltransferase (TPMT) genotype does not predict adverse drug reactions to thiopurine drugs in patients with inflammatory bowel disease. Aliment Pharmacol Ther 2003;18:395–400. [PubMed] [Google Scholar]
68. Lennard L . TPMT in the treatment of Crohn’s disease with azathioprine. Gut 2002;51:143–6. [PMC free article] [PubMed] [Google Scholar]
69. Schreiber S , Wedel S. Diagnosis and treatment of anemia in inflammatory bowel disease. Inflamm Bowel Dis 1997;3:204–16. [PubMed] [Google Scholar]
70. Decaux G , Prospert F, Horsmans Y, et al. Relationship between red cell mean corpuscular volume and 6-thioguanine nucleotides in patients treated with azathioprine. J Lab Clin Med 2000;135:256–62. [PubMed] [Google Scholar]
71. Eschbach JW, Downing MR, Egrie JC, et al. USA multicenter clinical trial with recombinant human erythropoietin (Amgen). Results in hemodialysis patients. Contrib Nephrol 1989;76:160–5. [PubMed] [Google Scholar]
72. Fishbane S , Galgano C, Langley RC jr. et al. Reticulocyte hemoglobin content in the evaluation of iron status of hemodialysis patients. Kidney Int 1997;52:217–22. [PubMed] [Google Scholar]
73. Fishbane S , Shapiro W, Dutka P, et al. A randomized trial of iron deficiency testing strategies in hemodialysis patients. Kidney Int 2001;60:2406–11. [PubMed] [Google Scholar]
74. Punnonen K , Irjala K, Rajamaki A. Serum transferrin receptor and its ratio to serum ferritin in the diagnosis of iron deficiency. Blood 1997;89:1052–7. [PubMed] [Google Scholar]
75. Gasche C , Waldhoer T, Feichtenschlager T, et al. Prediction of response to iron sucrose in inflammatory bowel disease-associated anemia. Am J Gastroenterol 2001;96:2382–7. [PubMed] [Google Scholar]
76. Babbs CF. Oxygen radicals in ulcerative colitis. Free Radic Biol Med 1992;13:169–81. [PubMed] [Google Scholar]
77. Millar AD, Rampton DS, Blake DR. Effects of iron and iron chelation in vitro on mucosal oxidant activity in ulcerative colitis. Aliment Pharmacol Ther 2000;14:1163–8. [PubMed] [Google Scholar]
78. Erichsen K , Hausken T, Ulvik RJ, et al. Ferrous fumarate deteriorated plasma antioxidant status in patients with Crohn disease. Scand J Gastroenterol 2003;38:543–8. [PubMed] [Google Scholar]
79. Naveh Y , Shalata A, Shenker L, et al. Absorption of iron in rats with experimental enteritis. Biometals 2000;13:29–35. [PubMed] [Google Scholar]
80. Harvey RS, Reffitt DM, Doig LA, et al. Ferric trimaltol corrects iron deficiency anaemia in patients intolerant of iron. Aliment Pharmacol Ther 1998;12:845–8. [PubMed] [Google Scholar]
81. Tuomainen T , Nyyssonen K, Porkkala-Sarataho E, et al. Oral supplementation with ferrous sulfate but not with non-ionic iron polymaltose complex increases the susceptibility of plasma lipoproteins to oxidation. Nutr Res 1999;19:1121–32. [Google Scholar]
82. Jacobs P , Wood L, Bird AR. Erythrocytes: better tolerance of iron polymaltose complex compared with ferrous sulphate in the treatment of anaemia. Hematology 2000;5:77–83. [PubMed] [Google Scholar]
83. Seligman PA, Moore GM, Schleicher RB. Clinical studies of HIP: an oral heme-iron product. Nutr Res 2000;20:1279–86. [Google Scholar]
84. Geisser P , Baer M, Schaub E. Structure/histotoxicity relationship of parenteral iron preparations. Arzneimittelforschung 1992;42:1439–52. [PubMed] [Google Scholar]
85. Zanen AL, Adriaansen HJ, van Bommel EF, et al. ‘Oversaturation’ of transferrin after intravenous ferric gluconate (Ferrlecit(R)) in haemodialysis patients. Nephrol Dial Transplant 1996;11:820–4. [PubMed] [Google Scholar]
86. Fishbane S , Wagner J. Sodium ferric gluconate complex in the treatment of iron deficiency for patients on dialysis. Am J Kidney Dis 2001;37:879–83. [PubMed] [Google Scholar]
87. Michael B , Coyne DW, Fishbane S, et al. Sodium ferric gluconate complex in hemodialysis patients: adverse reactions compared to placebo and iron dextran. Kidney Int 2002;61:1830–9. [PubMed] [Google Scholar]
88. Yee J , Besarab A. Iron sucrose: the oldest iron therapy becomes new. Am J Kidney Dis 2002;40:1111–21. [PubMed] [Google Scholar]
89. Chandler G , Harchowal J, Macdougall IC. Intravenous iron sucrose: establishing a safe dose. Am J Kidney Dis 2001;38:988–91. [PubMed] [Google Scholar]
90. Kooistra MP, Kersting S, Gosriwatana I, et al. Nontransferrin-bound iron in the plasma of haemodialysis patients after intravenous iron saccharate infusion. Eur J Clin Invest 2002;32 (suppl 1) :36–41. [PubMed] [Google Scholar]
91. Breymann C , Visca E, Huch R, et al. Efficacy and safety of intravenously administered iron sucrose with and without adjuvant recombinant human erythropoietin for the treatment of resistant iron-deficiency anemia during pregnancy. Am J Obstet Gynecol 2001;184:662–7. [PubMed] [Google Scholar]
92. Breymann C , Richter C, Huttner C, et al. Effectiveness of recombinant erythropoietin and iron sucrose vs. iron therapy only, in patients with postpartum anaemia and blunted erythropoiesis. Eur J Clin Invest 2000;30:154–61. [PubMed] [Google Scholar]
93. Krafft A , Breymann C, Huch R, et al. Intravenous iron sucrose in two pregnant women with inflammatory bowel disease and severe iron deficiency anemia. Acta Obstet Gynecol Scand 2000;79:720–2. [PubMed] [Google Scholar]
94. Weiss G , Meusburger E, Radacher G, et al. Effect of iron treatment on circulating cytokine levels in ESRD patients receiving recombinant human erythropoietin. Kidney Int 2003;64:572–8. [PubMed] [Google Scholar]
95. Kaltwasser JP, Kessler U, Gottschalk R, et al. Effect of recombinant human erythropoietin and intravenous iron on anemia and disease activity in rheumatoid arthritis. J Rheumatol 2001;28:2430–6. [PubMed] [Google Scholar]
96. Oldenburg B , Berge Henegouwen GP, Rennick D, et al. Iron supplementation affects the production of pro-inflammatory cytokines in IL-10 deficient mice. Eur J Clin Invest 2000;30:505–10. [PubMed] [Google Scholar]
97. Emerit J , Pelletier S, Likforman J, et al. Phase II trial of copper zinc superoxide dismutase (CuZn SOD) in the treatment of Crohn’s disease. Free Radic Res Commun 1991;12–13 (Pt 2) :563–9. [PubMed] [Google Scholar]
98. Papadaki HA, Kritikos HD, Valatas V, et al. Anemia of chronic disease in rheumatoid arthritis is associated with increased apoptosis of bone marrow erythroid cells: improvement following anti-tumor necrosis factor-alpha antibody therapy. Blood 2002;100:474–82. [PubMed] [Google Scholar]
99. Pincus T , Olsen NJ, Russell IJ, et al. Multicenter study of recombinant human erythropoietin in correction of anemia in rheumatoid arthritis. Am J Med 1990;89:161–8. [PubMed] [Google Scholar]
100. Glaspy J , Bukowski R, Steinberg D, et al. Impact of therapy with epoetin alfa on clinical outcomes in patients with nonmyeloid malignancies during cancer chemotherapy in community oncology practice. Procrit Study Group. J Clin Oncol 1997;15:1218–34. [PubMed] [Google Scholar]
101. Horina JH, Petritsch W, Schmid CR, et al. Treatment of anemia in inflammatory bowel disease with recombinant human erythropoietin: results in three patients. Gastroenterology 1993;104:1828–31. [PubMed] [Google Scholar]
102. Schreiber S , Howaldt S, Schnoor M, et al. Recombinant erythropoietin for the treatment of anemia in inflammatory bowel disease. N Engl J Med 1996;334:619–23. [PubMed] [Google Scholar]
103. Dohil R , Hassall E, Wadsworth LD, et al. Recombinant human erythropoietin for treatment of anemia of chronic disease in children with Crohn’s disease. J Pediatr 1998;132:155–9. [PubMed] [Google Scholar]
104. Smith RE jr, Jaiyesimi IA, Meza LA. et al. Novel erythropoiesis stimulating protein (NESP) for the treatment of anaemia of chronic disease associated with cancer. Br J Cancer 2001;84 (suppl 1) :24–30. [PMC free article] [PubMed] [Google Scholar]
105. Hodges P , Gee M, Grace M, et al. Vitamin and iron intake in patients with Crohn’s disease. J Am Diet Assoc 1984;84:52–8. [PubMed] [Google Scholar]
106. Gee MI, Grace MG, Wensel RH, et al. Nutritional status of gastroenterology outpatients: comparison of inflammatory bowel disease with functional disorders. J Am Diet Assoc 1985;85:1591–9. [PubMed] [Google Scholar]
107. Imes S , Pinchbeck BR, Thomson AB. Diet counseling modifies nutrient intake of patients with Crohn’s disease. J Am Diet Assoc 1987;87:457–62. [PubMed] [Google Scholar]
108. Geerling BJ, Badart-Smook A, Stockbrugger RW, et al. Comprehensive nutritional status in patients with long-standing Crohn disease currently in remission. Am J Clin Nutr 1998;67:919–26. [PubMed] [Google Scholar]
Anemia and diseases of the gastrointestinal tract
AAG – autoimmune atrophic gastritis
AD – gluten-free diet
HZ – gluten sensitive celiac disease
IDA – iron deficiency anemia
Gastrointestinal tract
PPI – proton pump inhibitor
CO – mucous membrane
Anemia is a clinical and hematological syndrome characterized by a decrease below the norm in the concentration of hemoglobin and / or erythrocytes per unit volume of blood.
The development of anemia may be due to a deficiency of iron in the body (iron deficiency) or vitamin B 12 and folic acid (megaloblastic). Anemia can be formed due to increased destruction of erythrocytes (hemolytic) or impaired erythropoiesis (aplastic) [1]. The most common anemia is due to iron deficiency (about 90% of all anemias). The causes of iron deficiency are as follows [2]:
– reduced intake from food;
– violation of the absorption of the microelement;
– increased bleeding loss;
– increased consumption of iron (for example, during pregnancy).
The gastrointestinal tract (GIT) is an organ directly associated with the formation of deficiency anemia. According to K.K. Noskovy et al. [3], when assessing the prevalence of anemia among patients undergoing examination and treatment in a specialized gastroenterological hospital, the incidence of anemic syndrome was 8.25–9.02%. Among all the causes of iron deficiency in the body in men and postmenopausal women, the most common is loss during bleeding from the gastrointestinal tract. The most important sources of blood loss from the gastrointestinal tract include the following [1]:
– peptic ulcers;
– damage to the mucous membrane (SO) against the background of taking non-steroidal anti-inflammatory drugs;
– malignant tumors;
– nonspecific ulcerative colitis;
– hemorrhoids;
– diaphragmatic hernia;
– diverticulosis.
Of course, when searching for the cause of anemia, it is first necessary to exclude diseases that create conditions for blood loss, however, iron deficiency, like vitamin B 12 , may be due to a violation of their absorption. Iron absorption is carried out in the duodenum and in the initial part of the jejunum and goes through the following stages: capture by CO cells (villi) of the small intestine of ferrous iron and its oxidation to trivalent in the microvilli membrane; the transfer of iron to its own shell, where it is captured by transferrin and quickly passes into the plasma.
Absorption of vitamin B 12 occurs in the ileum with the help of highly specific receptors located on the membrane of the villi of enterocytes, then endocytosis and intracellular binding of vitamin B 12 to transcobalamin II occur [4].
In this regard, the cause of the development of iron and vitamin B 12 -deficiency anemia may be the pathology of the small intestine. The most common disease of this organ is gluten-sensitive celiac disease (gluten enteropathy, “gluten-sensitive celiac disease”, GC). In patients with iron deficiency anemia (IDA) of unknown etiology or refractory to treatment, celiac disease occurs quite often. Studies by Israeli scientists show that in patients with unexplained IDA, celiac disease is diagnosed in 4-6% of cases [2]. Iranian doctors confirmed HC in 10% of patients with IDA [5], while S. Fayed et al. when examining 25 patients with treatment-refractory IDA, HC was found in 44% [6].
HC is an immune-dependent inflammation characterized by the development of atrophy of the small intestine mucosa in individuals with a genetically determined hypersensitivity to the vegetable protein gluten.
Gluten in the composition of gliadin and other proteins of cereals (wheat, rye, barley) penetrates the epithelial intestinal barrier, reaches the cells presenting the antigen, and activates them. In response, antibodies are formed to gliadin, tissue transglutaminase, endomysium; there is a synthesis of pro-inflammatory cytokines, in particular interleukin-15, which activates intraepithelial lymphocytes, leading to the destruction of the intestinal epithelium. Intraepithelial lymphocytes are a heterogeneous population of T cells, composed primarily of cytotoxic CD8 lymphocytes, whose main role is to maintain the integrity of the small intestinal mucosal epithelium by eliminating damaged cells and promoting the formation of new ones. Dysregulation of the activation of intraepithelial lymphocytes plays a key role in the death of the intestinal epithelium and the development of villous atrophy [7]. The association of the disease with class II histocompatibility genes HLA DQ2 and DQ8 has been proven [8]. As a result of immune inflammation, the villi are shortened and the SO crypts are significantly lengthened, the epithelium is flattened, and is abundantly infiltrated by intraepithelial lymphocytes. The lamina propria showed lymphoplasmacytic infiltration. From the toxic effects of gluten, the duodenum and proximal jejunum are most affected. It is in these departments that iron is absorbed [9].
In adults, the clinical picture of HC most often consists of symptoms of IDA, malaise, increased fatigue. The severity of anemia depends on the severity of damage to the intestinal epithelium. Diarrhea is noted, more often episodic or nocturnal. Most patients have no gastrointestinal symptoms [10]. Perhaps the formation of osteoporosis due to deficiency of vitamin D and calcium, coagulopathy with the development of vitamin K deficiency. The clinical picture may include dermatitis herpetiformis, liver steatosis, infertility and miscarriage, mental and neurological disorders. Latent forms occur 6–7 times more often than with clinical manifestations [11].
Diagnosis is based on the detection of antibodies to gliadin (sensitivity of the method is 75-90%, specificity – 82-95%), endomysium (sensitivity 85-98%, specificity 97-100%), tissue transglutaminase (sensitivity 93%, specificity 99% ). Genetic testing can only exclude Hcy (HLA DQ2/DQ8). Duodenal biopsy and morphological examination of the mucosa of the distal part of the duodenum remains the “gold standard” for diagnosing HC [5, 12, 13].
The basis of the treatment of the disease is a gluten-free diet (AD). The most dangerous cereals are wheat, rye, barley. Safe foods include rice, potatoes, soybeans, corn, buckwheat, and millet. The effect of AD is assessed after 1-6 months. Nutrient deficiency is corrected: enzyme preparations, preparations of vitamins A, B, D, E, K, PP, folic acid, iron. However, anemia can gradually disappear only if blood pressure is observed. F. Zamani et al. demonstrated an increase in mean hemoglobin levels from 9.9±1.6 to 12.8±1.0 g/dl (p<0.01) in patients with HC after 6 months of blood pressure compliance without receiving iron supplements [10].
Current research is focused on finding new options for the treatment of HC. Attempts are being made to reduce the immunogenicity of gluten-containing grains, to create enzymes that break down gluten, to inhibit the binding of gluten to antigen-presenting cells, and to limit T-cell migration in the small intestine [14]. However, this is a matter for the future.
In the absorption of iron and vitamin B 12 The stomach also plays an important role. Hydrochloric acid is necessary for the transition of ionic ferric iron to the ferrous form. Under the influence of hydrochloric acid and gastric juice proteases, vitamin B 12 is released from food, cyanocobalamin is transferred to the internal factor for further transportation. Intrinsic factor (gastric juice glycoprotein) is secreted by the parietal cells of the gastric fundus [1, 4]. In this regard, the reason for the formation of iron and vitamin B 12 – deficiency anemia can become atrophic gastritis. Atrophy is defined as the loss of the corresponding glands. There are two forms of atrophic gastritis, which are formed due to autoimmune processes, as well as under the influence of prolonged persistence of Helicobacter pylori [15].
C. Hershko and A. Ronson found autoimmune gastritis in 20-27% of patients with anemia of unknown etiology, 50% had evidence of active infection H. pylori [2].
Autoimmune atrophic gastritis (AAG) is an immune-mediated form of chronic gastritis with parietal cell reduction, hypo- or achlorhydria, and decreased cobalamin levels. It occurs much less frequently than other forms of gastritis: no more than 5% of all cases of chronic gastritis. In pathogenesis, antibodies to parietal cells, intrinsic factor, H + /K + -ATPase are formed, which leads to atrophy of CO, mainly the fundus of the stomach. There is lymphoplasmacytic infiltration of the lamina propria, pseudohypertrophy of parietal cells, hypertrophy and hyperplasia of enterochromaffin cells. In the absence of infection H. pylori no changes in CO in the antrum. AAH is a morphological diagnosis [16, 17]. Detection of antibodies to gastric parietal cells and intrinsic factor, the presence of both basal and stimulated achlorhydria, hypergastrinemia, decreased pepsinogen activity, and low serum cobalamin levels (<100 pg/mL) help in diagnosis [18].
The clinical picture shows idiopathic B 12 -deficiency anemia (pernicious, Addison-Birmer’s anemia). Possible hematological manifestation of the disease in the form of fatigue, striation and brittle nails, vitiligo, “crimson tongue”. Gastrointestinal manifestation: decreased appetite, diarrhea, development of malabsorption syndrome. Neurological manifestation: funicular myelosis. Possible asymptomatic course [19].
There is no clearly developed tactics for the treatment of patients with AAH. Rational nutrition (vegetables, fruits), smoking cessation are recommended. The management of patients with anemia associated with AAH is focused on lifelong cobalamin replacement therapy [18].
The second most common form of atrophic gastritis is associated with long-term exposure to H. pylori infection . After colonization of the stomach H. pylori chronic inflammation of the mucosal system is formed. There is an infiltration by plasma cells, the production of pro-inflammatory cytokines, the formation of specific antibodies. Through antigenic mimicry of antibody H. pylori act against the parietal cells of the stomach, resulting in the formation of atrophy mainly in its antrum [20]. Successful eradication of H. pylori significantly reduces the severity of atrophy both in the antrum and in the body of the stomach, which was proved by Japanese researchers in a long-term (for 8.6 years) observation of 118 patients with atrophic gastritis associated with H. pylori [21].
In recent years infection H. pylori is considered as a triggering factor in the development of idiopathic anemia. Microorganisms are detected in 48-50% of cases of refractory IDA [2, 6, 22]. W. Xia et al. examined adolescent girls with IDA and found H. pylori infection in 46.9%, while eradication therapy led to a faster response to treatment with iron preparations [23]. Similar results were obtained by G. Vitale et al.: eradication of H. pylori increased the level of iron and vitamin B 12 in blood serum [24]. A meta-analysis including 16 studies (956 patients) showed that eradication therapy for H. pylori infection in combination with iron preparations statistically significantly increased the level of hemoglobin by 1.48 times (p<0.00001), serum iron by 1. 15 times (p<0.00001) and ferritin 1.84 times (p<0.00001) compared with iron therapy alone. The study showed that eradication of H. pylori may be an effective treatment for anemia in patients infected with H. pylori [25]. All this allowed international experts studying H. pylori infection in 2010 to include IDA of unknown etiology as an additional indication for eradication therapy. [26]. According to the Recommendations of the Russian Gastroenterological Association for the diagnosis and treatment of H. pylori infection in adults, based on the Maastricht Agreement of the last (IV) revision, the main three-component treatment regimen includes a proton pump inhibitor (PPI) in a standard dose 2 times a day, clarithromycin 500 mg 2 times a day and amoxicillin 1000 mg 2 times a day or metronidazole 500 mg 2 times a day. To increase the effectiveness of standard three-component therapy, it is possible to increase the dose of PPI by 2 times, the duration of therapy up to 10-14 days, and the addition of a bismuth preparation. As second-line therapy, a four-component regimen can be prescribed, which includes PPI at a standard dose 2 times a day, bismuth tripotassium dicitrate 120 mg 4 times a day, tetracycline 500 mg 4 times a day and metronidazole 500 mg 3 times a day for 10 days. To overcome resistance H. pylori and improve the effectiveness of treatment, a three-component therapy with levofloxacin (PPI at a standard dose 2 times a day + levofloxacin 500 mg 2 times a day + amoxicillin 1000 mg 2 times a day for 10 days) and a sequential treatment regimen (in for 5 days PPI at a standard dose 2 times a day + amoxicillin 1000 mg 2 times a day, for the next 5 days PPI at the same dose and frequency rate + clarithromycin 500 mg 2 times a day + metronidazole 500 mg 2 times a day) [27 ].
Thus, pathology of the stomach and small intestine can play a role in the formation of iron and vitamin B 12 -deficiency anemia, leading to atrophy of the mucosa of these organs and leading to impaired absorption of nutrients. Patients with anemia of unspecified etiology or refractory to iron therapy should be evaluated for HC, autoimmune gastritis, and H. pylori infection. Recognition of the role of H. pylori , autoimmune gastritis and HC in the pathogenesis of iron and cobalamin deficiency may have significant implications in the development of a diagnostic algorithm for patients with anemia and the possibility of their successful treatment.
symptoms and signs, treatments
Anemic condition may result from iron deficiency at birth, unbalanced diet or rapid growth. In adults, anemia often occurs as a complication of diseases of internal organs and systems.
Several risk factors for the disease can be identified. For example, we are talking about a vegetarian diet that leads to vitamin B12 deficiency. Alcohol abuse can cause folic acid deficiency, which also increases the risk of anemia. Some types of pathology are hereditary in nature (for example, sickle cell anemia). In addition, the development of the disease can provoke the intake of certain medications and the presence of untreated infections.
What is anemia
As we have already noted, this pathological condition is characterized by a decrease in the level of red blood cells and / or hemoglobin in the blood. In men, anemia is considered to be a decrease in hemoglobin below 130 g / l, for women this indicator during the development of the disease is less than 120 g / l. For children – values are determined taking into account age.
According to the World Health Organization, 2 billion people worldwide have been diagnosed with the disease. Anemia is much more common in women, and pathology is also quite common among children. It affects up to 30-40% of newborns and about 25% of adolescents.
Erythrocytes are produced in the bone marrow and after maturation enter the blood in a “kit” with hemoglobin molecules. Each hemoglobin molecule includes a protein and non-protein iron group. The main biological function of hemoglobin is to carry oxygen to tissues and transport carbon dioxide from tissues to the lungs. With the development of anemia, this process is disrupted, which leads to the development of hypoxia (oxygen starvation of tissues).
In most cases, anemia is not an independent disease, but only a manifestation of another pathology. Therefore, even mild forms of anemia require diagnostics to exclude recurrences of such situations.
Causes of the disease
The development of anemia in humans is often associated with impaired formation of new red blood cells and increased destruction of red blood cells. In addition, this condition may be the result of the loss of red blood cells during heavy bleeding.
The lower the hemoglobin level, the more severe the disease. The patient may face a number of serious complications and a significant deterioration in well-being. But the main danger of pathology is that it is often accompanied by more severe internal diseases.
Based on this, three main mechanisms for the development of pathology can be distinguished:
- Violation of the formation of erythrocytes and hemoglobin synthesis.
- The result of loss of red blood cells (most often due to bleeding).
- Accelerated destruction of red blood cells.
The most common cause of anemia is blood loss. It may be acute or chronic. Acute bleeding is considered to be bleeding with a loss of more than 500-700 ml of blood (in an adult) in a short period of time. Such blood loss may be visible (for example, as a result of bleeding from a wound, epistaxis, or hematemesis) or hidden. The second option is more dangerous, since it cannot be noticed immediately. Hidden bleeding often occurs in the intestines or in the abdominal cavity.
Chronic bleeding is characterized by small but regular blood loss. It can be heavy menstruation in women, as well as stomach ulcers, oncological neoplasms, hemorrhoids and various intestinal lesions. Often this condition occurs after hemodialysis.
Impaired formation of red blood cells and hemoglobin synthesis is associated with the presence of a lack of iron, vitamin B12 or folic acid. Also the cause of anemia in this case may be diseases of the red bone marrow.
Iron deficiency is often the result of impaired intake, absorption or increased loss of iron in the body. In adult men, in half of the cases, this condition is caused by blood loss from the gastrointestinal tract. In women – heavy menstruation, pregnancy, lactation and recent childbirth. Particular attention should be paid to the diagnosis of iron deficiency in children, as it can be the result of a wide range of pathological processes.
If hematopoiesis is impaired, anemia can be provoked by the following reasons:
- Damage to the bone marrow by toxins or ionizing radiation.
- Insufficient intake or malabsorption of components necessary for the formation of new red blood cells (this is vitamin B12, folic acid, etc.).
- The appearance of secondary tumor foci (metastases) in the bone marrow.
- Violation of the formation of the non-protein part of hemoglobin.
- Hormonal disorders leading to reduced production of red blood cells.
- Development of antigen-antibody reaction after blood transfusion or allergy.
The list of possible causes of such disease as anemia can be continued. Unfortunately, there are many more factors that can cause the development of pathology…
Symptoms of anemia
Signs of anemia are often not sensitive or specific. Many types of anemia occur with minimal or no symptoms.
Possible non-specific symptoms include the following:
- General weakness and fatigue.
- Pale skin.
- Drowsiness.
- Frequent dizziness.
- Shortness of breath, palpitations.
- “Flies” before the eyes.
There are also signs that may indicate a specific cause of the disease:
- Dark urine and yellowing of the skin (in the absence of liver pathologies) indicate hemolysis.
- Weight loss may be one of the symptoms of malignancy.
- The presence of blood in the stool is evidence of gastrointestinal bleeding.
- Peripheral neuropathy develops in the presence of vitamin B12 deficiency.
Should alert dry skin, brittle nails and hair, cracks and “bites” in the corners of the lips, constant muscle weakness. In severe cases, the patient may experience convulsions, vomiting, nausea, and other symptoms.
One of the most common diseases among adults and children around the world is anemia, often referred to as anemia. However, this name does not fully reflect the features of the pathology, since the patient has a decrease in the number of erythrocytes and hemoglobin, and not all blood.
There are a lot of reasons that cause such a state. In women, the problem can be the result of heavy menstruation, pregnancy and breastfeeding. But there are also more serious causes, including hidden bleeding of the gastrointestinal tract and malignant neoplasms. Different degrees of anemia are often diagnosed in children, which can be the result of malnutrition, iron absorption disorders, or various diseases of the internal organs.
Let’s figure out why such a pathology occurs, how the diagnosis is made and what treatment methods exist.
Classification of the disease
Classification of anemia is carried out taking into account various factors. Pathologies associated with blood loss are usually divided into two categories:
- acute
- chronic
Depending on the nature of development, hereditary and acquired pathologies are distinguished. As for the origin of anemia, all forms can be divided into:
- Hemolytic. Such anemias appear as a result of active destruction of red blood cells. Various factors can lead to this condition.
- Aplastic. Directly related to the inability of the bone marrow to create new blood cells.
- Posthemorrhagic. They are the result of a large loss of blood during bleeding.
- Scarce. They arise due to a deficiency of various trace elements: iron, vitamins or proteins.
For anemia resulting from impaired hematopoiesis in the body, the following classification is used. Allocate anemia:
- Associated with impaired DNA and RNA synthesis.
- Caused by a disruption in the formation of hemoglobin.
- Associated with abnormal division of red blood cells.
- Caused by inhibition of bone marrow cell formation.
When diagnosing, it is important to determine the degree of anemia , as this will allow planning treatment tactics:
- Mild degree. Decrease in hemoglobin up to 90 g/l. The patient may have minor symptoms, in some cases the pathology is asymptomatic.
- Medium. Hemoglobin indicators remain in the range from 70 to 90 g / l. A person has general weakness and fatigue, often there are pronounced symptoms of the disease.
- Heavy. This stage is characterized by a decrease in the level of hemoglobin less than 70 g / l. Significantly increases the risk of complications from the cardiovascular system.
One of the fairly common forms of anemia is iron deficiency anemia. It is most common in women of childbearing age and children under 4 years of age. Such a anemia in children is most often associated with a vegetarian or unbalanced diet, some hereditary factors. The disease is characterized by the presence of hypoxic and sideropenic syndromes.
Hypoxic syndrome is manifested by symptoms common to all forms of anemia. The patient has pallor, palpitations, headache, tinnitus, severe weakness and tiredness.
Sideropenic syndrome is manifested by dry skin, hair loss and other symptoms that indicate an iron deficiency in the body. In addition, with the development of the disease, numerous metabolic disorders occur. This provokes such a variety of clinical symptoms. In severe cases, neurotic reactions and neurasthenia may occur. Very often, patients have lesions of the gastrointestinal tract, which manifest themselves in the form of chronic gastritis or intestinal malabsorption syndrome.
Another common form of anemia is folate deficiency. It occurs as a result of a deficiency of folic acid and folates (that is, its derivatives). This condition can be the result of alimentary insufficiency, malabsorption in the intestine, taking certain medications.
Unfortunately, there is no exact data on the prevalence of this pathology in our country. However, in the course of research, it was possible to establish a connection between this type of anemia and alcohol abuse. In patients with folate deficiency anemia, weakness, fatigue, dizziness, shortness of breath, lethargy and poor appetite are observed. Often there is angular stomatitis, nausea, vomiting, diarrhea, abdominal pain.
Of particular danger is anemia that occurs with malignant neoplasms. This condition can be caused by both the presence of a tumor and its treatment. The pathogenesis of anemia in this case is quite complex and may be associated with direct and indirect consequences of the tumor process.
Diagnosis features
Suspect anemia based on history and physical examination. Most often, the initial diagnosis is performed by a general practitioner or pediatrician. Next, you may need to consult a hematologist, oncologist.
At the consultation, the specialist assesses the general well-being of the person, pays special attention to the presence of fatigue, weakness, pallor, shortness of breath during exertion.
To clarify and confirm the diagnosis, the following laboratory tests are carried out:
- Clinical blood test with determination of the number of leukocytes and platelets.
- Erythrocyte indices and morphology.
- Peripheral blood smear.
- Study of the number of reticulocytes.
In some cases the diagnosis of anemia includes aspiration and bone marrow biopsy. But the examination begins with a general blood test, as it allows you to identify the number of leukocytes and platelets, as well as determine the indicator of the distribution of red blood cells by volume. The choice of further procedures is based on the results of a general analysis, since already at this stage it is possible to identify the presence of anemia, the possible causes of its development.
Normal hemoglobin values vary with sex and age of the patient, and sometimes with chronic diseases and underlying conditions. For men, additional diagnostics are prescribed when the values are already below 130 g/l; in women, the doctor may suspect anemia at values below 120 g/l. For children, the limits of the norm change significantly with age, so special tables are used to evaluate the results.
A peripheral blood smear is used to check for excess RBC production. Using this procedure, it is possible to identify various changes in the structure of erythrocytes and detect a number of other disorders.
The evaluation of the reticulocyte count plays an important role in the diagnosis of anemia. Normal values range from 0.5% to 1.5% (as a percentage) or from 50,000 to 150,000 / µl (in absolute terms). It is this parameter that makes it possible to evaluate the reaction of the bone marrow to insufficient production of red blood cells or their excessive destruction. A decrease in normal values indicates the presence of the first problem, an increase indicates an increased destruction of red blood cells.
In some cases, bilirubin and lactate dehydrogenase (LDH) levels may also be assessed. These indicators help to differentiate between hemolysis and bleeding. Since in the first case, the values \u200b\u200bare increased, and with blood loss they remain within the normal range.
If a violation of the process of cell maturation is suspected, the patient is prescribed a bone marrow biopsy. With the help of such diagnostics, it is possible to assess the distribution and number of erythrocyte precursors, the features of iron accumulation in cells, etc. Most often, manipulation is performed in the presence of unexplained anemia or a suspected primary bone marrow disease.
Additionally, the patient may be prescribed X-ray or CT scan of the chest, ultrasound of the abdominal cavity, ultrasound of the thyroid gland, ECG. Such studies will help assess the state of internal systems and identify concomitant diseases.
Treatment
Treatment of anemia is always selected individually and depends on the symptoms present , causes, stage of development of the disease.
Key clinical guidelines include:
- Management of acute or chronic blood loss.
- Restoration of normal factors of growth and division of erythrocytes.
- Elimination of the causes of destruction of red blood cells.
- Treatment of diseases that cause a decrease in hemoglobin levels.
If there is a micronutrient deficiency, the patient is prescribed iron, folic acid, vitamins B6 and B12. In some cases, erythrocyte growth and reproduction stimulants are used. The normalization of nutrition is important – it is important for the patient to diversify the diet with foods high in proteins and vitamins. This will make up for the deficiency of important trace elements.
Severe cases may require blood transfusion or surgery (eg bone marrow transplant).
Hemolytic anemia is diagnosed with hormonal therapy, treatment with immunosuppressants or cytostatics, and sometimes with blood or plasma transfusions. This is required in order to eliminate the hemolyzing factor of the disease. Sometimes antibiotic therapy is performed to prevent infectious complications. In severe cases, bone marrow transplantation is used.
Often, especially in children, anemia is associated with infection with worms or other parasites. In this case, competent antiparasitic treatment will be required.
To prevent disease, it is recommended to visit a doctor regularly (once a year) and take a general blood test. This will allow you to track the decrease in hemoglobin and start early treatment. The diet should include offal, red meat, vegetables, fruits. Refusal of alcohol and smoking, prevention of helminthic invasion, taking medications only as prescribed by a doctor will also become important measures for the prevention of anemia. Pregnant women are prescribed an additional intake of folic acid and iron to prevent pathology.
If you notice signs of anemia, you should not postpone your visit to the doctor. You can seek help from our medical center “Yunona” – the specialists of the clinic will help determine the causes of your condition and select an effective treatment!
Author
Kaplina E. |