What Does Mcv Stand For On A Blood Test?

What Does Mcv Stand For On A Blood Test

What does a low MCV mean in a blood test?

Low MCV (microcytosis) is less than 80 fl. It may be a sign of: Iron-deficiency anemia. Thalassemia. Other hemoglobin disorders.

How do you fix elevated MCV?

What causes enlarged red blood cells (macrocytosis)? – Answer From Rajiv K. Pruthi, M.B.B.S. Macrocytosis is a term used to describe red blood cells that are larger than normal. Also known as megalocytosis or macrocythemia, this condition typically causes no signs or symptoms and is usually detected incidentally on routine blood tests.

  • Vitamin B-12 deficiency
  • Folate deficiency
  • Liver disease
  • Alcoholism
  • Hypothyroidism
  • A side effect of certain medications, such as those used to treat cancer, seizures and autoimmune disorders
  • Increased red blood cell production by the bone marrow to correct anemia, for example, after blood loss
  • An underlying bone marrow cancer called myelodysplastic syndrome

If you have macrocytosis, blood tests can help determine its cause. In some cases, it may be necessary to remove a sample of your bone marrow — the spongy tissue inside your bones — for testing. Management of macrocytosis consists of finding and treating the underlying cause.

Does MCV increase with age?

4. DISCUSSION – This study included more patient data than any of the previous studies, 12, 13, 14, 17, 18 and the findings revealed a distinct age‐related increase in MCV compared with other CBC parameters. The MCV increased gradually from 1 to 88 years of age, and the increase could be represented by two different sets of linear regression Equations. MCV is used to classify anaemia as either microcytic, normocytic or macrocytic.5 In microcytic anaemia, the average erythrocyte volume is smaller than normal, generally under 80 fl, and this finding is commonly observed in cases of chronic iron‐deficient anaemia, anaemia of chronic disease and thalassemias. Macrocytic anaemia is characterized by elevated MCV (generally over 100 fl) and is subcategorized as megaloblastic or non‐megaloblastic. Megaloblastic anaemia is caused by impaired DNA synthesis and commonly occurs in folate deficiency and vitamin B12 deficiency, while non‐megaloblastic anaemia occurs due to hepatic insufficiency, chronic alcoholism and rare congenital diseases.5 The MCV has also been recently reported to be a risk factor for mortality and morbidity in some clinical settings. Borderline high MCV (MCV > 95 fl) was independently associated with arterial stiffness measured by brachial‐ankle pulse wave velocity in apparently healthy individuals.19 In patients with stage 3–5 chronic kidney disease (CKD), MCV was associated with all‐cause mortality, cardiovascular mortality and infection‐associated mortality.9 Other studies with CKD patients showed that an increase in MCV was independently associated with more impaired endothelial function and insulin resistance and showed higher cardiovascular event and mortality rates.20 In older patients, high MCV levels were also significantly associated with high rates of decline on tasks of global mental status, long‐delay memory and attention, even after adjusting for potential confounders.21 Age‐related changes in MCV may be a part of the normal ageing process. Young RBCs are released into circulation as reticulocytes from the bone marrow, and old RBCs will be removed from circulation within a few hours or days.22 The lifespan of RBCs in older individuals is shorter than that in young adults, and the RBC production increases to compensate for the shorter lifespan.14, 23 These younger RBCs tend to have larger volumes, as measured by MCV.14 Various cytokines and growth factors are involved in the formation of RBCs, including erythropoietin, which is essential for the survival and differentiation of erythropoietic progenitors.24, 25 Other growth factors and cytokines, such as insulin, insulin‐like growth factors (IGFs), hepatocyte growth factors and interleukins (IL‐3, IL‐4, IL‐6, IL‐9 and IL‐11), have also been known to co‐stimulate of growth of the RBCs.24, 26 The relationship between biological changes and ageing is not fully understood. One recent study revealed that prolonged growth hormone, insulin and IGF nutrient response signalling pathways were silent killers of stem cells and one the factors responsible for ageing.27 Ageing accelerates after reproductive age, and several mechanisms are known to accelerate this process.28 The age‐related changes in MCV showed two linear trends with different slopes, with the distinction appearing from 25 years of age. This result may provide evidence for accelerated ageing after reproductive age, but more biological studies are needed to validate this assumption. Moreover, additional research is required to explain the link among IGF and MCV. Our study had several limitations. First, the retrospectively obtained patient cohort included inpatients, outpatients and emergency room patients in addition to those who had undergone medical check‐ups. Therefore, these patients were more likely to have disease and may not represent the general population. Second, we could not control the influence of factors other than anaemia, including underlying diseases such as chronic hepatitis, chronic renal disease or malignancy disease, on MCV changes, and the influence of these factors should be verified in future studies. Third, we did not include most important clinical outcome, that is mortality. Further studies are needed to identify the relation between an increase in MCV with ageing and mortality.

How do you control MCV?

Get more vitamin B12 and folate in your diet – Vitamin B12 and folate (Vitamin B9) are nutrients needed to form healthy red blood cells. Hence, if you have deficiencies in these vitamins, it’s highly likely to develop low MCH and MCV. Include the following food sources of vitamin B12 and B9 in your diet:

Fish (salmon, tuna, and trout)Meat (beef, pork, and poultry)Leafy greens (spinach, cabbage, and kale)Broccoli Brussel sprouts Dairy productsFortified cereals

What diseases cause low MCV?

Differential Diagnosis – The differential diagnoses for microcytic, normocytic and macrocytic anemias are listed below based on MCV findings in a complete blood count. Differential diagnoses of MCV under 80 include iron deficiency anemia causes, anemia of chronic disease causes, sideroblastic anemia causes, H.

pylori infection, and thalassemias. Iron deficiency anemia can have many different differential diagnoses including menorrhagia, colorectal adenocarcinoma, bleeding colonic polyp, bleeding peptic ulcer disease, Helicobacter pylori infection, hematemesis, chronic epistaxis, and duodenal malabsorption or resection.

Anemia of chronic disease can have differential diagnoses including malignancy, rheumatologic conditions such as SLE and rheumatoid arthritis, autoimmune diseases such as primary biliary cirrhosis or multiple sclerosis, chronic kidney disease, and chronic infection.

  • Chronic alcoholism, vitamin B6 deficiency, isoniazid use, myelodysplastic disorder, lead poisoning, copper deficiency, and congenital sideroblastic anemia are all differential diagnoses for sideroblastic anemia, causing microcytic anemia.
  • The main types of thalassemia are alpha1, alpha2, alpha3/ hemoglobin H disease, alpha4, which is fatal, beta-thalassemia minor, beta-thalassemia major, and HbS/β thalassemia heterozygote.

Differential diagnoses of MCV above 100 include megaloblastic anemia and non-megaloblastic anemia. Megaloblastic anemia causes include folate deficiency which can be caused by chronic alcoholism, barbiturate use, phenytoin use, sulfasalazine use, methotrexate use, triamterene use, trimethoprim/sulfamethoxazole use, pyrimethamine use, and duodenal or jejunal malabsorption or resection.

  1. Differential diagnoses for vitamin B12 deficiency would include Crohn disease ileitis, short bowel syndrome, strict vegan diet without supplementation, diphyllobothrium latum infection, chronic metformin use, pernicious anemia, atrophic gastritis, orotic aciduria, and Diamond Blackfan anemia.
  2. Non-megaloblastic differential diagnoses include those causing hepatic insufficiency or cirrhosis which can be secondary to chronic alcoholism, fulminant hepatitis secondary to drug toxicity, alpha 1 antitrypsin disease, galactosemia, Wilson disease, chronic hepatitis B viral infection, chronic hepatitis C infection, hemochromatosis, autoimmune hepatitis, amyloidosis, chronic decompensated right heart failure, and parasitic infections such as Schistosoma haematobium,

Differential diagnoses of MCV 80 to 100 include those that cause intravascular hemolytic anemia and extravascular hemolytic anemia and aplastic anemia. Intravascular hemolytic anemia can be caused by paroxysmal nocturnal hemoglobinuria and micro/macroangiopathic hemolytic anemia due to Thrombotic thrombocytopenic purpura, Hemolytic Uremic Syndrome, HELLP Syndrome, disseminated intravascular coagulation, aortic stenosis, and defective prosthetic cardiac valve.

Extravascular hemolytic anemia can result from hereditary spherocytosis, sickle cell anemia, glucose 6-phosphate dehydrogenase deficiency, infections like malaria and babesiosis, and autoimmune hemolytic anemia. Some differential diagnoses for autoimmune hemolytic anemia causes would be chronic leukocytic leukemia, systemic lupus, erythematosus, and hematopoietic stem cell transplant.

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Also, differential diagnoses for aplastic anemia would include Fanconi anemia, paroxysmal nocturnal hemoglobinuria, radiation exposure, the toxicity of drugs like chloramphenicol, sulfonamides, benzene exposure, viral infections such as parvovirus B19, especially in immunocompromised patients, HIV, Ebstein-Barr virus, hairy cell leukemia, and myelodysplastic disorders.

Does low MCV mean iron deficiency?

Interpreting test results – MCV test results are interpreted by comparing your MCV to a reference range, or the set of values that the laboratory expects for a healthy person. Reference ranges are based on the results of a large sample of healthy people and are associated with the equipment and procedures of the laboratory that conducts the test.

  • MCV is usually reported in femtoliters (fL).
  • The American Board of Internal Medicine lists a typical MCV reference range as 80-98 fL.
  • MCV levels are reported as within the reference range if they fall within the expected range for a healthy individual.
  • If the MCV result is outside of the reference range, it may be reported as high or low.

If you have anemia or other health conditions you can have normal or abnormal MCV results. It is also possible for healthy people to have a normal or abnormal MCV result. In patients with anemia, MCV results are categorized as follows:

  • Low MCV means that RBC are smaller than normal and may indicate microcytic anemia. This condition may be caused by iron deficiency, lead poisoning, or thalassemia, a genetic condition that causes your body to have less hemoglobin than normal.
  • Normal MCV may indicate normocytic anemia. This can occur when an individual experiences symptoms of anemia due to sudden blood loss, kidney failure, or aplastic anemia, a rare disorder where the body does not produce enough RBC.
  • High MCV means that the RBC are too large and indicates macrocytic anemia. This condition can be caused by several factors including low folate or vitamin B12 levels or chemotherapy.

MCV is usually not interpreted as an isolated measurement. Rather, it is compared to the results of your other RBC indices and CBC values, like hemoglobin and hematocrit. Your doctor will also consider any symptoms or changes in your health when interpreting these test results.

  • What do my MCV levels indicate about my health?
  • Can any diagnoses be made based on my MCV results?
  • Do I need any follow-up tests based on my MCV results?
  • If my MCV test results come back abnormal, is there anything you would suggest to improve my health?
  • Blood Smear Learn More
  • CBC Blood Test (Complete Blood Count) Learn More
  • MCH Blood Test (Mean Corpuscular Hemoglobin) Learn More
  • MCHC Blood Test (Mean Corpuscular Hemoglobin Concentration) Learn More
  • Platelet Count (PLT) Blood Test Learn More
  • Red Blood Cell Count (RBC) Test Learn More
  • White Blood Cell Count (WBC Blood Test) Learn More

Does MCV go away?

How is molluscum contagiosum treated? – Some treatments exist for molluscum that may prevent spread of the infection to other parts of the body and to other people. A health care provider can remove the growths with surgery or laser therapy. A health care provider may prescribe a cream to apply on the bumps or a medicine to take by mouth.

However, treatment is not usually required because the bumps disappear on their own within six months. However, they may not go away completely for up to four years. In addition, not all treatments are successful for all people. For example, it is more difficult to treat persons who have a weak immune system.

This includes people who are infected with HIV or who are receiving drugs to treat cancer. Some molluscum treatments that are advertised on the Internet are not effective and may even be harmful! Therefore, always discuss any therapy with a health care provider before using it.

What drugs cause high MCV?

Discussion – The causes of macrocytosis reported varies in different populations studied. Savage et al. in their study of 300 hospitalized patients in a New York City teaching hospital have reported drug therapy and alcohol abuse as the most frequent causes, and Vitamin B12/folate deficiency as uncommon (6%). Davidson et al. have also reported medications as the most frequent cause. Keenan et al. have observed that alcoholism followed by hematological disorders as the most frequent causes. However, their study has excluded drug induced causes. Mahmoud et al. have studied 124 patients in the age group of ≥75 years and found a higher incidence of hematological diseases and malignancy associated with macrocytosis. Breedveld et al. and Seppa et al. have reported Vitamin deficiency and alcoholism as the most frequent etiological factors, which is similar to the findings in the present study. Drugs reported to cause macrocytosis include reverse transcriptase inhibitors (Zidovudine, lamivudine, stavudine), anticonvulsants (valproic acid, phenytoin), folate antagonists (methotrexate), chemotherapeutics (alkylating agents, pyrimidine and purine inhibitors), sulfasalazine (anti inflammatory), pyrimethamine, trimethoprim, sulfamethoxazole, metformin and nitrous oxide. Most patients with HIV, being treated with reverse transcriptase inhibitors will display macrocytosis without anemia. In these patients, macrocytosis is considered a surrogate marker indicating the patients compliance in taking medications, Colon-Otero et al. have reported that 60% patients with macrocytosis present without anemia. In the present study, 83 cases (46.7%) presented without anemia and the remaining 95 cases (53.3%) had associated anemia. The relative incidence of anemia in our study varied among different etiologies, being most frequent in Vitamin B12/folate deficiency (Fig.1 ). Alcoholism was commonly associated with nonanemic macrocytosis. Another important observation in this study was that 9 cases (20.9%) of Vitamin B12 deficiency manifested isolated macrocytosis, without anemia. This re-emphasises the fact that macrocytosis can be an early diagnostic harbinger of Vitamin B12 deficiency, preceding anemia by months. It must be noted that MCV is an average value, and can be masked by a coexisting microcytic anemia like iron deficiency anemia, anemia of chronic illness and thalassemia trait, In the present study, the maximum MCV observed in Vitamin B12/folate deficiency was 146.8 fl, whereas in alcoholism it was 114 fl. In alcoholism, the MCV is usually reported to range between 100 and 110 fl, Ethanol appears to have a direct toxic effect on the marrow erythroid precursors. As the life-span of erythrocytes is 120 days, it may take 3–4 months for MCV to return to normal following abstinence from alcohol, The mean RDW (21.6%) in megaloblastic cases was significantly higher compared to nonmegaloblastic conditions (13.7%). Gupta et al. have compared the red cell parameters in macrocytosis of aplastic anemia and megaloblastic anemia and observed that RDW in megaloblastic anemia was significantly higher than the RDW in aplastic anemia. An increased RDW has been reported in megaloblastic anemia, myelodysplastic syndromes and chemotherapy, In liver disease and aplastic anemia, RDW is normal or mildly increased, Seppa et al. have compared the red cell parameters in macrocytosis of pernicious anemia and alcohol abuse. They found that a combination of low red cell count (<4 × 10 12 /l), high RDW (>15%), with a normal thrombocyte count and a normal thrombocyte mean cellular volume was highly sensitive in detecting Vitamin B12/folate deficiency. Bessmann et al. have developed an improved classification of anemias based on MCV and RDW. Megaloblastic processes are characterized by the presence of oval macrocytes (macro-ovalocytes) and hypersegmented neutrophils. However, hypersegmented neutrophils can sometimes be absent in megaloblastic conditions, if associated with marked left shift or severe neutropenia, Macro-ovalocytes are reported to be more sensitive but somewhat less specific than neutrophil hypersegmentation in predicting marrow megaloblastic changes, It is reported that an MCV >115 fl, increased RDW, macro-ovalocytes, and hypersegmented neutrophils suggest a megaloblastic disorder, Nonmegaloblastic conditions display uniformly round macrocytes and normal RDW, Round macrocytes are commonly seen in alcoholism and round, target-appearing macrocytes are characteristic of liver disease such as hepatitis and obstructive jaundice, In the present study, hypersegmented neutrophils and macro-ovalocytes were more frequently observed in megaloblastic macrocytosis. However, these features were also observed in a small percentage of alcoholism cases, who predominantly exhibited round, uniform macrocytes. Though not specific for one condition, an elevated MCV of >100 fl, is a useful parameter directing further investigations which can ultimately lead to a definitive diagnosis in 75% of cases, It may be the only indicator of vitamin deficiency and alcoholism, Mahmoud et al. believe that unexplained macrocytosis in the elderly (≥75 years) could be an early sign of Myelodysplastic syndrome. Joseph et al. have observed that refractory, unexplained macrocytosis may be an early sign of smoldering leukemia. Therefore regardless of the hemoglobin levels, close attention should be paid to MCV, Macrocytosis needs to be evaluated even in the absence of anemia, as it may be the first clue to an underlying pathology. Complete medical history including alcohol and drug intake, proper evaluation of red cell parameters and peripheral smear assist in arriving at a provisional diagnosis, thereby directing further management. This approach helps in determining the cause of macrocytosis, particularly in resource limited settings.

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What vitamin deficiency causes high MCV?

References – 1. Chanarin I, Metz J. Diagnosis of cobalamin deficiency: the old and new. Br J Haematol 1997; 97 :695–700.2. Kasper DL, Braunwald E, Fauci A, Hauser S, Longo D, Jameson JL. Harrison’s principles of internal medicine.16 th ed. New York: McGraw-Hill Medical Publishing Division; 2005.3.

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Lindenbaum J. Status of laboratory testing in the diagnosis of megaloblastic anemia. Blood 1983; 61 :624–627.6. Lawrence AC, Bevington JM, Young M. Storage of blood and the mean corpuscular volume. J Clin Pathol 1975; 28 :345–349.7. Breedveld FC, Bieger R, van Wermeskerken RK.

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Etiology and diagnostic evaluation of macrocytosis. Am J Med Sci 2000; 319 :343–352.10. Hoffbrand AV, Pettit, JE. Clinical hematology: Sandoz atlas. London: Glower; 1988.11. Nathan DG, Orkin SH, Look AT, Ginsburg D. Nathan and Oski’s hematology of infancy and childhood.6 th ed.

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Inflamm Bowel Dis 2003; 9 :237–245.15. Papadakis KA. Mean corpuscular volume: a simple and inexpensive way to monitor azathioprine/6-mercaptopurine treatment in patients with inflammatory bowel disease? Evidence-Based Gastroenterology 2004; 5 :22–23.16.

  • Petersen K, Hale BR, Wallace MR.
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Int J STD AIDS 2002; 13 :748–754.18. Bain BJ. Diagnosis from the blood smear. N Engl J Med 2005; 353 :498–507.19. Torres Gomez A, Casano J, Sanchez J, Madrigal E, Blanco F, Alvarez MA. Utility of reticulocyte maturation parameters in the differential diagnosis of macrocytic anemias.

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A problem-oriented approach. Baltimore: Williams & Wilkins.1996.25–54.47. Nyholm E, Turpin P, Swain D, Cunningham B, Daly S, Nightingale P, Fegan C. Oral vitamin B12 can change our practice. Postgrad Med J 2003; 79 :218–220.48. Bolaman Z, Kadikoylu G, Yukselen V, Yavasoglu I, Barutca S, Senturk T. Oral versus intramuscular cobalamin treatment in megaloblastic anemia: a single-center, prospective, randomized, open-label study.

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Does vitamin D deficiency cause high MCV?

3.1. Comparisons – Table 2 describes the computed differences of all determined parameters in groups I, II and III. There were only significant variations of vitamin D, MCV and MCHC between groups I, II and III. The increase of MCHC was significant lower, when vitamin D values went down, in comparison to the MCHC rise, when vitamin D was elevated.

Can low vitamin D cause high MCV?

There was no relationship between differences of vitamin D and MCV (see also Table 3).

What cancers cause high MCV levels?

In addition, recent studies have found an association between high MCV and the prognosis of colorectal, esophageal, and liver cancers.

What vitamin deficiency causes high MCV?

References – 1. Chanarin I, Metz J. Diagnosis of cobalamin deficiency: the old and new. Br J Haematol 1997; 97 :695–700.2. Kasper DL, Braunwald E, Fauci A, Hauser S, Longo D, Jameson JL. Harrison’s principles of internal medicine.16 th ed. New York: McGraw-Hill Medical Publishing Division; 2005.3.

  1. Davidson RJ, Hamilton PJ.
  2. High mean red cell volume: its incidence and significance in routine haematology.
  3. J Clin Pathol 1978; 31 :493–498.4.
  4. Hattersley PG, Gerard PW, Caggiano V, Nash DR.
  5. Erroneous values on the Model S Coulter Counter due to high titer cold autoagglutinins.
  6. Am J Clin Pathol 1971; 55 :442–446.5.

Lindenbaum J. Status of laboratory testing in the diagnosis of megaloblastic anemia. Blood 1983; 61 :624–627.6. Lawrence AC, Bevington JM, Young M. Storage of blood and the mean corpuscular volume. J Clin Pathol 1975; 28 :345–349.7. Breedveld FC, Bieger R, van Wermeskerken RK.

  • The clinical significance of macrocytosis.
  • Acta Med Scand 1981; 209 :319–322.8.
  • Colon-Otero G, Menke D, Hook CC.
  • A practical approach to the differential diagnosis and evaluation of the adult patient with macrocytic anemia.
  • Med Clin North Am 1992; 76 :581–597.9.
  • Savage DG, Ogundipe A, Allen RH, Stabler SP, Lindenbaum J.

Etiology and diagnostic evaluation of macrocytosis. Am J Med Sci 2000; 319 :343–352.10. Hoffbrand AV, Pettit, JE. Clinical hematology: Sandoz atlas. London: Glower; 1988.11. Nathan DG, Orkin SH, Look AT, Ginsburg D. Nathan and Oski’s hematology of infancy and childhood.6 th ed.

Philadelphia: Saunders; 2003; 1841.13. Sechi LA, De Carli S, Catena C, Zingaro L, Bartoli E. Benign familial macrocytosis. Clin Lab Haematol 1996; 18 :41–43.14. Thomas CW Jr, Lowry PW, Franklin CL, Weaver AL, Myhre GM, Mays DC, Tremaine WJ, Lipsky JJ, Sandborn WJ. Erythrocyte mean corpuscular volume as a surrogate marker for 6-thioguanine nucleotide concentration monitoring in patients with inflammatory bowel disease treated with azathioprine or 6-mercaptopurine.

Inflamm Bowel Dis 2003; 9 :237–245.15. Papadakis KA. Mean corpuscular volume: a simple and inexpensive way to monitor azathioprine/6-mercaptopurine treatment in patients with inflammatory bowel disease? Evidence-Based Gastroenterology 2004; 5 :22–23.16.

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