Macrocytic anemia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2]

The word “hematology,” which appears to have been first used in this country in 1811, is older than might be expected, for in 1743, Thomas Schwencke (1694-1768) wrote Hamatologia, sive Sanguinis Historia, Experimentis passim superstructa etc. Hagae Comitum. Hematology, like bacteriology, has developed as the result of laboratory methods and the applications of physics and chemistry. Macrocytic anemia are the anemia which has MCV>100fL. Macrocytic anemia may be classified into 2 subtypes/groups: Megaloblastic anemia and non megaloblastic anemia. Folate is important in the production of various building blocks necessary for the production of biologic macromolecules. By combining with carbon moieties, tetrahydrofolate (THF) becomes methelenetetrahydofolate. This molecule is then able to donate carbon moieties to form purines, dTMP, and methionine. Of note, Vitamin B12 is also a cofactor in the production of methionine. THF is the resulting molecule after donation of carbon moieties except in the synthesis of dTMP from dUMP. DHF (dihydrofolate) results from this reaction. DHF reductase must act on DHF to participate in reactions again. In 60% of anemic patients, megaloblastic anemia affects 2-4% of population. Patients of all age groups may develop megaloblastic anemia. The incidence of megaloblastic anemia increases with age. Megaloblastic anemia commonly affects older age group. Males are more commonly affected by megaloblastic anemia than females. In deficiencies of vitamin b12 and folate causing megaloblastic anemia, supplementation are made with Cyanocobalamine and Folic Acid respectively based on the severity and the cause. LDH falls in 2 days. Hypokalemia requiring replacement can occur in the acute phase as new cells are being generated rapidly. A reticulocytosis begins in 3-5 days and peaks in 10 days. The Hematocrit will rise within 10days. If it does not, suspect another disorder. Hypersegmented polymorphonuclear cells disappear in 10-14 days.

Megaloblastic anemia and pernicious anemia was first discovered by Osler and Gardner in 1877 at Montreal. Increase in bone marrow cells was noted by Cohnheim in 1876.

Macrocytic anemia are the anemia which has MCV>100fL. Macrocytic anemia may be classified into 2 subtypes/groups: Megaloblastic anemia and non megaloblastic anemia.

Folate is important in the production of various building blocks necessary for the production of biologic macromolecules. By combining with carbon moieties, tetrahydrofolate (THF) becomes methelenetetrahydofolate. This molecule is then able to donate carbon moieties to form purines, dTMP, and methionine. Of note, Vitamin B12 is also a cofactor in the production of methionine. THF is the resulting molecule after donation of carbon moieties except in the synthesis of dTMP from dUMP. DHF (dihydrofolate) results from this reaction. DHF reductase must act on DHF to participate in reactions again. The two metabolically active forms of Vitamin B12 are Methycobalamin and Adenosylcobalamin. The former is important in methionine synthesis. Methionine is necessary for the production of cholinephospholipids. Adenosylcobalamin is necessary to convert methylmalonyl CoA to succinyl-CoA. Interruption of this reaction eventually leads to nonphysiologic fatty acid production and abnormal neuronal lipid production. B12 deficiency also leads to folate metabolism derangement. Tissue folate levels are reduced in the setting of Vitamin B12 deficiency through a complicated biochemical pathway. This is known as the “folate trap hypothesis” and explains why large doses of folate will help the hematological manifestations. The mechanism of the neurologic manifestations remains independent of folate metabolism.

The common causes of megaloblastic anemia are less dietray intake, autoimmune disorders like pernicious anemia, alcoholism, increased demands like in pregnancy and due to drugs.

The most important differential is whether the patient has ACD alone or ACD with ongoing iron deficiency anemia (ACD/IDA). The following parameters will distinguish the two: Soluble transferrin receptor levels (sTfR) and/or the sTfR-ferritin index sTfR and the sTfR-ferritin index are normal in uncomplicated ACD, while both are elevated when IDA is also. Percentage of hypochromic red cells and reticulocyte hemoglobin may help.

In 60% of anemic patients, megaloblastic anemia affects 2-4% of population. Patients of all age groups may develop megaloblastic anemia. The incidence of megaloblastic anemia increases with age. Megaloblastic anemia commonly affects older age group. Males are more commonly affected by megaloblastic anemia than females.

Common risk factors of megaloblastic anemia include nutritional factors like alcoholism, elderly, pregnant, vegans, and malabsorptive syndromes

There is insufficient evidence to recommend routine screening for megaloblastic anemia

The symptoms of megaloblastic anemia typically develop many years after defieciency of Vitamin B12. If left untreated, patients with megaloblastic anemia may progress to develop Subacute combined degeneration of spinal cord, Peripheral neuropathy, and Dementia.

Homocysteine and methylmalonic acid levels can be helpful in confirmation. Both serum homocysteine and methylmalonic acid (MMA) levels are increased in helpful confirmatory tests for cobalamin and folate deficiencies. Homocysteine but not methylmalonic acid is increased in folate deficiency.

History may include higher MCV specially in neonates and infants, alcohol use, medications (eg, anticonvulsants, zidovudine, immunosuppressive agents), congenital heart disease, Down syndrome, reticulocytosis, bone marrow failure/dysplasia, liver disease, thyroid disease, hemolytic anemias with reticulocytosis and myelodysplastic syndromes (MDS). Macrocytosis is a common feature of MDS, especially in older adults. Patients with B12 deficiency show neurologic dysfunction, anemia symptoms such as fatigue, dyspnea, lightheadedness, and anorexia, high output cardiac failure, angina, diarrhea, cheilosis, glossitis, subacute combined degeneration, broad based gait, ataxia, numbness or paresthesias, Rhomberg and Babinski’s sign. Dementia may progress to frank “Megaloblastic Madness”

Common physical examination findings of megaloblastic anemia include glossitis, pallor, mouth ulcers, vitiligo, subacute combined degeneration, and positive Romberg’s sign.

The lab findings include measuring levels of vitamin b12, folate, methylmalonic acid, and homocysteine.

There are no echocardiogram/ultrasound findings associated with megaloblastic anemia. However, an echocardiogram may be helpful in the diagnosis of complications of megaloblastic anemia which include features of myocardial infarction when associated with hyperhomocysteinemia and dilated cardiomyopathy, and an ultrasound may show complication like splenomegaly.

There are no x-ray findings associated with megaloblastic anemia

There are no echocardiogram/ultrasound findings associated with megaloblastic anemia. However, an echocardiogram may be helpful in the diagnosis of complications of megaloblastic anemia which include features of myocardial infarction when associated with hyperhomocysteinemia and dilated cardiomyopathy, and an ultrasound may show complication like splenomegaly.

There are no CT scan findings associated with megaloblastic anemia.

There are no MRI findings associated with megaloblastic anemia. However, an MRI may be helpful in the diagnosis of complications of megaloblastic anemia, which include subacute combined degeneration

There are no other imaging findings associated with megaloblastic anemia

There are no other diagnostic findings associated with megaloblastic anemia

In deficiencies of vitamin b12 and folate causing megaloblastic anemia, supplementation are made with Cyanocobalamine and Folic Acid respectively based on the severity and the cause. LDH falls in 2 days. Hypokalemia requiring replacement can occur in the acute phase as new cells are being generated rapidly. A reticulocytosis begins in 3-5 days and peaks in 10 days. The Hematocrit will rise within 10days. If it does not, suspect another disorder. Hypersegmented polymorphonuclear cells disappear in 10-14 days.

Surgical intervention is not recommended for the management of megaloblastic anemia

Green leafy vegetables and meat are a good source of Vitamin B-12. Alcohol consumption can lead to macrocytic anemia. These are some of the primary ways to reduce the incidence of macrocytic anemia.

Folic acid supplementation in conditions which need more folate like pregnancy and lactation or in malabsorption e.g., celiac disease or a loss e.g., chronic hemolytic disorder. Folic acid supplementation in pregnant women can also prevent fetal neural tube defects.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2] Omer Kamal, M.D.[3]

Megaloblastic anemia and pernicious anemia was first discovered by Osler and Gardner in 1877 at Montreal. Increase in bone marrow cells was noted by Cohnheim in 1876.

Following facts were found in historical perspective:^[1]

• Megaloblastic anemia and pernicious anemia was first discovered by Osler and Gardner in 1877 at Montreal.
• Increase in bone marrow cells was noted by Cohnheim in 1876.

• The association between megaloblastic(pernicious) anemia and spinal cord lesions was made in 1887 by Lichtheim.
• Subacute combined degeneration of spinal cord was coined by Russell et al in 1900.
• In 1908, Cabot was the first to discover the association between megaloblastic anemia and the development of numbness and tingling of extremities.
• In 1923, Minot and Murphy started a diet for people with anemia which had animal sources like liver, muscle meat, leafy vegetables, eggs and milk. they discovered rises in cell count and hemoglobin levels.
• In 1934, Whipple, Minot and Murphy were awarded with Nobel prize for medicine and physiology for saving the lives of anemic people with dietary measures.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2], Omer Kamal, M.D.[3]

Macrocytic anemia are the anemia which has MCV>100fL. Macrocytic anemia may be classified into 2 subtypes/groups: Megaloblastic anemia and non megaloblastic anemia.

• Macrocytic anemia are the anemia which has MCV>100fL

• Macrocytic anemia may be classified into 2 subtypes/groups:^[1][2][3]
  • Megaloblastic anemia
    • Vitamin B12 deficiency
    • Folate deficiency
  • Non megaloblastic anemia
    • Intrinsic (Myelodyplasia)
    • Extrinsic (liver disease, hypothyroidism)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2] Omer Kamal, M.D.[3]

Folate is important in the production of various building blocks necessary for the production of biologic macromolecules. By combining with carbon moieties, tetrahydrofolate (THF) becomes methelenetetrahydofolate. This molecule is then able to donate carbon moieties to form purines, dTMP, and methionine. Of note, Vitamin B12 is also a cofactor in the production of methionine. THF is the resulting molecule after donation of carbon moieties except in the synthesis of dTMP from dUMP. DHF (dihydrofolate) results from this reaction. DHF reductase must act on DHF to participate in reactions again. The two metabolically active forms of Vitamin B12 are Methycobalamin and Adenosylcobalamin. The former is important in methionine synthesis. Methionine is necessary for the production of choline phospholipids. Adenosylcobalamin is necessary to convert methylmalonyl CoA to succinyl-CoA. Interruption of this reaction eventually leads to nonphysiologic fatty acid production and abnormal neuronal lipid production. B12 deficiency also leads to folate metabolism derangement. Tissue folate levels are reduced in the setting of Vitamin B12 deficiency through a complicated biochemical pathway. This is known as the “folate trap hypothesis” and explains why large doses of folate will help the hematological manifestations. The mechanism of the neurologic manifestations remains independent of folate metabolism.

Reticulocytosis: Reticulocytes are immature RBCs without nuclei but some retained some messenger RNA with a typical mean corpuscular volume (MCV) of approximately 103 to 126 fL. The increase in MCV could be attributed in part to the signals from erythropoietin to increase RBC production rapidly and skipping some divisions which in turn increases reticulocytes in blood which look much bigger than normal mature RBCs, oval and lacking central pallor with a bluish color due to retained RNA. As reticulocytes are much larger than the mature RBCs, the increasing percentage of total RBCs will raise the MCV proportionately.^{[1][2][3][4][5][6]}

• Folate is important in the production of various building blocks necessary for the production of biologic macromolecules. By combining with carbon moieties, tetrahydrofolate (THF) becomes methelenetetrahydofolate. This molecule is then able to donate carbon moieties to form purines, dTMP, and methionine. Of note, Vitamin B12 is also a cofactor in the production of methionine.
• THF is the resulting molecule after donation of carbon moieties except in the synthesis of dTMP from dUMP. DHF (dihydrofolate) results from this reaction. DHF reductase must act on DHF to participate in reactions again.^{[7][8] [9]}
• The two metabolically active forms of Vitamin B12 are Methycobalamin and Adenosylcobalamin. The former is important in methionine synthesis. Methionine is necessary for the production of choline phospholipids. Adenosylcobalamin is necessary to convert methylmalonyl CoA to succinyl-CoA. Interruption of this reaction eventually leads to nonphysiologic fatty acid production and abnormal neuronal lipid production.
• B12 deficiency also leads to folate metabolism derangement. Tissue folate levels are reduced in the setting of Vitamin B12 deficiency through a complicated biochemical pathway. This is known as the “folate trap hypothesis” and explains why large doses of folate will help the hematological manifestations. The mechanism of the neurologic manifestations remains independent of folate metabolism.

• Folate has minimum daily requirement of 50 mcg per day this requirement can increase substantially in settings such as pregnancy.^[10][11]
• Total body stores are approximately 5-20mg with half held in the liver. The serum folate level is not a reliable index of tissue folate levels.
• Serum folate levels can go up or down despite normal tissue levels depending on dietary intake and EtOH intake. The RBC (red blood cell) folate level is a better measure of tissue folate stores.

• The minimum daily requirement for B12 is 2.5 mcg.
• About 4mg is stored in the body with half in the liver.
• Obviously, it takes much longer to become B12 (3-6 years) versus folate (3 months) if intake ceased abruptly.
• The test for B12 is variable.

• Hyperhomocysteinemia
• Chemotherapy
• Polyglandular autoimmune syndrome
• Gastritis^[12]
• Hemodialysis

• On microscopic histopathological analysis, following are characteristic findings of megaloblastic anemia:
  • Macrocyte
  • Hypersegmented neutrophils
  • Cabot rings and basophillic stippling can also be seen.

<imagemap> Image:Macrocytosis.jpg|230px|thumb|Non-megaloblastic macrocytosis is characterized by the presence of large RBCs (macrocytes).Source: By Osarten, Wikimedia commons[13] </imagemap>

<imagemap> Image:Hypersegmented neutrophil.png|thumb|Megaloblastic macrocytosis is characterized by the presence of large RBCs (macrocytes) and hypersegmented neutrophils ≥ 5 lobes (red arrow).Source:Wikimedia commons[14] </imagemap>

<imagemap> File:Cabot ring and basophilic stippling.jpg|thumb|Cabot ring and basophillic stippling, By Dr. Roshan Nasimudeen, Source: Wikimedia commons[15] </imagemap>

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2] Omer Kamal, M.D.[3]

The common causes of megaloblastic anemia are less dietray intake, autoimmune disorders like pernicious anemia, alcoholism, increased demands like in pregnancy and due to drugs.

Common causes of macrocytic anemia may include: causes of megaloblastic anemia and non megaloblastic anemia:^[1][2][3]

• Vitamin B12 Deficiency:  
  1. Deficient intake
  2. Deficient intrinsic factor (pernicious anaemia or gastrectomy)
  3. Bilogical competition for B12 by diverticulosis, fistula, intestinal anastomosis, achlorhydria and infection by the marine parasite Diphyllobothrium latum
  4. Selective B12 malabsorption (congenital and drug-induced)
  5. Chronic pancreatitis
  6. Ileal resection and bypass
• Folate Deficiency:
  1. Deficient intake
  2. Alcoholism
  3. Increased needs: pregnancy, infant, rapid cellular proliferation, and cirrhosis
  4. Malabsorption (congenital and drug-induced)
  5. Intestinal and jejunal resection
• Toxins and Drugs:
  • Amobarbital sodium
  • Cycloserine
  • Cytarabine
  • Ethotoin
  • Folic acid antagonists (methotrexate)
  • Pergolide
  • Purine antagonists (6-mercaptopurine)
  • Pyrimidine antagonists (cytosine arabinoside)
  • Phenobarbital
  • Pyrimethamine
  • Secobarbital sodium
  • Trimethoprim
  • Erythroleukemia.

• Myelodysplasia
• Chronic liver disease
• Reticulocytosis
• Hypothyroidism

Less common causes of macrocytsic anemia include: ^[4]

• Combined deficiency(vitamin B12 & folate) Tropical sprue
• Inherited DNA Synthesis Disorders: Deficient thiamine and factors (e.g. enzymes) responsible for folate metabolism.
• Lesch-Nyhan Syndrome
• Methylmalonic aciduria
• Orotic aciduria

• Lesch-Nyhan Syndrome
• Orotic aciduria

Cardiovascular	No underlying causes
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	Amobarbital sodium, Cycloserine, Cytarabine, Ethotoin, Folic acid antagonists (methotrexate), Pergolide, Purine antagonists (6-mercaptopurine), Pyrimidine antagonists (cytosine arabinoside), Phenobarbital, Pyrimethamine, Secobarbital sodium, Trimethoprim
Ear Nose Throat	No underlying causes
Endocrine	Hypothyroidism
Environmental	No underlying causes
Gastroenterologic	Chronic liver diseases, diverticulosis, fistula, intestinal anastomosis, achlorhydria
Genetic	Lesch-Nyhan Syndrome, Methylmalonic aciduria, Orotic aciduria
Hematologic	Myelodysplasia, Pernicious anemia, Reticulocytosis
Iatrogenic	No underlying causes
Infectious Disease	Diphyllobothrium latum
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	Alcoholism, Folate deficiency,Orotic aciduria, Vitamin B12 deficiency
Obstetric/Gynecologic	Pregnancy
Oncologic	No underlying causes
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	No underlying causes
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	No underlying causes

List the causes of the disease in alphabetical order:

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2]

Megaloblastic anemia needs to be diffrentiated from other causes of anemia.

To review the differential diagnosis of anemia, click here.

Disease	Genetics	Clinical manifestation					Lab findings
		History	Symptoms	Signs	Hemolysis	Intrinsic/Extrinsic	Hb concentration	MCV	RDW	Reticulocytosis	Haptoglobin levels	Hepcidin	Iron studies					Specific finding on blood smear
													Serum iron	Serum Tfr level	Transferrin or TIBC	Ferritin	Transferrin saturation
Folate deficiency[1]	Impaired DNA synthesis	Alcohol consumption History of using drugs like methotrexate, trimethoprim, and phenytoin Low socioeconomic groups with poor nutrition Older people Pregnant and lactating women	No neurological symptoms vs B12 deficiency Odynophagia Angular stomatitis	Glossitis Signs of heart failure Anencephaly and spina bifida	−	−	Anisochromic	Macrocytic	↑	↓	Nl	Nl	↑	↑	↓	↑	↑	RBC macrocytosis Hypersegmented neutrophils Pancytopenia in severe cases
Vitamin B12 deficiency[2]	Impaired DNA synthesis	Pernicious anemia Crohn’s disease Gastrectomy Veganism Diphyllobothrium latum infection	Psychosis Insomnia Depression Cognitive slowing Restless leg syndrome	Neurological deficit Myelopathy Memory loss with reduced attention span Nystagmus Positive romberg sign Positive Lhermitte’s sign	−	−	Anisochromic	Macrocytic	↑	↓	Nl	Nl	↑	↑	↓	↑	↑	Senile neutrophil Anisocytosis Ovalocytes
Orotic aciduria[3]	Autosomal recessive Deficiency of enzyme UMPS	Episodic vomiting Rhabdomyolysis	Coma Gastrointestinal manifestation	Neurological manifestation	−	−	Anisochromic	Macrocytic	↑	↓	Nl	Nl	↑	↑	↓	↑	↑	NA
Fanconi anemia[4]	Autosomal recessive X-linked recessive	History of anemia at age 16	Hypopigmentation Cafe-au-lait patches Radial ray anomaly	Significant for bilateral short thumbs	−	−	Anisochromic	Macrocytic	↑	↓	Nl	Nl	↑	↑	↓	↑	↑	Nl appearing WBC, RBC and Platelets But the number is greatly reduced
Disease	Genetics	History	Symptoms	Signs	Hemolysis	Intrinsic/Extrinsic	Hb concentration	MCV	RDW	Reticulocytosis	Haptoglobin levels	Hepcidin	Serum iron	Serum Tfr level	IBC	Ferritin	Transferrin saturation	Specific finding on blood smear
Diamond-Blackfan anemia[5]	Mutations in: RPL5 RPL11 RPL35A RPS7 RPS10 RPS17 RPS19 RPS24 RPS26	Associated with myelodysplastic syndrome Increased risk of AML	Pale skin Sleepiness Heart murmurs	Triphalangeal thumbs Short stature Microcephaly Hypertelorism Ptosis Micrognathia	−	−	Anisochromic	Macrocytic	Nl	↓	Nl	Nl	↑	↑	↓	↑	↑	NA
Liver disease[6]	−	Hepatitis Binge drinking Gall bladder disease	Jaundice Abdominal pain Itchy skin	Ascites Right upper quadrant pain Hepatomegaly Swelling in the legs Ankle swelling	−	−	Anisochromic	Macrocytic	↑	↑	Nl	Nl	↑	↑	↓	↑	↑	Round macrocytes Target macrocytes
Alcoholism[7]	−	History of increased alcohol intake Folic acid deficiency	Memory impairment Nausea Sweating	Truncal obesity Asterixis Encephalopathy Spider angiomas Hematemesis Gynecomastia	−	−	Anisochromic	Macrocytic	↑	↑	Nl	Nl	↑	↑	↓	↑	↑	Oval macrocytes Hypersegmented neutrophils
Disease	Genetics	History	Symptoms	Signs	Hemolysis	Intrinsic/Extrinsic	Hb concentration	MCV	RDW	Reticulocytosis	Haptoglobin levels	Hepcidin	Serum iron	Serum Tfr level	IBC	Ferritin	Transferrin saturation	Specific finding on blood smear

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2] Associate Editor(s)-in-Chief: Amandeep Singh M.D.[3]

Megaloblastic anemia affects 2-4% of population. Patients of all age groups may develop megaloblastic anemia. The incidence of megaloblastic anemia increases with age. Males are more commonly affected by megaloblastic anemia than females.

• Megaloblastic anemia affects 2-4% of population.^[1][2][3]

• Patients of all age groups may develop megaloblastic anemia.
• The incidence of megaloblastic anemia increases with age.
• Megaloblastic anemia commonly affects older age group.

• Males are more commonly affected by megaloblastic anemia than females.^[4]

• Megaloblastic anemia is more common in developing countries due to lack of resources.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2] Associate Editor(s)-in-Chief: Amandeep Singh M.D.[3]

Common risk factors of megaloblastic anemia include nutritional factors, alcoholism, elderly, pregnant, vegans, and malabsorptive syndromes.

Common risk factors of megaloblastic anemia:^[1][2][3][4]

• Folate deficiency
• Nutritional deficiency
  • Strict vegan diet
  • Malabsorptive disorders such as blind loops/bacterial overgrowth, sprue, Whipple’s and crohn’s
  • Diphillobothrium latum infection (a competitor for B12 absorption)
• Elderly age
• Alcohol use
• Narcotic abuse
• Physiologic or pathologic states of increased metabolic demand
  • Pregnancy
  • Infancy
  • Low grade hemolysis
  • Malignancy
  • Chronic hemodialysis
• Autoimmune disease
  • Hashimoto’s
  • Vitiligo
  • Diabetes
  • Adrenal insufficiency (Schmitt’s Syndrome)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2]

There is insufficient evidence to recommend routine screening for megaloblastic anemia

There is insufficient evidence to recommend routine screening for megaloblastic anemia

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2]

The symptoms of megaloblastic anemia typically develop many years after defieciency of Vitamin B12. If left untreated, patients with megaloblastic anemia may progress to develop Subacute combined degeneration of spinal cord, Peripheral neuropathy, and Dementia.

• The symptoms of megaloblastic anemia typically develop many years after defieciency of Vitamin B12. ^[1]
• If left untreated, patients with megaloblastic anemia may progress to develop Subacute combined degeneration of spinal cord, Peripheral neuropathy, and Dementia.

• Common complications of megaloblastic anemia include:^[2]
  • Subacute combined degeneration of spinal cord
  • Pyrexia of unknown origin^[3]
  • Damage to the nervous system
  • Long-term neurologic complications.
  • Peripheral neuropathy
  • Dementia.

• Prognosis is generally good with folate and vitamin B12 supplemntation^[4]

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