Prevalence and Incidence of Pernicious anemia

Prevalance of Pernicious anemia:

399,455 people in the USA 1996 ¹ ... see also overview of Pernicious anemia.

Prevalance Rate:

approx 1 in 680 or 0.15% or 399,454 people in USA [Source statistic for calcuation: "399,455 people in the USA 1996 ¹" -- see also general information about data sources]

Ophanet, who are a consortium of European partners, currently defines a condition rare when if affects 1 person per 2,000. They list Pernicious anemia as a "rare disease". More information about Pernicious anemia is available from Orphanet

Prevalence/Incidence of Pernicious anemia: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the prevalence and/or incidence of Pernicious anemia.

Folic acid deficiency anemia: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

Folic acid deficiency anemia may result from:

❑ alcohol abuse (alcohol may suppress metabolic effects of folate)

❑ poor diet (common in alcoholics, elderly people living alone, and infants, especially those with infections or diarrhea)

❑ impaired absorption (due to intestinal dysfunction from disorders such as celiac disease, tropical sprue, regional jejunitis, or bowel resection)

❑ bacteria competing for available folic acid

❑ excessive cooking, which can destroy a high percentage of folic acids in foods (See Foods high in folic acid.)

❑ limited storage capacity in infants

❑ prolonged drug therapy (anticonvulsants and estrogens)

❑ increased folic acid requirements during pregnancy; during rapid growth in infancy (common because of recent increase in survival of premature infants); during childhood and adolescence (because of general use of folate-poor cow’s milk); and in patients with neoplastic diseases and some skin diseases (chronic exfoliative dermatitis).

It’s estimated that 10% of the United States population has low folate stores.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Iron deficiency anemia: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

Iron deficiency anemia may result from:

❑ inadequate dietary intake of iron (less than 1 to 2 mg/day), such as in prolonged unsupplemented breast-feeding or bottle-feeding of infants or during periods of stress such as rapid growth in children and adolescents

❑ iron malabsorption, such as in chronic diarrhea, partial or total gastrectomy, chronic diverticulosis, and malabsorption syndromes, such as celiac disease and pernicious anemia

❑ blood loss secondary to drug-induced GI bleeding (from anticoagulants, aspirin, and steroids) or due to heavy menses, hemorrhage from trauma, GI ulcers, esophageal varices, or cancer

❑ pregnancy, which diverts maternal iron to the fetus for erythropoiesis

❑ intravascular hemolysis-induced hemoglobinuria or paroxysmal nocturnal hemoglobinuria

❑ mechanical erythrocyte trauma caused by a prosthetic heart valve or vena cava filters.

A common disease worldwide, iron deficiency anemia affects 10% to 30% of the adult population of the United States. It occurs most commonly in premenopausal women, infants (particularly premature or low-birth-weight neonates), children, and adolescents (especially girls). Persons who are at increased risk for iron deficiency include those of low socioeconomic status who don’t get a well-balanced diet that includes iron-rich foods.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Sickle cell anemia: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

Sickle cell anemia results from homozygous inheritance of the gene that produces HbS (chromosome 11). It's inherited as an autosomal recessive trait. Heterozygous inheritance of this gene results in sickle cell trait, a condition that usually produces no symptoms. (See Sickle cell trait.) Sickle cell anemia is most common in tropical Africans and in people of African descent; about 1 in 10 American blacks carries the abnormal gene. However, sickle cell anemia also appears in other ethnic populations, including people of Mediterranean or East Indian ancestry.

If two parents who are both carriers of sickle cell trait (or another hemoglobinopathy) have offspring, each child has a 25% chance of developing sickle cell anemia. (See Inheritance patterns in sickle cell anemia, page 22.) Overall, 1 in every 400 to 600 black children has sickle cell anemia. The defective HbS-producing gene may have persisted because, in areas where malaria is endemic, the heterozygous sickle cell trait provides resistance to malaria and is actually beneficial.

The abnormal HbS found in such patients' RBCs become insoluble whenever hypoxia occurs. As a result, these RBCs become rigid, rough, and elongated, forming a crescent or sickle shape. (See Comparing normal and sickled red blood cells.) Such sickling can produce hemolysis (cell destruction). In addition, these altered cells tend to pile up in capillaries and smaller blood vessels, making blood more viscous. Normal circulation is impaired, causing pain, tissue infarctions, and swelling. Such blockage causes anoxic changes that lead to further sickling and obstruction.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Sideroblastic anemias: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

Hereditary sideroblastic anemia appears to be transmitted by X-linked inheritance, occurring mostly in young males; females are carriers and usually show no signs of this disorder.

The acquired form may be secondary to ingestion of or exposure to toxins, such as alcohol and lead, or to certain drugs. It can also occur as a complication of other diseases, such as rheumatoid arthritis, lupus erythematosus, multiple myeloma, tuberculosis, and severe infections.

The primary acquired form, known as refractory anemia with ringed sideroblasts, is most common in elderly people. It’s commonly associated with thrombocytopenia or leukopenia as part of a myelodysplastic syndrome.

In sideroblastic anemia, normoblasts fail to use iron to synthesize Hb. As a result, iron is deposited in the mitochondria of normoblasts, which are then termed ringed sideroblasts.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Pernicious anemia: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

Familial incidence of pernicious anemia suggests a genetic predisposition. (It may involve an inherited single dominant autosomal factor.) Significantly higher incidence in patients with immunologically related diseases, such as thyroiditis, myxedema, and Graves’disease, seems to support a widely held theory that an inherited autoimmune response causes gastric mucosal atrophy and, therefore, deficiency of hydrochloric acid and IF. IF deficiency impairs vitamin B₁₂ absorption. The resultant vitamin B₁₂ deficiency inhibits cell growth, particularly of red blood cells (RBCs), leading to insufficient and deformed RBCs with poor oxygen-carrying capacity. It also impairs myelin formation, causing neurologic damage. Iatrogenic induction can follow partial gastrectomy.

PEDIATRIC TIP Juvenile pernicious anemia, occurring in children younger than age 10, stems from a congenital stomach disorder that causes secretion of abnormal IF.

ELDER TIP With age, vitamin B₁₂ absorption may also diminish, resulting in reduced erythrocyte mass and decreased hemoglobin (Hb) levels and hematocrit (HCT).

Pernicious anemia primarily affects people of northern European ancestry. It’s rare in children and infants. Onset typically occurs after age 35, and incidence increases with age. It affects about 2% of people older than age 60.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Aplastic anemias: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

Aplastic anemias usually develop when damaged or destroyed stem cells inhibit red blood cell (RBC) production. Less commonly, they develop when damaged bone marrow microvasculature creates an unfavorable environment for cell growth and maturation. About one-half of such anemias result from drugs (antibiotics and anticonvulsants), toxic agents (such as benzene and chloramphenicol), or radiation. The rest may result from immunologic factors (unconfirmed), severe disease (especially hepatitis), or preleukemic and neoplastic infiltration of bone marrow.

Idiopathic anemias may be congenital. Two such forms of aplastic anemia have been identified: Congenital hypoplastic anemia (Blackfan-Diamond anemia) develops between ages 2 and 3 months; Fanconi’s syndrome, between birth and age 10. In Fanconi’s syndrome, chromosomal abnormalities are usually associated with multiple congenital anomalies, such as dwarfism, and hypoplasia of the kidneys and spleen. In the absence of a consistent familial or genetic history of aplastic anemia, researchers suspect that these congenital abnormalities result from an induced change in the fetus’development.

Incidence is 0.6 to 6.1 cases per 1 million people. There is no racial predilection.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

About prevalence and incidence statistics:

The term 'prevalence' of Pernicious anemia usually refers to the estimated population of people who are managing Pernicious anemia at any given time. The term 'incidence' of Pernicious anemia refers to the annual diagnosis rate, or the number of new cases of Pernicious anemia diagnosed each year. Hence, these two statistics types can differ: a short-lived disease like flu can have high annual incidence but low prevalence, but a life-long disease like diabetes has a low annual incidence but high prevalence. For more information see about prevalence and incidence statistics.

Footnotes:
1. Rose and Mackay, 1998, The Autoimmune Diseases, Third Edition