All statistics for Vitamin B12 Deficiency
Prevalence/Incidence of Vitamin B12 Deficiency: Online Medical Books
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Vitamin B deficiencies:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Thiamine deficiency results from malabsorption or inadequate dietary intake of vitamin B1. It also results from alcoholism, prolonged diarrhea, or from increased requirement, which can occur in pregnancy, lactation, and hyperthyroidism. Beriberi, a serious thiamine-deficiency disease, is most prevalent in Asians, who subsist mainly on diets of unenriched rice and wheat. Although this disease is uncommon in the United States, alcoholics may develop cardiac (wet) beriberi with high-output heart failure, neuropathy, and cerebral disturbances. In times of stress (pregnancy, for example), malnourished young adults may develop beriberi; infantile beriberi may appear in infants on low-protein diets or in those breast-fed by thiamine-deficient mothers.
Riboflavin deficiency (ariboflavinosis) results from a diet deficient in milk, meat, fish, legumes, and green, leafy vegetables. Alcoholism or prolonged diarrhea may also induce riboflavin deficiency. Exposure of milk to sunlight or treatment of legumes with baking soda can destroy riboflavin.
Niacin deficiency, in its advanced form, produces pellagra, which affects the skin, central nervous system (CNS), and GI tract. (See Recognizing pellagra.) Although this deficiency is now seldom found in the United States, it was once common among Southerners who subsisted mainly on corn and consumed minimal animal protein. (Corn is low in niacin and in available tryptophan, the amino acid from which the body synthesizes niacin.) Niacin deficiency is still common in parts of Egypt, Romania, Africa, Serbia, and Montenegro, where corn is the dominant staple food. Niacin deficiency can also occur secondary to carcinoid syndrome or Hartnup disease.
Pyridoxine deficiency usually results from destruction of pyridoxine in infant formulas by autoclaving. A frank deficiency is uncommon in adults, except in patients taking pyridoxine antagonists, such as isoniazid and penicillamine.
Cobalamin deficiency most commonly results from an absence of intrinsic factor in gastric secretions, or an absence of receptor sites after ileal resection. Other causes include malabsorption syndromes associated with sprue, intestinal worm infestation, regional ileitis, and gluten enteropathy, and a diet low in animal protein.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Vitamin C deficiency:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
This deficiency’s primary cause is a diet lacking in vitamin C-rich foods, such as citrus fruits, tomatoes, cabbage, broccoli, spinach, and berries. Because the body can’t store this water-soluble vitamin in large amounts, the supply needs to be replenished daily. Other causes include:
❑ destruction of vitamin C in foods by overexposure to air or by overcooking
❑ excessive ingestion of vitamin C during pregnancy, which causes the neonate to require large amounts of the vitamin after birth
❑ marginal intake of vitamin C during periods of physiologic stress — caused by infectious disease, for example — which can deplete tissue saturation of vitamin C.
Historically common among sailors and others deprived of fresh fruits and vegetables for long periods of time, vitamin C deficiency is uncommon today in the United States, except in alcoholics, people on restricted-residue diets, and infants weaned from breast milk to cow’s milk without a vitamin C supplement.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Vitamin D deficiency:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Vitamin D deficiency results from inadequate dietary intake of preformed vitamin D, malabsorption of vitamin D, or too little exposure to sunlight.
Once a common childhood disease, rickets is now rare in the United States but occasionally appears in breast-fed infants who don’t receive a vitamin D supplement or in infants receiving a formula with a nonfortified milk base. This deficiency may also occur in overcrowded urban areas in which smog limits sunlight penetration. Incidence is highest in black children who, because of their skin color, absorb less sunlight. (Solar ultraviolet rays irradiate 7-dehydrocholesterol, a precursor of vitamin D, to form calciferol.)
Osteomalacia, also uncommon in the United States, is most prevalent in Asia, among young multiparas who eat a cereal diet and have minimal exposure to sunlight. Other causes include:
❑ vitamin D–resistant rickets (refractory rickets, familial hypophosphatemia) from an inherited impairment of renal tubular reabsorption of phosphate (from vitamin D insensitivity)
❑ conditions that lower absorption of fat-soluble vitamin D, such as chronic pancreatitis, celiac disease, Crohn’s disease, cystic fibrosis, gastric or small bowel resections, fistulas, colitis, and biliary obstruction
❑ hepatic or renal disease, which interferes with the formation of hydroxylated calciferol, necessary to initiate the formation of a calcium-binding protein in intestinal absorption sites
❑ malfunctioning parathyroid gland (decreased secretion of parathyroid hormone), which contributes to calcium deficiency (normally, vitamin D controls calcium and phosphorus absorption through the intestine) and interferes with activation of vitamin D in the kidneys.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Vitamin E deficiency:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Vitamin E deficiency in infants usually results from consuming formulas high in polyunsaturated fatty acids that are fortified with iron but not vitamin E. Such formulas increase the need for antioxidant vitamin E because the iron supplement catalyzes the oxidation of RBC lipids. A neonate has low tissue concentrations of vitamin E to begin with because only a small amount passes through the placenta; the mother retains most of it. Because vitamin E is a fat-soluble vitamin, deficiency develops in conditions associated with fat malabsorption, such as kwashiorkor, celiac disease, or cystic fibrosis. These conditions may induce megaloblastic or hemolytic anemia and creatinuria, all of which are reversible with vitamin E administration.
Vitamin E deficiency is uncommon in adults but is possible in people whose diets are high in polyunsaturated fatty acids, which increase vitamin E requirements, and in people with vitamin E malabsorption, which impairs RBC survival.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Vitamin A deficiency:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Vitamin A deficiency usually results from inadequate intake of foods high in vitamin A (liver, kidney, butter, milk, cream, cheese, and fortified margarine) or carotene, a precursor of vitamin A found in dark green leafy vegetables and yellow or orange fruits and vegetables. (Six mg of beta-carotene is equal to 1 mg of vitamin A.) The recommended daily allowance for vitamin A is 1 mg for adult males and 0.8 mg for adult females.
Less common causes include:
❑ malabsorption due to celiac disease, sprue, cirrhosis, obstructive jaundice, cystic fibrosis, giardiasis, or habitual use of mineral oil as a laxative
❑ massive urinary excretion caused by cancer, tuberculosis, pneumonia, nephritis, or urinary tract infection
❑ decreased storage and transport of vitamin A due to hepatic disease.
Each year, more than 80,000 people worldwide — mostly children in underdeveloped countries — lose their sight from severe vitamin A deficiency. This condition is rare in the United States, although many disadvantaged children have substandard levels of vitamin A. With therapy, the chance of reversing symptoms of night blindness and milder conjunctival changes is excellent. When corneal damage is pres-ent, emergency treatment is necessary.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
About prevalence and incidence statistics:
The term 'prevalence' of Vitamin B12 Deficiency usually refers to the estimated population
of people who are managing Vitamin B12 Deficiency at any given time.
The term 'incidence' of Vitamin B12 Deficiency refers to the annual diagnosis rate,
or the number of new cases of Vitamin B12 Deficiency 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.
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