Causes of Vitamin B12 Deficiency
List of causes of Vitamin B12 Deficiency
Following is a list of causes or underlying conditions
(see also Misdiagnosis of underlying causes of Vitamin B12 Deficiency)
that could possibly cause Vitamin B12 Deficiency includes:
Causes of Vitamin B12 Deficiency (Diseases Database):
The follow list shows some of the possible medical causes of Vitamin B12 Deficiency
that are listed by the Diseases Database:
Source: Diseases Database
Vitamin B12 Deficiency Causes: Book Excerpts
Vitamin B12 Deficiency as a symptom:
Conditions listing Vitamin B12 Deficiency
as a symptom may also be potential underlying causes of Vitamin B12 Deficiency.
Our database lists the following as having
Vitamin B12 Deficiency as a symptom of that condition:
Drug interactions causing Vitamin B12 Deficiency:
When combined, certain drugs, medications, substances or toxins may react
causing Vitamin B12 Deficiency as a symptom.
The list below is incomplete and various other drugs or substances may cause your symptoms.
Always advise your doctor of any medications or treatments you are using,
including prescription, over-the-counter, supplements, herbal or alternative treatments.
- K-Dur and diuretic blood pressure tablet interaction
- K-Tab and diuretic blood pressure tablet interaction
- Micor-K and diuretic blood pressure tablet interaction
- Slow-K and diuretic blood pressure tablet interaction
- more interactions...»
Read more about medication causes of Vitamin B12 Deficiency
Related information on causes of Vitamin B12 Deficiency:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Vitamin B12 Deficiency may be found in:
Causes of Vitamin B12 Deficiency: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the causes of Vitamin B12 Deficiency.
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.
» READ BOOK EXCERPT ONLINE »
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.
» READ BOOK EXCERPT ONLINE »
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.
» READ BOOK EXCERPT ONLINE »
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.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Vitamin K deficiency:
Causes
(Professional Guide to Diseases (Eighth Edition))
Vitamin K deficiency is common among neonates in the first few days postpartum due to poor placental transfer of vitamin K and inadequate production of vitamin K-producing intestinal flora. Its other causes include prolonged use of drugs, such as the anticoagulant warfarin and antibiotics that destroy normal intestinal bacteria; decreased flow of bile to the small intestine from obstruction of the bile duct or bile fistula; malabsorption of vitamin K due to sprue, pellagra, bowel resection, ileitis, or ulcerative colitis; chronic hepatic disease, with impaired response of hepatic ribosomes to vitamin K; and cystic fibrosis, with fat malabsorption. Vitamin K deficiency seldom results from insufficient dietary intake of this vitamin.
» READ BOOK EXCERPT ONLINE »
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.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
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