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B12 Defeciency

Vitamin B12 Deficiency and Symptoms:
Vitamin B12 deficiency is usually due to mal-absorption.  The only other cause is inadequate dietary intake of the vitamin.  Dietary Vitamin B12 deficiency arises in vegans who omit meat, fish, eggs, cheese, and other animal products from their diet.  Vitamin B12 deficiency may also arise rarely in non-vegetarian individuals who exist on grossly inadequate diets because of poverty or psychiatric disturbance.
Selective mal-absorption of the Vitamin B12 with Proteinuria is the most common cause of megaloblastic anemia due to Vitamin B12 deficiency in infancy in Western Countries. The patients secrete normal amounts of IF and gastric acid but are unable to absorb the Vitamin B12. Nearly all patients with acute tropical sprue show mal-absorption of Vitamin B12, leading to B12 deficiency. The Fish tapeworm lives in the small intestine of humans and accumulates Vitamin B12 from food, rendering this unavailable for absorption. Severe Chronic Pancreatitis have lack of trypsin is thought to cause dietary Vitamin B12 attached to gastric non-IF binder to be unavailable for absorption. Serum Vitamin B12 levels tend to fall in patients with HIV infection and are subnormal in 10-35% of those with AIDS.
Mal-absorption of the Vitamin B12 has been reported in Zollinger-Ellison Syndrome.  It is thought that there is a failure to release Vitamin B12 from R-binding protein due to inactivation of pancreatic trypsin by high acidity, as well as interference with IF binding of the Vitamin B12.
Vitamin B12 deficiency can cause a type of anemia that is characterized by fewer. Other effects include walking and balance disturbances, a loss of vibration sensation, confusion, and, in seriously advanced cases, dementia. Since the body requires the Vitamin B12, an inadequate supply of the vitamin B12 can damage the nerves.
               
Symptoms of B-12 deficiency and vitamin B-12-related anemia include:
·         Feeling tired or weak
·         Pale appearance to the lining of lower eyelids
·         Palpitations, fast or irregular heart beat.
·         Faintness and breathlessness.
·         Hair loss
·         Bruising that occurs without reason
·         Dizziness
·         Long or unusually heavy menstrual periods
The megaloblastic anemias are a group of disorders characterized by the presence of distinctive morphologic appearance of the developing red cells in the bone marrow. The cause is either due to Vitamin B12 deficiency (cobalamin) or folate deficiency, but megaloblastic anemia may arise because of genetic or acquired abnormalities affecting the metabolism of these vitamins or because of defects in DNA synthesis not related to Vitamin B12 or folate. After the marrow, the next most affected tissues are the epithelial cell surfaces of the mouth, stomach, and small intestine and the respiratory, urinary, and female genital tracts.  The cells show macrocytosis, with increased numbers of multinucleate and dying cells.  The b12 deficiency may cause cervical smear abnormalities.
Pernicious anemia is defined as a severe lack of Intrinsic Factor due to gastric atropathy.   Pernicious anemia is one of the autoimmune conditions and is connected with autoimmune endocrine conditions, including Hashimoto's thyroitis, thyrotoxicosis, diabetes, Addison's disease and primary ovarian failure. People with these autoimmune conditions are at higher risk of pernicious anemia and vice versa. Pernicious anemia is an autoimmune disease in which the body is not able to absorb enough of the vitamin B12 from the digestive tract. It occurs after long-term autoimmune gastritis (inflammation of the mucosal lining of the stomach). The destruction of the gastric mucosal cells makes you unable to make intrinsic factor, a substance that enables the vitamin B12to be absorbed from the intestine, resulting in the in the B12 deficiency.
Pernicious anemia is most common in people of Celtic (i.e., English, Irish, Scottish) or Scandinavian descent. Pernicious anemia usually occurs in people aged 40 to 70 years. Among Caucasians, the mean age of onset is 60 years, but it shows up at an average of 50 with African-Americans.

While symptoms of pernicious anemia are usually slow and vague, making diagnosis difficult, the most common symptoms include weakness, sore tongue, and paresthesias (numbness, tingling, burning sensations). Other symptoms include:
·         Lack of appetite, weight loss of 10-15 pounds in about 50% of patients, due to lack of appetite
·         Low-grade fever
·         Anemia
·         Half of all patients have a smooth tongue which may be painful and red. Burning and soreness on the tongue may also be accompanied by changes in taste and loss of appetite.
·         Constipation or several semisolid bowel movements daily
·         Numbness and tingling in hands and feet
·         Nausea, vomiting, heartburn
·         Flatulence, diarrhea
·         Sense of fullness, abdominal pain
·         Fatigue, weakness
·         Pale skin, pallor, lemon-yellow waxy appearance to the skin
·         Impaired smell
·         Bleeding gums
·         Shortness of breath
·         Headache
·         Ringing in the ears (tinnitus)
·         Loss of bladder control
·         Impotence
·         Clumsiness and unsteady gait (worse in the dark)
·         Irritability, personality changes, memory loss
·         Delusions, hallucinations
·         Premature whitening of the hair
·         Rapid heartbeat
Vitamin B12 deficiency has been reported in infants born to mothers who had severe B12 deficiency.  These infants develop megaloblastic anemia at about 3-6 months of age, presumably because they are born with low stores of the Vitamin B12 and also because they are fed with breast milk of low Vitamin B12 content.  These babies have also shown growth retardation, impaired psychomotor development and other neurologic disorders. Vitamin B12 deficiency has also been associated with impaired bactericidal function of phagocytes. The Gonads are also affected, and infertility is common in both men and women with Vitamin B12 deficiency and b12 deficiency has been implicated in recurrent fetal loss and neural tube defects. Vitamin B12 deficiency may cause a bilateral peripheral neuropathy or degeneration of the posterior and pyramidal tracts of the spinal cord and, less frequently optic atrophy or cerebral symptoms. Long term nutritional B12 deficiency in infancy leads to poor brain development and impaired intellectual development. Psychiatric disturbance is common in both folate and B12 (cobalamin) deficiencies. This, like the neuropathy, has been attributed to a failure of the synthesis of SAM, which is needed in methylation of biogenic amines (e.g., dopamine) as well as of proteins, phospholipids, and neurotransmitters in the brain.  With association between lower serum folate or the Vitamin B12 levels and higher homocysteine levels, the development of Alzheimer’s disease has been reported.
Following total gastrectomy, b12 deficiency is inevitable, and prophylactic vitamin b12 therapy should be commenced immediately following the operation. After partial gastrectomy, 10–15% of patients also develop b12 deficiency. The exact incidence and time of onset are most influenced by the size of the resection and the preexisting size of the vitamin b12 body stores.