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      Low Initial Vitamin B 12 Levels in Helicobacter pylori-Positive Patients on Chronic Hemodialysis

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          Background: Helicobacter pylori has been identified as a possible cause of vitamin B<sub>12</sub> deficiency in the general population. We assessed any potential relationship between low cyanocobalamin serum levels and Helicobacter pylori status in hemodialysis patients and subsequently correlated these results with the existence of anemia (a common complication in hemodialysis patients), and macrocytosis. Methods: In 29 chronic hemodialysis patients, active H. pylori infection was diagnosed using two different methods regardless of digestive symptoms: by searching for bacterial antigens in stools and by the detection of urea breakdown through breath testing. If these results were non-coincident, gastroscopy was performed and antral biopsies obtained. Patients were subsequently divided into group A ( H. pylori-positive, n = 8, 28%) and group B ( H. pylori-negative, n = 21, 72%). The corresponding initial values of erythrocytic folic acid, vitamin B<sub>12</sub> and homocysteine prior to the first hemodialysis session of each patient were retrospectively collected. Results: Vitamin B<sub>12</sub> levels (normal 200– 900 pg/ml) were significantly lower in group A compared to group B (225.4 ± 111.9 vs. 707.9 ± 258.3 pg/ml, p < 0.011). In group A, 5 patients (63%) had vitamin B<sub>12</sub> deficiency (154 ± 24.6 pg/ml). Baseline hematocrits, erythrocyte folic acid and serum homocysteine levels were not different between the groups, but mean corpuscular volumes were significantly higher in group A compared to group B (109.7 ±14.1 vs. 91.8 ± 8.8 fl, p = 0.002). Conclusions: H. pylori-positive chronic hemodialysis patients may present with lower vitamin B<sub>12</sub> blood levels and macrocytosis. H. pylori infection should be suspected in this population when low or low-normal vitamin B<sub>12</sub> levels or macrocytosis exist.

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          Vitamin B12 deficiency in the elderly.

          Vitamin B12 deficiency is estimated to affect 10%-15% of people over the age of 60, and the laboratory diagnosis is usually based on low serum vitamin B12 levels or elevated serum methylmalonic acid and homocysteine levels. Although elderly people with low vitamin B12 status frequently lack the classical signs and symptoms of vitamin B12 deficiency, e.g. megaloblastic anemia, precise evaluation and treatment in this population is important. Absorption of crystalline vitamin B12 does not decline with advancing age. However, compared with the younger population, absorption of protein-bound vitamin B12 is decreased in the elderly, owing to a high prevalence of atrophic gastritis in this age group. Atrophic gastritis results in a low acid-pepsin secretion by the gastric mucosa, which in turn results in a reduced release of free vitamin B12 from food proteins. Furthermore, hypochlorhydria in atrophic gastritis results in bacterial overgrowth of the stomach and small intestine, and these bacteria may bind vitamin B12 for their own use. The ability to absorb crystalline vitamin B12 remains intact in older people with atrophic gastritis. The 1998 recommended daily allowance for vitamin B12 is 2.4 micrograms, but elderly people should try to obtain their vitamin B12 from either supplements or fortified foods (e.g. fortified ready-to-eat breakfast cereals) to ensure adequate absorption from the gastrointestinal tract. Because the American food supply is now being fortified with folic acid, concern is increasing about neurologic exacerbation in individuals with marginal vitamin B12 status and high-dose folate intake.
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            Helicobacter pylori--is it a novel causative agent in Vitamin B12 deficiency?

             R Finci,  K Kaptan,  A Ural (2000)
            Evidence for vitamin B12 deficiency usually involves combinations of low serum vitamin B12 levels, clinical and metabolic abnormalities, and therapeutic response. Identification of the underlying cause is important in the diagnosis of vitamin B12 deficiency that is usually attributed to malabsorption. Helicobacter pylori is one of the most common causes of peptic ulcer disease worldwide and a major cause of chronic superficial gastritis leading to atrophy of gastric glands. It is suggested that there may be a casual relationship between H. pylori and food-cobalamin malabsorption. To evaluate the H. pylori incidence in patients with vitamin B12 deficiency prospectively and to assess whether treatment for H pylori infection could correct this deficiency over time. We performed a prospective cohort study involving 138 patients who had anemia and vitamin B12 deficiency. An upper gastrointestinal endoscopy was performed to assess the severity of atrophic gastritis and biopsy specimens for Campylobacter-like organisms tests and histological examination for H pylori were obtained at the time of diagnosis. The diagnosis of H. pylori prompted a combination treatment. Helicobacter pylori was detected in 77 (56%) of 138 patients with vitamin B12 deficiency and eradication of H pylori infection successfully improved anemia and serum vitamin B12 levels in 31 (40 %) of 77 infected patients. Helicobacter pylori seems to be a causative agent in the development of adult vitamin B12 deficiency. Eradication of H. pylori infection alone may correct vitamin B12 levels and improve anemia in this subgroup of patients.
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              Non-gastrointestinal tract associations of Helicobacter pylori infection.

              Helicobacter pylori infection is linked to conditions of the upper gastrointestinal tract, including peptic ulcer and gastric adenocarcinoma. It has also been associated with a wide variety of non-gastrointestinal tract conditions. However, the evidence in support of H. pylori infection as a cause of the non-gastrointestinal tract conditions is not widely understood. We reviewed the medical literature for publications and abstracts dealing with putative non-gastrointestinal tract associations of H. pylori infection. We appraised the level of evidence and applied it to an established set of 9 criteria for determining causation. We found that many studies examining a possible causal relationship have been uncontrolled or inadequately controlled. Studies have often failed to control for socioeconomic status. Studies of treating H. pylori infection in patients with these disorders have been poorly designed and inappropriately controlled, and therefore add little to the evidence base. Attention should be focused on appropriate testing for and treatment of H. pylori infection in patients with conditions that are of proven association, notably peptic ulcer disease.

                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                January 2004
                17 November 2004
                : 96
                : 1
                : c28-c32
                Nephrology Section, Hospital Británico de Buenos Aires, Argentina
                75569 Nephron Clin Pract 2004;96:c28–c32
                © 2004 S. Karger AG, Basel

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