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PubMedDate not supplied

Synthetic and biosynthetic studies on vitamin B12.

Vitamin B12 is the anti-pernicious anemia vitamin. It functions as the main part of a coenzyme for a range of remarkable rearrangement reactions. The macrocycle for vitamin B12 is smaller by one carbon than that for chlorophyll and protoheme. Research is described involving numerous skills at the microscale level. In addition, synthesis of new pigments that have been encountered has been undertaken. A large part of the biosynthetic pathway to vitamin B12 has been revealed.

Chemical Phenomena↗
PubMed2003

Intermediate effects of the ileocaecal urinary reservoir (Charleston pouch 1) on serum vitamin B12 concentrations: can vitamin B12 deficiency be prevented?

OBJECTIVE: To assess the long-term effects of a form of ileocolic urinary reservoir (Charleston Pouch 1) on vitamin B12 serum levels, as vitamin B12 deficiency may be an important long-term risk after urinary diversion by this method. PATIENTS AND METHODS: The study included 60 patients (mean age 52 years, range 27-77; 33 men and 27 women) who had a follow-up of >or= 36 months (36-132 months) after the construction of an ileocaecal urinary reservoir. Vitamin B12 serum levels were determined at the time of diversion and again when the patients were evaluated every 6 months. RESULTS: Fifty-eight patients had a normal serum vitamin B12 concentration before surgery (two patients were excluded from the study because they had low levels); the mean level was 464 pg/mL (normal range 247-1000). At 6 and 12 months, the mean vitamin B12 levels were 367.5 and 468.5 pg/mL; at 1.5, 2, 3, 4, 5, 6, 7, 8, 10 and 11 years, the mean levels were 305, 495.5, 436.5, 379.5, 423.5, 393, 529.5, 631, 333.5 and 340 pg/mL, respectively. CONCLUSION: Ileocaecal urinary reservoirs have no adverse effects on serum vitamin B12 levels for up to 10 years after surgery. Patients with vitamin B12 deficiency must be identified and given adequate parenteral doses for life. Because body stores of vitamin B12 may not be depleted for many years, problems with B12 may be masked for a long time. We recommend that vitamin B12 levels be obtained annually, that a modest supplement twice yearly (by injection) may be beneficial and that serum vitamin B12 must be sampled before giving vitamin B12 injections, to avoid false results.

Adult↗
PubMed2006

Dietary folate, vitamin B12, and vitamin B6 and the risk of Parkinson disease.

BACKGROUND: Increased homocysteine levels might accelerate dopaminergic cell death in Parkinson disease (PD), through neurotoxic effects. Higher dietary intakes of folate, vitamin B12, and vitamin B6 (cofactors in homocysteine metabolism) might decrease the risk of PD through decreasing plasma homocysteine. Moreover, vitamin B6 might influence the risk of PD through antioxidant effects unrelated to homocysteine metabolism and through its role in dopamine synthesis. METHODS: In the Rotterdam Study, a prospective, population-based cohort study of people aged 55 years and older, the authors evaluated the association between dietary intake of folate, vitamin B12, and vitamin B6 and the risk of incident PD among 5,289 participants who were free of dementia and parkinsonism and underwent complete dietary assessment at baseline. PD was assessed through repeated in-person examination and continuous monitoring by computer linkage to medical records. Data were analyzed using Cox proportional hazards regression analysis. RESULTS: After a mean follow-up of 9.7 years, the authors identified 72 participants with incident PD. Higher dietary intake of vitamin B6 was associated with a significantly decreased risk of PD (hazard ratio per SD, 0.69 [95% CI 0.50 to 0.96]; for highest vs lowest tertile, 0.46 [0.22 to 0.96]). Stratified analyses showed that this association was restricted to smokers. No association was observed for dietary folate and vitamin B(12). CONCLUSIONS: Dietary vitamin B6 may decrease the risk of Parkinson disease, probably through mechanisms unrelated to homocysteine metabolism.

Administration, Oral↗
PubMed1977

HLA phenotype A2;B12 in vitamin B12 neuromyelopathy.

Severe neurological complications (either peripheral neuropathy, subacute combined degeneration of the cord or cerebral changes) are a characteristic feature in some patients with marked vitamin B12 deficiency. Although Addisonian pernicious anaemia (PA) is the major cause of this neurological syndrome, the disorder has been described in association with other conditions in which there is a profound depletion of vitamin B12 stores. Sixteen patients with vitamin B12 neuromyelopathy, associated with PA, have been HLA-typed for 27 alleles of the A and B loci and compared with 53 cases of PA without neurological damage and 60 controls of the same ethnic group. There is a significantly increased frequency of the HLA phenotype. A12;B12 (44% instead of 4% in PA patients without neurological damage) in the disease group studied (P less than 0.0005). The signficance of these findings in relation to the pathogenesis of vitamin B12 neuromyelopathy is discussed.

Anemia, Pernicious↗