Mauktilar vitamina b12 hupovitaminose Oral diseases caused by candida species. Definition CSP condition due to a deficiency of one or more essential vitamins. How to cite this article. The coenzyme forms of vitamin B Vitamin B12 deficiency as a worldwide problem.
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Search Menu Abstract Hypercobalaminemia high serum vitamin B12 levels is a frequent and underestimated anomaly. Clinically, it can be paradoxically accompanied by signs of deficiency, reflecting a functional deficiency linked to qualitative abnormalities, which are related to defects in tissue uptake and action of vitamin B The aetiological profile of high serum cobalamin predominantly encompasses severe disease entities for which early diagnosis is critical for prognosis.
These entities are essentially comprised of solid neoplasms, haematological malignancies and liver and kidney diseases. This review reflects the potential importance of the vitamin B12 assay as an early diagnostic marker of these diseases. A codified approach is needed to determine the potential indications of a search for high serum cobalamin and the practical clinical strategy to adopt upon discovery of elevated cobalamin levels.
While low serum cobalamin levels do not necessarily imply deficiency, an abnormally high serum cobalamin level forms a warning sign requiring exclusion of a number of serious underlying pathologies. Functional cobalamin deficiency can thus occur at any serum level. Strengths High serum cobalamin vitamin B12 is a frequent and underestimated anomaly.
Hypercobalaminemia can yield clinical signs indicating functional and qualitative vitamin B12 deficiency. Methylmalonic acid and homocysteinemia are key biomarkers for the diagnosis of functional deficits in vitamin B The majority of causes of hypercobalaminemia is related to quantitative anomalies pertaining to transcobalamins. Solid neoplasms, myeloproliferative blood disorders, liver metastases, liver diseases and kidney failure are the main aetiologies to look for when dealing with high serum cobalamin levels.
Introduction High serum cobalamin vitamin B12 has long been a misunderstood and underestimated anomaly, being considered as irrelevant from a diagnostic and clinical standpoint. Both fundamental and clinical research efforts were indeed concentrated, for a long time, on cobalamin deficiency.
However, the growing awareness by clinicians of the frequency and clinical impact of this deficiency resulted in an increasing demand for a biological assay of vitamin B This enabled to highlight firsthand the non-negligible frequency of patients presenting high cobalamin blood levels. In this article, we review the current concepts of the metabolism and physiology of vitamin B12 to address, in a second instance, the diagnostic implications in clinical practice of the discovery of excess vitamin B The high frequency of high serum cobalamin was recently exemplified in a retrospective study by Deneuville et al.
Large-scale studies are thus needed to assess the actual incidence and prevalence of this anomaly in the general population. Pathophysiological basis Vitamin B12 and its absorption factors Vitamin B12 was discovered as the antipernicious anaemia factor that was found in the liver. In the mean time, the importance of gastric juice for inducing reticulocytosis in pernicious anaemia patients was identified. Without this absorption factor vitamin B12 deficiency follows.
Only during the s, this vitamin B12 absorption factor, called intrinsic factor IF as opposed to the extrisic factor vitamin B12 itself had been to some extent purified.
The second gene appeared to be coding for the protein amnionless, which is essential for gastrulation in mice. This is accompanied by proteinuria, because cubam is also mediating the tubular reabsorption of protein from the primary urine. It has long time been thought that without the functional sophisticated mechanism for vitamin B12 absorption, such as, for example, in patients with pernicious anaemia or in patients after a total gastrectomy, parenteral treatment with vitamin B12 was indispensable.
However, neither fungi and plants nor animals are able to synthesize vitamin B Only bacteria and archaea, also single-celled microorganisms but with an evolutionary history different from that of bacteria, have the enzymes required for its synthesis. Many foods are, however, a natural source of vitamin B12 because of bacterial symbiosis.
Clinically, measuring this active fraction of vitamin B12, bound to TCB II is ensured by the determination of holotranscobalamin. Hence, a better knowledge of these proteins, their sites of production, their distribution and their physiological functions is vital to understand the pathophysiological mechanisms and aetiological implications of high serum cobalamin. They belong to the haptocorrin HC superfamily in which they represent the serum forms. Before vitamin B12 can be measured it has to be freed of protein and converted to cyanocobalamin.
Different methods exist for the measurement of the free cyanocobalamin. Older assays, still in use in some laboratories, depended on the growth of microorganisms. For obvious reasons the presence of antibiotics in serum risks to lead to falsely low results with these assays.
Most vitamin B12 determinations today are performed using automated equipment. These assays are mostly based on competition for IF between radioactive vitamin B12 and the cyanocobalamin in the serum sample. Discrepancies between results of vitamin B12 levels determined by different methods are not uncommon. It is therefore necessary to use the reference values of the laboratory that performed the measurement for reviews, see Vogeser and Lorenzl 48 and Karmi et al.
Regrettably neither specific clinical symptoms nor precise serum vitamin B12 levels allow the straightforward diagnosis of a case of deficiency. Originally megaloblastic anaemia was believed to be a specific symptom for vitamin B12 deficiency. After eight decades of reluctance it has been widely accepted only since that neurologic dysfunction can be the only clinical symptom of vitamin B12 deficiency. Methylmalonic acid and homocysteine are used.
Functional deficiency of vitamin B12 leads to increased levels of methylmalonic acid because the vitamin plays a role in the conversion of methylmalonyl coenzyme A to succinyl coenzyme A by the enzyme methylmalonyl coenzyme A mutase. Homocysteine levels are raised because methionine synthase requires methylcobalamin for the conversion of homocysteine to methionine. Only in the s, the techniques for measuring these metabolites became sufficiently sensitive. Mechanisms related to high serum cobalamin levels High serum levels of cobalamin involve three essential pathophysiological mechanisms, which meet virtually all aetiologies to search for and that will be detailed later on.
These mechanisms are 1 , 37 : a direct increase in plasma vitamin B12 by excess intake or administration, a direct increase in plasma vitamin B12 by liberation from an internal reservoir, an increase in TCB via excess production or lack of clearance and a quantitative deficiency or lack of affinity of TCB for vitamin B Figure 1 outlines the metabolism of vitamin B12 and the various aetiological mechanisms of high serum cobalamin.
Figure 1 Metabolism of vitamin B12 and pathophysiological correlations with high serum cobalamin. Pathological consequences of high serum cobalamin Vitamin B12 is a ubiquitous coenzyme mainly involved in reactions leading to the synthesis of DNA and of that of methionine from homocysteine. Contrary to vitamin B12 deficiency, the pathophysiology and clinical consequences of high serum cobalamin have, until now, been very little studied. It is however currently considered that an increase in plasma levels of vitamin B12 may be an indicator of a functional deficit with clinical consequences paradoxically similar to those of vitamin B12 deficiency.
Indeed, an increase in the binding of vitamin B12 to HCs, secondary to an elevation in their plasma levels especially for TCB I and III which are by far the majority , leads to a potential decline in its attachment to TCB II and therefore alters its delivery to the cells.
From a practical standpoint, the finding of high serum cobalamin should first and foremost be followed by the search for the cause of this condition. Specific correction of the hypervitaminemia B12 can frequently be obtained by treatment of the underlying disorder. Moreover, although high cobalamin blood levels are not unusual they are significantly associated to both malignant hemopathies and solid tumours.
It is noteworthy that most of diagnosed neoplastic diseases were previously unknown and at a non-metastatic stage. As described earlier, it is necessary in clinical practice to consider the three aforementioned basic pathophysiological mechanisms, which meet virtually all aetiologies to search for. Excess vitamin B12 intake Excessive oral intake of vitamin B12 is usually relatively easy to identify in the course of the anamnesis.
This self-medication, sometimes overlooked by the patient, should be systematically investigated at examination, as it is often not spontaneously reported. Parenteral administration of vitamin B This was previously most often the result of exogenous intake during the course of a Schilling test not currently used because no longer available , which includes by definition an intramuscular loading dose of vitamin B In this regard, it should be reminded that the parenteral route is decreasingly justified in the majority of aetiologies of vitamin B12 deficiency and that, as mentioned earlier, oral treatment has been found to be both effective and sufficient, including in the case of pernicious anaemia.
A simple cobalamin excess should remain a diagnosis of exclusion. These latter studies have also attempted to identify the practical diagnostic and prognostic implications of this association. The carcinomas most frequently involved are hepatocellular carcinoma HCC and secondary liver tumours, breast cancer, colon cancer, cancer of the stomach and pancreatic tumours.
In the series of Fremont et al. In other solid tumours, high serum cobalamin is thought to be mainly related to an excess synthesis of TCB by the tumour or to an increase in HCs due to induction of hyperleukocytosis.
Table 1 summarizes the key data in the literature regarding high serum cobalamin observed in haematological disorders. It should be noted that lymphoproliferative disorders are rarely providers of high serum cobalamin except for multiple myeloma, where both hypervitaminemia and hypovitaminemia B12 can be observed personal observation 1.
Table 1 High serum cobalamin related to haematological disorders and their clinical characteristics. Extent of high serum cobalamin. Mechanism of high serum cobalamin. Potential clinical implications.
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Gorg Issues of sensitivity for holotranscobalamin and the low specificity of total homocysteine limit their utility. A disorder that is caused by the deficiency of a vitamin. The aim of the present study is to establish a diagnostic algorithm by using a combination of these markers in place of a single measurement. Biochemical, haematological and morphological data were used to categorize people with or without vitamin B12 deficiency. Riboflavin, a component of the B 2 vitaminic complex, plays important roles in biochemistry, especially in redox reactions, due to the ability to participate in both one- and two-electron transfers as well as acting as a photosensitizer. Disease or Syndrome T Serum cobalamin does not necessarily reflect a normal B12 status. Enviado por Luiza flag Denunciar.
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