The aim of this study was to investigate the subclinical involvement of the optic nerve in asymptomatic patients with vitamin B12 deficiency using visual evoked potentials.

This study included 40 asymptomatic patients diagnosed with vitamin B12 deficiency (considered as serum levels below 150 pg/mL) and a control group of 40 healthy individuals. All participants underwent a visual evoked potential examination. Routine screening for homocysteine was performed for patients with vitamin B12 deficiency. The levels of vitamin B12 and homocysteine and the presence of megaloblastic anemia were analyzed statistically compared with P100, N75, and N135 latencies and amplitudes.

The mean vitamin B12 level was 96 pg/mL in the patient group and 374 pg/mL in the control group. In the patient group, 24 (60%) patients had hyperhomocysteinemia and 8 (20%) patients had megaloblastic anemia. The P100 wave latency of patients with vitamin B12 deficiency was significantly prolonged compared with the control group ( P < 0.01). There was no significant difference in the P100 amplitude between the patient group and the control group. P100 latencies were significantly longer in patients with hyperhomocysteinemia ( P = 0.002).

Our study showed that patients with vitamin B12 deficiency may have visual evoked potential abnormalities without visual symptoms or examination findings. In addition, high homocysteine levels led to a prolonged P100 latency in the patient group independent of vitamin B12 levels.

Frailty is a clinical syndrome with a worldwide prevalence of 5-27% among those aged over 65 years. Frailty is characterised by loss of muscle strength and impaired physical function, and is associated with increased falls, hospitalisation and death. Nutritional deficiencies and low physical activity are common in this age group due to ill health, disability and reductions in enthusiasm, food intake and therefore, energy availability. Both low physical activity and inadequate dietary intake have a significant role to play in the onset and progression of frailty, primarily through bone and muscle health implications. Frailty is, however, preventable and reversible, and several interventions have been carried out to offset and reverse the condition. This article reports the recent evidence on the role of nutrition and physical activity in the pathogenesis of frailty and provides a critical review of previously implemented interventions focussed on physical activity and nutrition to prevent and reduce frailty among older adults.

Black cohosh rhizome, available as a dietary supplement, is most commonly marketed as a remedy for dysmenorrhea and menopausal symptoms. A previous subchronic toxicity study of black cohosh dried ethanolic extract (BCE) in female mice revealed a dose-dependent ineffective erythropoiesis with a macrocytosis consistent with the condition known as megaloblastic anemia. The purpose of this study was to investigate potential mechanisms by which BCE induces these particular hematological changes. B6C3F1/N female mice (32/group) were exposed by gavage to vehicle or 1,000 mg/kg BCE for 92 days. Blood samples were analyzed for hematology, renal and hepatic clinical chemistry, serum folate and cobalamin, red blood cell (RBC) folate, and plasma homocysteine and methylmalonic acid (MMA). Folate levels were measured in liver and kidney. Hematological changes included decreased RBC count; increased mean corpuscular volume; and decreased reticulocyte, white blood cell, neutrophil, and lymphocyte counts. Blood smear evaluation revealed increased Howell-Jolly bodies and occasional basophilic stippling in treated animals. Plasma homocysteine and MMA concentrations were increased in treated animals. Under the conditions of our study, BCE administration caused hematological and clinical chemistry changes consistent with a functional cobalamin, and possibly folate, deficiency. Further studies are needed to elucidate the mechanism by which BCE causes increases in homocysteine and MMA.

Biermer disease or pernicious anemia is an autoimmune atrophic gastritis characterized by the lack of secretion of gastric intrinsic factor. This leads to an insufficient absorption of vitamin B12 in the ileum. Clinical manifestations are mainly hematologic. Neuropsychiatric manifestations are known but are less frequent especially early in the disease. Inaugural neuropsychiatric arrays are rare and various thus making diagnosis difficult. In this article, we report through two clinical cases different neuropsychiatric manifestations revealing pernicious anemia. Mrs. C.O., aged 56, presented after surgery for gallstones, an acute psychiatric array associated with gait disorders. She had no history of neurological or psychiatric problems. The psychiatric interview revealed delirious syndrome, depressive symptoms and anxiety. Neurological examination noted a flaccid paraplegia with peripheral neuropathic syndrome and myoclonus in the upper limbs. At the full blood count, a macrocytosis (VGM: 112.2fl) without anemia was found. The level of vitamin B12 in the blood was low. Cerebro-spinal MRI was suggestive of a neuro-Biermer and showed hyper signal in the cervical cord on T2-weighted sagittal section. In axial section, hyper signal appears at the posterior columns in the form of V. There were no brain abnormalities. A sensorimotor axonal polyneuropathy was diagnosed. The patient received vitamin B12 intramuscularly for ten days associated with neuroleptic treatment. Mrs. R.M., aged 40, was brought to the psychiatry consultation for acute behavioral disorders progressively worsening over a month. An anxiety syndrome, depressive syndrome and delirious syndrome were identified. Neurological examination showed a posterior cordonal syndrome with quadripyramidal syndrome. Full blood count showed a macrocytic anemia. Serum B12 level was collapsed. Cerebro-spinal MRI was normal. She received vitamin B12 with clinical and biological improvement. Features of pernicious anemia vary according to studies and age range. Digestive and hematological manifestations are well known. Neurological and psychiatric manifestations of pernicious anemia were also described in the early literature. They can be the initial symptoms or the only ones. However, inaugural neuropsychiatric features are often unrecognized. The most common psychiatric symptoms were depression, mania, psychotic symptoms, cognitive impairment and obsessive compulsive disorder. Neurological involvement includes mainly combined spinal sclerosis, peripheral neuropathy and dementia. Cerebellar ataxia and movement disorders are reported less often. Severity of neuropsychiatric features and therapeutic efficacy depends on the duration of signs and level of B12 deficiency. Macrocytic anemia may lack. Neuropsychiatric manifestations could be isolated or be the first manifestation of vitamin deficiency and occur without any hematological or gastrointestinal context. Pernicious anemia and serum B12 assay should be discussed in all patients with organic mental disorders, atypical psychiatric symptoms and fluctuation of symptomatology. Nevertheless, B12 level could be normal in genuine pernicious anemia diseases and macrocytic anemia may lack. Substitutive vitaminotherapy is required when diagnosis is strongly suspected and etiologic assessment is negative.

Cobalamin deficiency is frequent in elderly patients and the main aetiologies are food-cobalamin malabsorption and pernicious anaemia. The aim of our retrospective study was to identify the causes and methods of management of cobalamin deficiency at Nice geriatric university hospital.

A retrospective monocentric study was conducted over 14 months at Nice geriatric hospital, which included patients with cobalamin deficiency having received supplementation. The clinical and paraclinical data, etiological diagnosis, treatment and follow-up modalities were analyzed retrospectively.

We studied 125 elderly patients whose median age was 85.5 ± 7 years. The etiological diagnosis was food-cobalamin malabsorption for 72 patients (57.6 %), nutritional cobalamin deficiency for 15 patients (12 %), pernicious anaemia for 12 patients (9.6 %) and there was no etiological diagnosis for 26 patients (20.8 %). Concerning cobalamin therapy, 111 patients (88.8 %) received oral therapy and 14 (11.2 %) intramuscular therapy. Vitamin B12 levels increased significantly after supplementation (p<0.001) but cobalamin administration varied according to the diagnoses (p<0.001) and was less effective in patients with dementia (p=0.04) and food-cobalamin malabsorption.

Our study showed the importance of food-cobalamin malabsorption in etiological diagnosis in accordance with the literature, but also the non-negligible share of nutritional cobalamin deficiency. Mainly oral cobalamin supplementation was used in our study with a significant increase in vitamin B12 levels. An oral cobalamin regimen is proposed for elderly patients with cobalamin deficiency but with no severe neurological signs.

Standard treatment of cobalamin (vitamin B12) deficiency involvesregular (1000 μg/mo) IM cyanocobalamin administration. It has been suggested that high-dose (>2000 μg/d) oral cyanocobalamin may be effective in patients with pernicious anemia.

The aim of this study was to assess the efficacy and tolerability of oral crystalline cyanocobalamin 1000 μg/d in patients with cobalamin deficiency related to established pernicious anemia.

This open-label, prospective study was conducted at StrasbourgUniversity Hospital, Strasbourg, France. Patients aged ≥18 years with well-documented cobalamin deficiency related to pernicious anemia were enrolled. Patients received crystalline cyanocobalamin 1000 μg QD PO (capsule) for at least 3 months. Serum cobalamin, folate, iron, and homocysteine concentrations were measured, and a complete blood count was obtained, before (month 0; baseline) and after treatment.

Ten patients (7 women, 3 men; mean [SD] age, 72.1 [15.5] years) entered the study. After 3 months of treatment, serum cobalamin concentration increased in all 9 patients in whom it was measured (mean [SD] increase, 117.4 [30.8] pg/mL; P < 0.001 vs baseline). Serum cobalamin concentrations were normalized (>200 pg/mL) in 6 patients. The serum cobalamin concentration was unavailable in 1 patient because of technical problems. Eight patients had increased hemoglobin concentrations (mean [SD] increase, 2.5 [2.4] g/dL; P < 0.01 vs baseline). All 10 patients had decreased mean erythrocyte corpuscular volumes (mean [SD] decrease, 10.4 [6.2] fL; P < 0.003 vs baseline). Four patients received concomitant blood transfusions or folate and iron supplementation. Three patients experienced clinical improvement in paresthesia, reflex abolition, or combined medullary sclerosis (each, 1 patient).

The results of this small study in patients with cobalamin deficiencyrelated to pernicious anemia suggest that oral crystalline cyanocobalamin 1000 μg/d may be an effective treatment.

Metabolic and deficiency neuropathies retain a growing interest because of their important prevalence. The dismemberment of diabetic neuropathies is proceeded, letting distinct pathophysiological mechanisms appear. So, even if glycaemic control remains determining for preventing the neuropathy associated with type 1 diabetes, it seems to have a restricted role with type 2 diabetes in which other metabolic factors are involved. The diagnosis of neuropathy due to B12 vitamin deficiency remains a real challenge for the clinician. Indeed, positive and negative predictive values of serum B12 and metabolites assay are weak, only a good therapeutic response allows a reliable diagnostic. It is so recommended to know the clinical and contextual particularities of this etiology in order to not delay the vitamin substitution, determining for the functional outcome. Finally, copper deficiency remains an unknown cause of neuropathy which is suitable to raise in case of malabsorption but also and especially in case of abuse of dental adhesive rich in zinc.

Many epidemiologic studies have considered whether markers of B-vitamin status are associated with cognitive function and cognitive decline. This avenue of research was sparked by the homocysteine (Hcy) theory of cardiovascular disease, which was extended to Alzheimer's disease when a link between vascular dementia and Alzheimer's disease was discovered. Hcy could cause cognitive impairment via direct neurotoxicity. However, decreased remethylation of Hcy to methionine might also compromise cognitive function by means other than mere Hcy lowering. Folate and vitamin B-12 participate in Hcy remethylation and largely determine Hcy status. Consequently, much of the relevant research has focused on these 2 B vitamins. The many subtly different hypotheses that investigators have addressed by attempting to link several B-vitamin status indicators to diverse cognition-related outcomes have created a confusing body of conflicting studies that seems to defy summarization. Nevertheless, themes are discernible that aid interpretation, foster hypothesis generation, and inform future study design. For example, despite a shared metabolic pathway, Hcy, vitamin B-12, and folate are differently related to specific cognitive outcomes. Although consistency of findings across studies is often touted as essential to distinguishing causal from coincidental relationships, discrepancies among study findings can be even more informative.

To investigate the status of vitamin B12 deficiency in elderly inpatients in the department of neurology.

A total number of 827 patients in the department of neurology of Shanghai Punan hospital, from March 2007 to July 2008, were employed in the present study. They were 60 years or older, and the average age was 77.1+/-7.5 years old. All the patients were diagnosed with no severe hepatic or renal dysfunction, without any usage of vitamin B12 during the previous 3 months before the detection. The levels of serum vitamin B12, folate and homocysteine (Hcy) were evaluated. The patients with vitamin B12 deficiency were screened. The resulting symptoms, positive signs of neurological examination, and the neuroelectricphysiological results were compared between patients with or without vitamin B12 deficiency.

Vitamin B12 deficiency was found in 163 patients (19.71% of the total patients), and was more prevalent in female than in male patients, also with increased incidences with aging. Patients with low levels of serum vitamin B12 exhibited higher rate of gastrointestinal diseases, while only 9.82% of the vitamin B12 deficient patients had megaloblastic anemia. Symptoms of vitamin B12 deficiency included unsteadily walking in the darkness and hypopallesthesia, and some chronic diseases such as cerebral ischemia, hypertension, Parkinson's disease (Parkinsonism), diabetes mellitus and coronary heart disease. Most of the vitamin B12 deficient patients had neuroelectricphysiological abnormalities.

Vitamin B12 deficiency is remarkably common in elderly patients in neurology department, with various and atypical clinical manifestations, and the neurological symptoms are more common than megaloblastic anemia symptoms.

Iron and/or vitamin B12 deficiency anemias, which have adverse effects on patients' quality of life, are commonly observed and often overlooked complications after restorative proctocolectomy. We performed a systematic review of publications on the prevalence of anemia as well as on the impact of anemia on a range of clinical, functional, quality of life, and economic outcomes in restorative proctocolectomy patients. This information is important to help healthcare providers through a comprehensive overview to increase awareness about a condition that could require therapy to improve patient healthcare and quality of life.

We reviewed the English language publications on the incidence of anemia and its adverse effect after restorative proctocolectomy The United States National Library of Medicine database (MEDLINE), the Excerpta Medica database (EMBASE), the Cochran Library, and the Google search engine were searched for published articles on the prevalence and impact of anemia in post-restorative proctocolectomy surgical patients.

The long-term complication most frequently described after RPC is pouchitis. Pouchitis is significantly associated with iron deficiency anemia caused by pouch mucosal bleeding. Other causes are insufficient and/or impaired iron absorption. It has also been observed, however, that restorative proctocolectomy patients with underlying familial adenomatous polyposis rarely develop pouchitis yet show higher rates of iron deficiency anemia compared to those patients with underlying ulcerative colitis. Other causes shown as independent risk factors for iron deficiency anemia in restorative proctocolectomy patients are malignancy, desmoid tumors, and J-pouch configuration. Vitamin B12 deficiency anemia is also common after restorative proctocolectomy. About one-third of restorative proctocolectomy patients show abnormal Schilling test and 5 percent have low referenced serum cobalamin. It has been observed that the degree resection of the terminal-ileum, malabsorption, bacterial overgrowth, and dietary factors are among the known causes of cobalamin deficiency. Folate deficiency has not been reported in restorative proctocolectomy patients. Describing restorative proctocolectomy surgery and its outcomes, in patients without anemia, the quality of life is reported excellent regardless of operative technique.

Anemia is not uncommon following restorative proctocolectomy and has been shown to have negative effects on the patient's quality of life and the economy and may substantially increase healthcare costs. The treatment of anemia and its underlying causes is important to improving clinical and economic outcomes.

Restorative proctocolectomy (RP) involves terminal ileal resection and formation of a small bowel reservoir that predisposes to bacterial overgrowth. It was anticipated that these patients would be at risk of vitamin B12 deficiency.

Vitamin B12 levels were measured sequentially in 171 patients who underwent RP. Prospective results were obtained from all 20 patients undergoing pouch formation after the commencement of the study. Further results were obtained retrospectively from case notes and computerized laboratory records of the 151 patients who underwent RP prior to the commencement of the study and these were correlated with the results of follow-up samples taken prospectively from the same patients after the commencement of the study. The median age of the patients was 40 years (range: 13-67) and the median duration of follow up was 5.4 years (range: 1-12). Patients with an abnormally low serum B12 level underwent both a Schilling and a hydrogen breath test. Eight of these patients were then treated with oral vitamin B12.

Abnormally low serum B12 levels were found in 25% of patients. Forty per cent of our patient group had three or more sequential B12 measurements and of these, 66% showed steadily declining B12 levels. Ninety-four per cent of patients with low B12 had a normal Schilling test and were negative for bacterial overgrowth.

Subnormal vitamin B12 levels develop in almost one-quarter of patients after pouch surgery. The exact mechanism for B12 deficiency in these patients is uncertain. In the majority of patients undergoing RP, vitamin B12 levels fall on sequential measurement. Serum B12 levels should be measured during follow up and pouch patients with subnormal B12 levels, should see them successfully restored to a normal value after treatment with oral B12 replacement therapy.

The BOSSANOVA study, a randomized double-blind trial, was designed to test the ability of very low oral doses of vitamin B-12 to increase the serum vitamin B-12 concentration in elderly subjects with food-bound vitamin B-12 malabsorption, and to determine whether there was a dose response. We also aimed to quantitatively assess the most efficient dose to be added to flour in addition to folic acid (flour cofortification with vitamin B-12 and folic acid). Sixty-seven patients were randomly assigned to 1 of 6 groups receiving various daily oral doses of vitamin B-12 (i.e., 2.5, 5, 10, 20, 40, or 80 microg/d) for 30 d. The dose-response was tested for different biological variables using a mixed model, taking into account the variable's initial value (between-subject effect), a linear log-dose effect, and a linear log (dosextime) interaction, where time was d 15 or d 30. We planned to determine the amount of oral vitamin B-12 that would increase the serum vitamin B-12 concentration by 37 pmol/L (50 ng/L). Significant between-subject effects were found for serum vitamin B-12, plasma homocysteine, and methylmalonic acid concentrations, but a log-dose effect was found only for vitamin B-12 (P<0.001). The slope of the line tended to be higher (P=0.07) at d 30 than at d 15. For a mean serum vitamin B-12 increase of 37 pmol/L, a dose of 5.9 (95% CI, 0.9-12.1) microg/d was needed. We concluded that very low oral doses of vitamin B-12 increased serum vitamin B-12 concentrations in elderly subjects with subclinical vitamin B-12 deficiency, following a log-dose pattern. Our results could be beneficial in the design of a public health program for safe flour cofortification with folic acid.

With the introduction of automated assays for measuring serum cobalamin levels over the last decades, the hematological manifestations related to cobalamin deficiency have been changed from the description reported in 'old' studies or textbooks. We studied the hematological manifestations or abnormalities in 201 patients (median age: 67 +/- 6 years) with well-documented cobalamin deficiency (mean serum vitamin B12 levels 125 +/- 47 pg/ml) extracted from an observational cohort study (1995-2003). Assessment included clinical features, blood count and morphological review. Hematological abnormalities were reported in at least two-third of the patients: anemia (37%), leukopenia (13.9%), thrombopenia (9.9%), macrocytosis (54%) and hypegmented neutrophils (32%). The mean hemoglobin level was 10.3 +/- 0.4 g/dl and the mean erythrocyte cell volume 98.9 +/- 25.6 fl. Approximately 10% of the patients have life-threatening hematological manifestations with documented symptomatic pancytopenia (5%), 'pseudo' thrombotic microangiopathy (Moschkowitz; 2.5%), severe anemia (defined as Hb levels <6 g/dl; 2.5%) and hemolytic anemia (1.5%). Correction of the hematological abnormalities was achieved in at least two-thirds of the patients, equally well in patients treated with either intramuscular or oral crystalline cyanocobalamin. This study, based on real data from a single institution with a large number of consecutive patients with well-documented cobalamin deficiency, confirms several 'older' findings that were previously reported before the 1990s in several studies and in textbooks.

During last decades, several progresses have been made in the diagnosis of cobalamin (vitamin B12) deficiency. Routine used of cobalamin standardized assays have potentially modified the frequency and the type of hematologic abnormalities.

Current studies on cobalamin deficiency, including more precise definitions and the description of new etiologies of cobalamin deficiency in adults, as the food-cobalamin malabsorption syndrome, show that hematological abnormalities are generally incomplete compared to historical descriptions of megaloblastic anemia. Nevertheless, they include severe manifestations in 10% of the patients: pancytopenia, severe anemia (hemoglobin < 6 g/dl) or hemolytic anemia and pseudo thrombotic microangiopathy related to cobalamin deficiency. These studies also show the efficacy of new treatment modalities including oral cobalamin administration.

Future studies will confirm these data with the routine use of the new cobalamin assay: holotranscobalamin and validate the usefulness of oral cobalamin therapy.

Neurological symptoms of B12 vitamin deficiency are polymorph. Causes are dominated by Biermer's disease and B12 vitamin non dissociation that is frequent in the elderly.

We realized a retrospective study during 11 years. Patients with neurological symptoms associated to megaloblastosis were included. Treatment with B12 vitamin lead to haematological manifestation regression.

26 cases were analyzed. Mean age was 50+/-14.5 years and there were 11 women and 15 men. Neurological signs included combined medullar sclerosis (N = 10), peripheral neuropathy (N = 10), isolated paresthesia (N = 5) and inferior limb pyramidal syndrome (N = 1). Neurological signs revealed vitamin B12 deficiency in 4 cases. Mean haemoglobin rate was 6.2+/-2.6 g/dl, mean MCV was 109+/-56 fl. Eight patients had macrocytic anaemia, nine bi-cytopenia and eight deep pancytopenia. Electromyography (N = 8) confirmed neuropathy and medullar MRI (N = 2) showed antero-posterior cordonal demyelinisation of cervico-dorsal medulla. Causes of B12 vitamin deficiency were Biermer's disease (N = 11), non dissociation of B12 vitamin's syndrome (N = 8) and partial gastrectomy (N = 1). In 6 patients, no aetiology was found. Treatment with parenteral vitamin B12 induced neurological symptoms regression in 14 cases. Patient with neurological disorder had significantly higher platelet count and haemoglobin level as compared with patients without neurological disorder. Reticulocyte crisis was more precocious in patients with neurological disorders.

Neurological symptoms in vitamin B12 deficiency are frequent. We insist on isolated forms, inaugural forms and on the interest of medullar MRI for early diagnosis.

Update of the adult cobalamin deficiencies.

More precise definitions establish the true cobalamin deficiencies and determine their real epidemiology. The current clinical data suggest the concept of food-cobalamin malabsorption as the leading etiology of cobalamin deficiency. The new features of cobalamin deficiency include neurological, gynecological and vascular manifestations. Current treatment modalities include nasal, sublingual and oral cobalamin administration.

Studies are in the way to establish the relevance of the new clinical manifestations and to validate the usefulness of oral cobalamin therapy.

Approximately 15% of people aged more than 60 years old have a cobalamin (vitamin B12) deficiency, mainly in relation with food-cobalamin malabsorption (FCM). To date, no study has documented this disorder in the elderly. There is also little information on clinical consequences.

We studied 92 elderly patients with well-established FCM who were extracted from an observational cohort study (1995-2004) of 172 consecutive elderly patients with documented cobalamin deficiency.

The median patient age was 76 +/- 8 years; 60 patients were women. The most common clinical manifestations were neurologic or psychologic: mild sensory polyneuropathy (44.6%), confusion or impaired mental functioning (22.8%), and physical asthenia (20.7%). Hematologic abnormalities were reported in at least one third of the patients: anemia (21%), leukopenia (10.9%), thrombopenia (8.7%), and pancytopenia (6.5%). All patients had low serum vitamin B12 levels (<200 pg/mL), with a mean value (+/- standard deviation) of 131 +/- 38 pg/mL and total serum homocysteine level of 22.1 +/- 9.3 micromol/L. The mean hemoglobin level was 10.9 +/- 2.5 g/dL and the mean erythrocyte cell volume 95.7 +/- 12.7 fL. Correction of the serum vitamin B12 levels and hematologic abnormalities was achieved equally well in patients treated with either intramuscular or oral crystalline cyanocobalamin.

This study suggests that in elderly patients, FCM may be associated with significant neurologic, psychologic, and hematologic abnormalities, which seem to respond equally well to either oral or parenteral vitamin B12 therapy.

Sweden is the only country in which oral high dose vitamin B12 has gained widespread use in the treatment of deficiency states.

The aim of the study was to describe prescribing patterns and sales statistics of vitamin B12 tablets and injections in Sweden 1990-2000.Design, setting, and sources: Official statistics of cobalamin prescriptions and sales were used.

The use of vitamin B12 increased in Sweden 1990-2000, mainly because of an increase in the use of oral high dose vitamin B12 therapy. The experience, in statistical terms a "total investigation", comprised 1,000,000 patient years for tablets and 750,000 patient years for injections. During 2000, 13% of residents aged 70 and over were treated with vitamin B12, two of three with the tablet preparation. Most patients in Sweden requiring vitamin B12 therapy have transferred from parenteral to oral high dose vitamin B12 since 1964, when the oral preparation was introduced.

The findings suggest that many patients in other post-industrial societies may also be suitable for oral vitamin B12 treatment.

A relation between food-cobalamin malabsorption and pernicious anemia has been suggested, particularly in the event of food-cobalamin malabsorption related to hypochlorhydric atrophic gastritis.

This work describes three cases of well-documented cobalamin deficiency related to food-cobalamin malabsorption in three women aged 56, 82 and 68 Years who had atrophic gastritis (not associated with Helicobacter pylori infection) and later developed authentic pernicious anemia.

This work illustrates the potential relation between these two disorders responsible for cobalamin deficiency.

The aim of this study was to describe the present clinical characteristics of the pernicious anemia (PA).

It is a retrospective (1996-2002) multicenter (five departments of internal medicine) study of 49 patients presenting an established cobalamin deficiency related to PA.

The median age of the patients was 74 years (25-93), the female/male ratio 2:9. Several autoimmune disorders were noted in 35% of the patients. Various clinical manifestations, mainly neurological, cutaneous and thrombotic, were found in 65.4% of the patients, at least one hematological abnormalities in 100%. Average serum vitamin B12 and homocystein levels were with 73 pg/ml (20-1960) and 42.9 micromol/l (7, 8-124). Anti-intrinsic factor or anti-parietal gastric cells antibodies were found in 87.5% and 62% of the patients (at least one antibody, in 96%) abnormal Schilling's test results in 86%. All the followed patients were successful treated with intramuscular (n = 27) or oral crystalline cyanocobalamin (n = 5).

PA was associated with several autoimmune disorders; PA may be responsible of various clinical manifestations or biological abnormalities; and oral crystalline cyanocobalamin treatment may be successful.

Vitamin B12 or cobalamin deficiency occurs frequently (> 20%) among elderly people, but it is often unrecognized because the clinical manifestations are subtle; they are also potentially serious, particularly from a neuropsychiatric and hematological perspective. Causes of the deficiency include, most frequently, food-cobalamin malabsorption syndrome (> 60% of all cases), pernicious anemia (15%-20% of all cases), insufficient dietary intake and malabsorption. Food-cobalamin malabsorption, which has only recently been identified as a significant cause of cobalamin deficiency among elderly people, is characterized by the inability to release cobalamin from food or a deficiency of intestinal cobalamin transport proteins or both. We review the epidemiology and causes of cobalamin deficiency in elderly people, with an emphasis on food-cobalamin malabsorption syndrome. We also review diagnostic and management strategies for cobalamin deficiency.