Oral Cobalamin Research Articles

Short-term oral cobalamin therapy for food-related cobalamin malabsorption

Short-term oral cobalamin therapy for food-related cobalamin malabsorption

Pulmonary Embolism in a Patient with Pernicious Anemia and Hyperhomocysteinemia

We report the case of a 60-year-old woman with a history of ataxia who sought evaluation after a syncopal episode. A diagnostic workup revealed pulmonary emboli, pernicious anemia (PA), hyperhomocysteinemia, and a G20210A prothrombin gene mutation. She was successfully treated with homocysteine-lowering therapy, including high doses of oral cobalamin. She also received oral anticoagulation for 6 months. At 1 year of follow-up, no further thrombotic episodes had occurred. Our report highlights the thrombotic risk of hyperhomocysteinemia secondary to PA in a patient with the G20210A prothrombin gene mutation.

Is low-dose oral cobalamin enough to normalize cobalamin function in older people?

To investigate whether the use of low-dose oral cobalamin (Cbl) supplements by older persons, as frequently found in multivitamin preparations, affects their Cbl serum concentrations and function, determined by measurements of the serum Cbl-related metabolites methylmalonic acid (MMA), homocysteine (HCYS), and methylcitric acid (MCTR). Cross-sectional study. Community. Two hundred forty-two independent, active, community-living, older adult volunteers recruited from community events and activities for seniors. We systematically collected data on vitamin supplement intake, diet, medications, and medical and surgical history. Serum was obtained for Cbl, MMA, HCYS, and MCTR, and creatinine and hematological parameters. Serum levels of Cbl were significantly higher in subjects on oral Cbl supplements (2-37.5 microg/day). Similarly, serum levels of the metabolites MMA, HCYS, and MCTR were also lower in subjects on Cbl supplementation. Intake of low-dose oral supplements of Cbl significantly reduced the odds of low Cbl levels or high MMA. The relationship between Cbl supplement dosage and the biochemical parameters was dose dependent. Oral Cbl (2-37.5 microg/day) intake by community-dwelling healthy older adults is associated with higher serum levels of Cbl and improved or normalized Cbl function, as indicated by lower concentrations of the metabolites MMA, HCYS, and MCTR. Use of low-dose oral Cbl replacement therapy might be sufficient to prevent Cbl deficiency in a large proportion of this population.

Oral cobalamin therapy for the treatment of patients with food-cobalamin malabsorption

Background The standard treatment for cobalamin (vitamin B 12) deficiency involves regular intramuscular cobalamin injection. It has been suggested that oral cobalamin therapy may be effective for treating patients who have food-cobalamin malabsorption. Subjects and methods We prospectively studied 10 patients with cobalamin deficiency and well-established food-cobalamin malabsorption who received 3000 μg or 5000 μg of oral crystalline cyanocobalamin once a week for at least 3 months. Complete blood counts and serum cobalamin, homocysteine, and folate levels were determined at baseline and after 3 months of treatment. Patients were reexamined after 6 months. Results After 3 months of treatment, all patients had increased hemoglobin levels (mean increase, 1.9 g/dL; 95% confidence interval: 0.9 to 3.9 g/dL; P <0.01 compared with baseline) and decreased erythrocyte cell volume (mean decrease, 7.8 fL; 95% confidence interval: 0.9 to 16.5 fL; P<0.001). However, 2 patients had only minor, if any, responses. Serum cobamin levels were increased in all 8 patients in whom it was measured. Conclusion Our findings suggest that moderate doses of crystalline cyanocobalamin given orally may be an effective treatment for food-cobalamin malabsorption.

Pernicious anemia (PA) subsequent to insulin‐dependent diabetes mellitus and idiopathic thrombocytopenic purpura, and effects of oral cobalamin on PA

American Journal of HematologyVolume 62, Issue 1 p. 61-62 Letters & CorrespondenceFree Access Pernicious anemia (PA) subsequent to insulin-dependent diabetes mellitus and idiopathic thrombocytopenic purpura, and effects of oral cobalamin on PA Haruki Kondo, Division of Hematology and Oncology, Department of Medicine, Shimizu Kosei Hospital, Shimizu, Shizuoka, JapanSearch for more papers by this authorTakaaki Imamura, Division of Hematology and Oncology, Department of Medicine, Shimizu Kosei Hospital, Shimizu, Shizuoka, JapanSearch for more papers by this author Haruki Kondo, Division of Hematology and Oncology, Department of Medicine, Shimizu Kosei Hospital, Shimizu, Shizuoka, JapanSearch for more papers by this authorTakaaki Imamura, Division of Hematology and Oncology, Department of Medicine, Shimizu Kosei Hospital, Shimizu, Shizuoka, JapanSearch for more papers by this author First published: 31 August 1999 https://doi.org/10.1002/(SICI)1096-8652(199909)62:1<61::AID-AJH12>3.0.CO;2-1Citations: 4AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat Citing Literature Volume62, Issue1September 1999Pages 61-62 ReferencesRelatedInformation

Sublingual therapy for cobalamin deficiency as an alternative to oral and parenteral cobalamin supplementation

Effectiveness of sublingual cobalamin-replacement therapy was studied in 18 people with cobalamin deficiency. Administration was efficacious and convenient, and compliance was high.

Oral Cobalamin Therapy in Patients Who Absorb It Normally

To the Editor: Although massive doses of oral cobalamin seem to work well in a research setting with compliant, motivated patients, the study by Kuzminski et al[1][1] is misleading in important ways. The question surrounding oral therapy has always concerned its effectiveness in patients with

Oral cobalamin for pernicious anemia: back from the verge of extinction.

High dose oral cobalamin therapy was shown to be effective for pernicious anemia and other cobalamin deficiency states 30 years ago, and physicians and patients state that they would find oral therapy useful, but a survey conducted in 1989 found that physicians were generally unaware of it. To assess physician awareness and use of oral cobalamin since 1989. Minneapolis area internists not listed as having subspecialties or academic business addresses were surveyed in 1989 and in 1996. There were 245 responses to the 1989 survey and 223 responses to the 1996 survey for response rates of 68% and 69%, respectively. The percentage of internists who ever used oral cobalamin to treat pernicious anemia increased from 0 in 1989 to 19% in 1996 (P < .001). The percentage who were aware of an effective oral cobalamin preparation for treating cobalamin deficiency states also increased significantly from 4 to 29% (P < .001). The percentage of internists who agreed with the incorrect view that sufficient quantities of cobalamin cannot be absorbed when given orally declined from 91% in 1989 to 71% in 1996 (P < .001). Minneapolis internists' awareness and use of oral cobalamin treatment for pernicious anemia increased substantially between 1989 and 1996, but the majority of internists remained unaware of this treatment option.

Effective Treatment of Cobalamin Deficiency With Oral Cobalamin

Because cobalamin deficiency is routinely treated with parenteral cobalamin, we investigated the efficacy of oral therapy. We randomly assigned 38 newly diagnosed cobalamin deficient patients to receive cyanocobalamin as either 1 mg intramuscularly on days 1, 3, 7, 10, 14, 21, 30, 60, and 90 or 2 mg orally on a daily basis for 120 days. Therapeutic effectiveness was evaluated by measuring hematologic and neurologic improvement and changes in serum levels of cobalamin (normal, 200 to 900 pg/mL) methylmalonic acid (normal, 73 to 271 nmol/L), and homocysteine (normal, 5.1 to 13.9 μmol/L). Five patients were subsequently found to have folate deficiency, which left 18 evaluable patients in the oral group and 15 in the parenteral group. Correction of hematologic and neurologic abnormalities was prompt and indistinguishable between the 2 groups. The mean pretreatment values for serum cobalamin, methylmalonic acid, and homocysteine were, respectively, 93 pg/mL, 3,850 nmol/L, and 37.2 μmol/L in the oral group and 95 pg/mL, 3,630 nmol/L, and 40.0 μmol/L in the parenteral therapy group. After 4 months of therapy, the respective mean values were 1,005 pg/mL, 169 nmol/L, and 10.6 μmol/L in the oral group and 325 pg/mL, 265 nmol/L, and 12.2 μmol/L in the parenteral group. The higher serum cobalamin and lower serum methylmalonic acid levels at 4 months posttreatment in the oral group versus the parenteral group were significant, with P &lt; .0005 and P &lt; .05, respectively. In cobalamin deficiency, 2 mg of cyanocobalamin administered orally on a daily basis was as effective as 1 mg administered intramuscularly on a monthly basis and may be superior. © 1998 by The American Society of Hematology.

Effective Treatment of Cobalamin Deficiency With Oral Cobalamin

AbstractBecause cobalamin deficiency is routinely treated with parenteral cobalamin, we investigated the efficacy of oral therapy. We randomly assigned 38 newly diagnosed cobalamin deficient patients to receive cyanocobalamin as either 1 mg intramuscularly on days 1, 3, 7, 10, 14, 21, 30, 60, and 90 or 2 mg orally on a daily basis for 120 days. Therapeutic effectiveness was evaluated by measuring hematologic and neurologic improvement and changes in serum levels of cobalamin (normal, 200 to 900 pg/mL) methylmalonic acid (normal, 73 to 271 nmol/L), and homocysteine (normal, 5.1 to 13.9 μmol/L). Five patients were subsequently found to have folate deficiency, which left 18 evaluable patients in the oral group and 15 in the parenteral group. Correction of hematologic and neurologic abnormalities was prompt and indistinguishable between the 2 groups. The mean pretreatment values for serum cobalamin, methylmalonic acid, and homocysteine were, respectively, 93 pg/mL, 3,850 nmol/L, and 37.2 μmol/L in the oral group and 95 pg/mL, 3,630 nmol/L, and 40.0 μmol/L in the parenteral therapy group. After 4 months of therapy, the respective mean values were 1,005 pg/mL, 169 nmol/L, and 10.6 μmol/L in the oral group and 325 pg/mL, 265 nmol/L, and 12.2 μmol/L in the parenteral group. The higher serum cobalamin and lower serum methylmalonic acid levels at 4 months posttreatment in the oral group versus the parenteral group were significant, with P < .0005 and P < .05, respectively. In cobalamin deficiency, 2 mg of cyanocobalamin administered orally on a daily basis was as effective as 1 mg administered intramuscularly on a monthly basis and may be superior.© 1998 by The American Society of Hematology.

Haematological Effects of Oral Cobalamin Preparations on Patients with Megaloblastic Anaemia

We investigated the haematological effects of a massive dose of oral cobalamin (vitamin B₁₂) on patients with cobalamin deficiency anaemia who had severe anaemia with a few neurological impairments and found that oral treatment was almost as effective as conventional injection therapy. The recovery of haematological indices with oral cobalamin preparations was slightly slower than with parenteral preparations, although the subjective symptoms disappeared soon after the start of therapy. The results of this study indicate that oral treatment keeps the cobalamin body stores satisfactorily filled and might be useful for older patients in whom injecting might be difficult.

Intranasal Cobalamin: A Warning

To the Editor.— The Commentary by Dr Lederle 1 and the accompanying editorial of Drs Hathcock and Troendle 2 provide a straightforward and compelling argument for the use of oral cobalamin for the treatment of pernicious anemia whenever possible. In my experience, the vicissitudes and costs of monthly intramuscular cobalamin injections often result in discontinuation of the therapy entirely, putting patients at risk for recurrent deficiency. Oral therapy should ameliorate this problem. However, there may be another alternative that the authors did not describe, and of which few physicians are aware: nasal cobalamin. For a number of years, an intranasal cyanocobalamin gel called Ener-B has been available over the counter. It is sold in packages of 12 unit-dose tubes, each containing 400 μg of cyanocobalamin. The manufacturer (Nature's Bounty, 90 Orville Dr, Bohemia, NY 11716) has targeted the product at the health-foods market and has not promoted it among physicians

Intranasal Cobalamin: A Warning-Reply

In Reply.— Dr Heimburger states that the summary report of Nature's Bounty's clinical studies indicates that the rise in serum cobalamin level after a single 400-μg intranasal dose approximates that from a 100-μg intramuscular dose. Dr Heimburger then suggests that the use of an intranasal gel would have a compliance advantage over daily oral cobalamin and would not entail the inconvenience or cost of intramuscular injections. He concludes that the use of Ener-B, with proper monitoring of cobalamin status, should be considered by physicians treating patients with pernicious anemia. It is the Food and Drug Administration's (FDA) position that Ener-B Intra-Nasal Gel is a drug, a new drug, and is illegally marketed. The FDA has consistently regulated parenteral vitamin-mineral and topically administered nutritional products as drugs. On February 26, 1987, the FDA sent a regulatory letter to Nature's Bounty informing them that Ener-B was an unapproved new drug and was

Oral cobalamin for treatment of pernicious anemia?

Oral cobalamin for treatment of pernicious anemia?

Oral Cobalamin for Treatment of Pernicious Anemia?

Pernicious anemia is a cobalamin deficiency disease caused by a lack of intrinsic factor (IF), which is necessary for the absorption of this vitamin. Because of the extensive hepatic storage of cobalamin, primary dietary deficiency is uncommon, occurring only in strict vegetarians after avoidance of animal products for many months. The most common cause of IF deficiency is gastric atrophy. Total gastrectomy leads to pernicious anemia, and partial gastrectomy does so occasionally. A rare congenital form of pernicious anemia may be the result of an autosomal recessive failure in IF production. It is possible to treat pernicious anemia with oral IF. This was standard practice at one time, but has lost favor because of the difficulty and expense of obtaining IF. For the last 30 or more years, the usual treatment has been 1000 μg of cobalamin administered intramuscularly once every 1 to 3 months. With a retention efficiency of

Oral cobalamin for pernicious anemia. Medicine's best kept secret?

THE TREATMENT of pernicious anemia with cobalamin is one of medicine's great success stories. However, the usual practice of giving the drug as an intramuscular injection has several drawbacks. Injections can be painful, difficult to provide for some patients who are elderly or living alone, 1 and costly if given by health professionals. 2 It is therefore not surprising that the search for an oral preparation began soon after cobalamin was isolated and introduced for parenteral use in 1948. Preparations containing oral intrinsic factor were tried, but antibody production caused some patients to become refractory and relapse. 3 Other studies revealed that a small but constant proportion of an oral dose of cyanocobalamin was absorbed without intrinsic factor, so that by sufficiently increasing the dose, adequate absorption could be attained. 4,5 Promising results from early studies of oral cyanocobalamin therapy led to the use of increasingly larger doses, and several

Transcobalamin II deficiency and oral cobalamin therapy [letter

Transcobalamin II deficiency and oral cobalamin therapy [letter