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Vitamin B12 replacement. To B12 or not to B12?
To review the evidence for an expanded approach to identifying and treating patients with cobalamin deficiency. Controversy surrounds this issue. Some authors claim that seven times more patients are treated than have true deficiency. New diagnostic tests and identification of patients who have neur...
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Published in: | Canadian family physician 1997-05, Vol.43, p.917-922 |
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description | To review the evidence for an expanded approach to identifying and treating patients with cobalamin deficiency. Controversy surrounds this issue. Some authors claim that seven times more patients are treated than have true deficiency. New diagnostic tests and identification of patients who have neurologic consequences without hematologic abnormalities suggest that some of these patients have a vitamin B12 tissue deficiency.
A MEDLINE search of English-language literature from 1990 to 1995 revealed retrospective and prospective studies of diagnostic tests; prospective surveys; a cohort study; and retrospective and prospective case series, some with control groups. No double-blind controlled trials of treatment were found.
Some patients with neuropsychiatric abnormalities develop a cobalamin tissue deficiency that can be detected by elevated serum homocysteine and methylmalonic acid levels despite normal serum vitamin B12 levels without macrocytic anemia. Serum cobalamin testing is neither sensitive nor specific in the low normal range for cobalamin deficiency. Treatment recommendations vary because no controlled trials support any recommendations. Oral cobalamin is an underused alternative to parenteral treatment.
Until the newer diagnostic tests become widely available, family physicians must continue to take a traditional approach to diagnosing vitamin B12 deficiency. There is, however, support for a clinical trial of treatment in patients with neuropsychiatric symptoms. |
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A MEDLINE search of English-language literature from 1990 to 1995 revealed retrospective and prospective studies of diagnostic tests; prospective surveys; a cohort study; and retrospective and prospective case series, some with control groups. No double-blind controlled trials of treatment were found.
Some patients with neuropsychiatric abnormalities develop a cobalamin tissue deficiency that can be detected by elevated serum homocysteine and methylmalonic acid levels despite normal serum vitamin B12 levels without macrocytic anemia. Serum cobalamin testing is neither sensitive nor specific in the low normal range for cobalamin deficiency. Treatment recommendations vary because no controlled trials support any recommendations. Oral cobalamin is an underused alternative to parenteral treatment.
Until the newer diagnostic tests become widely available, family physicians must continue to take a traditional approach to diagnosing vitamin B12 deficiency. There is, however, support for a clinical trial of treatment in patients with neuropsychiatric symptoms.</description><identifier>ISSN: 0008-350X</identifier><identifier>EISSN: 1715-5258</identifier><identifier>PMID: 9154363</identifier><language>eng</language><publisher>Canada: College of Family Physicians of Canada</publisher><subject>Family Practice ; Homocysteine - blood ; Humans ; Methylmalonic Acid - blood ; Prevalence ; Research Design ; Sensitivity and Specificity ; Vitamin B 12 - metabolism ; Vitamin B 12 - therapeutic use ; Vitamin B 12 Deficiency - complications ; Vitamin B 12 Deficiency - diagnosis ; Vitamin B 12 Deficiency - drug therapy ; Vitamin B 12 Deficiency - metabolism ; Vitamins & minerals</subject><ispartof>Canadian family physician, 1997-05, Vol.43, p.917-922</ispartof><rights>Copyright College of Family Physicians of Canada May 1997</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2255508/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2255508/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9154363$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Delva, M D</creatorcontrib><title>Vitamin B12 replacement. To B12 or not to B12?</title><title>Canadian family physician</title><addtitle>Can Fam Physician</addtitle><description>To review the evidence for an expanded approach to identifying and treating patients with cobalamin deficiency. Controversy surrounds this issue. Some authors claim that seven times more patients are treated than have true deficiency. New diagnostic tests and identification of patients who have neurologic consequences without hematologic abnormalities suggest that some of these patients have a vitamin B12 tissue deficiency.
A MEDLINE search of English-language literature from 1990 to 1995 revealed retrospective and prospective studies of diagnostic tests; prospective surveys; a cohort study; and retrospective and prospective case series, some with control groups. No double-blind controlled trials of treatment were found.
Some patients with neuropsychiatric abnormalities develop a cobalamin tissue deficiency that can be detected by elevated serum homocysteine and methylmalonic acid levels despite normal serum vitamin B12 levels without macrocytic anemia. Serum cobalamin testing is neither sensitive nor specific in the low normal range for cobalamin deficiency. Treatment recommendations vary because no controlled trials support any recommendations. Oral cobalamin is an underused alternative to parenteral treatment.
Until the newer diagnostic tests become widely available, family physicians must continue to take a traditional approach to diagnosing vitamin B12 deficiency. There is, however, support for a clinical trial of treatment in patients with neuropsychiatric symptoms.</description><subject>Family Practice</subject><subject>Homocysteine - blood</subject><subject>Humans</subject><subject>Methylmalonic Acid - blood</subject><subject>Prevalence</subject><subject>Research Design</subject><subject>Sensitivity and Specificity</subject><subject>Vitamin B 12 - metabolism</subject><subject>Vitamin B 12 - therapeutic use</subject><subject>Vitamin B 12 Deficiency - complications</subject><subject>Vitamin B 12 Deficiency - diagnosis</subject><subject>Vitamin B 12 Deficiency - drug therapy</subject><subject>Vitamin B 12 Deficiency - metabolism</subject><subject>Vitamins & minerals</subject><issn>0008-350X</issn><issn>1715-5258</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><recordid>eNpdkFtLxDAQhYMoa139CULxwbcuuU2Svii6eIMFX1bxLaRpql3apqat4L83rIuoMDDMmY_DmdlDCZEEMqCg9lGCMVYZA_xyiI6GYYMxFZyRGZrlBDgTLEGL53o0bd2l14SmwfWNsa513bhI136r-ZB2fkzH7XR5jA4q0wzuZNfn6On2Zr28z1aPdw_Lq1XWEwYqs6AqUhiFKeESKq6Y4goKQ0xFSkKFyBUoi4UUVekULSThhbVSclkWQIRhc3Tx7dtPRetKGxMF0-g-1K0Jn9qbWv_ddPWbfvUfmlIAwCoanO8Mgn-f3DDqth6saxrTOT8NWqo8jyiO4Nk_cOOn0MXjNMUQiwGL0OnvOD85dm9kXxWMa5E</recordid><startdate>199705</startdate><enddate>199705</enddate><creator>Delva, M D</creator><general>College of Family Physicians of Canada</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>199705</creationdate><title>Vitamin B12 replacement. To B12 or not to B12?</title><author>Delva, M D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p1358-c58f1ba8021475f4838485ba1af1d12669858c0676fde82b714bcc7747db516a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Family Practice</topic><topic>Homocysteine - blood</topic><topic>Humans</topic><topic>Methylmalonic Acid - blood</topic><topic>Prevalence</topic><topic>Research Design</topic><topic>Sensitivity and Specificity</topic><topic>Vitamin B 12 - metabolism</topic><topic>Vitamin B 12 - therapeutic use</topic><topic>Vitamin B 12 Deficiency - complications</topic><topic>Vitamin B 12 Deficiency - diagnosis</topic><topic>Vitamin B 12 Deficiency - drug therapy</topic><topic>Vitamin B 12 Deficiency - metabolism</topic><topic>Vitamins & minerals</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Delva, M D</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Canadian family physician</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Delva, M D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vitamin B12 replacement. To B12 or not to B12?</atitle><jtitle>Canadian family physician</jtitle><addtitle>Can Fam Physician</addtitle><date>1997-05</date><risdate>1997</risdate><volume>43</volume><spage>917</spage><epage>922</epage><pages>917-922</pages><issn>0008-350X</issn><eissn>1715-5258</eissn><abstract>To review the evidence for an expanded approach to identifying and treating patients with cobalamin deficiency. Controversy surrounds this issue. Some authors claim that seven times more patients are treated than have true deficiency. New diagnostic tests and identification of patients who have neurologic consequences without hematologic abnormalities suggest that some of these patients have a vitamin B12 tissue deficiency.
A MEDLINE search of English-language literature from 1990 to 1995 revealed retrospective and prospective studies of diagnostic tests; prospective surveys; a cohort study; and retrospective and prospective case series, some with control groups. No double-blind controlled trials of treatment were found.
Some patients with neuropsychiatric abnormalities develop a cobalamin tissue deficiency that can be detected by elevated serum homocysteine and methylmalonic acid levels despite normal serum vitamin B12 levels without macrocytic anemia. Serum cobalamin testing is neither sensitive nor specific in the low normal range for cobalamin deficiency. Treatment recommendations vary because no controlled trials support any recommendations. Oral cobalamin is an underused alternative to parenteral treatment.
Until the newer diagnostic tests become widely available, family physicians must continue to take a traditional approach to diagnosing vitamin B12 deficiency. There is, however, support for a clinical trial of treatment in patients with neuropsychiatric symptoms.</abstract><cop>Canada</cop><pub>College of Family Physicians of Canada</pub><pmid>9154363</pmid><tpages>6</tpages></addata></record> |
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subjects | Family Practice Homocysteine - blood Humans Methylmalonic Acid - blood Prevalence Research Design Sensitivity and Specificity Vitamin B 12 - metabolism Vitamin B 12 - therapeutic use Vitamin B 12 Deficiency - complications Vitamin B 12 Deficiency - diagnosis Vitamin B 12 Deficiency - drug therapy Vitamin B 12 Deficiency - metabolism Vitamins & minerals |
title | Vitamin B12 replacement. To B12 or not to B12? |
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