Drug and Environmental Factors Associated with Adverse Pregnancy Outcomes Part III: Folic Acid: Pharmacology, Therapeutic Recommendations, and Economics

Lewis, D P; Dyke, Don C. Van; Stumbo, Phyllis J.; Berg, Mary

doi:10.1345/aph.17427

Cited by 19 publications

(7 citation statements)

References 101 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It is less clear whether or not low dose folic acid masks B12 deficiency 285,401. Although the United States FDA requires 140 μg of folic acid per 100 g of grain or flour,424,425 an amount chosen because it was considered high enough to prevent NTDs, but low enough to not mask B12 deficiency, some have advocated increasing this amount 426. Due to insufficient sensitivity, neither Hgb nor MCV are useful in ruling out B12-deficient dementia or SCD 7,13,33,58,124,289,300,371,373,378,385,427.…”

Section: Discussionmentioning

confidence: 99%

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Werder¹

2010

NDT

View full text Add to dashboard Cite

IntroductionAlthough consensus guidelines recommend checking serum B12 in patients with dementia, clinicians are often faced with various questions: (1) Which patients should be tested? (2) What test should be ordered? (3) How are inferences made from such testing? (4) In addition to serum B12, should other tests be ordered? (5) Is B12 deficiency compatible with dementia of the Alzheimer’s type? (6) What is to be expected from treatment? (7) How is B12 deficiency treated?MethodsOn January 31st, 2009, a Medline search was performed revealing 1,627 citations related to cobalamin deficiency, hyperhomocysteinemia, and dementia. After limiting the search terms, all abstracts and/or articles and other references were categorized into six major groups (general, biochemistry, manifestations, associations and risks, evaluation, and treatment) and then reviewed in answering the above questions.ResultsThe six major groups above are described in detail. Seventy-five key studies, series, and clinical trials were identified. Evidence-based suggestions for patient management were developed.DiscussionEvidence is convincing that hyperhomocysteinemia, with or without hypovitaminosis B12, is a risk factor for dementia. In the absence of hyperhomocysteinemia, evidence is less convincing that hypovitaminosis B12 is a risk factor for dementia. B12 deficiency manifestations are variable and include abnormal psychiatric, neurological, gastrointestinal, and hematological findings. Radiological images of individuals with hyperhomocysteinemia frequently demonstrate leukoaraiosis. Assessing serum B12 and treatment of B12 deficiency is crucial for those cases in which pernicious anemia is suspected and may be useful for mild cognitive impairment and mild to moderate dementia. The serum B12 level is the standard initial test: 200 picograms per milliliter or less is low, and 201 to 350 picograms per milliliter is borderline low. Other tests may be indicated, including plasma homocysteine, serum methylmalonic acid, antiparietal cell and anti-intrinsic factor antibodies, and serum gastrin level. In B12 deficiency dementia with versus without pernicious anemia, there appear to be different manifestations, need for further workup, and responses to treatment. Dementia of the Alzheimer’s type is a compatible diagnosis when B12 deficiency is found, unless it is caused by pernicious anemia. Patients with pernicious anemia generally respond favorably to supplemental B12 treatment, especially if pernicious anemia is diagnosed early in the course of the disease. Some patients without pernicious anemia, but with B12 deficiency and either mild cognitive impairment or mild to moderate dementia, might show some degree of cognitive improvement with supplemental B12 treatment. Evidence that supplemental B12 treatment is beneficial for patients without pernicious anemia, but with B12 deficiency and moderately-severe to severe dementia is scarce. Oral cyanocobalamin is generally favored over intramuscular cyanocobalamin.

show abstract

Section: Discussionmentioning

confidence: 99%

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Werder¹

2010

NDT

View full text Add to dashboard Cite

show abstract

“…It is recognized that high-dose folic acid taken by a patient who is vitamin B 12 deficient may interfere with/delay the diagnosis of a vitamin B 12 deficiency since the hematological but not neurological abnormalities may be reversed by folic acid. There is no known maternal risk as long as vitamin B 12 deficiency is not coexisting, and there is general agreement that the toxicity risk in pregnancy is minimal [17]. The risk to the fetus has been studied in a small number of studies with no adverse events.…”

Section: Risks Of Folic Acidmentioning

confidence: 99%

Recent advances in the prevention of congenital heart disease

Huhta

Linask

Bailey

2006

Current Opinion in Pediatrics

View full text Add to dashboard Cite

“…With decreased folate, homocysteine would be increased. This would have an affect on peripheral vascular disease, stroke, myocardial infarction, coronary artery disease, and congenital birth defects such as NTDs ( 62 ). Perhaps in the fu ture, the status of homocysteine will be routinely monitored in patients taking AEDs that lower the folate status because the implication is that folate-lowering drugs may cause iatrogenic diseases.…”

Section: Lmplications For Homocysteinementioning

confidence: 99%

Effects of Antiepileptics on Nutritional Status

Berg¹

2004

Handbook of Drug-Nutrient Interactions

View full text Add to dashboard Cite

Drug and Environmental Factors Associated with Adverse Pregnancy Outcomes Part III: Folic Acid: Pharmacology, Therapeutic Recommendations, and Economics

Cited by 19 publications

References 101 publications

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Recent advances in the prevention of congenital heart disease

Effects of Antiepileptics on Nutritional Status

Contact Info

Product

Resources

About