Folic acid therapy

There is, moreover, the field of hypervitaminoses, which has been explored for the fat-soluble vitamins, but hardly touched in the water-soluble vitamins. The production of combined system disease by folic acid therapy of pernicious anemia belongs to this group, but many more instances wait to be recognized. The indiscriminate use of polyvitamin preparations by poorly informed clinicians is bound to mask such states and to delay their discovery. Also, the use of flushing doses of vitamins in diagnostic tests may cause acute hypervitaminoses. 

HYDROXOCOBALAMIN, CRYSTALLINE Adm n ster IM only. The recommended dosage is 30 meg/day for 5 to 10 days, followed by 100 to 200 meg/month. Children may be given a total of 1 to 5 mg over 2 weeks or more in doses of 100 meg, then 30 to 50 meg every 4 weeks for maintenance. Institute concurrent folic acid therapy at the beginning of treatment if needed. 

Hematologic Hematopoietic complications, some fatal, include thrombocytopenia, leukopenia, granulocytopenia, agranulocytosis, and pancytopenia. Macrocytosis and megaloblastic anemia usually respond to folic acid therapy. Eosinophilia monocytosis leukocytosis simple anemia hemolytic anemia aplastic anemia ecchymosis. 

Sunder-Plassmann G, et al. Effect of high dose folic acid therapy on hyperhomocysteinemia in hemodialysis patients Results of the Vienna multicenter study. J Am Soc Nephrol 2000 11 1106-1116. 

B13. Butterworth, C. E., Hatch, K. D., Core, H., Mueller, H., and Krumdieck, C. L., Improvement in cervical dysplasia associated with folic acid therapy in users of oral contraceptives. Am. J. Clin. Nutr. 35, 73-82 (1982). 

Namazi, M.H., Motamedi, M.R., Safi, M., Vakili, H., Saadat, H., and Nazari, N., 2006. Elficacy of folic acid therapy for prevention of instent restenosis a randomized clinical trial. Archive of Iranian Medicine. 9 108-110. 

Bile acid sequestrants may interfere with die digestion of fats and prevent die absorption of die fat-soluble vitamins (vitamins A, D, E, and K) and folic acid. When die bile acid sequestrants are used for long-term therapy, vitamins A and D may be given in a water-soluble form or administered parenterally. If bleedingtendencies occur as die result of vitamin K deficiency, parenteral vitamin K is administered for immediate treatment, and oral vitamin K is given for prevention of a deficiency in the futum... 

The underlying cause of anemia (e.g., blood loss iron, folic acid, or B12 deficiency or chronic disease) must be determined and used to guide therapy. 

The underlying cause of anemia (e.g., blood loss iron, folic acid, or vitamin B12 deficiency or chronic disease) must be determined and used to guide therapy. As discussed previously, patients should be evaluated initially based on laboratory parameters to determine the etiology of the anemia (see Fig. 63-3). Subsequently, the appropriate pharmacologic treatment should be initiated based on the cause of anemia. 

Other than transfusion, nonpharmacologic therapy plays a limited role in the management of anemia. Certainly, some causes of anemia can be attributed to diets poor in iron, folic acid, or vitamin B12. However, in the United States, nutrient-poor diets are rarely the sole cause of anemia in a patient. Therefore, ingesting a diet that is rich in iron, folic acid, or vitamin B12 should be encouraged but should not be the only... 

When treating folic acid deficiency, an initial daily dose of 1 mg/day by mouth typically is effective. Absorption of folic acid generally is rapid and complete. However, patients with malabsorption syndromes may require larger doses (up to 5 mg/day). Similar to vitamin B12 deficiency, resolution of symptoms and reticulocytosis is prompt, occurring within days of commencing therapy. Hgb will start to rise after 2 weeks of therapy and may take from 2 to 4 months to resolve the deficiency completely. Afterwards, if the underlying deficiency is corrected, folic acid replacement can be discontinued. However, in cases where folic acid is consumed rapidly or absorbed poorly, chronic replacement may be required. 

In patients with folic acid deficiency, methylmalonic acid may be normal, and homocysteine may be high. Monitor hemoglobin periodically, and reevaluate patients who fail to normalize hemoglobin levels after 2 months of therapy. 

Anaemia often becomes a characteristic feature of several chronic diseases, such as rheumatoid arthritis. In most instances this can be linked to lower than normal endogenous serum EPO levels (although in some cases a deficiency of iron or folic acid can also represent a contributory factor). Several small clinical trials have confirmed that administration of EPO increases haematocrit and serum haemoglobin levels in patients suffering from rheumatoid arthritis. A satisfactory response in some patients, however, required a high-dose therapy that could render this therapeutic approach unattractive from a cost benefit perspective. 

Patients sustain convulsions and neurological deterioration. The urine contains low levels of the metabolites of serotonin, norepinephrine and dopamine. The reductase also plays a role in the maintenance of tetrahydrofolate levels in brain, and some patients have had low folate levels in the serum and CNS. Treatment has been attempted with tryptophan and carbidopa to improve serotonin homeostasis and with folinic acid to replete diminished stores of reduced folic acid. This therapy is sometimes effective. Diagnosis involves assay of DHPR in skin fibroblasts or amniotic cells. Phenylalanine hydroxylase activity is normal. 

Toxicities are GI (stomatitis, diarrhea, nausea, vomiting), hematologic (thrombocytopenia, leukopenia), pulmonary (fibrosis, pneumonitis), and hepatic (elevated enzymes, rare cirrhosis). Concomitant folic acid may reduce some adverse effects without loss of efficacy. Liver injury tests (aspartate aminotransferase or alanine aminotransferase) should be monitored periodically, but a liver biopsy is recommended during therapy only in patients with persistently elevated hepatic enzymes. MTX is teratogenic, and patients should use contraception and discontinue the drug if conception is planned. 

Methotrexate, an antimetabolite, is indicated for moderate to severe psoriasis. It is particularly beneficial for psoriatic arthritis. It is also indicated for patients refractory to topical or UV therapy. Methotrexate can be administered orally, subcutaneously, or intramuscularly. The starting dose is 7.5 to 15 mg per week, increased incrementally by 2.5 mg every 2 to 4 weeks until response maximal doses are approximately 25 mg/wk. Adverse effects include nausea, vomiting, mucosal ulceration, stomatitis, malaise, headache, macrocytic anemia, and hepatic and pulmonary toxicity. Nausea and macrocytic anemia can be ameliorated by giving oral folic acid 1 to 5 mg/day. Methotrexate should be avoided in patients with active infections and in those with liver disease. It is contraindicated in pregnancy because it is teratogenic. 

A vitamin is often the etiological center of a disease as vitamin Bi2 and folic acid in macrocytic anemias. Here, because of the obvious implications for diagnosis and therapy the determination of the nucleo-genic vitamins, Bi2 and folic acid, is imperative in the routine of clinical hematology. 

H12. Hoogstraten, B., Baker, H., and Reizenstein, P., Correlation between serum folic acid activity and response to antifolate therapy. Blood 17, 787 (1961). 

Folic acid is used as an adjunct to methotrexate therapy to limit methotrexate-induced side-effects such as mucositis and stomatitis. 

Cl. Carpenter, E. M., Anticonvulsant therapy and folic acid metabolism. D. M. Thesis, University of Oxford, 1972. 

Parenteral Treatment of megaloblastic anemias due to folic acid deficiency when oral therapy is not feasible. 

Addisonian pernicious anemia - Parenteral therapy is required for life oral therapy is not dependable. Administer 100 meg daily for 6 or 7 days by IM or deep subcutaneous injection. If there is clinical improvement and a reticulocyte response, give the same amount on alternate days for 7 doses, then every 3 to 4 days for another 2 to 3 weeks. By this time, hematologic values should have become normal. Follow this regimen with 100 meg monthly for life. Administer folic acid concomitantly if needed. 

Other patients with vitamin 8 2 deficiency - In seriously ill patients, administer both vitamin B-12 and folic acid. It is not necessary to withhold therapy until the precise cause of B-12 deficiency is established. For hematologic signs, children may be given 10 to 50 meg/day for 5 to 10 days followed by 100 to 250 meg/dose every 2 to 4 weeks for neurologic signs, 100 meg/day for 10 to 15 days, then once or twice weekly for several months, possibly tapering to 250 to 1,000 meg/month by 1 year. 

Anemia Administration has been associated in a few cases with vitamin B-12 or folic acid deficiency, megaloblastic anemia, and sideroblastic anemia. If evidence of anemia develops, institute appropriate studies and therapy. 

Folic acid is used for the treatment of folate deficiency. Oral folic acid is usually the therapy of choice. For megaloblastic anemia doses of 5 mg daily for 4 months should be effective. Folinic acid is available in a parenteral formulation which may be indicated when oral therapy is not feasible and for rescue treatments following certain anti-cancer regimens. 

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