Folic acid deficiency

There appears to be considerable evidence that folic acid is essential for growth and development, as well as hemopoiesis. This is presumably because of its role in the synthesis of protein and nucleic acids. In the synthesis of protein folic acid appears to facilitate the ability of the body to use formate for the production of amino acids (Plant et aZ. ° ). It is thought that both folic acid and vitamin B12 are concerned in the synthesis of desoxyribonucleic acid (Woods ). 

---

Folic acid deficiency Hyperthermia Phenylketonuria Rheumatic disease Virilizing tumors Drugs and chemicals Androgenic chemicals Angiotensin-converting enzyme inhibitors Captopril, enalapril Antibiotics... 

The anemias discussed in this chapter include iron deficiency anemia, anemia in patients witii chronic renal disease pernicious anemia, and anemia resulting from a folic acid deficiency. Table 45-1 defines these anemias. Drugp used in treatment of anemia are summarized in die Summary Drug Table Drugp Used in die Treatment of Anemia. 

Follow die diet recommended by die primary healdi care provider because diet and drug are necessary to correct a folic acid deficiency. 

Folic acid deficiency is also related to megaloblastic anemia. Tetrahydrobiopterin is a co-factor for phenylalanine, tyrosine, and tryptophane hydroxilases — enzymes... 

Anemia from vitamin B12 or folic acid deficiency is treated effectively by replacing the missing nutrient. 

Folic add (plasma) 3.1-12.4 ng/mL or mcg/L (7-28 nmol/L) Used to determine folic acid deficiency. 

Anemia from vitamin BI2 or folic acid deficiency is treated effectively by replacing the missing nutrient. Both folic acid and vitamin B12 are essential for erythrocyte production and maturation. Replacing these factors allows for normal DNA synthesis and, consequently, normal erythropoiesis. 

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. 

Serum uric acid and folic acid concentrations should be monitored yearly in patients prone to hyperuricemia or folic acid deficiency. Blood glucose must be monitored carefully in diabetic patients. 

Macrocytic anemias Megaloblastic anemias Vitamin B12 deficiency Folic acid deficiency anemia Microcytic hypochromic anemias Iron-deficiency anemia Genetic anomaly Sickle cell anemia Thalassemia... 

Common but usually transient side effects are lethargy, incoordination, blurred vision, higher cortical dysfunction, and drowsiness. At concentrations greater than 50 mcg/mL, phenytoin can exacerbate seizures. Chronic side effects include gingival hyperplasia, impaired cognition, hirsutism, vitamin D deficiency, osteomalacia, folic acid deficiency, carbohydrate intolerance, hypothyroidism, and peripheral neuropathy. 

In tropical sprue, both in Hong Kong and in Puerto Rico, folic acid deficiency is a constant and early feature (B25, F18). Its importance in sprue was first demonstrated by Spies and his colleagues (S18) in the West Indies. However, it cannot be concluded that tropical sprue is simply due to dietary folic acid deficiency. In Hong Kong the condition may develop in a previously healthy individual on an adequate... 

The chemistry, metabolism, and clinical importance of folic acid have been the subject of many excellent reviews (A7, Gil, H14, H20, Rl). Folic acid deficiency leads to a macrocytic anemia and leucopenia. These symptoms are due to inadequate synthesis of nucleic acid. The synthesis of purine bases and of thymine, required for nucleic acid synthesis, is impaired in folic acid deficiency. Detection of folic acid activity in biologic fluids and tissues is of the utmost importance it distinguishes between the various anemias, e.g., those due to vitamin Bi2 or folic acid deficiency. Because morphology of the abnormal red cell does not help in diagnosing vitamin deficiency, one must rely on assay methods for differential diagnosis. Treatment of pernicious anemia with folic acid has led to subacute combined degeneration of the spinal cord despite... 

Nearly all microbiologic assays for folic acid activity have used Streptococcus faecalis and Lactobacillus casei. Earlier it appeared that these organisms could not detect folic acid deficiency in man (C2, L8) for example, in one study using S. faecalis there was no detectable activity in the fasting serum of humans (C3). Administration of a loading dose of folic acid with subsequent assay by S. faecalis (G9) has served as a workable means of determining folic acid deficiency (C6), a technique having definite drawbacks (G10). 

B12 from those due to folic acid deficiency. In all cases the folic acid determinations agreed with the clinical findings more detailed results are given elsewhere (B12). 

B36. Broquist, H. P., and Luhby, A. L., Detection and isolation of formimino-glutamic acid from urine in folic acid deficiency in humans. Proc. Soc. Exptl. Biol. Med. 100, 349-354 (1959). 

B37. Brown, D. D., Silva, O. L., Gardiner, R. C., and Silverman, M., Metabolism of formiminoglutamic acid by vitamin B12 and folic acid deficient rats fed excess methionine. J. Biol. Chem. 235, 2058-2062 (1960). 

K7. Kohn, J., Mollin, D. L., and Rosenbach, L. M., Conventional voltage electrophoresis for formiminoglutamic acid determination and folic acid deficiency. /. Clin. Pathol. 14, 345-350 (1961). 

In view of the reported growing importance ascribed to folic acid deficiency in the prevention of various disease conditions, such as neural tube defects, megaloblastic anemia, colon cancer, and colorectal cancer, a dissolution requirement is specified for folic acid when it is present in multivitamin-mineral combination products. Currently, the dissolution standard required in the official articles of dietary supplements (including vitamin-mineral combination products) places folic acid outside the index vitamin hierarchy. Therefore, a mandatory dissolution test for folic acid is required that is independent of and in addition to the mandatory index vitamin test for multivitamin preparations containing folic acid. 

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

Megaloblastic anemia due to folic acid deficiency No more than 1 mg leucovorin/day. There is no evidence that doses greater than 1 mg/day have greater efficacy than 1 mg doses. 

Vitamin 8 2 deficiency Vitamin B-12 deficiency due to malabsorption syndrome as seen in pernicious anemia Gl pathology, dysfunction or surgery fish tapeworm infestation malignancy of pancreas or bowel gluten enteropathy sprue small bowel bacterial overgrowth total or partial gastrectomy accompanying folic acid deficiency. Increased vitamin B-12 requirements Increased vitamin B-12 requirements associated... 

Inadequate response A blunted or impeded therapeutic response may be due to infection, uremia, bone marrow suppressant drugs, concurrent iron or folic acid deficiency, or misdiagnosis. 

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. 

Patients with folic acid deficiency may have diarrhea and nausea, but the principal symptoms are weakness and easy fatigability due to megaloblastic anemia arising from impaired cell division in the bone marrow. 

The answer is D. Several vitamin deficiencies can cause anemia due to reduced DNA synthesis in the erythropoietic cells of the bone marrow, especially folic acid and vitamin Bj2 (cobalamin), which are particularly prevalent among elderly patients due to poor diet and reduced absorption. In addition, deficiencies of either folic acid or vitamin Bj2 could produce the megaloblastic anemia seen in this patient. However, the absence of neurologic symptoms, a hallmark of vitamin Bj2 deficiency, makes that diagnosis less likely than folic acid deficiency. 

Folate deficiency can be dietary, especially in the eiderly, due to increased demand like in pregnancy, or due to maiabsorption syndromes. Agents which can cause folic acid deficiency with long-term use include phenytoin, oral contraceptives, isoniazid and glucocorticosteroids. In rare instances the use of dihydrofolate reductase inhibitors like trimethoprim, methotrexate or pyrimethamine can contribute to the occurrence of folate deficiency. Folinic acid can circumvent the need for the inhibited dihydrofolate reductase. 

Because the actions of triamterene and amiloride are independent of plasma aldosterone levels, their prolonged administration is likely to result in hyperkalemia. Both amiloride and triamterene are contraindicated in patients with hyperkalemia. Triamterene should not be given to patients with impaired renal function. Potassium intake must be reduced, especially in outpatients. A folic acid deficiency has been reported to occur occasionally following the use of triamterene. 

---