FIGLU excretion in pregnancy.
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Anemia, Macrocytic↗
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Relative importance of formiminoglutamic and urocanic acid excretion after a histidine load.
A thin-layer chromatographic method for the simultaneous assessment of formimino-glutamic (Figlu) and urocanic acid excretion after loading with 15 g. histidine has been applied to 15 control subjects and to 49 selected patients. Upper limits of normal excretion were determined for urocanic acid and Figlu alone (15 mg. and 30 mg/8 hr. respectively), and for the combined metabolites (40 mg./8 hr.). Of the 49 patients studied, 27 excreted total metabolites above 40 mg./8 hr.; of these 19 would have been revealed by their abnormal excretion of Figlu and 22 by their abnormal excretion of urocanic acid. Of 74 tests in the 64 subjects, urocanic acid was present in all but 27% of the tests, and in 29.8% of the tests urocanic acid was in excess of the amount of Figlu excreted. In six normal and six abnormal tests urocanic acid was the sole metabolite present. These results re-emphasize the value of estimating both histidine metabolites in tests for folate deficiency in man, and underline the greater relative importance of urocanic acid.
Anemia, Pernicious↗
Cobalamin-dependent metabolism in chronic myelogenous leukemia determined by deoxyuridine suppression test and the formiminoglutamic acid and methylmalonate excretion in urine.
The cobalamin metabolism in chronic myelogenous leukemia (CML) was evaluated in 18 newly diagnosed and untreated patients by formiminoglutamic acid (FiGlu) and methyl malonic acid excretion (MMA) tests. A deoxyuridine (dU) suppression test of bone marrow cells was compared in patients with acute myelogenous leukemia (N = 5), myelodysplastic disease (N = 3), untreated pernicious anemia (N = 16), folate deficiency (N = 7), and a hospital reference group without signs of cobalamin or folate deficiency (N = 22). All had normal MMA excretion but 3 of 15 patients had increased FiGlu excretion. In vitro thymidine uptake in bone marrow cells of CML patients were lower (mean 40 fmol/106 cells) than pernicious anemia patients (115 fmol/106 cells). Methotrexate (MTX) increased the uptake in all cases. Addition of formyl-THF, methyltetrahydrofolate (methyl-THF), and pteroylglutamic acid (PGA) tended to normalize the effect of MTX. In pernicious anemia methyl-THF only decreased the uptake in combination with CN-Cbl. dU suppression values were significantly higher (6.3%) in CML than in the reference group (4.4%), but significantly lower than in pernicious anemia (41.6%) and folate deficiency (28.5%). The dU suppression values in bone marrow cells of CML patients correlated significantly with the transferrin saturation. In buffy coat cells dU suppression values were even higher (9.3%) than in bone marrow cells of the same CML patients. Addition of folate forms and CN-Cbl did not change the dU suppression values in CML, as it did in pernicious anemia. MTX increased dU suppression values significantly in all patients, but more in CML (64.5%) than in pernicious anemia (48.6%) and controls (49.8%). The MTX effect was to some extent neutralized by folate analogues with formyl-THF as the most effective followed by methyl-THF and lastly PGA. Methyl-THF also neutralized MTX in pernicious anemia, but its effect was certainly enhanced by addition of CN-Cbl. Thymidine uptake and dU suppression patterns were not significantly changed in CML after treatment with busulfan for 1 week or in accelerated phase. We concluded that signs of cobalamin or folate deficiency (apart from one patient) cannot be demonstrated in untreated CML. However, dU suppression was significantly increased and more so in circulating myeloid cells than in bone marrow. This indicates a deranged metabolism of deoxynucleotides which is independent of cobalamin and folates, and a difference between bone marrow cells and circulating cells. dU suppression is a valuable indicator of cobalamin deficiency.(ABSTRACT TRUNCATED AT 400 WORDS)
Adolescent↗
Conventional voltage electrophoresis for formiminoglutamic-acid determination in folic acid deficiency.
A new method for the determination of urinary formiminoglutamic acid (FIGLU) using conventional electrophoresis at 200 to 500 v. on cellulose acetate strips is reported. Experience in 166 determinations on 137 patients shows the method to be a simple, practical, and apparently sensitive one for the determination of FIGLU in the urine. Results of the application of the measurement of urinary FIGLU with histidine loading as a test for folic acid deficiency are also reported.
Cellulose↗
Effect of methionine on in vivo histidine metabolism in rats.
Experiments were conducted to examine the effects of methionine supplementation on histidine metabolism in rats. All animals were fed 10% casein diets with a methionine content of either 0.6 or 1.1%. Experiments in which the animals were fed their diets containing an additional 1% histidine ad libitum for at least 10 days revealed that methionine-supplemented animals had a 49% reduction of plasma histidine and an 80% reduction in urinary excretion of formiminoglutamic acid (FIGLU) on day 10. This effect was not observed on day 5. In subsequent experiments rats were fed the control or test diet ad libitum prior to receiving their diets, containing a histidine load, by force-feeding. When a 100-mg histidine load was given on day 5, 24-hour urinary FIGLU excretion was 83% lower in methionine-supplemented animals. When rats were force-fed a 75-mg [ring-2-14C]histidine load on day 10, those receiving supplemental methionine oxidized 21% more of the histidine label to 14CO2 and excreted 61% less of the dose as urinary FIGLU in 24 hours. The activities of histidase and urocanase were unaffected by the methionine supplement. The results suggest that dietary methionine supplementation enhances the in vivo catabolism of histidine by stimulating one-carbon metabolism. Delivery of the methionine supplement by ad libitum feeding requires at least 5 days for this effect to be achieved.
Animals↗
[Clinical studies of histidinemia (author's transl)].
This study was performed to investigate 1) technical modification of Guthrie method for mass screening to detect histidinemia, 2) patients with histidinemia in view of genetic and biochemical aspects, and 3) therapy of histidinemia in newborn infants. Guthrie method was the useful method for mass screening of histidinemia in newborn infants. It is possible to measure blood level of histidine using by Subutilis spore ATTCC 6633 instead of ATCC 6051. Mass screening of histidinemia was done in about 20,000 newborn infants in Hokkaido, and one case of histidinemia, which was first case in Japan found by this method, was observed. In a case of 5 year-old boy with clinical histidinemia, in whom serum histidine level was 12.1 mg/kl, histidase activity of stratum corneum was not detectable, FIGLU and urocanic acid in urine and urocanic acid in sweat were not detected, the half life of histidine at intravenous histidine loading test was too long to measure. But in other case of 13 year-old boy without clinical signs of histidinemia, elder brother of former case, serum histidine level was 4.7 mg/dl, histidase activity was 11% of normal control, excretion of FIGLU and urocanic acid in urine, and urocanic acid in sweat were observed, and the half life of histidine was 5 hours and 50 minutes (normal: 2 hours and 20 minutes). In both cases, Tryptophan absorption and metabolism were not influenced by high level of blood histidine. Therapy with low histidine milk was made in 3 cases of affected infants. When histidine was given orally in dose of 30-35 mg/kg/day, serum histidine level was down to 3-5 mg/dl in a week in all cases, but in one case low proteinemia an anemia were observed. When histidine was orally given in a dose of 40-50 mg/kg/day, serum histidine level was well controlled. In all cases with histidine limited diets, mental retardation and growth retardation were not found.
Adolescent↗
Effect of nitrous oxide on folate and vitamin B12 metabolism in patients.
Exposure to nitrous oxide (N2O) markedly enhances excretion of formic acid and formiminoglutamic acid (FIGLU) in the urine of rats, suggesting a disruption in the normal pathways of folic acid metabolism secondary to an N2O-induced inactivation of methionine synthase. We tested whether surgical patients (23 having total hip replacements and 26 having resection of acoustic neuromas) exposed to isoflurane alone or combined with N2O responded similarly. We found no increase in urinary formic acid and FIGLU in patients exposed to N2O for hip replacement, but a small, transient increase in the FIGLU-to-creatinine ratio in those undergoing resection of acoustic neuromas (mean duration of anesthesia = 9.3 h). This increase peaked at the end of anesthetic exposure and returned toward control levels by the first day after anesthesia and surgery. Low preoperative levels of red blood cell folate and low-normal levels of serum vitamin B12 did not predict an increase in formic acid or FIGLU in response to N2O. Although an occasional patient may prove highly susceptible to and develop signs of severe vitamin B12 and folic acid deficiency after exposure to N2O, our findings suggest that this is a rare event.
Adult↗
Excretion of formimino-glutamic acid in steatorrhoea.
Minor degrees of folic acid deficiency are very common in idiopathic steatorrhoea. The urinary excretion of formimino-glutamic acid (Figlu) after a histadine load is a satisfactory means of detecting this deficiency and may be used as a screening test for idiopathic steatorrhoea.
Celiac Disease↗