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At least 37 records · Page 2Linked to original sources
PubMed1982

Skin histidase activity and urine formiminoglutamic acid (FIGLU) in patients with histidinemia found by screening newborn infants.

Skin histidase activities and urine formiminoglutamic acid (FIGLU) levels were measured in 20 patients with histidinemia, identified by Guthrie's screening method, and their family members as well as control subjects. There was a significant positive correlation between skin histidase activities and the amounts of urine FIGLU. Although the difference of skin histidase activity and the amount of urinary FIGLU was significant between any two of the three groups (i.e. controls, parents and patients; p less than 0.005), these levels ranged widely and a considerable number of the cases overlapped among groups. When a discriminant function was computed to obtain the minimum probability of misclassification between the groups using the above two parameters, a better segregation was observed. However, even though the number of misclassifications decreased, the overlapping cases were still present, especially between the parent and patient groups. It is concluded that either skin histidase activity, urine FIGLU, or both, can be used as genetic markers of the disease to a large but still limited extent.

Amino Acid Metabolism, Inborn Errors↗
PubMed1978

Blood and liver folacin activity, formiminoglutamic acid excretion, growth and hematology in guinea pigs fed a folacin deficient diet with and without sulfonamides.

Dietary folacin deficiency in the presence and absence of dietary sulfonamides was studied in the guinea pig for the purpose of relating the growth and hematologic effects of folacin deficiency to tissue and biochemical changes. Six-week old female guinea pigs fed control and folacin deficient diets with and without 0.1% sulfonamides for 6 to 7 weeks. Growth was significantly reduced in both groups fed the folacin deficient diets, and 25% of all deficient animals died. Macrocytic anemia was not present, but reduced leukocyte numbers were observed in folacin deficiency. Plasma and red blood cell folacin activities were reduced by about 50% in deficient guinea pigs in the presence and absence of dietary sulfonamides. Both liver total folacin activity and urinary formiminoglutamic acid excretion were not significantly altered by the degree of folacin deficiency obtained in this study.

Animals↗
PubMed1995

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↗