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Serum methylmalonic acid

Serum vitamin B12 levels decrease with age, and serum methylmalonic acid concentrations increase with age. These findings reflect a decline in vitamin B12 status in elderly people. [Pg.344]

On the day of admission, the patient had developed a deep venous thrombosis in his right calf, a site not involved in the injury. In investigating the underlying cause of the deep venous thrombosis, serum homocysteine was measured and found to be 17.4 pmol/L (normal is < 14 pmol/I.).To distinguish between folic acid and vitamin B12 deficiencies, a serum methylmalonic acid (MMA) assay was performed it yielded a result of 0.59 pmol/I. MMA (normal is < 0.30 pmol/L). This confirmed the presence of vitamin B12 deficiency, despite a serum B12 concentration that was within the normal range. [Pg.301]

Transcorrin II bound vitamin B12 Mean cell volume Serum methylmalonic acid Serum homocysteine Urine FIGLU more than 8 h after histidine load — <0.15 <0.22 >100 fL >1 i.mol/L >20 i.mol/L >50 [ig /mL ... [Pg.315]

Savage DG, Lindenbaum J, Stabler SP, Allen RH. Sensitivity of serum methylmalonic acid and total homocysteine determinations for diagnosing cobalamin and folate deficiencies. Am J Med 1994 96 239-46. [Pg.978]

Indirect tests assess the functional adequacy of vitamin Bi2. Serum methylmalonic acid concentration is increased when a lack of adenyl-Cbl causes a block in the conversion of methylmalonyl-CoA to succinyl-CoA. It is a sensitive test of status, being often the first analyte to be raised in sub-clinical vitamin B12 deficiency. It has a further advantage in that it is unaffected by folate deficiency. Early methods for methylmalonic acid lacked sensitivity and specificity, a situation that has been resolved by the adoption of gas chromatographic-mass spectrometric methods,though these require specialized handling. Plasma total homocysteine concentration is a sensitive indicator of vitamin B status, because methyl-Cbl is required for the remethylation of... [Pg.1104]

Serum methylmalonic acid concentrations below 376nmol/L have been considered acceptable in an elderly U.S. population,as have concentrations below 320 nmoI/L in a group of older Dutch subjects. ... [Pg.1105]

Marsh, D.B., and Nutall, K.L. Serum methylmalonic acid by capillary zone electrophoresis using electrokinetic injection and indirect photometric detection. J. Capillary Electmphor, 2, 63,1995. [Pg.809]

Nilsson K, Gustafson L, Hultberg B. The plasma homocysteine concentration is better than that of serum methylmalonic acid as a marker for sociopsychological performance in a psychogeri-atric population. Clin Chem 2000 46 691-696. [Pg.452]

Some forms of MMA may be responsive to vitamin Bjj. Responsiveness can be determined by administration of 1.0 mg hydroxocobalamin (IM or IV) for 5 days. A reduction in serum methylmalonic acid concentrations of 50 % or greater suggests responsiveness [14]. For those with cobalamin-responsive forms of MMA, intramuscular (IM) hydroxocobalamin injections of 1.0-2.0 mg are often administered daily. A decreased frequency of IM injections or use of oral supplements may be appropriate for older individuals. The hydroxocobalamin form rather than the standard cyanocobalamin form must be used [15]. [Pg.225]

Serum methylmalonic acid, an intermediary product of vitamin B12 metabolism, is a sensitive indicator of vitamin B12 deficiency reflecting the functional status of vitamin B12 and folate in the tissues. [Pg.809]

Serum methylmalonic acid Serum homocysteine Serum methylmalonic acid... [Pg.809]

Serum methylmalonic acid (as metabolic changes precede over low vitamin B levels)... [Pg.809]

Vitamin B12 deficiency is generally assessed based on serum vitamin B12 concentration, plasma homocysteine concentration and serum methylmalonic acid (MMA) concentration (Savage et al. 1994). Serum vitamin B12 concentration has been reported by many researchers, including us, to be similar in patients with CKD and healthy individuals (Koyama et al. 2002). However, plasma total homocysteine level is elevated in an inverse relationship with the reduction in renal function (Bostom and Lathrop 1997). [Pg.822]

In a meantime, primiparous cows were fed the same basal diet than in the experiment described previously and supplemented daily with folic acid and rumen-protected methionine. The effects of weekly intramuscular injections of saline (0.95 NaCl) or 10 mg of vitamin Bj2 on milk production were monitored from 4 to 18 weeks of lactation. Supplementary vitamin Bj2 tended to increase milk yield from 28.5 to 31.1 kg/d and increased energy-corrected milk as well as milk yields of solids, fat and lactose but had no effect on dry matter intake or milk composition. Furthermore, packed cell volume and blood haemoglobin increased and serum methylmalonic acid decreased in cows that received vitamin Bj2 injections. The first observation suggests that low vitamin B 2 supply interfered with folate metabolism because folic acid deficiency, through its role in DNA synthesis, affects hematopoiesis (Bills et al., 1992). The second one indicates that low vitamin Bj2 supply interfered with the other vitamin B j 2-dependent enzyme, methylmalonyl-CoA mutase. These findings supported the hypothesis that vitamin Bj2 supply is suboptimal in early lactation (Girard and Matte, 2005) and may have limited the potential role of folic acid in these first studies. [Pg.239]

Vitamin B12 Low serum cobalamin (< 150 pmol/L) accompanied by increased serum homocysteine (> 13 Nnol/L), and increased serum (> 0.4 -mol/L) and urine (> 3.6 mmol/mol creatinine) methylmalonic acid... [Pg.732]

When Rinaldo analyzed Ryan s blood serum, he found high concentrations of methylmalonic acid, a breakdown product of the branched-chain amino acids isoleucine and valine, which accumulates in MMA patients because the enzyme that should convert it to the next product in the metabolic pathway is defective. And particularly telling, he says, the child s blood and urine contained massive amounts of ketones, another metabolic consequence of the disease. Like Shoemaker, he did not find any ethylene glycol in a sample of the baby s bodily fluids. The bottle couldn t be tested, since it had mysteriously disappeared. Ri-naldo s analyses convinced him that Ryan had died from MMA, but how to account for the results from two labs, indicating that the boy had ethylene glycol in his blood Could they both be wrong ... [Pg.684]

Whlean et al. (W7) described a follow-up, extending over several years, of two infants with methylmalonic aciduria unresponsive to treatment with vitamin B12. The first patient, a boy, was the child of two first cousins delivery followed an uneventful pregnancy. The child had convulsions 4 days after birth and was found to have a profound metabolic acidosis, and was excreting a large amount of methylmalonic acid in his urine. His serum vitamin B12 concentration was normal. Further studies confirmed a diagnosis of methylmalonic aciduria. [Pg.201]

A 6-month-old child was breast-fed exclusively by a mother who had been a strict vegetarian for at least 7 years. He was totally unresponsive to stimuli. His hemoglobin was 5.7 g/dL, and his bone marrow aspirates showed megaloblastic changes in blood cells. His serum folate and iron were normal. His urine contained increased amounts of homocystine, methylmalonic acid, and glycine. Propose a reason for this infant s illness, and discuss its biochemical etiology. Discuss other possible reasons for the same or similar symptoms in a patient. Explain the abnormal serum and urine chemistries. [Pg.151]

Indirect indicators of vitamin B12 deficiency include measurements of the metabolites homocysteine and methylmalonic acid (MMA) in serum and MMA in urine (see the Biochemical Perspectives section). Whereas the serum homocysteine concentration increases during folate or vitamin B12 deficiencies, the serum and urine MMA concentrations increase only in vitamin B12 deficiency. Therefore, MMA determinations can be used to differentiate vitamin B12 deficiency from folate deficiency. The normal concentration of MMA in serum ranges from 0.08 to 0.28 pmol/L. MMA is quantified using gas-liquid chromatography and mass spectrometry. Elevated concentrations of MMA and homocysteine in serum may precede the development of hematological abnormalities and reductions in serum vitamin B12 concentrations. One should be aware that other conditions, including renal in sufficiency and inborn errors of metabolism, can also result in elevated serum levels of MMA. [Pg.303]

Test for serum levels of methylmalonic acid (functional test). [Pg.522]

Both direct and indirect (ftmctional) methods are available for assessing vitamin B status. The indirect tests include assays for urinary and serum concentrations of methylmalonic acid, plasma homocysteine, the deoxyuridine suppression test, and the vitamin B12 absorption test. Cyto-chemical staining of red blood cell (RBC) precursors and the test for IF blocking antibodies are also ancillary methods for assessing vitamin B12 status. [Pg.1103]

Stabler SP, Marcell PD, Podell ER, Allen RH, Linden-baum J. Assay of methylmalonic acid in the serum of patients with cobalamin deficiency using capillary gas chromatography-mass spectrometry. J Clin Invest 1986 77 1606-12. [Pg.1161]

The answer is d. (Murray, pp 238-249. Scriver, pp 2165-2194. Sack, pp 121-144. Wilson, pp 287-324.) Propionic acidemia (232000) results from a block in propionyl CoA carboxylase (PCC), which converts propionic to methylmalonic acid. Excess propionic acid in the blood produces metabolic acidosis with a decreased bicarbonate and increased anion gap (the serum cations sodium plus potassium minus the serum anions chloride plus bicarbonate). The usual values of sodium (-HO meq/L) plus potassium ( 4 meq/T) minus those for chloride (-105 meq/L) plus bicarbonate (—20 meq/L) thus yield a normal anion gap of -20 meq/L. A low bicarbonate of 6 to 8 meq/L yields an elevated gap of 32 to 34 meq/L, a gap of negative charge that is supplied by the hidden anion (propionate in propionic acidemia). Biotin is a cofactor for PCC and its deficiency causes some types of propionic acidemia. Vitamin B deficiency can cause methylmalonic aciduria because vitamin Bn is a cofactor for methylmalonyl coenzyme A mutase. Glycine is secondarily elevated in propionic acidemia, but no defect of glycine catabolism is present. [Pg.391]

A vitamin B12 coenzyme is needed to convert methyknalonyl coenzyme A to succinyl co-enzyme A. Patients with vitamin B12 deficiency almost always have increased urinary excretion of methylmalonic acid (MMA). MMA is amore specific marker for vitamin B12 deficiency compared to homocysteine. MMA levels are not elevated in folate deficiency, as folate does not participate in MMA metabolism. Levels of both MMA and homocysteine are usually elevated prior to the development of hematologic abnormalities and reductions in serum vitamin B12 levels. MMA levels need to be interpreted cau-... [Pg.1813]

Bea Twelvlow, a 75-year-old woman, went to see her physician because of a numbness and tingling in her arms. A diet history indicated a normal and healthy diet, but Bea was not taking any supplemental vitamin pills. Laboratory results indicated a slight elevation of methylmalonic acid, and this led the physician to suspect a vitamin B12 deficiency. Direct measurement of serum B12 levels did indicate a deficiency, but the results of a Schilling test were normal. [Pg.733]

Nutritional anemia (hemoglobin, hematocrit, MCV, serum vitamin Bi2 and/or methylmalonic acid, total homocysteine, ferritin, iron, folate, total iron-binding capacity)... [Pg.109]


See other pages where Serum methylmalonic acid is mentioned: [Pg.315]    [Pg.315]    [Pg.944]    [Pg.196]    [Pg.226]    [Pg.230]    [Pg.315]    [Pg.315]    [Pg.944]    [Pg.196]    [Pg.226]    [Pg.230]    [Pg.118]    [Pg.737]    [Pg.203]    [Pg.518]    [Pg.518]    [Pg.188]    [Pg.922]    [Pg.803]    [Pg.226]   
See also in sourсe #XX -- [ Pg.1104 ]




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Methylmalonic

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