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1 strongly influenced by both renal status and cobalamin deficiency.
2 s identified the entity of mild, preclinical cobalamin deficiency.
3  not all abnormal metabolite results reflect cobalamin deficiency.
4 seem at increased risk for mild, preclinical cobalamin deficiency.
5  megaloblastic anemia, often associated with cobalamin deficiency.
6 plasma MMA values have been used to diagnose cobalamin deficiency.
7 y years before the establishment of clinical cobalamin deficiency.
8                                           In cobalamin deficiency, 2 mg of cyanocobalamin administere
9 ed to ascertain the prevalence of folate and cobalamin deficiencies and hyperhomocysteinemia in Bangl
10               tHcy is a marker of folate and cobalamin deficiencies and is also related to several li
11 row mononuclear cells of eight patients with cobalamin deficiency and compared this with that found i
12 chemical basis for neurologic dysfunction in cobalamin deficiency and the frequent divergence between
13                        Ethnic differences in cobalamin deficiency and the Hcys patterns associated wi
14 unusual states of neurologically symptomatic cobalamin deficiency are being recognized, such as nitro
15 were increased and only GSH was decreased in cobalamin deficiency as a whole, compared with 17 contro
16 mes more common in the elderly than clinical cobalamin deficiency but also differs from it in arising
17 toms commonly but not specifically linked to cobalamin deficiency, even with low-normal levels.
18 nborn errors of metabolism and indicators of cobalamin deficiency in older persons.
19                   The importance of treating cobalamin deficiency in pregnancy is considered.
20 y and bariatric surgery rates, prevalence of cobalamin deficiency in pregnancy is rising.
21 determine the demographic characteristics of cobalamin deficiency in the elderly and its role in thei
22 the very common problem of mild, preclinical cobalamin deficiency in the elderly await further clarif
23                                         Mild cobalamin deficiency is most common in elderly white men
24    This study is the first to show that true cobalamin deficiency is not more common in HHT than in t
25                                              Cobalamin deficiency is relatively common, but the great
26                                      Because cobalamin deficiency is routinely treated with parentera
27 ile megaloblastic anemia due to vitamin B12 (cobalamin) deficiency is caused by intestinal malabsorpt
28      The challenges in medical management of cobalamin deficiency lie in attention to the unique path
29                                Vitamin B-12 (cobalamin) deficiency may produce severe neurologic and
30 to the unique pathophysiology that underlies cobalamin deficiency, more than in the mechanics of ther
31                 In the diagnosis of juvenile cobalamin deficiency, mutational analysis of the CUBN, A
32 re of this knockout and the lack of systemic cobalamin deficiency point to other mechanisms for cellu
33  individual components: correctly diagnosing cobalamin deficiency, reversing it, defining its underly
34 es in epidemiologic surveys have subclinical cobalamin deficiency (SCCD), not classical clinical defi
35  consequences, and management of subclinical cobalamin deficiency (SCCD), which affects many elderly
36                                              Cobalamin deficiency (serum cobalamin <258 pmol/L and MM
37 entrations or the mild metabolic evidence of cobalamin deficiency so often seen in the elderly.
38  cohort of elderly with a high prevalence of cobalamin deficiency to determine whether SAH, SAM, or t
39 ave broadened and complicated the picture of cobalamin deficiency while providing greater opportuniti
40                                              Cobalamin deficiency with elevated serum MMA concentrati