PURPOSE: Vitamin B12 (VB12) deficiency is an inevitable sequela of a total gastrectom, which results in general symptoms, including easy fatigue, and hematological, neurological, and gastrointestinal complications. Especially in cases of neurological injury, it may be irreVersible if the timely treatment is delayed. Therefore the early diagnosis and treatment is essential. However, no guidelines exist for the incidence or treatments. METHODS: We investigated the symptoms and serum VB12 concentrations of 296 patients who underwent a total gastrectomy for a gastric malignancy. We defined 200~300 pg/ml as the mild decrease group, under 200 pg/ml as the severe decrease group, and over 300 pg/ml as the normal limit. RESULTS: The cumulative incidence of VB12 deficiency were 5.1, 11.2, 29.9, 44.7, 64.5% at 6 month, 1, 2 and 3 years, and at 4 or more years, respectively. The 90% of patients reported at least 1 symptom. The group under 200 pg/ml was supplemented at 1 month intervals; 10 of the 16 patients (63%) had their VB12 elevated to above 300 pg/ml. The group between 200~300 pg/ml was supplemented at 1 or 3 month intervals; 21 out of 23 (91%), and 12 out of 15 patients (80%) had their B12 elevated to above 300 pg/ml at the 1 and 3 month intervals, respectively, but with no statistical significance. CONCLUSION: The group with a V12 under 200 pg/ml should be supplemented 6 times, at 1 month intervals, regardless of the symptom presentation, and when the rechecked serum VB12 level has been increased above 300 pg/ml, it should be supplemented at 3 month intervals. In the group with a VB12 between 200 and 300 pg/ml, the VB12 should be supplemented at 3 month intervals if the symptom is present, and the asymptomatic group should be observed.
Early Diagnosis ; Fatigue ; Gastrectomy* ; Humans ; Incidence* ; Vitamin B 12 Deficiency* ; Vitamin B 12* ; Vitamins*

Megaloblastic anemia induced by Vitamin B12 deficiency is a disorder caused by impaired DNA synthesis. It has been previously thought to be rare in children, however, recent studies suggest that this condition is more common than previously recognized. Deficiency can lead to a wide spectrum of hematologic and neuropsychiatric disorders. Especially in children, it often presents with nonspecific manifestations, such as developmental delay, irritability, weakness, and failure to thrive. Early diagnosis and prompt treatment might resolve these complications, but permanent neurologic damage may have already occurred. We experienced two cases of Megaloblastic Anemia induced by Vitamin B12 deficiency and report them with a brief review of the literature.
Anemia, Megaloblastic* ; Child* ; DNA ; Early Diagnosis ; Failure to Thrive ; Humans ; Megaloblasts* ; Vitamin B 12 Deficiency* ; Vitamin B 12* ; Vitamins*

BACKGROUND: The traditional treatment of cobalamin deficiency anemia is performed by intramuscular injections. However, it has been suggested that oral replacement of cobalamin is also effective as an intramuscular injection. We studied the effectiveness of oral mecobalamin treatment in patients with cobalamin deficiency. METHODS: Patients with newly diagnosed cobalamin deficiency (<200 pg/mL) or who were previously maintained on intramuscular injection were given 2,000 microgram of oral mecobalamin daily. RESULTS: Sixteen patients were enrolled. The common causes of cobalamin deficiency were total gastrectomy (75%) and pernicious anemia (12.5%). Twelve patients received oral mecobalamin, except for four patients who were lost from follow-up after initial diagnosis. The mean pretreatment values of serum cobalamin and hemoglobin level were 58.3+/-21.9pg/mL and 8.1+/-1.9g/dL, respectively. After one, two, and six months of oral therapy, the respective mean values were 1,691.8+/-260.4pg/mL, 1,085.8+/-1,110.3pg/mL and 990.2+/-249.8pg/mL of serum cobalamin, and 10.4+/-1.3g/dL, 11.3+/-2.2g/dL and 12.1+/-2.3g/dL of hemoglobin. Initially elevated serum homocysteine were normalized after one month of oral therapy. Symptoms such as glossitis were relieved rapidly by oral treatment. CONCLUSION: High-dose oral mecobalamin supplement was a simple and effective treatment in patients with cobalamin deficiency, especially in total gastrectomized patients.
Anemia ; Anemia, Pernicious ; Diagnosis ; Follow-Up Studies ; Gastrectomy ; Glossitis ; Homocysteine ; Humans ; Injections, Intramuscular ; Vitamin B 12 Deficiency ; Vitamin B 12*

Iron deficiency anemia (IDA) and megaloblastic anemia due to vitamin B12 deficiency are well-characterized prototypes of anemia. There is no doubt that IDA is the most common hematologic disorder in Korea and worldwide as well. The diagnosis and treatment of IDA is not a difficult practice usually, however, a caution is required in detecting early-stage iron deficiency and in distinguishing IDA from anemia of chronic disorders such as chronic inflammatory disease, malignancies, chronic liver disease, and chronic renal disease. Administration of a standard iron preparation at a proper dosage over an adequate period is a prerequisite for the successful treatment of IDA, which is sometimes overlooked by both physicians and patients. Early detection and treatment as well as prevention of iron deficiency per se are also required. Pernicious anemia is the most common cause of vitamin B12 deficiency in Western populations. By contrast, the disorder is rare in Korea, although the number of cases seems to be increasing these days. The majority of patients with megaloblastic anemia reveal a history of gastrectomy. Thus, it should be reminded that vitamin B12 supplementation is important to prevent the development of overt deficiency or anemia in these susceptible individuals, since a delay in the treatment of vitamin B12 deficiency may result in an irreversible neurologic deficit.
Anemia* ; Anemia, Iron-Deficiency ; Anemia, Megaloblastic ; Anemia, Pernicious ; Diagnosis ; Gastrectomy ; Humans ; Iron ; Korea ; Liver Diseases ; Neurologic Manifestations ; Renal Insufficiency, Chronic ; Vitamin B 12 ; Vitamin B 12 Deficiency

Humans ; Infant ; Male ; Severity of Illness Index ; Vitamin B 12 Deficiency ; complications ; diagnosis

Subacute combined degeneration (SCD) of the spinal cord is a neurological complication arising from vitamin B12 deficiency. Typical findings are demyelination and axonal loss of the posterior and lateral columns of the thoracic and cervical spinal cord, leading to sensory ataxia and paresthesia. Clinical and neurological features and MRI findings all contribute to the diagnosis of this entity. In the Korean medical literature, only one case of SCD involving pre-treatment MRI has been reported. We describe one case of SCD in a post-gastrecto-my patient who initially presented with progressive sensory abnormality in both upper and lower extremities and showed T2 hyperintensity in the posterior and lateral columns of the spinal cord; this diminished, with clinical improvement, after vitamin B12 therapy. Our report includes the MR images obtained during follow up.
Ataxia ; Axons ; Demyelinating Diseases ; Diagnosis ; Follow-Up Studies ; Humans ; Lower Extremity ; Magnetic Resonance Imaging* ; Paresthesia ; Spinal Cord* ; Subacute Combined Degeneration* ; Vitamin B 12 ; Vitamin B 12 Deficiency ; Vitamins

We report a patient who was diagnosed as subacute combined degeneration (SCD) with elevated homocysteine and methylmalonic acid levels in the situation of a spurious elevation of the vitamin B12 concentration. A false-positive elevation of the vitamin B12 level could lead to a delayed diagnosis and cause irreversible changes in the nervous systems. We therefore suggest that the homocysteine and methylmalonic acid levels should be checked in patients with a normal or elevated vitamin B12 level for whom there is a high clinical suspicion for vitamin B12 deficiency, as a further evaluation for SCD.
Delayed Diagnosis ; Gastritis, Atrophic* ; Homocysteine ; Humans ; Methylmalonic Acid ; Nervous System ; Subacute Combined Degeneration* ; Vitamin B 12 Deficiency ; Vitamin B 12* ; Vitamins*

BACKGROUND: Methylmalonic acid (MMA) is one of the metabolites of the DNA synthesis metabolic pathway wherein vitamin B12 acts as a coenzyme. Vitamin B12 deficiency leads to inhibition of methyl-malonyl CoA mutase, and sequential elevation of blood and urine concentrations of MMA. It has been known that the urine concentration of MMA is a more specific and sensitive marker than the hema-tologic indices and the serum concentration of vitamin B12 for the diagnosis of vitamin B12 deficiency. We investigated the sensitivity of urine concentration of MMA and the usefulness as a differential mark-er for myelodysplastic syndrome (MDS) and megaloblastic anemia (MA). METHODS: We identified 37 cases that were examined for both urine concentrations of MMA and bone marrow studies from January 1996 to December 2000. Serum concentrations of vitamin B12 and folate were measured by the chemiluminescence immunoassay using ACS:180 (Bayer Diag-nostics). Urine concentration of MMA was measured by isotope dilution gas chromatography-mass spectrometry (GC 8000-gas chromatography MD800). RESULTS: Of 36 patients, 12 patients were diagnosed with MA, 8 patients with MDS, 5 patients with aplastic anemia based on the bone marrow study. Increased urine concentration of MMA was observed in all the patients with MA, but none of the patients with MDS. Using a cut-off value of 5 mmol/mol creatinine urine concentration MMA, the sensitivity and specificity in diagnosis for MA were 100% and 80%. The correlation between the urine concentration of MMA and the serum con-centration of vitamin B12 was insignificant (r=-0.25, P=0.21). The highest correlation index with urine concentration of MMA was the red cell distribution width (r=0.74, P < 0.01). CONCLUSIONS: We concluded that the urine concentration of MMA was a sensitive marker for diagno-sis of MA caused by vitamin B12 deficiency and could be a useful test in the differentiation for MA from MDS. Although a consensus for a diagnostic value of the urine concentration of MMA would be nec-essary, we recommend using both the urine concentration of MMA and the serum vitamin B12 as prima-ry tests for diagnosis of MA caused by vitamin B12 deficiency.
Anemia, Aplastic ; Anemia, Megaloblastic* ; Bone Marrow ; Chromatography ; Consensus ; Creatinine ; Diagnosis ; DNA ; Erythrocyte Indices ; Folic Acid ; Gas Chromatography-Mass Spectrometry ; Humans ; Immunoassay ; Luminescence ; Megaloblasts* ; Metabolic Networks and Pathways ; Methylmalonic Acid* ; Myelodysplastic Syndromes ; Sensitivity and Specificity ; Vitamin B 12 Deficiency* ; Vitamin B 12* ; Vitamins*

BACKGROUND & OBJECTIVES: Subacute combined degeneration (SCD) is a disease of spinal cord involving the posterior and lateral column due to vitamin B12 deficiency. The clinical and electrophysiologic findings of SCD are various. METHODS: From 1989 to 1996, 7 patients were diagnosed with SCD in our hospitals. The diagnosis was made by the neurologic and laboratory findings and electrophysiolgic studies such as nerve conduction studies(NCS) and evoked potential(EP). RESULT: Four patients received gastrectomy. Two had chronic atrophic, gastritis; one of them was assumed to have food-cobalamin malabsorrtion. The remaining one was a heavy drinker. The mean duration of neurologic symptoms was 35.7 months. The most common initial complaint was paresthesia (in 4) and impairment of cutaneous sensation was the most common neurologic sign At the time of diagnosis, 5 patients had myelopathy with was supported by EP in 3(60%). There were abnormal NCS findings in 5 f 6 patients with peripheral neuropathy. In one patient, there was no symptom and sign compatible with myelopathy but median nerve SEP showed bilateral central conduction delay. No one had visual symptoms but prolongation of P 100 was detected in 2 patients. Sural nerve biopsy was done in 2 case, which revealed chronic nonspecific neuropatby in one and chronic axonopathy in the other. Megaloblastic anemia was found in 4 cases and improved by cobalamin therapy in all the parents, in which the follow up hematologic data were available. There as a tendency that nonanemic patients had more severe neurologic symptoms than anemic ones. We could not find any relationship between the duration and severity of neurologic menifestations was best in the patients with the shortest duration of neurologic manifestations and hematologic feature festations. CONCLUSIONS: The authors suggest that early detection and treatment is very important for the improvement of symptoms in SCD.
Anemia, Megaloblastic ; Biopsy ; Diagnosis ; Follow-Up Studies ; Gastrectomy ; Gastritis ; Humans ; Median Nerve ; Neural Conduction ; Neurologic Manifestations ; Parents ; Paresthesia ; Peripheral Nervous System Diseases ; Sensation ; Spinal Cord ; Spinal Cord Diseases ; Subacute Combined Degeneration* ; Sural Nerve ; Vitamin B 12 ; Vitamin B 12 Deficiency

To date, the determination of serum vitamin B12 levels has been the most common laboratory test for the assessment of vitamin B12 status; however, the diagnostic accuracy of this test is low. To obtain a more sensitive marker, a new test to measure holotranscobalamin (holoTC) levels has been introduced. In this study, we assessed 45 patients for whom a vitamin B12 test had been requested and 139 anemic patients. We investigated the associations between the levels of homocysteine (Hcy) and those of holoTC, serum vitamin B12, and folate and assessed the diagnostic value of holoTC levels as a marker for vitamin B12 deficiency. We also determined the precision of the AxSYM holoTC assay by calculating the coefficient of variance (CV). The within-run and between-run precision values were excellent, as all CV values were less than 3.5%. The holoTC levels were low (<35 pmol/L) in 7 samples, and 6 of these samples had normal total serum vitamin B12 levels. In 2 of these samples, high Hcy levels (>12 micromol/L) indicated vitamin B12 deficiency. Thus, the holoTC levels were more sensitive than the serum vitamin B12 levels for indicating vitamin B12 status. If the serum vitamin B12 level is 151-300 pmol/L, the levels of holoTC alone or in combination with serum vitamin B12 levels are likely to be more useful markers than serum vitamin B12 levels alone.
Adult ; Aged ; Aged, 80 and over ; Analysis of Variance ; Biological Markers/blood ; Female ; Folic Acid/blood ; Homocysteine/blood ; Humans ; Male ; Middle Aged ; Transcobalamins/*analysis ; Vitamin B 12/*blood ; Vitamin B 12 Deficiency/diagnosis ; Young Adult