Polyneuropathy includes a lot of diseases damaging peripheral nerves. It shows roughly the same areas on both sides of the body, featuring weakness, numbness, and burning pain. Polyneuropathy is known to usually begin in the hands and feet and progress to the arms and legs. Sometimes it can involve other parts of the body such as the autonomic nervous system. Lots of causes can induce acute or chronic polyneuropathy, so finding the original cause is most important for the treatment of polyneuropathy. There are too many different types of polyneuropathies to be discussed in this review, so we will discuss some of various acquired polyneuropathies such as diabetic neuropathy, vasculitic neuropathy, alcoholic neuropathy, Vitamin B12 deficiency neuropathy, and drug-induced neuropathy, with special focus on symptoms, pathogenesis, diagnosis, treatment, and prognosis.
Alcoholic Neuropathy ; Arm ; Autonomic Nervous System ; Burns ; Diabetic Neuropathies ; Diagnosis* ; Foot ; Hand ; Hypesthesia ; Leg ; Peripheral Nerves ; Polyneuropathies* ; Prognosis* ; Vitamin B 12 Deficiency

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*

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

We evaluated the prevalence of vitamin B12 deficiency and associated factors in type 2 diabetes patients using metformin. A total of 799 type 2 diabetes patients using metformin was enrolled. Vitamin B12 and folate levels were quantified by chemiluminescent enzyme immunoassay. Vitamin B12 deficiency was defined as vitamin B12 < or = 300 pg/mL without folate deficiency (folate > 4 ng/mL). The prevalence of vitamin B12 deficiency in metformin-treated type 2 diabetes patients was 9.5% (n = 76), and the mean vitamin B12 level was 662.5 +/- 246.7 pg/mL. Vitamin B12 deficient patients had longer duration of metformin use (P < 0.001) and higher daily metformin dose (P < 0.001) than non-deficient patients. Compared with daily metformin dose of < or = 1,000 mg, the adjusted odds ratio for 1,000-2,000 mg, and > or = 2,000 mg were 2.52 (95% CI, 1.27-4.99, P = 0.008) and 3.80 (95% CI, 1.82-7.92, P < 0.001). Compared with metformin use of < 4 yr, the adjusted odds ratios for 4-10 yr, and > or = 10 yr were 4.65 (95% CI, 2.36-9.16, P < 0.001) and 9.21 (95% CI, 3.38-25.11, P < 0.001), respectively. In conclusion, our study indicates that patients with type 2 diabetes treated with metformin should be screened for vitamin B12 deficiency, especially at higher dosages (> 1,000 mg) and longer durations (> or = 4 yr) of treatment.
Aged ; Area Under Curve ; Diabetes Mellitus, Type 2/complications/diagnosis/*drug therapy ; Female ; Folic Acid/blood ; Humans ; Hypoglycemic Agents/adverse effects/*therapeutic use ; Immunoassay ; Male ; Metformin/adverse effects/*therapeutic use ; Middle Aged ; Odds Ratio ; Patients ; Prevalence ; ROC Curve ; Time Factors ; Vitamin B 12/blood ; Vitamin B 12 Deficiency/diagnosis/epidemiology/*etiology

<b>OBJECTIVEb>Combined methylmalonic acidemia with homocystinuria is a common form of methylmalonic acidemia in China. Patients with this disease can progress to death without timely and effective treatment. This study aimed to analyze the treatment outcomes of patients with combined methylmalonic acidemia and homocystinuria.

<b>METHODb>From September 2004 to April 2012, 58 patients with combined methylmalonic acidemia and homocystinuria (34 males and 24 females) were diagnosed and treated in our hospital. Fifty cases were from clinical patients including 42 early-onset cases and 8 late-onset cases. Their age when they were diagnosed ranged from 18 days to 30.8 years. The other 8 cases were from newborn screening. All the patients were treated with vitamin B12, betaine, folic acid, vitamin B6, and L-carnitine. The physical and neuropsychological development, general laboratory tests, the levels of amino acids, acylcarnitines, and homocysteine in blood, and organic acids in urine were followed up.

<b>RESULTb>The follow-up period ranged from 1 month to 7.1 years. Three cases died (all were early-onset cases). In the other patients after treatment, the symptoms such as recurrent vomiting, seizures, lethargy, and poor feeding disappeared, muscle strength and muscle tension were improved, and general biochemical abnormalities such as anemia and metabolic acidosis were corrected. Among the surviving 55 cases, 49 had neurological impairments such as developmental delay and mental retardation. The median levels of blood propionylcarnitine and its ratio with acetylcarnitine, serum homocysteine, and urine methylmalonic acid were significantly decreased (P < 0.01), from 7.73 µmol/L (ranged from 1.5 to 18.61 µmol/L), 0.74 (ranged from 0.29 to 2.06), 97.3 µmol/L (ranged from 25.1 to 250 µmol/L) and 168.55 (ranged from 3.66 to 1032.82) before treatment to 2.74 µmol/L (ranged from 0.47 to 12.09 µmol/L), 0.16 (ranged from 0.03 to 0.62), 43.8 µmol/L (ranged from 17 to 97.8 µmol/L) and 6.81 (ranged from 0 to 95.43) after treatment, respectively.

<b>CONCLUSIONb>Patients with combined methylmalonic acidemia and homocystinuria respond to a combined treatment consisting of supplementation of hydroxycobalamin, betaine, folic acid, vitamin B6 and L-carnitine with clinical and biochemical improvement. But the long-term outcomes are unsatisfactory, with neurological sequelae in most patients.

Adolescent ; Adult ; Amino Acid Metabolism, Inborn Errors ; blood ; diagnosis ; therapy ; Betaine ; administration & dosage ; therapeutic use ; Carnitine ; analogs & derivatives ; blood ; Child ; Child, Preschool ; Female ; Follow-Up Studies ; Homocystine ; blood ; Homocystinuria ; blood ; diagnosis ; therapy ; Humans ; Hydroxocobalamin ; administration & dosage ; therapeutic use ; Infant ; Infant, Newborn ; Male ; Methylmalonic Acid ; urine ; Neonatal Screening ; Treatment Outcome ; Vitamin B 12 ; administration & dosage ; therapeutic use ; Vitamin B 12 Deficiency ; congenital ; Young Adult

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

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

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*

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*