Normal Serum Vitamin B12 Levels Research Articles

Relationship of Serum Vitamin B12 and Serum Homocysteine Levels with Pseudo Exfoliation Syndrome

Objective: To evaluate the relationship of serum Vitamin B12 and serum Homocysteine levels with Pseudo Exfoliation Syndrome. Study Design: Cross-sectional study. Place and Duration of Study: Department of Ophthalmology, Armed Forces Institute of Ophthalmology, Rawalpindi Pakistan, from Jun to Nov 2022. Methodology: We included 55 individuals with unilateral Pseudo Exfoliation Syndrome without glaucoma and 50 healthy individuals as controls. All participants were subjected to the assessment of serum Homocysteine levels by high-performance liquid chromatography and Vitamin B12 levels by chemi-luminescent enzyme immunoassay. Results: Thirty-two (58.18%) individuals out of 55 with unilateral Pseudo Exfoliation Syndrome had increased serum Homocysteine levels (>5umol/L). Of these 32, 25(78.12%) individuals had moderately high serum Homocysteine levels, while 7(21.87%) had severely high serum Homocysteine levels. Twenty-six (47.27%) out of 55 individuals with Pseudo Exfoliation Syndrome had decreased serum Vitamin B12 levels, while the rest 29(52.72%) had normal-range serum Vitamin B12 levels. In comparison, 7(14%) had reduced serum Vitamin B12 levels, while the rest, 43(86%), had normal serum Vitamin B12 levels. Conclusion: Our study showed that raised Hcy levels were present in individuals with PXS without glaucoma and reduced serum Vitamin B12 levels. Assessment of Hcy level in individuals presenting with PXS may be undertaken as it is a known risk factor for vasuclopathies.

Nangs, balloons and crackers: Recreational nitrous oxide neurotoxicity.

Nitrous oxide is a colourless, odourless gas that has been used in medicine for more than 150 years for its anaesthetic and analgesic properties. Its first recorded use as a recreational drug was in early 19th century Britain at 'laughing gas parties', where it was used to provide short-lived euphoria to the bored upper class. A recent resurgence of its abuse among Australian youth has led to marked neurological morbidity. The aim of this article is to provide an overview of the clinical presentation, differential diagnosis, investigation and treatment of patients presenting with neurotoxicity due to recreational nitrous oxide abuse. Nitrous oxide exerts its neurotoxicity through vitamin B12 inactivation, which disrupts myelin sheath maintenance, leading to peripheral and central nervous system demyelination. Importantly, patients often present with non-specific sensorimotor signs and symptoms with normal serum vitamin B12 levels. Early recognition and treatment are crucial to limit long-term neurological sequelae.

Is serum vitamin B12 decrease a necessity for the diagnosis of subacute combined degeneration?: A meta-analysis.

To determine the prevalence of subacute combined degeneration (SCD) patients with normal or elevated serum vitamin B12 level and to identify clinical characteristics of these patients. We searched PubMed, EMBASE, and Cochrane library, without language restriction up to June 2019 and included studies with SCD patients who were diagnosed with normal or elevated serum vitamin B12 levels. Meta-analysis was performed to estimate the prevalence of SCD in patients with normal or elevated serum vitamin B12 levels and compare the differences of clinical data between patients with low and no-low serum vitamin B12 level. Six studies were included in our analysis, with a total number of 181 patients involved. The pooled proportion in patients with no-low serum vitamin B12 level was 31.0% (95% confidence interval [CI]: 22.5-40.8). There was no significant difference in the level of hemoglobin (Mean difference (MD): -3.05, 95% CI: -12.42 to 6.33. P = 0.52) and erythrocyte mean corpuscular volume (MD: -2.37, 95% CI: -11.17 to 6.43, P = 0.60) between SCD patients with no-low and those with low serum vitamin B12 levels. The meta-analysis showed that the functional disability rating scale on admission in patients with low serum vitamin B12 level was no worse than that with normal or elevated serum vitamin B12 level (MD: 0.29, 95% CI: -0.58 to 1.16, P = 0.51). Decreased level of serum vitamin B12 may not be a necessity for the diagnosis of SCD. Approximately one third of the SCD patients have normal or elevated serum vitamin B12 level. No differences were found in clinical severity between patients with normal or elevated serum vitamin B12 level and those with low level of serum vitamin B12 on admission.

118 Case series: subacute combined degeneration of the spinal cord in vitamin B12-replete recreational nitrous oxide abusers

IntroductionWithin a few years of its discovery in late 18th century, nitrous oxide was being used recreationally for its pleasurable effects. It remains in widespread use as an inhaled stimulant today, and can be legally acquired in bulk quantities with relative ease. In the body prolonged exposure to nitrous oxide leads to the oxidization of vitamin B12, rendering it unusable in key enzymatic reactions necessary for myelin synthesis. Over time this qualitative deficiency leads to a central demyelination syndrome that characteristically develops despite normal serum vitamin B12 levels and, with continued exposure to nitrous oxide, resists treatment with vitamin B12 supplementation.MethodNitrous oxide abusers presenting with a central demyelination syndrome were enrolled in this case series. Serum levels of vitamin B12, active B12, folate and homocysteine were measured. Nitrous oxide exposure was discontinued, and all patients were treated in accordance with evidence-based guidelines.ResultsEight patients presented with predominantly moderate-to-severe clinical deficits. The majority were vitamin B12 replete. In most cases individuals had actively engaged in prolonged vitamin B12 supplementation in an attempt to circumvent the harmful pathophysiology, of which they were loosely aware. Following treatment and rehabilitation several patients were discharged into full-time care, and most had significant residual disability at follow-up.ConclusionsThis case series not only illustrates the tragic consequences of abuse of this widely available and legally procured stimulant, but also highlights the futility of pursuing a nominally ‘protective’ strategy of vitamin B12 supplementation in the context of continued nitrous oxide exposure.

Sa1112 CT Attenuation Value of the Fluid Collection Site to Diagnose Infected Pancreatic Fistula After Distal Pancreatectomy

BACKGROUND: It is unclear whether serum vitamin B12 level accurately reflects its deficiency at the cellular level in the low normal range (200-400pg/ml). Serum homocysteine is a cheap, widely available and sensitive test (95.9%) which has been shown to be a reliable marker for cellular deficiency of vitamin B12. AIMS AND OBJECTIVES: To determine whether patients with low normal serum vitamin B12 levels have vitamin B12 deficiency at cellular level, using serum homocysteine as a surrogate marker MATERIALS AND METHOD: Consecutive patients attending Gastroenterology department at a tertiary care hospital in south India, and found to have serum vitamin B12 levels between 200 to 400 pg/ml, during the period from November 2009 to November 2010, were prospectively enrolled after informed consent. Patients were excluded if any of the following was present: age 1.4, serum folic acid 200pg/ml) and high performance liquid chromatography was used for serum homocysteine (normal<13μM). Data was analyzed using SPSS 16.0. The study was approved by the institutional review board. RESULTS: 50 participants (27male, 23female) with serum vitamin B12 level in low normal range(200-400pg/ml) were enrolled. 74% of the participants had hyperhomocysteinemia suggestive of cellular deficiency of vitamin B12. There was no significant correlation between serum levels of homocysteine and vitamin B12 in the study group (spearman correlation coefficient,r = -0.22, p=0.11). Further analysis was done after including 47 consecutive patients with vitamin B12 deficiency (serum vitamin B12 < 200pg/ml) which revealed a strong inverse correlation between serum vitamin B12 and serum homocysteine levels in patients with vitamin B12 deficiency, ie <200 pg/ml (Spearman correlation coefficient, r = -0.44, p<0.01), unlike the patients with low normal serum vitamin B12 levels, ie 200-400 pg/ml (figure 1). This suggests that serum vitamin B12 may not reflect its deficiency at celluar level, in the low normal range CONCLUSIONS: A majority of patients with low normal serum vitamin B12 levels (200-400pg/ml) have hyperhomocysteinemia, suggestive of vitamin B12 deficiency at cellular level. Serum homocysteine is a useful ancillary test to detect intracellular vitamin B12 deficiency in patients with low normal serum vitamin B12 levels and thereby identify a subgroup with potential benefit from vitamin B12 supplementation.

Sa1111 Serum Vitamin B12 Levels: Does it Reflect Cellular Deficiency of the Vitamin in Low Normal Range?

BACKGROUND: It is unclear whether serum vitamin B12 level accurately reflects its deficiency at the cellular level in the low normal range (200-400pg/ml). Serum homocysteine is a cheap, widely available and sensitive test (95.9%) which has been shown to be a reliable marker for cellular deficiency of vitamin B12. AIMS AND OBJECTIVES: To determine whether patients with low normal serum vitamin B12 levels have vitamin B12 deficiency at cellular level, using serum homocysteine as a surrogate marker MATERIALS AND METHOD: Consecutive patients attending Gastroenterology department at a tertiary care hospital in south India, and found to have serum vitamin B12 levels between 200 to 400 pg/ml, during the period from November 2009 to November 2010, were prospectively enrolled after informed consent. Patients were excluded if any of the following was present: age 1.4, serum folic acid 200pg/ml) and high performance liquid chromatography was used for serum homocysteine (normal<13μM). Data was analyzed using SPSS 16.0. The study was approved by the institutional review board. RESULTS: 50 participants (27male, 23female) with serum vitamin B12 level in low normal range(200-400pg/ml) were enrolled. 74% of the participants had hyperhomocysteinemia suggestive of cellular deficiency of vitamin B12. There was no significant correlation between serum levels of homocysteine and vitamin B12 in the study group (spearman correlation coefficient,r = -0.22, p=0.11). Further analysis was done after including 47 consecutive patients with vitamin B12 deficiency (serum vitamin B12 < 200pg/ml) which revealed a strong inverse correlation between serum vitamin B12 and serum homocysteine levels in patients with vitamin B12 deficiency, ie <200 pg/ml (Spearman correlation coefficient, r = -0.44, p<0.01), unlike the patients with low normal serum vitamin B12 levels, ie 200-400 pg/ml (figure 1). This suggests that serum vitamin B12 may not reflect its deficiency at celluar level, in the low normal range CONCLUSIONS: A majority of patients with low normal serum vitamin B12 levels (200-400pg/ml) have hyperhomocysteinemia, suggestive of vitamin B12 deficiency at cellular level. Serum homocysteine is a useful ancillary test to detect intracellular vitamin B12 deficiency in patients with low normal serum vitamin B12 levels and thereby identify a subgroup with potential benefit from vitamin B12 supplementation.

Poster Abstracts from the AAAP 20th Annual Meeting and Symposium

Poster Abstracts from the AAAP 20th Annual Meeting and Symposium

Relationship between the Levels of Holotranscobalamin and Vitamin B12

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.

Poliklinik Hastalarında Vitamin B12 Eksikliği ve Özellikleri

Objective: The aim of this study is to evaluate the properties of vitamin B12 deficiency and predisposing factors in the patients of an outpatient clinic. Material and Methods: Four hundred patients with vitamin B12 deficiency were studied. Anthropometric measures, biochemical analysis, gastric parietal cell antibodies and parasites in stool of the patients, antigliadin antibody survey and upper gastrointestinal system endoscopy were performed. Additionally, randomly selected 100 patients with low and 100 healthy subjects with normal serum vitamin B12 levels were questioned about food intake. Results: Overall ratio of vitamin B12 deficiency among outpatients was 4%. Coexisting diseases such as diabetes mellitus (12.3%), hypertension (42.0%), hyperlipidemia (42.0%) and obesity (42.0%) were determined. Nearly a quarter (22,8%) had autoimmune thyroid disease. A group of patients had other problems that may have caused malabsorption such as Helicobacter pylori gastritis (66/85= 77.6%), antigastric parietal cell antibody positivity (37/85= 43.5%), antigliadin antibody positivity (40/61= 65.6%), and others (3.3%). The patient group with vitamin B12 deficiency consumed significantly less meat (p< 0.001), chicken (p< 0.001), fish (p= 0.002), milk (p= 0.027) and eggs (p< 0.001), smaller number of meals (p= 0.013) and significantly higher amounts of fiber (p< 0.001) and vegetables (p= 0.037) when compared with the control group. Conclusion: Vitamin B12 deficiency was considered to be related mainly with improper and defective alimentation. However, malabsorption-related diseases may also contribute to vitamin B12 deficiency.

Retinopathy in Inherited Transcobalamin II Deficiency

Transcobalamin II (TCII) is a primary plasma protein that binds vitamin B12 and facilitates its cellular uptake by many tissues.1 Inherited deficiency of TCII is a rare autosomal recessive disorder that results in severe megaloblastic anemia in early infancy despite normal serum vitamin B12 levels.

A Complex Pattern of Melanonychia and Onycholysis After Treatment With Pemetrexed for Lung Cancer

A 53-year-old black man was diagnosed with poorly differentiated adenocarcinoma of the lung and treated initially with 4 cycles of paclitaxel in combination with carboplatin and external-beam radiation therapy with a good clinicoradiologic response. The patient tolerated the chemotherapy well and did not develop any skin or nail changes during that period of time. His lung cancer recurred 10 months later, when he was found to have bone metastases. Second-line chemotherapy with pemetrexed 500 mg/m2 intravenously every 3 weeks was commenced. A week prior, the patient was started on folic acid 1 mg orally daily and given an injection of vitamin B12 1000 microg intramuscularly that was continued every 3 cycles thereafter. Dexamethasone 4 mg orally twice daily was given around the time of chemotherapy administration to prevent the dermatitis associated with the drug. The patient denied taking other drugs. Two months into his second-line chemotherapy, he developed multiple, concomitant, transverse and longitudinal black lines in all of his fingernails and toenails. After an interval of 3 months, he presented a complex pattern of nail hyperpigmentation, from combined dense horizontal and longitudinal streaks in some nails to diffuse black discoloration in others (Figure). Other associated changes included koilonychia, dystrophy, and friability of nail plates. Along with normal results of a hepatorenal panel and normal serum vitamin B12 and folate levels, no metabolic or endocrinologic alterations were present to explain the nail pigmentation and dystrophic changes. Results of his mycologic examination and cultures came back negative. When questioned, he denied taking any other drugs including other alternative medicine approaches or vitamin supplements, particularly retinoids, well known for causing severe nail dystrophy.

Rheumatoid arthritis, Pyrexia of Unknown Origin (PUO) and pancytopenia

A 61-yr-old previously fit lorry driver was referred by his general practitioner in October 1999 to an orthopaedic clinic with a 6-month history of painful hands, shoulders and feet. His general practitioner had treated him with ibuprofen without much improvement. He admitted to a recent history of loss of appetite with loss of two stones (12.7 kg) in weight. His joint pains had been increasing in severity with visible swelling of his fingers and knees. He had no relevant family history. He was an ex-smoker and drank little alcohol. Physical examination revealed a healthy-looking man with signs of synovitis in the symptomatic joints. The orthopaedic surgeon referred him to the rheumatologist (K.C.). The preliminary blood tests showed haemoglobin of 10.4 g/dl with normal haematocrit, leucocyte and platelet counts and normal serum vitamin B12 and red-cell folate levels. His serum ferritin was 468 g/l (normal range 18–400 g/l). He also had transient random hyperglycaemia, which was followed by a normal glucose tolerance test. His rheumatoid factor was elevated at 1:2560. His chest X-ray was normal except for some thickening of the bronchiolar wall. He was seen in the rheumatology clinic 2 months later, in December 1999, with classical symptoms and signs of a symmetrical inflammatory polyarthritis suggestive of rheumatoid disease. His knees were drained and injected with methyl prednisolone and local anaesthetic. He was also given intramuscular methyl prednisolone (120mg) to induce remission of active disease. Investigations revealed haemoglobin 10.3 g/dl, white cell count 6.4 10/l, platelet count 449 l0/l and ESR of 100mm in the first hour. The biochemical screens were all normal, including liver, renal and bone panels. The rheumatoid factor was 2460 IU (normal range 30 IU) and CRP was elevated at 85.1mg/dl (normal range <10mg/dl). The X-rays of his hands and feet showed no obvious erosions. The option of commencing methotrexate as a second-line drug was discussed but he preferred to wait until he returned from a planned Christmas holiday in Spain. Soon after his return from holiday he developed sudden severe cramp-like pains associated with numbness in his legs. He was virtually unable to walk. An MRI scan of his whole spine was done on the advice of the neurosurgeons, and, as the scans were normal, he was referred to the neurologists, who performed a lumbar puncture to exclude acute infective polyneuritis. The neurologists also noted a skin rash on his legs associated with left foot drop (Fig. 1). An autoimmune disease was suspected and the rheumatologist (K.C.) was consulted. On examination he had a vasculitic rash with peripheral neuropathy. There was no lymphadenopathy or organomegaly. Given the recent diagnosis of seropositive rheumatoid arthritis (RA), systemic rheumatoid vasculitis (SRV) seemed to be the most plausible diagnosis. Investigations at this time revealed haemoglobin 9.0 g/dl, white cell count 12.1 10/l and neutrophils 9.6 10/l with normal platelet and lymphocyte count. The ESR was 110mm in the first hour and CRP was 121mg/dl (normal range <5mg/dl). The biochemical, serological and microbiological screens including hepatitis A, B and C were all normal/negative. His anti nuclear antibodies, anti DNA antibodies, extractable nuclear antigens, anti cardiolipin antibodies, anti neutrophil cytoplasmic antibodies and cryoglobulins were all negative. Echocardiogram was normal. A cerebrospinal fluid study showed a mild increase in cerebrospinal fluid protein but no oligoclonal band or albumino-cytological dissociation. Electromyography showed severe sensorimotor polyneuropathy of the axonal type with some denervation changes in the peroneal muscles. A skin biopsy confirmed active necrotizing vasculitis, consistent with SRV (Fig. 2). He was commenced on pulse intravenous methyl prednisolone (500mg) and cyclophosphamide (500mg) with some symptomatic improvement, and was discharged home on a 2-weekly regime.

Relationship of Normal Serum Vitamin B12 and Folate Levels to Cognitive Test Performance in Subtypes of Geriatric Major Depression

This retrospective study evaluated the relationships between normal serum vitamin B12 and folate levels and neuropsychologic measures in a sample of 60 geriatric inpatients with psychotic depression, nonpsychotic depression, bipolar disorder, and dementia--all consecutively referred for cognitive testing. The psychotic depression subgroup demonstrated numerous significant positive correlations between B12 and cognitive subtests not seen in other diagnostic subgroups, especially those of IQ, and verbal and visual memory. Metabolic factors including vitamin B12 may play specific roles in the cognitive dysfunctions of different geropsychiatric disorders.

Folate-responsive neuropathy: report of 10 cases.

Ten patients with severe neurological disease that was clinically indistinguishable from subacute combined degeneration of the spinal cord were found to have normal serum vitamin B12 levels. All were folate deficient. Specific folate treatment led to significant reversal of the neuropathy. These findings indicate the need to review orthodox concepts of the role of folic acid in maintaining the integrity of the nervous system.

Observations on the incidence and cause of macrocytosis in patients on azathioprine therapy following renal transplantation.

A high mean corpuscular volume (MCV) was found in 74% of a group of 69 patients with functioning renal allografts. All 69 patients had normal red cell folate and serum vitamin B12 levels and normal liver function tests. A study of marrow aspirates from 28 of these patients, with MCV values ranging between 87 and 129 fl, indicated that all the patients with a high MCV and several of the patients with a normal MCV had megaloblastie erythropoiesis. Deoxyuridine suppression tests were performed on the marrow cells from 20 patients and showed no impairment in the conversion of deoxyuridylate to thymidylate. It was concluded that the macrocytosis encountered in patients with renal grafts was usually caused by therapy with azathioprine and not by folate deficiency or interference with folate metabolism. There was no correlation between renal function and the MCV in patients with creatinine clearance values between 35 and 149 ml/min.

Letter: Thrombocytopenia and iron deficiency.

Letters1 January 1974Thrombocytopenia and Iron DeficiencyDAVID SONNEBORN, PH.D.DAVID SONNEBORN, PH.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-80-1-111 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The platelet count in iron-deficiency anemia is typically elevated. Severe iron deficiency may cause thrombocytopenia (1, 3); this has been shown in children (4). We have been unable to discover any report of low platelets associated with iron-deficiency anemia in an adult. The response to iron in an adult with a severe iron-deficiency anemia and thrombocytopenia but with normal serum folate and vitamin B12 levels is described below; an apparent case of iron-deficiency thrombocytopenia.A 31-year-old black women presented to the emergency room with flank pain and hematuria of 1 month's duration. For the previous year she...