Cobalamin Deficiency In Patients Research Articles

A Brief Review on the Association of Prolonged Metformin Therapy and Vitamin B12 Deficiency

Type 2 Diabetes Mellitus is a fast-growing health challenge, signaled by hyperglycemia. There are two types of diabetes mellitus, Type 1 and Type 2; both are equally life threatening condition. Type 1 diabetes is a persistent autoimmune disease as a consequence of insulin deficiency, whereas in Type 2 diabetes the body either does not produce enough insulin or develops resistance to insulin. Metformin is the exclusive pharmacologic management for Type 2 diabetes mellitus and frequently prescribed drug either single or in combination with insulin or other hypoglycemic agents. Metformin has immensely improved insulin sensitivity and defend against vascular complications. Vitamin B 12 (cobalamin) has a vital role in DNA synthesis, cellular metabolism and the deficiency will lead to megaloblastic anemia. Several studies state that metformin can cause cobalamin deficiency in doses greater than 2000 mg/ day and for a time period of more than 4 years. Hence, cobalamin and calcium supplementation will reduce the occurrence of cobalamin deficiency in patients with metformin therapy. Keywords: Type 2 diabetes mellitus, Metformin, Vitamin B 12, Vitamin B 12 deficiency, Cobalamin.

The prevalence of gastrointestinal symptoms and cobalamin deficiency in patients with chronic urticaria

BackgroundThere is a paucity of studies reporting the presence of systemic symptoms and micronutrient deficiency in patients with chronic urticaria, and these data are lacking in a Canadian population.ObjectiveTo report the prevalence of gastrointestinal symptoms and vitamin B12 (cobalamin) deficiency in a Canadian patient population diagnosed with chronic urticaria.MethodsA retrospective chart review of 100 adult patients with chronic urticaria was conducted. Demographic characteristics, medications, presence of gastrointestinal symptoms, and laboratory findings were abstracted from electronic medical records.ResultsSeventy percent of patients with chronic urticaria reported experiencing gastrointestinal symptoms. The most common symptom identified was gastroesophageal reflux (42%). Vitamin B12 (cobalamin) deficiency, defined as serum vitamin B12 level ≤ 250 pmol/L, was identified in 31.7% of the patients. Among those patients with urticaria and vitamin B12, 68% reported gastrointestinal symptoms.ConclusionsThis is the first study to provide data on the high prevalence of gastrointestinal symptoms and vitamin B12 (cobalamin) deficiency in a Canadian population diagnosed with chronic urticaria. Early recognition and management of systemic symptoms and micronutrient deficiency may lead to a more comprehensive approach to management of these patients.Trial registration Not applicable

Relationship between cobalamin deficiency and delirium in elderly patients undergoing cardiac surgery.

BackgroundDelirium is common after cardiac surgery and is independently associated with increased morbidity, mortality, prolonged hospital stays, and higher costs. Cobalamin (vitamin B12) deficiency is a common cause of neuropsychiatric symptoms and affects up to 40% of elderly people. The relationship between cobalamin deficiency and the occurrence of delirium after cardiac surgery has not been examined in previous studies. We examined the relationship between cobalamin deficiency and delirium in elderly patients undergoing coronary artery bypass grafting (CABG) surgery.Material and methodsA total of 100 patients with cobalamin deficiency undergoing CABG were enrolled in this retrospective study. Control group comprised 100 patients without cobalamin deficiency undergoing CABG. Patients aged 65 years or over were included. Diagnosis of delirium was made using Intensive Care Delirium Screening Checklist. Delirium severity was measured using the Delirium Rating Scale-revised-98.ResultsPatients with cobalamin deficiency had a significantly higher incidence of delirium (42% vs 26%; P=0.017) and higher delirium severity scores (16.5±2.9 vs 15.03±2.48; P=0.034) than patients without cobalamin deficiency. Cobalamin levels were significantly lower in patients with delirium than patients without delirium (P=0.004). Delirium severity score showed a moderate correlation with cobalamin levels (ρ=−0.27; P=0.024). Logistic regression analysis demonstrated that cobalamin deficiency was independently associated with postoperative delirium (OR 1.93, 95% CI 1.03–3.6, P=0.038).ConclusionThe results of our study suggest that cobalamin deficiency may be associated with increased risk of delirium in patients undergoing CABG. In addition, we found that preoperative cobalamin levels were associated with the severity of delirium. This report highlights the importance of investigation for cobalamin deficiency in patients undergoing cardiac surgery, especially in the elderly.

Laboratory testing for cobalamin deficiency in megaloblastic anemia

Cobalamin (vitamin B12) deficiency is a common cause of megaloblastic anemia in Western populations. Laboratory evaluation of megaloblastic anemia frequently includes the assessment of patient cobalamin and folate status. Current total serum cobalamin measurements are performed in the clinical laboratory with competitive binding luminescence assays, whose results may not always accurately reflect actual cobalamin stores. Surrogate markers of cobalamin deficiency such as methylmalonic acid and homocysteine have been utilized to improve diagnostic accuracy; however, the specificity of these tests by themselves is rather low. Measurement of the biologically active fraction of cobalamin, holotranscobalamin, has been proposed as a replacement for current total cobalamin assays. Although holotranscobalamin measurements appear to have slighter better sensitivity, the specificity of this assay remains to be determined. The relative merits and demerits of commonly available methods to assess cobalamin deficiency in patients with suspected megaloblastic anemia are discussed.

Macrocytosis and Cobalamin Deficiency in Patients Treated with Sunitinib

To the Editor: Sunitinib malate is a multitargeted tyrosine kinase inhibitor approved for the treatment of advanced renal-cell carcinoma. We report on an asymptomatic increase in the mean corpuscular volume of erythrocytes and cobalamin deficiency in six patients with metastatic renal-cell carcinoma who were treated for more than 5 months with sunitinib as part of a clinical trial evaluating the efficacy and safety of continuous daily administration of the drug. The starting dose of sunitinib was 37.5 mg daily; three patients required a dose reduction to 25 mg, and one patient had a dose escalation to 50 mg daily. An . . .

Cobalamin Profiles In Patients After Urinary Diversion

We assessed the risk of tissue cobalamin (vitamin B12) deficiency in patients after various types of urinary diversion. Serum vitamin B12, methylmalonic acid and homocysteine were measured in 41 patients with urinary diversion, including an ileal neobladder in 12, ileal reservoir in 2, ileocecal reservoir in 10 and ileal conduit in 17. Followup was 0 to 10 years. The complete cobalamin profiles revealed a much higher incidence of tissue cobalamin deficiency in patients with each type of urinary diversion than measuring the vitamin B12 level alone. The risk of chronic tissue cobalamin deficiency after urinary diversion is higher than previously reported based on measuring serum vitamin B12 alone. Long-term patient monitoring for cobalamin deficiency or empirical supplemental therapy is indicated to prevent clinical cobalamin deficiency and irreversible sequelae.

Metabolic cobalamin deficiency in patients with low to low-normal plasma cobalamins

Over a 2-year period, we examined 48 patients with P-cobalamin levels in the difficult “grey zone” at the lower reference limit detected by a competitive protein binding assay using intrinsic factor as binder. In 21 of 30 patients (70%) with low P-cobalamins we could not establish the diagnosis of metabolic cobalamin deficiency, but 1 of 18 patients (6%) with low-normal P-cobalamin values was confirmed metabolically cobalamin-deficient. Half of these 30 patients with low P-cobalamins had neuropsychiatric disorders, but only one-third of the latter patients had metabolic cobalamin deficiency. Ten of the remaining 15 patients (67%) were characterized as non-deficient. In patients with low-normal P-cobalamin level, we found neuropsychiatric disorders in 5 of the 18 (28%), but none of these had metabolic cobalamin deficiency. We conclude that P-cobalamins below the reference interval combined with typical neuropsychiatric symptoms or findings are not diagnostic of cobalamin deficiency and that further analyses are necessary