Manifestation Of Vitamin B12 Deficiency Research Articles

Vitamin B12 Deficiency Masquerading as Clozapine-Resistant Psychotic Symptoms in Schizophrenia

Vitamin B₁₂ Deficiency Masquerading as Clozapine-Resistant Psychotic Symptoms in Schizophrenia

Brief Report: Childhood Disintegrative Disorder as a Likely Manifestation of Vitamin B12 Deficiency

Childhood disintegrative disorder is a rare disorder, characterized by regression of acquired skills after a period of normal development. The case of childhood disintegrative disorder presented here was found to have vitamin B12 deficiency and hyperhomocysteinemia on extensive evaluation to find a probable cause for regression. This case illustrates the need for a thorough evaluation of all cases of childhood disintegrative disorder so that treatable causes of regression, like vitamin B12 deficiency, are not missed.

Evaluation of Vitamin B12 Monitoring in a Veteran Population on Long-Term, High-Dose Metformin Therapy

Metformin can result in vitamin B(12) deficiency, potentially leading to complications such as neuropathy. Annual monitoring of vitamin B(12) has been suggested; however, it is unknown whether current practice reflects this recommendation. To identify vitamin B(12) monitoring patterns in patients on long-term, high-dose metformin. Secondary objective was to determine the frequency of new vitamin B(12) deficiency, anemia, and neuropathy documented after initiation of high-dose metformin. Electronic medical records of veterans treated at the Veterans Affairs Maryland Healthcare System with high-dose metformin (≥2000 mg/day) as of November 1, 2010, were reviewed. Data regarding metformin treatment, vitamin B(12) measurements, and documentation of vitamin B(12) deficiency, cyanocobalamin supplementation, anemia, and neuropathy were collected. Subjects treated with metformin for less than 1 year or those with documented peripheral neuropathy, megaloblastic anemia, vitamin B(12) deficiency, or a condition associated with vitamin B(12) malabsorption prior to metformin initiation were excluded. Subjects (N = 235) had a mean metformin dose of 2050 mg/day and mean duration of treatment of 5.2 years. Sixty percent did not have vitamin B(12) measured. Of subjects receiving metformin for 10 years or more, nearly half (46%) never had vitamin B(12) measured. New documentation of vitamin B(12) deficiency or cyanocobalamin supplementation was found in 5.5% of the population, and anemia was found in 12%. Of the 14% with new neuropathy, 42% did not have vitamin B(12) measured. Vitamin B(12) was not routinely monitored in patients on high-dose metformin, even in those at highest risk (≥10 years of therapy), or in those with potential manifestations of vitamin B(12) deficiency (neuropathy). Cases of vitamin B(12) deficiency and resulting anemia or neuropathy may be undiagnosed and untreated because of lack of monitoring. Prospective studies examining the effect of increased vitamin B(12) monitoring on identification and treatment of vitamin B(12) deficiency in patients on metformin are warranted.

P.3.e.006 Sudden onset of psychosis as the sole manifestation of vitamin B12 deficiency

Human papillomavirus (HPV) has been shown to represent a major independent risk factor for head and neck squamous cell cancer, in particular for oropharyngeal carcinoma. This type of cancer is rapidly evolving in the Western world, with rising trends particularly in the young, and represents a distinct epidemiological, clinical, and molecular entity. It is the aim of this review to give a detailed description of genomic, epigenomic, transcriptomic, and posttranscriptional changes that underlie the phenotype of this deadly disease. The review will also link these changes and examine what is known about the interactions between the host genome and viral genome, and investigate changes specific for the viral genome. These data are then integrated into an updated model of HPV-induced head and neck carcinogenesis.

Psychotic disorder, hypertension and seizures associated with vitamin B12 deficiency: a case report

This report highlights a rare presentation of vitamin B(12) deficiency (concurrent psychotic disorder, seizures and hypertension). A 16-year-old girl presented with nervousness that had been persisting for 2 weeks. She had stopped eating and there was decreased self-care and she could not walk and sleep. Two days prior to admission, generalized tonic-clonic convulsions were noted. On physical examination, vital signs were normal, except for hypertension (150/100 mm Hg). She did not respond to conversation; she could not answer the questions. Mood was depressive and hallucinations were noted. Laboratory analyses were normal, except for a low vitamin B(12) level (<150 pg mL(-1)). The patient was not given any treatment of hypertension, psychosis or seizures, except vitamin B(12) injections. After that, she showed improvement within 1 week. In the 7 days of hospitalization, the arterial blood pressure returned to normal, psychotic symptoms were resolved, the visual hallucinations and the depressive mood subsided, and she could eat and speak clearly. No hypertension or convulsions have been detected on the control examinations, and she has now been followed-up without any symptoms or findings. In conclusion, with this report we emphasized that psychosis, seizures and hypertension can be a rare manifestation of vitamin B(12) deficiency, which is reversible with therapy and serum vitamin B(12) level should be checked in patients who do not have an obvious cause for psychosis, seizures or hypertension.

Nutritional B12 Deficiency in Infants of Vitamin B12-Deficient Mothers

Nutritional vitamin B₁₂ deficiency in infants may occur because the maternal diet contains inadequate animal products. Clinical presentations of the infants who had nutritional vitamin B₁₂ deficiency were analyzed in this study. Patients with nutritional vitamin B₁₂ deficiency were enrolled in the study between 2003 and 2010. The diagnosis was based on a nutritional history of mothers and infants, clinical findings, hematological evaluation, and low level of serum vitamin B₁₂. Thirty children aged 1 - 21 months constituted the study group. Poverty was the main cause of inadequate consumption of animal products of the mothers. All infants had predominantly breastfed. The most common symptoms were developmental delay, paleness, apathy, lethargy, anorexia, and failure to thrive. Hematological findings were megaloblastic anemia (83.3 %), thrombocytopenia (30 %), and severe anemia (13.3 %). All of the mothers had low serum B₁₂ levels; eight of them had megaloblastic anemia. The unusual clinical manifestations of vitamin B₁₂ deficiency may also be seen apart from neurological and hematological findings. Nutritional vitamin B₁₂ deficiency due to maternal deficiency might be a serious health problem in infants. Therefore, screening and supplementation of pregnant and lactating women to prevent infantile vitamin B₁₂ deficiency should be considered.

Vitamin B12 deficiency: an unusual cause of vocal fold palsy

We report an extremely rare case of vocal fold palsy secondary to vitamin B12 deficiency. Case report and English-Language review of the world literature concerning vitamin B12 deficiency and its neurological manifestations. We discuss the physiological role of vitamin B and its specific relationship to the presented patient's symptoms. We describe a rare instance of a patient presenting with bilateral lower limb weakness and unilateral vocal fold palsy, as a manifestation of vitamin B12 deficiency. Quick recognition and treatment resulted in a full recovery. To our knowledge, this is the first reported case of unilateral vocal fold palsy secondary to vitamin B12 deficiency. Central and peripheral neuropathies have been described; however, other than the optic nerve, the cranial nerves are very rarely affected. It is important to consider vitamin B12 deficiency as a cause, as speedy identification and treatment can help prevent permanent neurological damage.

Negative symptoms presenting as neuropsychiatric manifestation of vitamin B12 deficiency

Long lists of psychiatric illness or symptoms have been documented to be caused by vitamin B12 deficiency. We describe an atypical case of a young adult who presented with predominant negative symptoms followed by neurological symptoms consistent with vitamin B12 deficiency. The symptoms showed complete remission after vitamin B12 supplementation. The uniqueness of this case is that vitamin B12 deficiency presented with predominant negative symptoms without other psychotic and manic symptoms, which has not been reported previously.

Acute presentation of dizziness in vitamin B12 deficient old patient of cardiac disease: A case report

Background Neuropsychiatric and hematogical manifestations of vitamin B12 deficiency are well known. The present report highlights the biochemical basis for the impaired synthesis of DNA and neurological disorders associated with vitamin B12 deficiency. Methods We present a case of an old patient who developed acute ataxia, dizziness and imbalance 2 days after pacemaker implantation in a cardiac care unit . Results On evaluation, the patient was found to have low vitamin B12 levels (121 pmol/l) with raised plasma homocysteine levels (28 μmol/l) and methylmalonic acid levels (17 μmol/l). Neurological examination revealed signs and symptoms of peripheral neuropathy. CT scan of the brain was found to be normal. The usual hematological presentation was absent in this case. The patient responded dramatically to parenteral vitamin B12 supplementation. Conclusion Though frequent, the vitamin B12 deficiency often goes unnoticed in elderly population. So, with this report we emphasize that deficiency of serum vitamin B12 levels should be suspected and evaluated in elderly patients presenting with neuropsychiatric symptoms.

Vitamin B12 deficiency presenting with Myeloneuropathy

The neurologic manifestations of vitamin B12 deficiency, although uncommon, are the result of its effects on the brain, optic nerves, peripheral nerves, and spinal cord. Myeloneuropathy, resulting in sensory disturbances, weakness, and spasticity, is known as subacute combined degeneration and primarily involves the dorsal, and lateral spinal columns as well as the peripheral nerves. Subacute combined degeneration is treatable and the symptoms are potentially reversible if detected at an early stage. We present the clinical as well as the laboratory findings in a patient with subacute combined degeneration who had resolution of the clinical neurological manifestations with B12 therapy.

Rare sensory and autonomic disturbances associated with vitamin B12 deficiency

Vitamin B12 deficiency is an important nutritional disorder causing neurological manifestations of myelopathy, neuropathy and dementia. Sub-acute combined degeneration (SCD) with involvement of the posterior columns in the cervical and thoracic cord is a common presentation of this disorder. In this case report, we describe a 43 year old woman with pernicious anemia and myelopathy with atypical clinical features. The patient presented with motor symptoms, a sensory level and bladder dysfunction. She had severe autonomic disturbances including an episode of unexplained bronchospasm, which has not been previously reported as a manifestation of vitamin B12 deficiency. We review the literature regarding these rarely reported features of vitamin B12 deficiency, and discuss aspects of management of this reversible condition. We emphasize the importance of awareness of autonomic disturbances in B12 deficient individuals.

Sub-acute combined degeneration with an initially normal level of vitamin B12: a case report

IntroductionThe neurological manifestation of vitamin B12 deficiency can occur as a result of peripheral nerve pathology or lateral and posterior column involvement, also known as “sub-acute combined degeneration”. This case report demonstrates an unusual presentation of SCD with normal B12 level.Case presentationA 39-year-old man was referred to the outpatient neurology clinic with a two month history of distal upper extremities numbness and fine motor movement difficulties. Initial vitamin B12 level was normal. A repeat MR imaging of the cervical and thoracic spine showed extensive posterior cervical cord flame-shaped lesions. His repeat vitamin B12 level was 41 pg/ml (normal; 200 ph/ml). He received monthly injections of vitamin B12. After six months his symptoms were resolved and his repeat spinal MRI showed resolution of the previous lesions.ConclusionWe recommend that every patient presenting with numbness and lesions on a spinal MR imaging should have their vitamin B12 level checked.

MRI Diagnosis Of Subacute Combined Degeneration Of Spinal Cord

Neurological manifestations of vitamin B12 deficiency are less common compared to hematological manifestations.Subacute combined degeneration of cord (SACD) is a neuropathologic manifestation of vitamin B12 deficiency characterized by loss of posterior column functions and lower limb weakness. Earlier, the diagnosis was based largely on clinical findings. With the advent of finer neuroimaging technique like MRI, it is possible to define the exact area involved. We report a case of SACD with MRI evidence of spinal cord involvement.

Nitrous oxide “Whippit” abuse presenting with cobalamin responsive psychosis

Nitrous oxide is a commonly abused inhalant drug. It is known to precipitate vitamin B12 deficiency when used chronically and acutely, especially in people having marginal vitamin B12 reserve. We are presenting a case of nitrous oxide "whippit" abuse in a thirty-three-year-old male with bizarre behavior and delusions. The patient had low normal levels of vitamin B12 (202 pg/ml), but he had markedly high methylmalonyl CoA (1078 nmol/L) and homocysteine (48.4 mcmol/L). Treatment with intramuscular cobalamin led to a resolution of his psychosis. This case report highlights the need to consider vitamin B12 deficiency in patients who arrive at a hospital with psychiatric manifestations and who report having a history of nitrous oxide exposure or abuse in the recent or remote past. A review of the literature on the neuropsychological manifestations of vitamin B12 deficiency is provided.

Initial diagnosis of vitamin B12 deficiency by sore mouth and assessment of the red blood cell distribution width, mean corpuscular volume, and hemoglobin level ── a preliminary study

The oral manifestations of glossodynia, glossitis, and stomatitis in vitamin B12 deficiency have long been recognized. These oral changes may occur in the preanemic stage. The aim of this paper was to study the red blood cell distribution width (RDW), mean corpuscular volume (MCV), and hemoglobin (Hb) level in 34 patients with a wide range of oral symptoms and signs as the initial manifestations of vitamin B12 deficiency. Of the 34 patients, 29 were normal to mildly anemic, and 5 were moderately to severely anemic; none had generalized symptoms sufficient to arouse suspicion of micronutrient deficiency or anemia before they visited the Oral Medicine Clinic. Nine (26.4%) of the 34 patients had normal RDWs and 8 (88.9%) of these 9 patients also had normal MCVs. Overall, 13 (38.2%) of the 34 patients had normal MCVs and 3 (8.8%) had low MCVs. Our findings indicate that the classic presentation of macrocytic heterogeneous anemia in vitamin B12 deficiency does not hold true in a large proportion of cases, and the increase of RDW is not necessarily the earliest indicator of vitamin B12 deficiency. Therefore, a diagnosis of vitamin B12 deficiency should be considered even in patients with normal Hb levels and low or normal MCVs. Nevertheless, the combined increase in the RDW and MCV in patients with a sore mouth is still a useful indicator of possible vitamin B12 deficiency after folate deficiency and chronic diseases have been ruled out.

Glossodynia as an Unusual Manifestation of Vitamin B12 Deficiency -A case report-

Glossodynia as an Unusual Manifestation of Vitamin B12 Deficiency -A case report-

Mielopatía por déficit de vitamina B12: caracterización clínica de 11 casos

Subacute combined degeneration is a clinical manifestation of vitamin B12 deficiency, that we observe with unusual frequency. To report a series of eleven patients with subacute combined degeneration. Retrospective analysis of 11 patients hospitalized in a public hospital in Santiago, between March 2001 and February 2003. All had a myelopathy of more than three weeks of evolution with serum vitamin B12 levels of less than 200 pg/ml. A risk factor was identified in 10 cases and the most common was an age over 60 years old. The main presenting symptom was the presence of paresthesias. On admission, sphincter dysfunction, posterior column and pyramidal syndromes coexisted in nine patients. A level of sensitive deficit was detected in six. Ten patients had macrocytosis and eight were anemic. Serum vitamin B12 was measured in ten and in nine, it was below 200 pg/ml. The mean lapse between onset of symptoms and treatment was eight months. All received intramuscular vitamin B12 in doses on 1,000 to 10,000 IU/day. Sphincter dysfunction and propioception were the first symptoms to improve. Subacute combined degeneration must be suspected in patients older than 60 years with a subacute myelopathic syndrome and low serum vitamin B12 levels.

A comprehensive evaluation of food fortification with folic acid for the primary prevention of neural tube defects.

BackgroundPericonceptional use of vitamin supplements containing folic acid reduces the risk of a neural tube defect (NTD). In November 1998, food fortification with folic acid was mandated in Canada, as a public health strategy to increase the folic acid intake of all women of childbearing age. We undertook a comprehensive population based study in Newfoundland to assess the benefits and possible adverse effects of this intervention.MethodsThis study was carried out in women aged 19–44 years and in seniors from November 1997 to March 1998, and from November 2000 to March 2001. The evaluation was comprised of four components: I) Determination of rates of NTDs; II) Dietary assessment; III) Blood analysis; IV) Assessment of knowledge and use of folic acid supplements.ResultsThe annual rates of NTDs in Newfoundland varied greatly between 1976 and 1997, with a mean rate of 3.40 per 1,000 births. There was no significant change in the average rates between 1991–93 and 1994–97 (relative risk [RR] 1.01, 95% confidence interval [CI] 0.76–1.34). The rates of NTDs fell by 78% (95% CI 65%–86%) after the implementation of folic acid fortification, from an average of 4.36 per 1,000 births during 1991–1997 to 0.96 per 1,000 births during 1998–2001 (RR 0.22, 95% CI 0.14–0.35). The average dietary intake of folic acid due to fortification was 70 μg/day in women aged 19–44 years and 74 μg/day in seniors. There were significant increases in serum and RBC folate levels for women and seniors after mandatory fortification. Among seniors, there were no significant changes in indices typical of vitamin B12 deficiencies, and no evidence of improved folate status masking haematological manifestations of vitamin B12 deficiency. The proportion of women aged 19–44 years taking a vitamin supplement containing folic acid increased from 17% to 28%.ConclusionsBased on these findings, mandatory food fortification in Canada should continue at the current levels. Public education regarding folic acid supplement use by women of childbearing age should also continue.

Catatonia and other psychiatric symptoms with vitamin B12 deficiency

To study unusual psychiatric manifestation of vitamin B12 deficiency and related issues. A case study of 52-year-old female and review of relevant literature. Complete remission of psychiatric symptoms without recurrence for the next 4 years with vitamin B12 as the only specific therapy instituted. Importance of B12 estimation and replacement in patients with varied psychiatric manifestations.

Prevention of Neural Tube Defects by Periconceptional Use of Folic Acid

Prevention of Neural Tube Defects by Periconceptional Use of Folic Acid