vitamin-b-12 and Psychotic-Disorders

This paper aims to broadly overview catatonia and vitamin B12 deficiency and highlight this association as a possible hidden cause. A review of published articles which examined the association between vitamin B12 deficiency and catatonia was performed. The articles for this review were selected by searching the electronic databases of the MEDLINE from March 2022 until August 2022 using catatonia (and related terms such as psychosis; psychomotor) and vitamin B12 (and related terms such as vitamin B12 deficiency; neuropsychiatry) as keywords. Articles had to be written in English to be included in this review. The direct relationship between levels of B12 and catatonic symptoms is difficult to confirm, as catatonia has different etiologies and can be triggered under the influence of multifactorial stressors. In this review, few published reports showed the reversibility of the catatonic symptoms once the level of B12 levels increased to more than 200 pg/ml. This could explain the responsibility of deficiency of B12 in the catatonic presentation of the few published case reports. B12-level screening in cases of catatonia of unclear etiology needs to be considered, particularly in a group at risk of B12 deficiency. Of particular concern is that vitamin B12 can be close to the normal range, which may delay the diagnosis. Detection and treatment of catatonic illness usually result in a rapid resolution of the condition, which, if untreated, can lead to potentially fatal outcomes.

Topics: Catatonia; Humans; Psychotic Disorders; Vitamin B 12; Vitamin B 12 Deficiency

Nitrous oxide (NO) is a commonly used drug in medical practice, restoration, and the automobile industry. Recreational abuse is an emerging public health problem owing to its accessibility and drug properties.. A 25-year-old male was hospitalized with acute psychosis and lower-extremity sensorimotor proprioceptive ataxia due to nitrous oxide abuse.. Laboratory studies confirmed a vitamin B12 deficiency. Magnetic resonance imaging of the spinal cord showed normal findings. Electrophysiological testing confirmed length-dependent sensorimotor polyneuropathy, with a predominant motor component and axonal degeneration.. Abstinence from toxic substances was suggested, and vitamin B12 substitution was introduced. The patient was lost to follow up.. Nitrous oxide toxicity is multisystemic and is thought to result from vitamin B12 inactivation. Recent case reports postulated direct paranodal lesions resulting from nitrous oxide consumption. Neurological, neuropsychiatric, and hematological toxicities are among those explored in this case report. Correction of the functional vitamin B12 status and nitrous oxide abstinence are essential in the treatment process.

Topics: Adult; Graft vs Host Disease; Humans; Male; Nitrous Oxide; Polyneuropathies; Psychotic Disorders; Vitamin B 12; Vitamin B 12 Deficiency

This review gives an overview of clinical characteristics, treatment and outcome of nutritional and acquired cobalamin (Cbl; synonym: vitamin B12) deficiencies, inborn errors of Cbl absorption and intracellular trafficking, as well as methylenetetrahydrofolate dehydrogenase (MTHFD1) and methylene tetrahydrofolate reductase (MTHFR) deficiencies, which impair Cbl-dependent remethylation. Acquired and inborn Cbl-related disorders and MTHFR deficiency cause multisystem, often severe disease. Failure to thrive, neurocognitive or psychiatric symptoms, eye disease, bone marrow alterations, microangiopathy and thromboembolic events are characteristic. The recently identified MTHFD1 defect additionally presents with severe immune deficiency. Deficient Cbl-dependent enzymes cause reduced methylation capacity and metabolite toxicity. Further net-effects of perturbed Cbl function or reduced Cbl supply causing oxidative stress, altered cytokine regulation or immune functions are discussed.

Topics: Folic Acid; Folic Acid Deficiency; Homocystinuria; Humans; Infant, Newborn; Metabolic Networks and Pathways; Methylenetetrahydrofolate Dehydrogenase (NADP); Methylenetetrahydrofolate Reductase (NADPH2); Muscle Spasticity; Psychotic Disorders; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Adult; Age Factors; Aged; Anemia, Hypochromic; Epilepsy; Female; Folic Acid; Humans; Male; Middle Aged; Psychotic Disorders; Schizophrenia; Vitamin B 12

Elevated homocysteine is observed in schizophrenia and associated with illness severity. The aim of this study was to determine whether vitamins B. A randomized, double-blind, placebo-controlled trial was used. A total of 120 patients with first-episode psychosis were randomized to an adjunctive B-vitamin supplement (containing folic acid [5 mg], B. B-vitamin supplementation reduced homocysteine levels (p = .003, effect size = -0.65). B-vitamin supplementation had no significant effects on Positive and Negative Syndrome Scale total (p = .749) or composite neurocognition (p = .785). There were no significant group differences in secondary symptom domains. A significant group difference in the attention/vigilance domain (p = .024, effect size = 0.49) showed that the B-vitamin group remained stable and the placebo group declined in performance. In addition, 14% of the sample had elevated baseline homocysteine levels, which was associated with greater improvements in one measure of attention/vigilance following B-vitamin supplementation. Being female and having affective psychosis was associated with improved neurocognition in select domains following B-vitamin supplementation. Genetic variation did not influence B-vitamin treatment response.. While 12-week B-vitamin supplementation might not improve overall psychopathology and global neurocognition, it may have specific neuroprotective properties in attention/vigilance, particularly in patients with elevated homocysteine levels, patients with affective psychosis, and female patients. Results support a personalized medicine approach to vitamin supplementation in first-episode psychosis.

Topics: Cognition; Dietary Supplements; Double-Blind Method; Female; Folic Acid; Humans; Male; Psychotic Disorders; Vitamin B 12; Vitamin B 6; Young Adult

Topics: Celiac Disease; Humans; Psychotic Disorders; Vitamin B 12; Vitamin B 12 Deficiency; Vitamins

Severe hyperhomocysteinemia (>100 µmol/L) is often associated with inborn errors of homocysteine metabolism. It manifests typically in neonatal period with developmental delay, hypotonia, feeding problems or failure to thrive. Adult-onset forms are rare and include less severe manifestations. Early diagnosis is crucial because effective treatment is available. A 23-year-old man presented with a 3-week history of speech and gait impairment, and numbness in lower limbs. Neurological examination revealed dysarthria, decreased vibratory sensation in both legs and appendicular and gait ataxia. Brain MRI revealed T2-hyperintense symmetric white matter lesions and cortical atrophy. He had folate and vitamin B

Topics: Age of Onset; Betaine; Dysarthria; Folic Acid; Gait Ataxia; Homocystinuria; Humans; Male; Methylenetetrahydrofolate Reductase (NADPH2); Muscle Spasticity; Psychotic Disorders; Tremor; Vitamin B 12; Young Adult

Topics: Aged; Betaine; Female; Homocysteine; Homocystinuria; Humans; Hyperhomocysteinemia; Leucovorin; Methylenetetrahydrofolate Reductase (NADPH2); Muscle Spasticity; Psychotic Disorders; Vitamin B 12; Vitamin B 12 Deficiency; Vitamin B Complex

In order to propose a course of action to be taken in the face of any hyperhomocysteinemia, we have reported for the first time in a French journal the recommendations made within the framework of the European E-HOD project for the diagnosis and treatment of remethylation disorders. The remethylation route ensures homocysteine-methionine conversion. It is linked to the folate cycle and the intracellular metabolism of cobalamins. Remethylation disorders can be classified into three groups: 1) isolated disorders (cblD-HC, cblE, cblG) corresponding to an isolated deficit in the production of methylcobalamin, cofactor of methionine synthase; 2) combined disorders (cblC, cblD-MMA/HC, cblF, cblJ) corresponding to an alteration of the transport and intracellular metabolism of cobalamins, which causes a defect in the synthesis of the two functional forms of cobalamin: methylcobalamin and adenosylcobalamin, a cofactor for methyl malonylCoA mutase; 3) MTHFR deficit, an abnormality of the folate cycle. The biological anomalies observed are hyperhomocysteinemia and hypomethioninaemia associated in the case of disorders combined with increased urinary excretion of methylmalonic acid. The clinical presentation is however heterogeneous according to the remethylation disorder but also for the same pathology according to the age. Given the large number of pathologies grouped together in remethylation disorders, this point is illustrated by only two clinical cases concerning the same deficit (deficit in MTHFR) but with different discovery circumstances: a neonatal form and a late form.

Topics: Alcoholism; Amino Acid Metabolism, Inborn Errors; Diagnosis, Differential; Female; Folic Acid; Folic Acid Deficiency; Homocysteine; Homocystinuria; Humans; Infant, Newborn; Metabolic Networks and Pathways; Methionine; Methylation; Methylenetetrahydrofolate Reductase (NADPH2); Middle Aged; Muscle Spasticity; Psychotic Disorders; Vitamin B 12

Topics: Anemia, Pernicious; Delusions; Diagnosis, Differential; Female; Hand; Head; Humans; Magnetic Resonance Imaging; Middle Aged; Neurologic Examination; Paresthesia; Psychotic Disorders; Radiography; Vitamin B 12

To explore the clinical presentation, course, treatment and impact of early treatment in patients with remethylation disorders from the European Network and Registry for Homocystinurias and Methylation Defects (E-HOD) international web-based registry.. This review comprises 238 patients (cobalamin C defect n = 161; methylenetetrahydrofolate reductase deficiency n = 50; cobalamin G defect n = 11; cobalamin E defect n = 10; cobalamin D defect n = 5; and cobalamin J defect n = 1) from 47 centres for whom the E-HOD registry includes, as a minimum, data on medical history and enrolment visit. The duration of observation was 127 patient years. In 181 clinically diagnosed patients, the median age at presentation was 30 days (range 1 day to 42 years) and the median age at diagnosis was 3.7 months (range 3 days to 56 years). Seventy-five percent of pre-clinically diagnosed patients with cobalamin C disease became symptomatic within the first 15 days of life. Total homocysteine (tHcy), amino acids and urinary methylmalonic acid (MMA) were the most frequently assessed disease markers; confirmatory diagnostics were mainly molecular genetic studies. Remethylation disorders are multisystem diseases dominated by neurological and eye disease and failure to thrive. In this cohort, mortality, thromboembolic, psychiatric and renal disease were rarer than reported elsewhere. Early treatment correlates with lower overall morbidity but is less effective in preventing eye disease and cognitive impairment. The wide variation in treatment hampers the evaluation of particular therapeutic modalities.. Treatment improves the clinical course of remethylation disorders and reduces morbidity, especially if started early, but neurocognitive and eye symptoms are less responsive. Current treatment is highly variable. This study has the inevitable limitations of a retrospective, registry-based design.

Topics: Adolescent; Adult; Age of Onset; Amino Acid Metabolism, Inborn Errors; Child; Child, Preschool; Cross-Sectional Studies; Disease Progression; Europe; Female; Homocystinuria; Humans; Infant; Infant, Newborn; Male; Methylation; Methylenetetrahydrofolate Reductase (NADPH2); Methylmalonic Acid; Muscle Spasticity; Phenotype; Pregnancy; Psychotic Disorders; Registries; Retrospective Studies; Vitamin B 12; Young Adult

Vitamin B

Topics: Anemia, Pernicious; Delayed Diagnosis; Dementia; Female; Humans; Middle Aged; Psychotic Disorders; Seizures; Vitamin B 12; Vitamin B Complex

Topics: Double-Blind Method; Folic Acid; Humans; Psychotic Disorders; Vitamin B 12; Vitamin B Complex

Topics: Anemia, Megaloblastic; Diet, Vegan; Dietary Supplements; Female; Humans; Middle Aged; Neglected Diseases; Psychotic Disorders; Treatment Outcome; Vitamin B 12; Vitamin B 12 Deficiency

Previous studies approved the important roles of CD68, as scavenger receptors, in Alzheimer's disease (AD). The aim of this study was to evaluate the effect of treatment with anti-psychotic drugs and vitamin B12 on the expression levels of CD68 in monocytes of psychotic AD patients.. Expression of CD68 on the monocytes was evaluated in the following groups: 1. age and sex matched healthy controls (Group 1), 2. non-psychotic AD patients (Group 2), 3. psychotic AD patients (Group 3), 4. psychotic AD patients treated with Risperidone (Group 4), 5. psychotic AD patients treated with Risperidone plus vitamin B12 (Group 5), 6. psychotic AD patients treated with Quetiapine (Group 6), psychotic AD patients treated with Quetiapine plus vitamin B12 (Group 7). The expression of CD68 has been performed using flow cytometry technique.. The results showed that CD68 levels were significantly increased in AD patients in comparison to healthy controls and in psychotic AD patients in comparison to non-psychotic AD patients. Treatment with anti-psychotic drugs decreased the expression of CD68. Expression of CD68 has a positive correlation with pain, dementia and mental disorders symptoms in psychotic AD patients.. CD68 may play key roles in the pathogenesis of AD and its complications may be via induction of inflammation. Therefore, it may be concluded that CD68 may be considered as a risk factor for development of AD and also psychotic symptoms in the patients.

Topics: Aged; Aged, 80 and over; Alzheimer Disease; Antigens, CD; Antigens, Differentiation, Myelomonocytic; Antipsychotic Agents; Case-Control Studies; Drug Therapy, Combination; Female; Flow Cytometry; Humans; Inflammation; Male; Monocytes; Psychotic Disorders; Quetiapine Fumarate; Risk Factors; Risperidone; Vitamin B 12

Severe methylenetetrahydrofolate reductase (MTHFR) deficiency is a rare inborn defect disturbing the remethylation of homocysteine to methionine (<200 reported cases). This retrospective study evaluates clinical, biochemical genetic and in vitro enzymatic data in a cohort of 33 patients.. Clinical, biochemical and treatment data was obtained from physicians by using a questionnaire. MTHFR activity was measured in primary fibroblasts; genomic DNA was extracted from cultured fibroblasts.. Thirty-three patients (mean age at follow-up 11.4 years; four deceased; median age at first presentation 5 weeks; 17 females) were included. Patients with very low (<1.5%) mean control values of enzyme activity (n = 14) presented earlier and with a pattern of feeding problems, encephalopathy, muscular hypotonia, neurocognitive impairment, apnoea, hydrocephalus, microcephaly and epilepsy. Patients with higher (>1.7-34.8%) residual enzyme activity had mainly psychiatric symptoms, mental retardation, myelopathy, ataxia and spasticity. Treatment with various combinations of betaine, methionine, folate and cobalamin improved the biochemical and clinical phenotype. During the disease course, patients with very low enzyme activity showed a progression of feeding problems, neurological symptoms, mental retardation, and psychiatric disease while in patients with higher residual enzyme activity, myelopathy, ataxia and spasticity increased. All other symptoms remained stable or improved in both groups upon treatment as did brain imaging in some cases. No clear genotype-phenotype correlation was obvious.. MTHFR deficiency is a severe disease primarily affecting the central nervous system. Age at presentation and clinical pattern are correlated with residual enzyme activity. Treatment alleviates biochemical abnormalities and clinical symptoms partially.

Topics: Ataxia; Betaine; Child; Female; Folic Acid; Genetic Association Studies; Homocystinuria; Humans; Intellectual Disability; Male; Methionine; Methylenetetrahydrofolate Reductase (NADPH2); Muscle Spasticity; Mutation; Phenotype; Psychotic Disorders; Retrospective Studies; Spinal Cord Diseases; Vitamin B 12

The aim of this study was to investigate the prevalence of metabolic disturbances in patients with first-episode schizophrenia (FES) and test the hypothesis that genetic variation in one-carbon metabolism may account for metabolic dysregulation in early psychosis. We measured fasting glucose, lipid profile parameters, homocysteine, folate and vitamin B12 in 135 patients with FES and 146 healthy controls (HCs). Polymorphisms in the following genes were determined: MTHFR (C677T and A1298C), MTHFD1 (G1958A), MTRR (A66G) and BHMT (G742A). Serum levels of folate and high-density lipoproteins (HDL) were significantly lower in patients with FES compared to HCs. In turn, serum levels of homocysteine and triglycerides were significantly higher in patients with FES than in HCs. Prevalence of hyperhomocysteinemia, low folate and HDL levels together with dyslipidemia was significantly higher in patients with FES compared to HCs. Higher homocysteine levels, lower vitamin B12 levels and the presence of metabolic syndrome were associated with higher severity of negative symptoms. None of studied polymorphisms was associated with schizophrenia risk. Several associations between studied polymorphisms and cardio-metabolic parameters were found. None of them remained significant after Bonferroni correction. Our results indicate that metabolic dysregulation in patients with FES is not associated with genetic variation in one-carbon metabolism.

Topics: Adult; Betaine-Homocysteine S-Methyltransferase; Blood Glucose; Carbon; Case-Control Studies; Dyslipidemias; Fasting; Female; Ferredoxin-NADP Reductase; Folic Acid; Homocysteine; Humans; Hyperhomocysteinemia; Lipoproteins, HDL; Male; Metabolic Syndrome; Methylenetetrahydrofolate Dehydrogenase (NADP); Methylenetetrahydrofolate Reductase (NADPH2); Minor Histocompatibility Antigens; One-Carbon Group Transferases; Polymorphism, Genetic; Prevalence; Psychotic Disorders; Schizophrenia; Triglycerides; Vitamin B 12; Young Adult

A 35-year-old woman was admitted with subacute intellectual deterioration. Laboratory studies showed elevated total homocysteine and decreased folic acid. MRI revealed leukoencephalopathy with a posterior predominance, and hyperintensity in the pyramidal tracts on T2-weighted and FLAIR images. The enzyme assay showed a deficiency of methylenetetrahydrofolate reductase (MTHFR) activity with low residual activity of 4.2% of the mean control value in cultured fibroblasts. Sequence analysis of the MTHFR gene demonstrated two homozygous missense mutations, c.677C>T (p.Ala222Val) and c.685A>C (p.Ile225Leu). c.677C>T (p.Ala222Val) is known as a common polymorphism and c.685A>C (p.Ile225Leu) is considered to be a novel polymorphism. A diagnosis of MTHFR deficiency was made. Treatment with folic acid, vitamin B12 and B6 made significant improvement of intellectual deterioration and reduction in the total homocysteine level. They also made marked resolution of leukoencephalopathy. Posterior-predominant leukoencephalopathy was found to be an excellent marker of MTHFR deficiency, and may help to establish the diagnosis.

Topics: Adult; Biomarkers; Female; Folic Acid; Homocysteine; Homocystinuria; Humans; Leukoencephalopathies; Magnetic Resonance Imaging; Methylenetetrahydrofolate Reductase (NADPH2); Muscle Spasticity; Mutation, Missense; Polymorphism, Single Nucleotide; Psychotic Disorders; Treatment Outcome; Vitamin B 12; Vitamin B 6

Although cobalamin (cbl) C deficiency is the most common inherited disorder of vitamin B12 metabolism, the late-onset form of the disease can be difficult to recognize because it has a broad phenotypic spectrum. In this report, we describe an adolescent female exposed to unknown illicit substances and sexual abuse who presented with psychosis, anorexia, seizures, and ataxia. The patient's diagnosis was delayed until a metabolic workup was initiated, revealing hyperhomocysteinemia, low normal plasma methionine, and methylmalonic aciduria. Ultimately, cblC deficiency was confirmed when molecular testing showed compound heterozygosity for mutations (c.271dupA and c.482G>A) in the MMACHC gene. This diagnosis led to appropriate treatment with hydroxocobalamin, betaine, and folate, which resulted in improvement of her clinical symptoms and laboratory values. This patient demonstrates a previously unrecognized presentation of late-onset cblC deficiency. Although neuropsychiatric symptoms are common in late-onset disease, seizures and cerebellar involvement are not. Furthermore, anorexia has not been previously described in these patients. This case emphasizes that inborn errors of metabolism should be part of the differential diagnosis for a teenager presenting with altered mental status, especially when the diagnosis is challenging or neurologic symptoms are unexplained. Correct diagnosis of this condition is important because treatment is available and can result in clinical improvement.(1.)

Topics: Adolescent; Anorexia; Carrier Proteins; Child Abuse, Sexual; Comorbidity; Cooperative Behavior; Diagnosis, Differential; Epilepsy, Temporal Lobe; Female; Genetic Carrier Screening; Humans; Illicit Drugs; Interdisciplinary Communication; Oxidoreductases; Psychotic Disorders; Substance-Related Disorders; Vitamin B 12; Vitamin B 12 Deficiency

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.

Topics: Adolescent; Female; Humans; Hypertension; Psychotic Disorders; Seizures; Treatment Outcome; Vitamin B 12; Vitamin B 12 Deficiency

Fahr's syndrome is characterized by symmetrical and bilateral intracerebral calcifications, located in the basal ganglia and mostly associated with a phosphorus calcium metabolism disorder. It must be distinguished from genetic or sporadic Fahr's disease.. We report two cases of this syndrome, the first was revealed by psychotic and cognitive disorders and the other by epilepsy. In both cases, brain imaging and biology resulted in the diagnosis of Fahr's syndrome. The outcome was favorable after treatment in both cases.. These two observations illustrate various clinical signs of Fahr's syndrome.

Topics: Adult; Aged; Basal Ganglia Diseases; Calcinosis; Calcium; Calcium Metabolism Disorders; Cognition Disorders; Female; Humans; Male; Psychotic Disorders; Syndrome; Tomography, X-Ray Computed; Treatment Outcome; Vitamin B 12; Vitamin D

There is considerable evidence that elevated plasma homocysteine levels are associated with a prothrombotic milieu, whereas activation of the coagulation cascade is an important component of the pathogenesis of sepsis. The protein C pathway has been reported to play a central role both in the propagation of sepsis and a hyperhomocysteinemia-induced hypercoagulable state. Our primary aim was to measure plasma homocysteine levels in mechanically ventilated patients with severe sepsis/septic shock and to assess the association of these levels with relevant clinical outcomes.. The study cohort included 102 mechanically ventilated patients with severe sepsis or septic shock. Demographics, comorbidities, clinical data and severity scores were recorded. Plasma homocysteine, vitamin B12, folate, creatinine, and protein C levels were measured in all study subjects upon enrollment, and genotyping for the C677T and A1298C polymorphisisms of the methylenetetrahydrofolate reductase (MTHFR) gene and for factor V Leiden (FVL) mutations was performed as well. The primary outcomes were mortality at 28 and 90 days; secondary outcomes included the number of days without renal or cardiovascular failure and the ventilator-free days during the study period.. Homocysteine levels were not significantly associated with any primary or secondary outcomes in the multivariable analysis. In addition, a synergistic effect of homocysteine with protein C levels was not detected.. Our data suggest that plasma homocysteine levels may not inform the prognosis of mechanically ventilated patients with severe sepsis/septic shock.

Topics: Activated Protein C Resistance; Aged; Blood Coagulation Tests; Cohort Studies; Comorbidity; Factor V; Female; Folic Acid; Homocysteine; Homocystinuria; Hospital Mortality; Humans; Hyperhomocysteinemia; Male; Methylenetetrahydrofolate Reductase (NADPH2); Middle Aged; Muscle Spasticity; Point Mutation; Protein C; Psychotic Disorders; Respiration, Artificial; Sepsis; Shock, Septic; Thrombophilia; Vitamin B 12

Vitamin B12 and folate deficiency causing neuropsychiatric and thrombotic manifestations, such as peripheral neuropathy, subacute combined degeneration of cord, dementia, ataxia, optic atrophy, catatonia, psychosis, mood disturbances, myocardial infarction and portal vein thrombosis are well known. This present report highlights an unusual presentation of vitamin B12 deficiency-psychotic disorder, extrapyramidal symptoms in a 12-year-old boy. His symptoms responded to parenteral vitamin B12 therapy. So with this report we emphasized that serum vitamin B12 and folate levels should be measured, especially in those patients who present with other known neuropsychiatric features of vitamin B12 and folate deficiency.

Topics: Basal Ganglia Diseases; Child; Folic Acid; Folic Acid Deficiency; Humans; Male; Psychotic Disorders; Vitamin B 12; Vitamin B 12 Deficiency

Although increased plasma total homocysteine (tHcy) concentrations were reported in psychiatric diseases, currently the reasons of elevated tHcy levels were not clearly understood. In this study we aimed to investigate the contribution of renal clearance of homocysteine on plasma tHcy load in patients with depression and first episode psychosis.. Thirty depression, 14 first episode psychosis patients and 34 healthy individuals (control group) were involved in the study. In patients and control groups, plasma and urine tHcy levels, urine methylmalonic acid (uMMA), serum vitamin B12 and folate concentrations were measured.. Although there was not any difference between depression, psychosis and control groups with respect to mean (SD) values of vitamin B12 (289(131), 230 (72) and 249(79) pg/mL, respectively) and folate (6.4(4.0), 5.3(2.3) and 5.7(2.3) ng/mL, respectively), plasma tHcy levels of depression and psychosis group were higher than the control values (16.3(6.2), 15.5(4.3) and 9.9(2.1) micromol/L, respectively). Urine tHcy values of patient groups were significantly lower than those in the control group (14.5(7.6), 15.8(6.8) and 29.6(16.9) micromol/g creatinine, respectively). There were elevated uMMA levels in depression and psychosis groups compared with control group (4.9(2.4), 6.6(3.2) and 2.8(1.2) mmol/mol creatinine, respectively). There were a significant and negative correlation between urinary tHcy and plasma tHcy levels (r=-0.258 and p=0.011).. In conclusion, reduced urinary tHcy levels in psychiatric patients could be one of the reasons of plasma tHcy elevations with normal folate and vitamin B12 levels. Altered renal handling mechanisms of homocysteine may lead to elevated plasma tHcy levels by reduced clearance of homocysteine via glomerular filtration.

Topics: Acute Disease; Adult; Biomarkers; Chronic Disease; Female; Folic Acid; Homocysteine; Humans; Male; Meta-Analysis as Topic; Middle Aged; Psychotic Disorders; Vitamin B 12

The present report highlights an unusual presentation of vitamin B12 deficiency--recurrent seizures in a 26-year-old man. His symptoms responded to parenteral vitamin B12 therapy. The relevant literature is reviewed.

Topics: Adult; Epilepsy, Complex Partial; Humans; Injections, Intramuscular; Male; Psychotic Disorders; Recurrence; Vitamin B 12; Vitamin B 12 Deficiency

The case of a 69 years old female patient is reported, who developed paranoid behaviour due to cobalamin-deficiency without megaloblastosis based on a chronic gastric atrophy. The psychosis showed complete remission after vitamin B 12 supplementation. The discussion leads to the question, whether or not chronic use of tricyclic antidepressants may be one cause of atrophic gastritis. Furthermore, differentialdiagnostic reflections consider the role of cobalamine and folate in the synthesis of monoamine neurotransmitters in the brain.

Topics: Aged; Diagnosis, Differential; Female; Gastritis; Humans; Paranoid Behavior; Psychotic Disorders; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Administration, Sublingual; Humans; Psychotic Disorders; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Child; Child Behavior Disorders; Female; Humans; Psychotic Disorders; Vitamin B 12

Topics: Anemia, Pernicious; Bipolar Disorder; Chronic Disease; Depression; Gastrointestinal Diseases; Humans; Malabsorption Syndromes; Psychosurgery; Psychotic Disorders; Schizophrenia; Vitamin B 12; Vitamin B 12 Deficiency; Vitamin B 6 Deficiency

Topics: Adult; Gastrectomy; Humans; Male; Postoperative Complications; Psychotic Disorders; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Female; Humans; Pregnancy; Psychotic Disorders; Puerperal Disorders; Vitamin B 12

Topics: Amblyopia; Female; Humans; Pregnancy; Psychotic Disorders; Puerperal Disorders; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Anticonvulsants; Epilepsy; Folic Acid; Humans; Mental Disorders; Psychotic Disorders; Schizophrenia; Vitamin B 12

Topics: Adjustment Disorders; Barbiturates; Depression; Female; Gastrectomy; Humans; Male; Middle Aged; Neurocognitive Disorders; Phenothiazines; Psychotic Disorders; Schizophrenia; Vitamin B 12

Topics: Adolescent; Adult; Anticonvulsants; Epilepsy; Erythrocyte Count; Female; FIGLU Test; Folic Acid; Folic Acid Deficiency; Hematocrit; Humans; Male; Middle Aged; Neutrophils; Phenobarbital; Phenytoin; Primidone; Psychotic Disorders; Vitamin B 12

Topics: Gastric Acidity Determination; Humans; Medical History Taking; Methods; Neurologic Manifestations; Paresthesia; Psychotic Disorders; Spinal Cord Diseases; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Age Factors; Anemia, Macrocytic; Anticonvulsants; Brain; Epilepsy; Female; Folic Acid; Folic Acid Deficiency; Humans; Intellectual Disability; Male; Mental Disorders; Peripheral Nerves; Phenobarbital; Phenytoin; Primidone; Psychotic Disorders; Sex Factors; Spinal Cord; Vitamin B 12

Topics: Aged; Antidepressive Agents; Female; Humans; Male; Middle Aged; Prognosis; Psychotic Disorders; Tranquilizing Agents; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Feeding and Eating Disorders; Humans; Injections, Intramuscular; Insulin; Psychotic Disorders; Vitamin B 12

Topics: Anemia, Macrocytic; Diagnosis, Differential; Female; Humans; Infusions, Parenteral; Male; Middle Aged; Psychotic Disorders; Spinal Cord Diseases; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Adolescent; Ascorbic Acid; Brain Diseases; Electroencephalography; Emaciation; Female; Humans; Psychotic Disorders; Puberty; Pyridoxine; Riboflavin; Thiamine; Vitamin B 12

Topics: Ascorbic Acid; Benzaldehydes; Central Nervous System Stimulants; Delirium; Folic Acid; Fructose; Humans; Prednisolone; Psychoses, Alcoholic; Psychotic Disorders; Pyridoxine; Rutin; Sorbitol; Vitamin B 12; Vitamin B Complex; Vitamin K 1

Topics: Adrenocorticotropic Hormone; Alcohol Withdrawal Delirium; Chlordiazepoxide; Chlorpromazine; Drug Therapy; Humans; Magnesium; Mental Disorders; Meprobamate; Mortality; Primidone; Promazine; Psychoses, Alcoholic; Psychotic Disorders; Vitamin B 12; Water-Electrolyte Balance

Topics: Anemia; Anemia, Pernicious; Cobalt Isotopes; Diagnosis, Differential; Hematinics; Humans; Myelitis; Neuritis; Neurologic Manifestations; Psychotic Disorders; Schilling Test; Urine; Vitamin B 12

Topics: Alzheimer Disease; Confusion; Corrinoids; Dementia; Humans; Psychotic Disorders; Vitamin B 12

Topics: Humans; Mental Disorders; Psychotic Disorders; Vitamin B 12

Topics: Alcohol Withdrawal Delirium; Alcoholism; Corrinoids; Humans; Psychoses, Alcoholic; Psychotic Disorders; Pyridoxine; Vitamin B 12; Vitamin B Complex

Topics: Aged; Cardiac Glycosides; Chlorpromazine; Ergot Alkaloids; Folic Acid; Hematinics; Humans; Mental Disorders; Povidone; Psychoses, Alcoholic; Psychotic Disorders; Vitamin B 12; Vitamin B Complex

Topics: Anemia; Anemia, Pernicious; Folic Acid; Hematinics; Humans; Mental Disorders; Psychotic Disorders; Spinal Cord; Spinal Cord Diseases; Vitamin B 12

Topics: Anemia; Anemia, Pernicious; Corrinoids; Hematinics; Humans; Psychotic Disorders; Spinal Diseases; Vitamin B 12

Topics: Delirium; Hematinics; Humans; Mental Disorders; Psychoses, Alcoholic; Psychotic Disorders; Vitamin B 12

Topics: Anemia; Anemia, Pernicious; Corrinoids; Humans; Psychotic Disorders; Syndrome; Vitamin B 12

Topics: Anemia; Anemia, Pernicious; Central Nervous System; Corrinoids; Folic Acid; Hematinics; Humans; Nervous System; Psychotic Disorders; Vitamin B 12