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Introduction: G6PD is essential for the production of NADPH, which is a cofactor for many enzymes involved in antioxidant defense and neurotransmitter synthesis. A deficiency in this enzyme could lead to increased oxidative stress, impaired neurotransmitter and immune function. The latter have been implicated in the pathophysiology of schizophrenia. Objectives: The present case is presented to underscore the infrequent and uncharacteristic manifestation of this condition, in the context of clinical symptoms and the trajectory of evolution of schizophrenia when associated with G6PD Deficiency. Moreover, it sheds light on the challenges clinicians encounter in the management of such cases. Methods: A case report of a patient who was admitted to the Psychiatry Department ("Ibn Omrane") of Razi Hospital". Results: Mr. M.T is a 26 year-old unmarried man. He comes from a non-consanguineous marriage and has an educational level of a bachelor's degree plus three additional years of study. He has a significant family medical history. His maternal uncle is under treatment for a chronic psychotic disorder. He has a personal history of G6PD deficiency and no specific habits to note. At the age of 24, he insidiously developed anxiety with incoherent statements of persecution accompanied by behavioral manifestations leading to mistrust and social isolation. He discontinued his studies for a year and began verbalizing suicidal thoughts accompanied by self-harm behaviors. The family sought help from a psychiatrist who prescribed 5 mg of olanzapine, which was covertly administered to the patient. At the age of 28, after a suicide attempt, he was involuntarily admitted to Razi Hospital. The clinical presentation was dominated by disorganization, with a partial response to treatment. Conclusions: More research is needed to confirm the association between G6PD deficiency and schizophrenia and to determine the underlying mechanisms. Larger studies with well-defined populations and methodologies are needed. It is also important to study the interaction between G6PD deficiency and other genetic and environmental factors that contribute to schizophrenia. Disclosure of Interest: None Declared [ABSTRACT FROM AUTHOR]

Introduction: Vitamin B12 deficiency gives rise to a wide spectrum of hematological, gastrointestinal, psychiatric, and neurological disorders. Notable among the neuropsychiatric symptoms are mood disturbances, cognitive decline, and psychotic manifestations. Objectives: We present a case of a woman with neuropsychiatric symptoms linked to vitamin B12 deficiency to highlight certain organic aetiologies with psychiatric symptoms in the foreground. Methods: We discussed through a clinical case and a literature review, the relationship between neuropsychiatric symptoms and vitamine B12 deficiency in the context of biermer's disease. Results: We presented a patient aged 51-years-old without neurological or psychiatric history, she was hospitalised in a psychiatry department for behavioral disturbances, hetero-aggression, and incoherent speech. The psychiatric examination revealed distant contact, inappropriate affects, disorganized speech with persecutory delusions, memory problems, and poor insight. Neurological et physical examinations were normal, and cerebral magnetic resonance imaging (MRI) showed no abnormalities. First, haloperidol 25mg was prescribed, however, there was only partial improvement. Complete blood counts revealed macrocytic anemia (Hemoglobin: 8 g/dL, mean corpuscular volume: 106 fL). Her serum B12 assay was 48.19 pmol/L.Given these results we proceed to a Fundic biopsy, performed by fibroscopy, that revealed fundic atrophy and intestinal metaplasia compatible with Biermer's disease. Vitamin B12 replacement therapy began with hydroxocobalamin at 1000 μg/day intramuscularly for 15 days, followed by 1000 μg every 15 days for one month. Subsequently, there was a remarkable improvement in psychotic symptoms and cognitive function. Follow-up assessments demonstrated a return to baseline functioning. Conclusions: This case, coupled with prior studies, emphasizes the importance of considering vitamin B12 deficiency in the differential diagnosis of neuropsychiatric symptoms. Therefore, prompt diagnosis and treatment of vitamin B12 deficiency are imperative in preventing potential irreversible neurological damage. Disclosure of Interest: None Declared [ABSTRACT FROM AUTHOR]