Prevalence, Behaviours and Burden of Irritable Bowel Syndrome in Medical Students and Junior Doctors.

BACKGROUND: Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder which can have a strong impact on patients' quality of life including influence on various social aspects and psychological ramifications. The aim of the study was to assess the prevalence and consequences of IBS in medical students and junior doctors in Malta. METHOD: An online survey was sent out to all medical students enrolled at University of Malta and all doctors training with the Malta Foundation Programme. KEY RESULTS: The prevalence of IBS was 17.7% (total number =192), with 6.2% being previously diagnosed with IBS and the rest (11.5%) having symptoms consistent with IBS according to the Rome IV criteria. There was no statistically significant difference in BMI and in activity level as determined by the Godin Leisure-Time Exercise Questionnaire between IBS and non-IBS group.Absenteeism was significantly commoner in students/ doctors with IBS (47.1%) than in those without IBS (9.5%; p=0.0001). Of those previously diagnosed with IBS, 66.7% self-medicated compared to 45.4% of those diagnosed through the questionnaire. 71.6% of those in the IBS group tried dietary modification as to control their symptoms.On the Kessler 6 Distress scale, 91.2% of the IBS group had a score >6, with 44.1% having a score >13. The mean Visceral Sensitivity Index Score was 40.1 (95% CI 33.6 - 46.6). CONCLUSION: IBS is prevalent, yet under-recognized, in medical students and junior doctors. Measures should be instituted for timely, confidential detection and management of IBS and its related psychological consequences.

A New Look on an Old Issue: Comprehensive Review of Neurotransmitter Studies in Cerebrospinal Fluid of Patients with Schizophrenia and Antipsychotic Effect on Monoamine’s Metabolism

Neurotransmitters metabolism has a key role in the physiopathology of schizophrenia as demonstrated by studies measuring monoamine metabolites in patient’s cerebrospinal fluid (CSF) since the beginning of the antipsychotic use. This comprehensive review aims to understand the anomalies of CSF monoamines in schizophrenia and their correlation with clinical and paraclinical features. We also review the influence of antipsychotic treatment on CSF monoamines and discuss the connection with metabolic and inflammatory processes. Studies comparing CSF homovanillic acid (HVA) levels between patients and controls are miscellaneous, due to the heterogeneity of samples studies. However, low HVA is associated with more positive symptoms and a poorer outcome and negatively correlated with brain ventricle size. Based on humans and animals’ studies, antipsychotic treatments increase HVA during the first week of administration and decrease progressively over the time with a fall-off after withdrawal. 5‐hydroxyindolacetic acetic acid levels do not seem to be different in the patient’s CSF compared to controls. Considering metabolic co-factors of neurotransmitters synthesis, there is evidence supporting an increase of kynurenic acid in the CSF of patients with schizophrenia. Few studies explore folate metabolism in CSF. Literature also emphasizes the relationship between folate metabolism, inflammation and monoamine’s metabolism. Those results suggest that the CSF monoamines could be correlated with schizophrenia symptoms and treatment outcome. However, further studies, exploring the role of CSF monoamines as biomarkers of disease severity and response to treatment are needed. They should assess the antipsychotic prescription, inflammatory markers and folate metabolism as potential confounding factors.

A New Look on an Old Issue: Comprehensive Review of Neurotransmitter Studies in Cerebrospinal Fluid of Patients with Schizophrenia and Antipsychotic Effect on Monoamine’s Metabolism

Neurotransmitters metabolism has a key role in the physiopathology of schizophrenia as demonstrated by studies measuring monoamine metabolites in patient’s cerebrospinal fluid (CSF) since the beginning of the antipsychotic use. This comprehensive review aims to understand the anomalies of CSF monoamines in schizophrenia and their correlation with clinical and paraclinical features. We also review the influence of antipsychotic treatment on CSF monoamines and discuss the connection with metabolic and inflammatory processes. Studies comparing CSF homovanillic acid (HVA) levels between patients and controls are miscellaneous, due to the heterogeneity of samples studies. However, low HVA is associated with more positive symptoms and a poorer outcome and negatively correlated with brain ventricle size. Based on humans and animals’ studies, antipsychotic treatments increase HVA during the first week of administration and decrease progressively over the time with a fall-off after withdrawal. 5‐hydroxyindolacetic acetic acid levels do not seem to be different in the patient’s CSF compared to controls. Considering metabolic co-factors of neurotransmitters synthesis, there is evidence supporting an increase of kynurenic acid in the CSF of patients with schizophrenia. Few studies explore folate metabolism in CSF. Literature also emphasizes the relationship between folate metabolism, inflammation and monoamine’s metabolism. Those results suggest that the CSF monoamines could be correlated with schizophrenia symptoms and treatment outcome. However, further studies, exploring the role of CSF monoamines as biomarkers of disease severity and response to treatment are needed. They should assess the antipsychotic prescription, inflammatory markers and folate metabolism as potential confounding factors.

Immune Activation and Deficit in Neurotransmitters Synthesis in Treatment Resistant Depression: About a Case of Hashimoto Encephalopathy

We report a case of Hashimoto encephalopathy initially presented as a drug-resistant depression with predominant apathy and asthenia, successfully treated with cyclophosphamide. We suspected that the psychiatric symptoms were due to a deficit in neurotransmitter synthesis related to immune activation. We hypothesized that the immunomodulatory treatment helped to restore the neurotransmitter synthesis and thus decreased the patient’s depressive symptoms. In this case report we propose an innovative model in which immunity might disturbs neurotransmitters synthesis leading to depressive symptoms.