Psychiatric comorbidity in the treatment of patients with inflammatory bowel disease

Abstract

Ulcerative colitis and Crohn’s disease, commonly known as inflammatory bowel disease (IBD), draw attention from specialists of various disorders, including gastroenterology, psychiatry, and radiology. The involvement of a cortical influence in the brain-gut axis as well as the interaction of the hypothalamic-pituitary-adrenal axis and the peripheral nervous system provide an initial explanation of the psychological symptoms associated with IBD. The involvement of structures the limbic system, such as the anterior cingulate cortex, the prefrontal cortex, and the amygdala, paves the way for the discovery of the mechanisms underlying depression depression, anxiety, alexithymia, personality traits, and other psychological impairments following the onset of IBD. Psychiatric therapy in IBD patients is almost as important as the gastroenterological approach and consists of pharmacological treatment and psychotherapy. Neither of the available psychiatric treatment methods is considered the golden standard because both methods have side effects, and psychotropic medication can provoke the worsening of IBD symptoms. Thus, both approaches must be applied with awareness of the possibility of side effects. We suggest that psychiatrists and gastroenterologists work together to reach a consensus on IBD therapy to ensure success and to reduce side effects and relapse to the lowest possible rates.

Keywords: Inflammatory bowel disease, Psychiatry, Treatment, Personality traits, Depression, Anxiety

Core tip: The involvement of a dysfunction of brain-gut interactions in the pathogenesis of inflammatory bowel disease (IBD) is represented by a dysfunction of the autonomic nervous system, an abnormal hypothalamic-pituitary-adrenal axis and cholinergic anti-inflammatory pathway, a deleterious effect of stress and depression, an abnormal coupling of the prefrontal cortex-amygdaloid complex, and an abnormal relation between the microbiota and the brain as pro-inflammatory factors. New investigations have provided a critical link between forebrain changes and abdominal pain independent of active disease and drug treatment, providing a potential basis for an explanation of the psychological symptoms and brain influence in the pathogenesis of IBD.