The etiology of inflammatory bowel disease is unclear, and the role played by anxiety and depression is highly controversial. Anxiety and depression in patients with inflammatory bowel disease could be secondary to disabling symptoms, but the interaction between physical morbidity and psychologic illness in these subjects has not been sufficiently investigated. Patients with inflammatory bowel disease are nevertheless frequently undernourished, but there are no studies on the association between anxiety and depression and malnutrition. This study was designed to characterize anxiety and depression in subjects affected by inflammatory bowel disease and to establish the influence of physical morbidity and/or nutritional status on psychologic disorders.
Seventy-nine consecutive patients, 43 with Crohn's disease (CD) and 36 with ulcerative colitis (UC), were enrolled in the study. An index of the disease activity and physical morbidity was obtained by the simplified Crohn's Disease Activity Index and Truelove-Witts criteria and using the Clinical Rating Scale. Thirty-six healthy volunteers were studied as controls. All the subjects were given the State and Trait Anxiety Inventory (STAI) test and the Zung self-rating Depression Scale.
The percentage of subjects with state anxiety was significantly higher in the CD (P < 0.001) and UC (P < 0.001) groups than in control subjects. There was no significant difference in trait anxiety among groups. The percentage of subjects with depression was significantly higher in the CD (P < 0.05) and UC (P < 0.05) groups than in control subjects. State anxiety and depression were significantly associated with physical morbidity and correlated with malnutrition in CD and UC patients.
Anxiety and depression in patients with inflammatory bowel disease could be reactive to the disabling symptoms and to malnutrition. As measured with the STAI, personality trait of anxiety does not seem to play an important role in inflammatory bowel disease.
"Symptoms include fever, malaise, anorexia, lethargy and, in severe cases, neuropsychiatric disorders, such as depression and anxiety
. Sickness behaviours occur during acute bacterial or viral infections, but also during chronic inflammatory diseases, such as rheumatoid arthritis, inflammatory bowel disease and psoriasis
[2-4]. In the case of the latter, what would be a beneficial, self-limiting, system can become dysregulated. "
[Show abstract][Hide abstract] ABSTRACT: Although the central nervous system (CNS) was once considered an immunologically privileged site, in recent years it has become increasingly evident that cross talk between the immune system and the CNS does occur. As a result, patients with chronic inflammatory diseases, such as rheumatoid arthritis, inflammatory bowel disease or psoriasis, are often further burdened with neuropsychiatric symptoms, such as depression, anxiety and fatigue. Despite the recent advances in our understanding of neuroimmune communication pathways, the precise effect of peripheral immune activation on neural circuitry remains unclear. Utilizing transcriptomics in a well-characterized murine model of systemic inflammation, we have started to investigate the molecular mechanisms by which inflammation originating in the periphery can induce transcriptional modulation in the brain.
Several different systemic and tissue-specific models of peripheral toll-like-receptor-(TLR)-driven (lipopolysaccharide (LPS), lipoteichoic acid and Imiquimod) and sterile (tumour necrosis factor (TNF) and 12-O-tetradecanoylphorbol-13-acetate (TPA)) inflammation were induced in C57BL/6 mice. Whole brain transcriptional profiles were assessed and compared 48 hours after intraperitoneal injection of lipopolysaccharide or vehicle, using Affymetrix GeneChip microarrays. Target gene induction, identified by microarray analysis, was validated independently using qPCR. Expression of the same panel of target genes was then investigated in a number of sterile and other TLR-dependent models of peripheral inflammation.
Microarray analysis of whole brains collected 48 hr after LPS challenge revealed increased transcription of a range of interferon-stimulated genes (ISGs) in the brain. In addition to acute LPS challenge, ISGs were induced in the brain following both chronic LPS-induced systemic inflammation and Imiquimod-induced skin inflammation. Unique to the brain, this transcriptional response is indicative of peripherally triggered, interferon-mediated CNS inflammation. Similar models of sterile inflammation and lipoteichoic-acid-induced systemic inflammation did not share the capacity to trigger ISG induction in the brain.
These data highlight ISG induction in the brain as being a consequence of a TLR-induced type I interferon response. As considerable evidence links type I interferons to psychiatric disorders, we hypothesize that interferon production in the brain could represent an important mechanism, linking peripheral TLR-induced inflammation with behavioural changes.
Journal of Neuroinflammation 04/2014; 11(1):73. DOI:10.1186/1742-2094-11-73 · 5.41 Impact Factor
"Psychological status has
been found to influence the timing of disease relapse [1,2]. Studies show a 30% rate of depression
during remission , with 80% and 55% of
patients reporting anxiety and depression, respectively, during relapse . While studies into psychological therapies
 have recently been conducted,
antidepressants have not been widely studied in the context of IBD. "
[Show abstract][Hide abstract] ABSTRACT: Studies with healthy volunteers have demonstrated that antidepressants can improve immunoregulatory activity and thus they may have a potential to positively impact the disease course in inflammatory bowel disease (IBD), a chronic and incurable condition. However, patients' views on the role of antidepressants in the management of their IBD are unknown. Thus, this study aimed to explore patients' experiences and opinions regarding the effect of antidepressants on IBD course before possibly undertaking future treatment trials with antidepressants.
Semi-structured in-depth interviews with open-ended questions were conducted with a randomly selected sample of IBD patients recruited at the Australian public hospital IBD clinic and currently receiving antidepressants. A qualitative content analysis was undertaken to summarise patients' responses. A Visual Analogue Scale was used to provide a quantitative assessment of patients' experiences with antidepressants.
Overall, 15 IBD sufferers currently on antidepressants (nine females, six males) were interviewed. All 15 reported a positive response to antidepressants reporting they improved their quality of life, with minimal side-effects. Five patients (33.3%) felt the antidepressant had specifically improved their IBD course. Three patients noted how they believed the reduction in feelings of stress mediated the positive influence of the antidepressant on IBD course. Ten patients (66.7%) felt the antidepressants had not specifically influenced their IBD. Nine patients (60.0%) had a generally positive attitude towards antidepressants, four patients (26.7%) were ambivalent, and two patients (13.3%) held a negative view towards antidepressants. Twelve patients (80.0%) stated that they would be willing to participate in clinical trials.
Antidepressants seem to be well tolerated by IBD patients. One third of patients reported an observable improvement of their IBD under the influence of this treatment. The positive attitude towards antidepressants in these participants may make the conduct of clinical trials to further assess for any specific role on IBD course feasible. However, due to a small sample size, a qualitative nature of this study and in light of the results of studies on other populations indicating reluctance to taking antidepressants at least in some patients, these results should be interpreted with caution until confirmed in quantitative studies.
"While some researchers [38, 58, 59] found no evidence of any association between these psychiatric disorders and either UC or CD, others [60–63] confirmed that depression and anxiety are common in IBD patients. The prevalence of anxiety and/or depression has been estimated to be as high as 29–35% during remission  and 80% for anxiety and 60% for depression during relapse . Robertson et al.  and Mikocka-Walus et al.  distinguished between these disorders and reported that anxiety is more prevalent than depression in IBD. "
[Show abstract][Hide abstract] ABSTRACT: Inflammatory bowel disease (IBD) including Crohn's disease (CD) and ulcerative colitis (UC) is a chronic and disabling disease with unknown etiology. There have been some controversies regarding the role of psychological factors in the course of IBD. The purpose of this paper is to review that role. First the evidence on role of stress is reviewed focusing on perceived stress and patients' beliefs about it in triggering or exacerbating the course of IBD. The possible mechanisms by which stress could be translated into IBD symptoms, including changes in motor, sensory and secretory gastrointestinal function, increase intestinal permeability, and changes in the immune system are, then reviewed. The role of patients' concerns about psychological distress and their adjustment to disease, poor coping strategies, and some personality traits that are commonly associated with these diseases are introduced. The prevalence rate, the timing of onset, and the impact of anxiety and depression on health-related quality of life are then reviewed. Finally issues about illness behavior and the necessity of integrating psychological interventions with conventional treatment protocols are explained.
Gastroenterology Research and Practice 06/2012; 2012(3):106502. DOI:10.1155/2012/106502 · 1.75 Impact Factor
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