Inflammatory Bowel Disease: A Study of the Association between Anxiety and Depression, Physical Morbidity, and Nutritional Status

Institute of Internal Medicine, Università Cattolica del Sacro Cuore, Rome, Italy.
Scandinavian Journal of Gastroenterology (Impact Factor: 2.36). 10/1997; 32(10):1013-21. DOI: 10.3109/00365529709011218
Source: PubMed


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.

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    • "Symptoms include fever, malaise, anorexia, lethargy and, in severe cases, neuropsychiatric disorders, such as depression and anxiety [1]. 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. "
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    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
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    • "Psychological status has been found to influence the timing of disease relapse [1,2]. Studies show a 30% rate of depression during remission [1], with 80% and 55% of patients reporting anxiety and depression, respectively, during relapse [3]. While studies into psychological therapies [4] have recently been conducted, antidepressants have not been widely studied in the context of IBD. "
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    BMC Gastroenterology 07/2012; 12(1):93. DOI:10.1186/1471-230X-12-93 · 2.37 Impact Factor
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    • "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 [64] and 80% for anxiety and 60% for depression during relapse [65]. Robertson et al. [17] and Mikocka-Walus et al. [40] distinguished between these disorders and reported that anxiety is more prevalent than depression in IBD. "
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    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.
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