Background and Summary. Chronic abdominal pain is a challenging complaint for both primary care providers and gastroenterologists alike, due to a broad differential diagnosis and sometimes extensive and negative workup. In the absence of red flag features that herald more acute conditions, the majority of patients with chronic abdominal pain have a benign cause or a functional disorder (e.g. Irritable bowel syndrome). The costs associated with a diagnostic workup are an expensive burden to healthcare. A systematic approach for evaluating patients and initiating a management plan are recommended in the primary care setting. Undiagnosed abdominal pain should be investigated starting with a detailed history and physical examination. Diagnostic investigations should be limited and adapted according to the clinical features, the alarm symptoms, and the symptom severity. This review will focus on the diagnostic tools which general practitioners (GP) utilize in the evaluation of chronic abdominal pain. Key Messages. The primary role of the general practitioner (GP) is to differentiate an organic disease from a functional one, to refer to a specialist, or to provide treatment for the underlying cause of pain. The functional disorders should be considered after the organic pathology has been confidently excluded. Once a diagnosis of functional pain is established, repetitive testing is not recommended and the patient should be referred to receive psychological support (e.g. cognitive therapy) associated with available pharmacological therapeutic options.
Diverticular disease (DD) is the most frequent condition in the Western world that affects the colon. Although chronic mild inflammatory processes have recently been proposed as a central factor in DD, limited information is currently available regarding the role of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α). Therefore, we conducted a systematic review and meta-analysis aiming to assess the mucosal TNF-α levels in DD. We conducted a systematic literature search using PubMed, Embase, and Scopus to identify observational studies assessing the TNF-α levels in DD. Full-text articles that satisfied our inclusion and exclusion criteria were included, and a quality assessment was performed using the Newcastle–Ottawa Scale (NOS). The principal summary outcome was the mean difference (MD). The results were reported as MD (95% confidence interval (CI)). A total of 12 articles involving 883 subjects were included in the qualitative synthesis, out of which 6 studies were included in our quantitative synthesis. We did not observe statistical significance related to the mucosal TNF-α levels in symptomatic uncomplicated diverticular disease (SUDD) vs. the controls (0.517 (95% CI −1.148–2.182)), and symptomatic vs. asymptomatic DD patients (0.657 (95% CI −0.883–2.196)). However, the TNF-α levels were found to be significantly increased in DD compared to irritable bowel disease (IBS) patients (27.368 (95% CI 23.744–30.992)), and segmental colitis associated with diverticulosis (SCAD) vs. IBS patients (25.303 (95% CI 19.823–30.784)). Between SUDD and the controls, as well as symptomatic and asymptomatic DD, there were no significant differences in the mucosal TNF-α levels. However, the TNF-α levels were considerably higher in DD and SCAD patients than IBS patients. Our findings suggest that TNF-α may play a key role in the pathogenesis of DD in specific subgroups and could potentially be a target for future therapies.
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