DISEASES OF THE DIGESTIVE SYSTEM

Digestive disorders may be functional (Drossman, 2006; Drossman et al., 2006), structural, or in some cases combinations of both (Grover et al., 2009). The functional gastrointestinal (GI) disorders (FGIDs), such as irritable bowel syndrome (IBS) or functional dyspepsia, are syndromes—that is, recurrent or prolonged clusters of symptoms that occur together. They result from known disturbances in GI functioning and central dysregulation of this GI function and should be differentiated from psychiatric multisymptom syndromes (for example, somatization disorder) that are determined by central amplification of normal somatic and visceral neural signaling (Drossman et al., 2002, 2006). The FGIDs range in severity from occasional mild episodes to more persistent and disabling symptoms with impaired health-related quality of life. These disorders fit a biopsychosocial construct (Drossman, 1998) and are understood as brain–gut axis dysfunction where psychosocial factors may disrupt gut functioning and vice versa (Jones et al., 2006). Genetic or early environmental predisposing factors including family enablement of illness behaviors (Levy et al., 2000) or early trauma or abuse history (Drossman et al., 1995), in many cases coupled with exposure to acute GI infection (Spiller and Campbell, 2006), can precipitate or exacerbate the clinical expression of FGIDs, causing them to manifest as disturbed motility (that is, constipation, diarrhea, nausea, vomiting), or visceral hypersensitivity (that is, pain, bloating, abdominal fullness). The symptoms can be sustained or perpetuated in the presence of psychological comorbidities including PTSD, anxiety, and depression; maladaptive coping style; or impaired social networks (Creed et al., 2006; Drossman et al., 2002; Levy et al., 2006).

Relevant to this review is the concept of postinfectious IBS, where the FGID is triggered by exposure to infectious agents, which normally cause acute gastroenteritis, but with coexistent stress, in this case deployment to the Gulf War, the symptoms are sustained (Drossman, 1999; Dunlop et al., 2003; McKeown et al., 2006; Spiller and Campbell, 2006). In a recently completed study using the Defense Medical Surveillance System, 31,866 cases of active-duty soldiers with FGIDs registered between 1999 and 2007 were matched to non-FGID active-duty controls. Researchers found a highly significant association of prior infectious gastroenteritis (greatest effect for bacterial gastroenteritis) to those with FGIDs (all p < 0.001), including functional diarrhea (OR 6.28), IBS (OR 3.72), functional constipation (OR 2.15), and functional dyspepsia (OR 2.39), and 28.8% of the active duty personnel studied still received care for the FGID 2 years after initial diagnosis. Thus there is a strong association of prior acute gastroenteritis (Riddle et al., 2009).

The pathophysiology of the FGIDs relate specifically to dysregulation of neural pathways between the brain and gut (that is, the brain–gut axis) that produce motility and sensory disturbances (visceral hypersensitivity), dysregulation of the hypothalamic-pituitary adrenal axis, altered corticolimbic pain modulation, and inflammation of the bowel mucosa associated with altered bacterial flora pain modulation, and inflammation of the bowel mucosa associated with altered bacterial flora (Drossman, 2006; Drossman et al., 2002; Kassinen et al., 2007).

The diagnosis of a functional GI disorder is made by fulfilling standardized symptom-based criteria (Rome criteria) for a minimal period of time, usually 6 months (Drossman, 2006). These criteria have not been used in published studies of Gulf War veterans with the exception of one physiological study (Dunphy et al., 2003). However, recently there have been several research abstracts published using Rome III criteria that describe increased incidence rates of



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