Initial levels of GI symptoms also differed among the FGID-POS, FGID-NEG, and well control groups, F (2, 241) = 18.44, P < 0.01. Tukey HSD tests revealed that both FGID-NEG and FGID-POS groups reported significantly more GI symptoms at initial evaluation compared with the well control participants (all <0.01). The FGID-POS group also reported significantly more GI symptoms than the FGID-NEG group at initial evaluation, P < 0.01 (Fig. 1). Figure 3 shows the percentage of participants in each group endorsing each of the 9 GI symptoms at initial evaluation.
Results of this prospective study showed that more than one-third (36%) of patients with Ped-FAP met symptom criteria for 1 or more FGIDs at a follow-up assessment 4 to 15 years after their initial medical evaluation. This finding is consistent with other reports (5) linking Ped-FAP to FGIDs in adulthood and has the benefit of a more rigorous prospective design and application of Rome III symptom criteria for FGIDs at follow-up.
Unique to the present study, we found that a high level of non-GI symptoms at the initial pediatric evaluation was associated with a greater likelihood of FGIDs in adolescence and young adulthood. In contrast, patients with Ped-FAP who did not subsequently meet criteria for FGIDs had baseline levels of non-GI symptoms similar to those of well controls. Thus, the presence of non-GI somatic symptoms such as back pain, weakness, and low energy may help differentiate a population of patients with Ped-FAP at high risk for FGIDs across the course of development.
It may be that individuals with functional somatic disorders are predisposed to a general heightened sensory responsiveness throughout the body (19). Enhanced responsiveness to pain and bodily sensations has been implicated in fibromyalgia, chronic fatigue syndrome (19,20), and headache (21). A recent study (22) showed evidence of neuronal changes in patients with functional pain disorders—specifically loss of gray matter in cortical areas (cingulate, insular, and prefrontal cortices) involved in the subjective, emotional experience of pain. Changes in the composition or function of these brain regions may affect how pain and bodily sensations are processed at the central level (22,23). Future studies should test the relation between somatic symptom reporting and responsiveness to painful visceral and somatic stimuli in pediatric FAP.
The Ped-FAP group that went on to develop FGIDs years later as adolescents and adults (FGID-POS) also reported significantly more GI symptoms at initial evaluation compared with well controls and those classified as FGID-NEG at follow-up. However, patients with Ped-FAP whose abdominal pain eventually resolved (FGID-NEG) also reported significantly more GI symptoms at initial evaluation compared with the well control group. Because both FGID-POS and FGID-NEG groups reported more GI symptoms than controls, the number of GI symptoms at initial evaluation may not be as useful as a predictor of future FGIDs as non-GI symptoms.
The present study had several limitations that suggest directions for future research. First, our patients with Ped-FAP were recruited from a tertiary care setting. Additional work is needed to evaluate whether findings generalize to patients with Ped-FAP in other settings. Second, we focused exclusively on non-GI somatic symptoms as a potential factor for long-term persistence of FGIDs. Assessment of non-GI symptoms may easily be incorporated into the medical evaluation during the clinical interview or by means of a questionnaire (17) and, therefore, has potential clinical utility. Non-GI symptoms, however, may be only 1 feature of a symptom complex that includes psychiatric comorbidities as well as family and environmental stressors. It is possible that all of these factors covary with non-GI symptoms during the course of development. Another limitation of the present study is that follow-up assessment was based on self-report of Rome III symptoms and did not include a medical evaluation to rule out organic disease. Therefore, we cannot rule out the possibility that, in some cases, GI symptoms reported at follow-up reflected underlying disease. Also, we do not know how treatment history (if any) may or may not have affected FGID outcome in the pediatric FAP group.
Multiple studies have shown that patients with FGIDs have increased health care use, and irritable bowel syndrome itself has been shown to be a large health care burden (24–28). The ability to identify children with FAP who are at risk for FGIDs in adulthood may provide the opportunity to alter the trajectory of these individuals' health outcomes. If at-risk children could be identified on the basis of assessment of somatic comorbidities, this population could be targeted for interventions such as cognitive behavioral therapy, which has been shown to benefit pediatric patients with FGIDs (9,29). These interventions may have a greater effect if done at an early age. Moreover, identification of pediatric patients at risk for persistent FGIDs may offer the opportunity to direct limited resources to these patients, resulting in later savings to the health care system.
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