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 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.
1. Apley J, Hale B. Children
with recurrent abdominal pain: how do they grow up? Br Med J 1973; 3:7–9.
2. Chitkara DK, Rawat DJ, Talley NJ. The epidemiology of childhood recurrent abdominal pain in Western countries: a systematic review. Am J Gastroenterol 2005; 100:1868–1875.
3. Konijnenberg AY, de Graeff-Meeder ER, van der Hoeven J, et al
. Psychiatric morbidity in children
with medically-unexplained chronic pain: diagnosis from the pediatrician's perspective. Pediatrics 2006; 117:889–897.
4. Rasquin A, Di Lorenzo C, Forbes D, et al
. Childhood functional gastrointestinal
disorders: child/adolescent. Gastroenterology 2006; 130:1527–1537.
5. Gieteling MJ, Bierma-Zeinstra SM, Passchier J, et al
. Prognosis of chronic or recurrent abdominal pain in children
. J Pediatr Gastroenterol Nutr 2008; 47:316–326.
6. Walker LS, Garber J, Van Slyke DA, et al
. Long-term health outcomes in patients with recurrent abdominal pain. J Pediatr Psychol 1995; 20:233–245.
7. Walker LS, Guite JW, Duke M, et al
. Recurrent abdominal pain: a potential precursor of irritable bowel syndrome in adolescents
and young adults. J Pediatr 1998; 132:1010–1015.
8. Christensen MF, Mortensen O. Long-term prognosis in children
with recurrent abdominal pain. Arch Dis Child 1975; 50:110–114.
9. Chitkara DK, van Tilburg MA, Blois-Martin N, et al
. Early life risk factors that contribute to irritable bowel syndrome in adults: a systematic review. Am J Gastroenterol 2008; 103:765–774.
10. Howell S, Poulton R, Talley NJ. The natural history of childhood abdominal pain and its association with adult irritable bowel syndrome: birth-cohort study. Am J Gastroenterol 2005; 100:2071–2078.
11. Claar RL, Walker LS. Functional assessment of pediatric pain patients: psychometric properties of the functional disability inventory. Pain 2006; 121:77–84.
12. Little CA, Williams SE, Puzanovova M, et al
. Multiple somatic symptoms
linked to positive screen for depression in pediatric patients with chronic abdominal pain
. J Pediatr Gastroenterol Nutr 2007; 44:528–562.
13. Mulvaney S, Lambert EW, Garber J, et al
. Trajectories of symptoms and impairment for pediatric patients with functional abdominal pain: a 5-year longitudinal study. J Am Acad Child Adolesc Psychiatry 2006; 46:737–744.
14. Walker LS, Garber J, Smith CA, et al
. The relation of daily stressors to somatic and emotional symptoms in children
with and without recurrent abdominal pain. J Consult Clin Psychol 2001; 69:85–91.
15. Walker LS, Smith CA, Garber J, et al
. Testing a model of pain appraisal and coping in children
with chronic abdominal pain
. Health Psychol 2005; 24:364–374.
16. Walker LS, Baber KF, Garber J, et al
. A typology of pain coping strategies in pediatric patients with chronic abdominal pain
. Pain 2008; 137:266–275.
17. Walker LS, Beck JE, Garber J, et al
. The Children
's Somatization Inventory: psychometric properties of the revised form (CSI-24). J Pediatr Psychol 2009; 34:430–440.
18. Drossman DA, Corazziari E, Delvaux M, et al. Rome III: The Functional Gastrointestinal Disorders
, 3rd ed. McLean, VA: Degnon Associates; 2006.
19. Geisser ME, Donnell CS, Petzke F, et al
. Comorbid somatic symptoms
and functional status in patients with fibromyalgia and chronic fatigue syndrome: sensory amplification as a common mechanism. Psychosomatics 2008; 49:235–242.
20. Yunus MB, Masi AT. Juvenile primary fibromyalgia syndrome. A clinical study of thirty-three patients and matched normal controls. Arthr Rheum 1985; 28:138–145.
21. Aamodt AH, Stovner LJ, Hagen K, et al
. Comorbidity of headache and gastrointestinal
complaints: the Head-HUNT study. Cephalalgia 2007; 28:144–151.
22. Valet M, Gundel H, Sprenger T, et al
. Patients with pain disorder show gray-matter loss in pain-processing structures: a voxel-based morphometric study. Psychosom Med 2009; 71:49–56.
23. Lane RD, Waldstein SR, Critchley HD, et al
. The rebirth of neuroscience in psychosomatic medicine, part II: clinical applications and implications for research. Psychosom Med 2009; 71:135–151.
24. Campo JV, Comer DM, Jansen-McWilliams L, et al
. Recurrent pain, emotional distress, and health service use in childhood. J Pediatr 2002; 141:76–83.
25. Camilleri M, Choi MG. Review article: irritable bowel syndrome. Aliment Pharmacol Ther 1997; 11:3–15.
26. Drossman DA, Camilleri M, Mayer EA, et al
. AGA technical review of irritable bowel syndrome. Gastroenterology 2002; 123:2108–2131.
27. Cash B, Sullivan S, Barghout V. Total costs of IBS: employer and managed care perspective. Am J Manag Care 2005; 11:S7–S16.
28. Levy RL, Von Korff M, Whitehead WE, et al
. Costs of care for irritable bowel syndrome patients in a health maintenance organization. Am J Gastroenterol 2001; 96:3122–3129.
29. Youssef NN, Rosh JR, Loughran M, et al
. Treatment of functional abdominal pain in childhood with cognitive behavioral strategies. J Pediatr Gastroenterol Nutr 2004; 39:192–196.