FromPatients with CD or UC ages 8 to 21 with mild or moderate disease activity as defined by pediatric Crohn’s disease activity index (PCDAI) score of 10 to 45 or pedia- tric ulcerative colitis index (PUCAI) of 10 to 60 were enrolled into this study. Before the study no change in medication(s) for IBD could occur for a minimum of 1 month for immunosuppressive medications and 2 months for biologics.
Twelve individuals (9 from Seattle Children’s and 3 from Children’s Center for Digestive Health Care, Atlanta, Georgia) enrolled in the study. Mean age of participants was 12.8 ± 2.2 years (range, 10 to 17 y). Six were male. Average disease duration before study was 1.3 ± 1.6 years (range, 0 to 5 y). For patients with CD, macroscopic disease at time of diagnosis per Paris classification was ileocolonic (L3) in 4 patients, ileal (L1) in 4 patients, and colonic (L2) in 1 patient. For patients with UC disease was extensive in 1 patient and pancolitis was present in 2 patients. At the time of entrance into the study, patients were on methotrexate (n=1), azathioprine (n=2), mesalamine (n=4), adali- mumab (n=1), ustekinumab (n=1), and no medication (n = 5)24 (Table 1).
So FOUR of the 12 had increase caloprotectin but they discount those .Four individuals had increased calprotectin at 12 weeks as compared with their 4-week level. The increase in mean calprotectin in the Atlanta group was largely driven by a single patient whose baseline calprotectin rose over 300 points from baseline. One individual confirmed eating non- SCD foods for 2 weeks before calprotectin. The other individual who had clinically performed quite well and maintained on the diet after the study had a normal repeat calprotectin 1 month after the study. The changes in cal- protectin for both the Seattle and Atlanta cohorts were not clinically significant (P = 0.10, 0.67, respectively).
Some EVEN LOST WEIGHTAlthough the results of the study suggest an overall benefit for patients on the SCD with the majority of patients going into clinical remission and many showing an alteration of the microbiome, there are limitations to this study. As an open-labeled study, recruited patients and parents had a strong personal belief that SCD would improve symptoms. It cannot be excluded that participant bias could account for some of the effect seen in the PCDAI/PUCAI. The degree of mucosal healing in this study was not assessed with ileocolonoscopy, but objective evaluation of inflam- mation with both CRP and fecal calprotectin did support the improvements seen in clinical disease activity. Another limitation to dietary therapy is the difficulty in ascertaining compliance with the diet. Although we had study partic- ipants meet with a dietitian at each visit to review the diet, there are no objective measures of dietary compliance. Also, variations in treatment from the different study sites, interpretation of dietary protocols and local resources, could potentially impact the results of the study. Finally the small sample size for this study limits the precision of estimated effects of the SCD within our IBD patients. The study itself also highlights some of the difficulty of dietary therapy. Two individuals were unable to finish the study given difficulty maintaining the diet. In addition, although most individuals gained weight, some did not.
So out of 5 patients with high sed rate(ESR ) only 2 had increased Sed rateWith respect to sedimentation rate, of those individ- uals who were able to maintain the diet for the full study, baseline sedimentation rate was elevated in 5 of 10 patients, and by 12 weeks only 2 individuals had continued elevation of sedimentation rate (Table 3). The mean sedimentation rate decreased from 15.3 ± 11.0 mm/h at baseline to 11.0 ± 9.6 mm/h at the 2-week visit in the Seattle cohort (normal sedimentation rate, 0 to 20mm/h) and decreased from 35.7 ± 1.2 mm/h at baseline to 26.7 ± 16.6 mm/h at the 2-week visit in the Atlanta cohort (normal sed- imentation rate, 0 to 32 mm/h). At 8 and 12 weeks the mean sedimentation rate still remained below baseline level at 8.3 ± 6.0 and 7.4 ± 5.5 mm/h in the Seattle Cohort and 11.7 ± 6.4 and 12.0 ± 12.7 mm/h, respectively, in the Atlanta Cohort. Although there were decreases of sed- imentation rate in both the Seattle and Atlanta groups, only Atlanta changes in sedimentation rate are statistically sig- nificant (P=0.047 at 2wk; P<0.001 at 8 and 12wk).
Serum albumin improved or was maintained for all except 1 patient. Three of 4 patients who presented with hypoalbuminemia had normal of albumin levels by the end of the study (Table 3). The mean albumin levels increased from 4.1±0.77g/dL at baseline to 4.4±0.44g/dL at the 12-week visit in the Seattle cohort (normal albumin, 3.8 to 5.4 g/dL) and increased from 3.2 ± 0.76 g/dL at baseline