Figures & data
Figure 1 Serum MPO concentration was measured in a typical ELISA. Five autistic children (A) with GI disease, two autistic children with no GI disease controls (C*), and three nonautistic children with no GI disease controls (C**) were tested. Four replicate samples were tested for each individual.
![Figure 1 Serum MPO concentration was measured in a typical ELISA. Five autistic children (A) with GI disease, two autistic children with no GI disease controls (C*), and three nonautistic children with no GI disease controls (C**) were tested. Four replicate samples were tested for each individual.](/cms/asset/3c42d20a-8689-4f76-a55c-cea6c6d180f4/dceg_a_6051_f0001_c.jpg)
Figure 2 MPO serum concentration was established for each individual by testing and correlating to known standards of various concentrations of MPO (15–1.875 ng/ml) as well as a negative control (serum diluent alone).
![Figure 2 MPO serum concentration was established for each individual by testing and correlating to known standards of various concentrations of MPO (15–1.875 ng/ml) as well as a negative control (serum diluent alone).](/cms/asset/d784e96e-2b43-458d-8b28-e21f1b4ca042/dceg_a_6051_f0002_c.jpg)
Figure 3 The mean ± SD MPO concentration (ng/ml) of 40 autistic children with chronic digestive disease (most with ileo-colonic LNH and inflammation of the colorectum, small bowel and/or stomach) (autistic GI), and 48 controls (12 age matched autistic children with no GI disease; control autistic, no GI), 20 age-matched siblings of autistic children, without autism or GI disease (control, no autism, no GI), and 16 nonautistic individuals with no family history of autism (control no family history autism).
![Figure 3 The mean ± SD MPO concentration (ng/ml) of 40 autistic children with chronic digestive disease (most with ileo-colonic LNH and inflammation of the colorectum, small bowel and/or stomach) (autistic GI), and 48 controls (12 age matched autistic children with no GI disease; control autistic, no GI), 20 age-matched siblings of autistic children, without autism or GI disease (control, no autism, no GI), and 16 nonautistic individuals with no family history of autism (control no family history autism).](/cms/asset/76f4daea-c8d5-4787-8389-5bfb2b94c2b7/dceg_a_6051_f0003_c.jpg)
Table 1 The total data from two assays of experimental and control groups is represented. The mean, standard deviation and standard error of the mean of MPO concentration (ng/ml) of 40 autistic children with chronic digestive disease (most with ileo-colonic LNH and inflammation of the colorectum, small bowel and/or stomach) (autistic GI), and 48 controls (12 age-matched autistic children with no GI disease; autistic, no GI), 20 age-matched siblings of autistic children, without autism or GI disease (nonautistic, no GI), and 16 nonautistic individuals with no family history of autism (no family history autism)
Table 2 MPO concentration of autistic children with GI disease with ANCA (anti-MPO or anti-MPO/anti-PR3; bold) and without ANCA are compared (p = 0.3718)
Table 3 MPO concentration of autistic children with GI disease with (bold) and without LNH, with (bold) and without erythema and with (bold) and without severe total GI disease are compared