Search

Growth impairment of undefined aetiology occurs in approximately 30% of children with chronic inflammatory bowel disease. We measured urinary growth hormone concentrations in 36 children with chronic inflammatory bowel disease and 51 normal controls. The median urinary concentration of growth hormone in the stunted children with chronic inflammatory bowel disease was 15.8 ng/g creatinine (range 4.3-32.6), compared with 11.7 ng/g creatinine (range 4.1-35.9) in those with normal growth. The difference was statistically not significant (p = 0.15). Moreover, there was no significant difference between the patients and the control group. One stunted patient had a urinary growth hormone (UGH) concentration below the normal range, whereas four patients with normal height were also below the normal range. Four of these five patients (80%) were on corticosteroid treatment at the time of urinary collection, whereas only 26% of the patients with normal UGH were also on corticosteroid treatment. We conclude that growth retardation in children with chronic inflammatory bowel disease is probably not related to growth hormone deficiency but must involve other mechanisms.

Twenty children with active ulcerative colitis were assessed before and after 8 weeks of medical therapy with 5-aminosalicylic acid (5-ASA) derivatives and corticosteroids. Local therapy was given for distal disease (seven cases) ; other disease was treated with oral prednisolone (1-2 mg/kg/day, maximum 40 mg). Eighteen of the children showed a clinical improvement on therapy, and complete remission of clinical disease activity by 8 weeks was seen in 17 (85%). C-reactive protein was elevated initially in 10 of 20 children and returned to normal posttreatment in all but one. Reassessment of the colon after treatment showed an improved endoscopic appearance in 15 and complete remission in eight (40%). Histological improvement was seen in 13, with full remission in only three (15%). In conclusion, remission of clinical disease activity by corticosteroid therapy in ulcerative colitis may not be accompanied by endoscopic remission and uncommonly by mucosal healing. This finding may be important prognostically because of the risk of dysplasia in long-standing persistent mucosal inflammation.

Eighteen children and adolescents, of a total of 90 treated in our unit between 1982 and 1992, underwent colectomy for ulceractive colitis. Six (6.7%) of the 90 patients had short stature, i.e., a height below the 3rd centile, and 8 of the 18 who had surgery had a subnormal height velocity, i.e., below the 25th centile for age at the time of surgery. Surgery was performed for resistance to medical therapy (n = 13) or toxic megacolon (n = 5). Surgery was followed by catch-up growth, i.e., increasing height velocity, in eight subjects and cessation of the trend of diminishing height velocity, but without catch-up growth, in five. In 11 of the subjects who were prepubertal, the median height velocity increased from 3.85 cm/year preoperatively to 7.35 cm/year postoperatively (p < 0.01). One year after surgery, 14 of the 18 patients were either asymptomatic or substantially improved. Surgery therefore led to improved linear growth and a prolonged symptom-free period in most of the children and adolescents with ulcerative colitis undergoing this treatment.

Intraepithelial lymphocytes (IEL) are present in fetal human small intestine from 14 weeks' gestation independent of exogenous dietary or microbial antigens. We have now studied the heterogeneity of IEL in 18-22-week-old human fetal intestine and in postnatal small intestine by single and sequential immunoenzyme histochemistry. In normal children and adults, there were 6-27 CD3+ IEL per 100 epithelial cells, whereas in fetal gut there were 3-5 CD3+ IEL per 100 epithelial cells. Postnatal intestine contained a population of CD3-,7+, non-T cell IEL (7-25% of total CD7+). These cells were absent from fetal IEL but were occasionally seen in the fetal lamina propria. About 6% of CD3+ postnatal IEL were CD4-,8-. In contrast in the fetus, 35-70% of CD3+ IEL were subset negative. Since CD3 and CD7 are always co-expressed on fetal IEL, 28-58% of fetal IEL were also CD7+,4-,8-. Only about 20% of the CD3+ IEL expressed the gamma delta chains of the T cell antigen receptor. We conclude from these studies that CD3+,4-,8- T cells migrate to the epithelium in the absence of exogenous antigen and that there is a population of CD3-,7+ non-T cells in postnatal gut which is absent in fetal gut.