Rectal prolapse in pediatrics has its highest incidence in infancy and is uncommonly seen in industrialized countries. The prolapse may involve only the mucosa (mucosal prolapse) or all layers of the rectum (complete prolapse or procidentia). It is usually detected by the child's parents and is brought urgently to medical attention; however, it is usually spontaneously reduced by the time they reach the practitioner's office. Rectal prolapse should be viewed as a symptom of an underlying condition rather than a discrete disease entity. Potential causes are increased intraabdominal pressure, diarrheal and neoplastic diseases, malnutrition, and conditions predisposing to pelvic floor weakness. Its strong association with cystic fibrosis makes the sweat test mandatory for infants and children with recurrent rectal prolapse. Of particular importance are three entities related to rectal prolapse that may easily escape diagnosis by practitioner: occult rectal prolapse, solitary ulcer of the rectum syndrome, and inflammatory cloacogenic polyps. The treatment of rectal prolapse is mainly conservative and is directed at the underlying conditions. Surgical intervention may be required for recurrent rectal prolapse refractory to conservative measures. The simplest, less invasive, yet highly effective approach, appears to be perirectal injection with a sclerosing agent. While the majority of children experience spontaneous resolution of the prolapse, the prognosis is worse when presentation occurs after the age of 4 years.

VEGF (vascular endothelial growth factor) is a multifunctional cytokine active on blood vessel cells. The present study measured VEGF in the aqueous phase of human milk and examined how the concentration varied with gestational age and the duration of lactation after birth. We hypothesized that VEGF-specific receptors were present on the apical surface of intestinal epithelial cells. The concentration of monomeric VEGF (containing 165 residues) measured by ELISA in the breast milk was 2 orders of magnitude greater than that measured in the serum of normal adults. The VEGF165 concentration in the first week of lactation was greater in the breast milk of mothers of full-term than in preterm babies (p < 0.05). The concentration in the breast milk of mothers of full-term infants decreased (p < 0.01) after the first week of lactation. Scatchard analysis of radioligand-receptor binding showed the presence of specific receptors for 125I-VEGF165 on the surface of Caco-2, an intestinal epithelial cell line, with a kd of 2.85 to 4 nM. Reverse transcriptase PCR of Caco-2 cell RNA showed mRNA for the VEGF receptor flt-1. In conclusion, VEGF is present in high concentrations in breast milk and binds to specific receptors on cells derived from intestinal epithelium.