True about solitary rectal ulcer syndrome is all/except

Histopathology of solitary rectal ulcer syndrome shows hypocellular lamina propria. There is relative absence of inflammatory cells. Surgical Pathology & Cytopathology writes - "There may be crypt architectural distortion and branching similar to that evident in idiopathic irritable bowel syndrome (IBD), but without the dense lamina propria inflammation". Solitary Rectal Ulcer Syndrome The pathogenesis of mucosal prolapse syndrome or solitary rectal ulcer syndrome is unclear. It has been postulated that there is a dysfunction of the neuromuscular control of defecation. This necessitates an increase in intraabdominal pressure to achieve expulsion of the stool. The pressure then forces a rectal mucosal fold to prolapse into the anal canal. Localized ischemia of the prolapsed mucosa as a result of local vascular compromise then produces the characteristic histological change of SRUS. SRUS affects both sexes, over a wide range, but is most common in women 20-40 years of age. Most lesions occur on the anterior or anterolateral rectal wall, but SRUS may involve the bowel anywhere from the sigmoid to the anorectal junction. Despite the designation solitary rectal ulcer, in 10 to 15% of cases multiple ulcers may be present within a single patch of diseased mucosa. Endoscopically only about half of the patients with SRUS have an actual ulcer. The remaining patients have an area of mucosal erythema, mucosal nodules, or frank polyps, which may or may not have surface ulceration. The histological features can be correlated to the underlying pathogenesis of the disorder. Prolapsed mucosa becomes ischemic due to compression of the vascular supply, particularly the small veins. This leads to detachment of the surface epithelium and withering of the superficial portion of the crypts, similar to ischemia from any cause. Since the prolapse is typically intermittent, during intervals of normal blood flow regrowth of the mucosa is stimulated, resulting in mucosal hyperplasia due to elongation of the crypts. As an additional response to the ischemic injury, fibrosis of the lamina propria occurs. There may be crypt architectural distortion and branching similar to that evident in idiopathic irritable bowel syndrome, but without the dense lamina propria inflammation. The muscularis mucosa also becomes thickened and disorganized and tongues of muscle extend upwards from the muscularis mucosa to the surface epithelium. In some cases the ischemia is severe enough to lead to erosion or ulceration, often with a scanty overlying pseudo membrane. The cells show enlarged, hyper chromatic nuclei, excess mitotic activity, and mucin-depleted goblet cells.