Making sense of polyps: inflammatory and hamartomatous
These notes help me build a clearer picture of the different kinds of colon polyps, their risk for developing into cancer and their management.
The UpToDate article Overview of colon polyps serves as primary reference.1
What’s the difference between neoplastic and non-neoplastic?
Neoplastic cells have a similar genetic makeup, originating from a transformed cell, whereas non-neoplastic proliferations have a polyclonal origin (different types of cells).2
Types of polyps
There are four main types of lesions depending on the tissues they arise from:
- inflammatory polyps
- hamartomatous polyps
- sessile serrated lesions
- adenomatous polyps
Right off the bat these polyps are non-neoplastic and are of two kinds: inflammatory pseudopolyps and prolapse type inflammatory polyps.
Inflammatory pseudopolyps arise after repeated ulceration and healing of the mucosa, commonly in patients with ulcerative colitis (and, to a lesser extent, Crohn’s disease), and usually no bigger than two centimeters. No need to resect them unless they cause obstruction or bleeding. No malignant potential either, but be wary of dysplasia lurking about. Histologically, they’re a mix of distorted colonic epithelium and an inflammed lamina propria.
Prolapse type inflammatory polyps are a consequence of peristalsis-induced trauma leading to twisting, traction and distortion. This, in turn, leads to ischemia and lamina propria fibrosis. There are a few types based on their location, some associated with diverticular disease. Such polyps are to be removed only if they’re symptomatic.
Hamartomatous polyps are disorganized growths of tissues originating from the same site. They occur either sporadically or as a part of several syndromes.
First on the list are juvenile polyps, made up of lamina propria and dilated cystic glands, and mostly diagnosed during childhood in the rectum, sigmoideum and sometimes proximal colon. As they carry no risk for cancer, they should only be treated if symptomatic. However, as part of an autosomal dominant juvenile polyposis syndrome (JPS) giving rise to polyps throughout the GI tract, there is an increased risk for colorectal and gastric cancer.
Moving on to more familiar ground, the polyps associated with the Peutz-Jeghers syndrome3 are a mix of glandular epithelium lining a tree-like smooth muscle frame that’s contiguous with the muscularis mucosa, due to STK11 mutations.4 A risk for both GI and non-GI (breast, ovarian and testicular) cancers is present. The polyps themselves can become cancerous, as well as symptomatic and can occur sporadically.
The Crohkhite-Canada syndrome has, beside GI polyps, a plethora of clinical manifestations.5 There’s a myxoid expansion in the lamina propria and eosinophils in the polyps (and they’re sometimes positive for IgG4), therefore the disease may be immune mediated. This means it may respond to immunosuppressive drugs.
Last on the list are rare hamartomatous tumor syndromes, of which the most relevant are Cowden and Bannayan-Riley-Ruvalcaba syndromes, both caused by mutations in the PTEN gene.6 These are associated with tumors in multiple organs and an increased risk for malignancy.
I’ll cover the other types of polyps in a subsequent post.
References & footnotes
Aside from polyps, clinical manifestations include melanin spots on the lips, perioral region, mouth, palms, soles, nose, perianal and genital areas. ↩
The STK11 gene, located on chromosome 19, codes serine/threonine kinase 11, which basically acts as a tumor suppressor. ↩
Alopecia, skin hyperpigmentation, onychodystrophy, diarrhea, weight loss and abdominal pain. ↩
The Phosphatase and tensin homolog (PTEN) gene is considered a tumor suppressor gene located on chromosome 10q23, down-regulating the PI3K-Akt and mTOR signaling pathways involved in cell proliferation and apoptosis. ↩