Table 4.
Reference, first author | Inflammation score | Fibrosis score | Main achievements |
---|---|---|---|
Dillman JR19 | 0 = o inflammation 1 = ow level of inflammation with scattered infiltrating mononuclear cells 2 = oderate inflammation with multiple foci 3 = igh level of inflammation with increased vascular density and marked wall thickening 4 = aximal severity of inflammation with transmural leukocyte infiltration and loss of goblet cellsa |
0 = o architectural distortion, no abnormal Masson trichrome staining 1 = o architectural distortion, mild abnormal Masson trichrome staining in mucosa/submucosa 2 = ubstantial abnormal mucosal/submucosal Masson trichrome staining with modest distortion of architecture but without obscuration of the mucosal/submucosal border 3 = ransmural fibrosis with abnormal Masson trichrome staining in all histological layers, transmural architectural distortion |
Statistically significant difference of SWE throughout the classes of fibrosis [low vs high fibrosis AUC max = 0.91] |
Baumgart DC20 | 1.presence of intraepithelial neutrophils [0 = none, 1 = few, 2 = excessive] 2.goblet cell reduction in crypts with surrounding neutrophils [0 = none, 1 = little, 2 = excessive] 3.excess of neutrophils in lamina propria [0 = none, 1 = few, 2 = excessive] 4.presence of crypt atrophy [0 = absent, 1 = present] 5.presence of fibrosis [0 = absent, 1 = present]b |
0 = o increased collagen deposition 1 = ncreased collagen deposition in submucosa 2 = ncreased collagen deposition in submucosa and mucosa 3 = ncreased collagen deposition in muscularis mucosa, submucosa, and mucosa, as well as thickening and disorganiation of the muscularis mucosa 4 = ncreased collagen deposition in muscularis propria, muscularis mucosa, submucosa, and mucosa 5 = increased collagen throughout all layers, including serosae |
Higher collagen content in affected versus unaffected segments associated with RTE-assessed strain [p <0..001] |
Fraquelli M21 | acute inflammatory score, and chronic inflammatory score ‡ | Mild/moderate versus severec | Strain ratio was significantly correlated with the bowel fibrosis [AUC for severe fibrosis = 0.917]. Bowel fibrosis was the only independent determinant of the strain ratio at multivariate analysis |
Lu C22 | 1.acute inflammatory score [ulceration, cryptitis, crypt abscess, lamina propria neutrophilic infiltration] 2.chronic inflammatory score [lamina propria lymphoplasmacytic cellularity, lamina propria eosinophilic infiltration, crypt architecture alteration] |
0 = one 1= <33% 2= >33% and <66% 3= 66% |
Correlation observed between SWE and muscular hypertrophy No correlation between SWE and fibrosis score |
Serra C23 | 0 = o polymorphonuclear or mononuclear leukocytes infiltrates 1 = Mild] cryptitis, leukocytes infiltrates limited to mucosa 2 = Moderate] cryptitis, crypt abscess, and leukocytes infiltrates until the submucosa 3 = [Severe] transmural inflammation with leukocytes infiltrates in all the layersc |
0 = one or normal fibrosis 1 = inimal fibrosis limited to submucosa 2 = Submucosaland muscular layer fibrosis <30% 3 = ubmucosal and muscular layer fibrosis between 30% and 60%, with preserved layers 4 = Massive transmural fibrosis >60%, effacement of normal layersc |
No correlation between SE and fibrosis score |
Chen YJ24 | 0 = o inflammation or distortion 1 = amina propria inflammation only 2 = ubmucosal foci of inflammation and/or foci of transmural inflammation 3 = ignificant, dissecting, confluent transmural inflammation |
0 = o fibrosis 1 = inimal fibrosis in submucosa or subserosa 2 = ncreased submucosal fibrosis, septa into muscularis propria and/or septa through muscularis propria, increase in sub-serosal collagen 3 = ignificant transmural scar, marked sub-serosal collagen |
SWE was significantly different throughout the classes of fibrosis [mild/moderate vs severe fibrosis AUC = 0.822; sensitivity = 69.6%; specificity = 91.7%]. No difference in SWE observed with respect to inflammation classes. Combined SWE + US showed a moderate agreement with the classes of strictures |
Quaia E25 | 1.mucosal ulceration [grade 0–3] 2.edema [grade 0–3] 3.quantity [grade 0–3] of neutrophilic infiltration 4.depth [grade 0–4] of neutrophilic infiltrationc |
Sections were scored as positive for fibrosis if at least moderate fibrosis was observed which involved the submucosa or deeper layersd | SE was able to differentiate between fibrosis and inflammation with a maximal AUC of 0.885 |
RTE; real-time elastography; SE, strain elastography; AUC, area under the curve; SWE, shear wave elastography.
According to Likert-like scales.
According to Bataille F, Klebl F, Rümmele P, et al. Histopathological parameters as predictors for the course of Crohn’s disease. Virchows Arch 2003;443:501–7.
According to Chiorean MV, Sandrasegaran K, Saxena R, et al. Correlation of CT enteroclysis with surgical pathology in Crohn’s disease. Am J Gastroenterol 2007;102:2541–50 and/or Borley NR, Mortensen NJ, Jewell DP, et al. The relationship between inflammatory and serosal connective tissue changes in ileal Crohn’s disease: evidence for a possible causative link. J Pathol 2000;190:196–202.
According to Gupta RB, Harpaz N, Itzkowitz S, et al. Histologic inflammation is a risk factor for progression to colorectal neoplasia in ulcerative colitis: a cohort study. Gastroenterology 2007;133:1099–105.
According to Theiss AL, Fuller CR, Simmons JG, Liu B, Sartor RB, Lund PK. Growth hormone reduces the severity of fibrosis associated with chronic intestinal inflammation. Gastroenterology 2005;129:204–19.