Published online Sep 7, 2026. doi: 10.3748/wjg.118486
Revised: April 1, 2026
Accepted: May 6, 2026
Published online: September 7, 2026
Processing time: 214 Days and 15.1 Hours
Chicken skin mucosa (CSM) is an endoscopic finding characterized by a speckled, pale-yellow appearance on the colorectal surface, which results from lipid accumulation in the lamina propria. The clinical role of CSM remains unclear.
To investigate the clinical significance of CSM by evaluating the clinical, endoscopic, pathological, and immunohistochemical transmembrane member 16A (TMEM16A, a calcium-activated chloride channel) characteristics of adenomas.
This retrospective study included 2237 consecutive patients who were pathologically diagnosed with colorectal adenomas and underwent endoscopic polypectomy at the First Affiliated Hospital of Dalian Medical University between September 2021 and January 2023. Clinical, colonoscopic, and pathological data from colorectal adenomas were collected and analyzed. TMEM16A protein expression was detected by immunohistochemical analysis in 37 consecutive adenomas with CSM and 38 consecutive adenomas without CSM.
The mean age of patients in the CSM group was higher than that in the non-CSM group (P = 0.02). The CSM group had a greater incidence of multiple adenomas (P < 0.001) and larger median adenoma size (P < 0.001). Adenomas with CSM were predominantly located in the distal colon and exhibited protruding morphology. There was a significant difference in the distribution and morphology of the adenomas between the two groups (P < 0.001). The incidence of advanced adenomas in the CSM group was greater than that in the non-CSM group (P < 0.001), and the presence of CSM was independently associated with advanced adenomas (adjusted odds ratio: 81.670; 95% confidence interval: 29.902-223.062; P < 0.001). TMEM16A expression was higher in the CSM group than in the non-CSM group (P = 0.034), and it was significantly elevated in the advanced adenomas group compared to non-advanced adenomas (P < 0.001).
This study demonstrates an independent association between the presence of CSM and advanced colorectal adenoma, potentially mediated by TMEM16A. These findings offer valuable insights for enhancing decision-making and patient management strategies.
Core Tip: Chicken skin mucosa (CSM) is an endoscopic, pale-yellow, speckled pattern appearing on colorectal mucosa, typically adjacent to colorectal neoplasm. Our study demonstrated that CSM is independently associated with advanced colorectal adenomas, featuring characteristics such as large size, multiple occurrences, distal location, protruding morphology, and dysplastic histology. Transmembrane member 16A (a calcium-activated chloride channel) expression was significantly higher in advanced than non-advanced adenomas based on immunohistochemistry. The independent link between CSM and advanced colorectal adenoma offers valuable insights for improved clinical decision-making and patient management.
- Citation: Wang RJ, Hu Y, Guo SB. Chicken skin mucosa is independently associated with advanced colorectal adenoma with transmembrane member 16A potentially involved in this association. World J Gastroenterol 2026; 32(33): 118486
- URL: https://www.wjgnet.com/1007-9327/full/v32/i33/118486.htm
- DOI: https://dx.doi.org/10.3748/wjg.118486
Initially described by Shatz et al[1] in 1998, colorectal chicken skin mucosa (CSM) is an endoscopic finding characterized by a speckled, pale-yellow appearance on colorectal mucosa, which results from lipid accumulation in the lamina propria. Unlike colonic xanthoma, CSM only appears adjacent to colorectal neoplasms[2]; however, the clinical significance of CSM remains unclear. CSM was initially used to describe morphological changes in the mucosa adjacent to colorectal tumors[3,4]. Previous studies have shown that CSM is more common on larger juvenile polyps and is considered a result of local mucosal damage rather than precancerous lesions[4]. Additionally, Nowicki et al[5] noted that CSM can appear in the mucosa surrounding various types of polyps due to local tissue damage, and is not a preneoplastic lesion.
However, recent studies have reported conflicting results[6]. While one study identified CSM as an independent endoscopic predictor of colorectal neoplastic polyps[7], Guan et al[8] reported that CSM exhibits increased proliferation [Ki-67 and cyclooxygenase 2 (COX-2)] and reduced apoptosis (caspase-3).
Transmembrane member 16A (TMEM16A), also referred to as anoctamin-1, is a calcium-activated chloride channel in the cell membrane. It is overexpressed in several malignant tumors, including colorectal cancer (CRC)[9]. High TMEM16A expression is involved in the tumorigenesis of CRC[10] and could be a predictive factor of lymph node metastasis[11].
This study analyzed the clinical data, colonoscopic, pathological, and immunohistochemical data from patients with colorectal adenomas, with or without CSM, to assess the relationship between CSM and the risk of adenoma carcinogenesis.
This retrospective cross-sectional study was conducted at the First Affiliated Hospital of Dalian Medical University (Dalian, Liaoning Province, China) in accordance with the Helsinki Declaration and local legislation. The study was approved by the Ethics Committee of the First Affiliated Hospital of Dalian Medical University, approval No. PJ-KS-KY-2022-327. Written informed consent was obtained from patients or their relatives.
A total of 2237 consecutive patients who had undergone endoscopic treatment and were pathologically diagnosed with adenomas from September 2021 to January 2023 were enrolled. Endoscopic treatments included endoscopic mucosal resection, cold snare polypectomy, and endoscopic submucosal dissection. The exclusion criteria were as follows: (1) Patients with severe benign and malignant intestinal stenosis; (2) Patients with severe cardiopulmonary diseases or other contraindications for colonoscopy; (3) Age < 18 years or > 80 years; (4) Pregnant and lactating women; (5) Severe coagulation dysfunction; (6) Poor bowel preparation; (7) Patients with CRC or a history of malignancy; (8) Inflammatory bowel disease; (9) Familial adenomatous polyposis; and (10) Incomplete case data.
A standard split-dose of 3 L polyethylene glycol solution was administered for bowel preparation. The procedure was performed under electrocardiogram monitoring by two experienced endoscopists, utilizing a standard colonoscope (CF-H290I; Olympus, Tokyo, Japan). The number, location, morphology (with or without CSM), and polyp size (measured during pathological sample processing) were recorded. Patient data, including age, sex, clinical manifestations, and concomitant diseases, were also collected, and pathological reports of adenomas were reviewed.
CSM is classified into two types[12]. Type 1 can be easily confirmed before injection, whereas type 2 is difficult to detect using conventional white light endoscopy, and requires submucosal injection (Figure 1).
The location of the adenoma was categorized into the proximal colon (cecum, ascending colon, hepatic flexure, and transverse colon) and distal colon (splenic flexure, descending colon, sigmoid colon, and rectum)[7].
Advanced adenoma was defined as any adenoma ≥ 1 cm, high-grade dysplasia, or villous or tubulovillous histology[13].
We also detected TMEM16A protein expression in adenomas with or without CSM using immunohistochemical analysis. A total of 37 consecutive specimens of adenomas with CSM from September 2021 to January 2022 and 38 consecutive specimens of adenomas without CSM were enrolled for immunohistochemical analysis. According to the criteria for advanced adenomas, the 75 specimens were divided into an advanced adenoma group (n = 39) and a non-advanced adenoma group (n = 36). TMEM16A expression in the two groups was detected by immunohistochemical analysis.
Immunohistochemical staining for TMEM16A was conducted as previously described[14]. The proportion of positively stained cells was graded as follows: A score of 4 for > 75% positive cells, 3 for 50%-75%, 2 for 25%-50%, and 1 for < 25%. Staining intensity was assessed based on coloration: 0 for no staining, 1 for faint yellow, 2 for light brown, and 3 for dark brown. Evaluation of TMEM16A protein expression was performed by two pathologists who were blinded to the patients’ clinical information. The overall score was calculated by multiplying the staining intensity score by the percentage of positive cells[15]. The primary outcome was comparing the size, quantity, morphology, location, and pathology of adenomas with and without CSM, whereas secondary outcomes focused on TMEM16A protein expression between the two groups.
All statistical analyses were conducted with SPSS software (version 25.0; IBM SPSS Statistics, Chicago, IL, United States). Continuous data are presented as the mean ± SD and were compared using the Student’s t-test. Categorical variables are shown as the frequencies and percentages, and were assessed with the χ2 or Fisher’s exact test, as appropriate. P < 0.05 was considered statistically significant.
Following the application of exclusion criteria, 2237 patients (4867 adenomas) were enrolled from September 2021 to January 2023. The study cohort was divided into a CSM group (138 patients, 474 adenomas) and a non-CSM group (2099 patients, 4393 adenomas), with the CSM group being significantly older (59.27 ± 10.89 years vs 56.90 ± 11.64 years; t = 2.32, P = 0.02). Males accounted for 55.8% (n = 77) of the CSM group compared to 56.6% (n = 1187) in the non-CSM group. There was no significant difference in sex between the two groups (P = 0.863). In the CSM group, 24 patients (17.4%) had a single adenoma and 114 (82.6%) had multiple adenomas (n ≥ 2). In the non-CSM group, 959 patients (45.7%) had a single adenoma and 1140 (54.3%) had multiple adenomas. The incidence of multiple adenomas was higher in the CSM group than in the non-CSM group (P < 0.001; Table 1).
| Characteristic | CSM group (n = 138) | Non-CSM group (n = 2099) | OR (95%CI) | P value |
| Age (year), mean ± SD | 59.27 ± 10.89 | 56.90 ± 11.64 | 2.37 (0.373-4.367) | 0.02 |
| Sex | 1.031 (0.729-1.459) | 0.863 | ||
| Male | 77 (55.8) | 1187 (56.6) | ||
| Female | 61 (44.2) | 912 (43.4) | ||
| No. of adenomas | - | - | 3.624 (2.345-5.600) | < 0.001 |
| Single | 24 (17.4) | 959 (45.7) | ||
| Multiple (n ≥ 2) | 114 (82.6) | 1140 (54.3) | ||
A total of 4867 adenomas were divided into two groups: Adenomas with CSM (n = 140) and adenomas without CSM (n = 4727). The median size of adenomas with CSM group was larger than that of adenomas without CSM (P < 0.001; Table 2).
| Characteristic | Adenoma with CSM (n = 130) | Adenoma without CSM (n = 2107) | OR (95%CI) | P value |
| Size (cm) | 1.0 (1.0, 1.5) | 0.5 (0.5, 0.6) | -6.968 (-8.187 to -5.749) | < 0.001 |
| Morphology | 11.715 (2.884-47.585) | < 0.001 | ||
| Flat (IIa, Is, LST) | 2 (1.5) | 326 (15.5) | ||
| Protruding (Ip, Isp) | 128 (98.5) | 1781 (84.5) | ||
| Location | 7.958 (4.854-13.004) | < 0.001 | ||
| Proximal colon | 19 (14.6) | 1215 (57.7) | ||
| Distal colon | 111 (85.4) | 892 (42.3) | ||
| Histology | < 0.001 | |||
| Tubular adenoma | 61 (46.9) | 2065 (98.0) | - | |
| Villous or tubulovillous adenoma | 39 (30.0) | 24 (1.1) | ||
| High-grade neoplasia | 30 (23.1) | 18 (0.9) | ||
| Adenoma type | 71.757 (43.325-118.846) | < 0.001 | ||
| Non-advanced adenoma | 20 (15.7) | 1957 (92.9) | ||
| Advanced adenoma | 110 (84.3) | 150 (7.1) | ||
Adenomas with CSM were primarily located in the distal colon (85.7%) compared to the proximal colon (14.3%), whereas adenomas without CSM exhibited a more varied distribution (62.3% proximal vs 37.7% distal), showing a statistically significant difference between the two groups (P < 0.001).
Adenoma morphology significantly differed between groups (P < 0.001). The group with CSM was predominantly characterized by a protruding morphology (98.6%), whereas the group without CSM showed both protruding (86.3%) and flat (13.7%) morphologies.
Microscopically, CSM was characterized by the accumulation of lipid-filled macrophages within the lamina propria (Figure 2). In the group of adenomas with CSM, 64 (45.7%) were tubular, 43 (30.7%) were villous or tubulovillous, and 33 (23.6%) displayed high-grade dysplasia. In the group of adenomas without CSM, 4651 (98.4%), 47 (1.0%), and 29 (0.6%), respectively, showed significant differences in pathology between the two groups (P < 0.001). The incidence of advanced adenomas was significantly higher in the group with CSM (84.3%) compared to the group without CSM (3.6%) (P < 0.001; Table 2). Furthermore, multivariable logistic regression analysis, adjusted for potential confounders such as patient age, lesion size, anatomical location, and morphological characteristics, identified CSM as an independent predictor of advanced adenoma (adjusted odds ratio = 81.670; 95% confidence interval: 29.902-223.062; P < 0.001) (Table 3).
| Characteristic | Multivariable logistic regression analysis | |
| OR (95%CI) | P value | |
| Age, year | 0.978 (0.950-1.007) | 0.136 |
| Sex | 0.630 (0.334-1.190) | 0.154 |
| Single vs multiple adenomas | 1.702 (0.806-3.591) | 0.163 |
| Size, cm | 1.086 (1.020-1.157) | 0.010 |
| Proximal vs distal colon | 52.214 (14.781-184.450) | < 0.001 |
| Flat vs protruding | 2.555 (0.508-12.837) | 0.255 |
| Histology | 33.934 (17.441-66.023) | < 0.001 |
| Non-advanced vs advanced adenoma | 81.670 (29.902-223.062) | < 0.001 |
Immunohistochemical staining showed that the 16A protein was mainly located in the membrane and cytoplasm of the adenoma cells, consistent with previous studies[16]. The immunohistochemistry score in the CSM group was significantly higher than that in the non-CSM group (5.54 ± 3.25 vs 4.21 ± 1.85; P = 0.034) (Figure 3, Table 4). The immunohistochemistry score in the advanced adenoma group was significantly higher than that in the non-advanced adenoma group (6.10 ± 2.77 vs 3.53 ± 1.87; P < 0.001) (Figure 4, Table 4).
| Group | Scores of IHC | OR (95%CI) | P value |
| CSM status | |||
| Adenoma with CSM (n = 37) | 5.54 ± 3.25 | 1.33 (0.103-2.557) | 0.034 |
| Adenoma without CSM (n = 38) | 4.21 ± 1.85 | - | - |
| Adenoma type | |||
| Advanced adenoma (n = 39) | 6.10 ± 2.77 | 2.57 (1.488-3.652) | < 0.001 |
| Non-advanced adenoma (n = 36) | 3.53 ± 1.87 | - | - |
CRC ranks among the most prevalent gastrointestinal malignancies worldwide[17]. As the adenoma-adenocarcinoma sequence is the primary pathway for CRC[18], removing precancerous adenomas via colonoscopy is an effective strategy to lower CRC-related morbidity and mortality[19,20]. With the widespread adoption of endoscopic screening, the clinical detection of colorectal polyps is common; therefore, lesions with significant malignant potential require heightened clinical attention. Advanced adenomas, in particular, are recognized as primary precursor lesions for CRC[21]. Studies have shown that advanced adenomas are associated with a roughly threefold higher long-term risk of CRC compared to having no adenomas, whereas non-advanced adenomas show no significant risk difference[13].
CSM is an endoscopic, pale-yellow, speckled pattern on colorectal neoplasm, typically adjacent to colorectal neoplasm; however, its pathophysiological significance and role in carcinogenesis remain unclear. Our findings align with previous research, demonstrating a higher prevalence of CSM in the vicinity of large adenomas and a significantly increased proportion of advanced adenomas compared to the non-CSM group[2]. In addition, we found that adenomas with CSM possess a higher carcinogenic risk than those without, driven by enhanced cell proliferation and suppressed apoptosis[8]. Thus, CSM is a potential endoscopic marker for predicting submucosal invasion in small left-sided CRCs[12].
Our findings indicate a significantly higher incidence of multiple adenomas in the CSM group compared to the non-CSM group. Therefore, identifying CSM-associated adenomas warrants careful screening for additional synchronous adenomas, as these represent an independent factor for synchronous advanced adenomas[22] and interval CRC[23,24].
CSM is histopathologically defined by the accumulation of lipid-laden macrophages within the lamina propria, immune cells that play a key role in cancer progression[25]. These lipid-loaded macrophages migrate towards tumors with high malignant potential[26], infiltrating the surrounding tissue. This mechanism likely explains the primary localization of CSM in the vicinity of advanced adenomas.
Interestingly, our study revealed a higher prevalence of CSM-positive adenomas in the distal colon, prompting us to investigate potential reasons for this distribution. One possibility is that chronic feces stasis in the distal colon and rectum promotes local mucosal inflammation and leads to macrophage infiltration[2]. Chronic bacterial inflammation has been linked to tumorigenesis[27], likely mediated by tumor-associated macrophages[28]. Furthermore, local mucosal macrophage density correlates with bacterial load, a relationship supported by evidence showing that macrophages are nearly undetectable in the intestinal mucosa of germ-free mice[29]. Animal studies have shown that peritoneal macrophages upregulate COX-2 expression[30], providing a mechanistic explanation for the elevated COX-2 levels observed in colorectal adenomas with CSM[8].
TMEM16A is highly expressed in many malignant tumors[31] and contributes directly to tumorigenesis and tumor progression by activating mitogen-activated protein kinase[32,33]. Previous studies have shown that TMEM16A promotes tumor growth by activating extracellular signal-regulated kinase 1/2 and inducing cyclin D1, whereas blocking this pathway - either pharmacologically or genetically - effectively reverses these cancer-promoting effects[31,32]. Our previous studies found that TMEM16A expression increases during colorectal tumor progression, with significantly higher levels in carcinoma compared to adenoma, and elevated levels in adenoma compared to normal tissues[34].
Additionally, increased TMEM16A protein expression in CRC correlates with lymph node metastasis, tumor invasion, and Dukes’ stage, serving as an independent predictor of prognosis[15]. Our study showed that TMEM16A expression was significantly higher in adenomas with CSM compared to those without, and was notably higher in advanced adenomas than in non-advanced lesions. Our findings suggest that CSM acts as an endoscopic predictor for advanced colorectal adenoma, potentially mediated by TMEM16A.
Impact on resection strategy: Adenomas accompanied by CSM are indicative of a higher likelihood of being advanced lesions, and timely endoscopic removal should be prioritized to minimize the risk of progression to CRC.
Alteration of follow-up intervals: The presence of CSM may necessitate a reduction in follow-up intervals. Given its association with an increased risk of malignancy, more frequent follow-up examinations are recommended to ensure timely detection and reduce the risk of developing interval CRC.
Caution during colonoscopy: Adenomas with CSM may have a higher likelihood of being multiple adenomas. Therefore, careful attention should be paid to the potential presence of any other additional adenomas. Because poor bowel preparation increases the risk of missing lesions, a meticulous search for additional adenomas is essential once CSM is identified.
Improvement in risk stratification: CSM assessment offers risk stratification for advanced adenomas, complementing established endoscopic features such as size and shape. Its identification helps physicians more accurately detect patients at higher risk, facilitating better clinical decision-making.
This study had several limitations related to its design and observational nature. First, the retrospective design may have introduced biases. CSM assessment was conducted by two endoscopists in a single-blind manner, introducing potential subjectivity due to reliance on visual characteristics, such as peri-lesional yellow speckling. Although histological confirmation (lipid-laden macrophages) provided a consensus for cases with endoscopist agreement, variation in detection practices - particularly for type 2 CSM, which may only be visible after submucosal injection - could lead to classification bias. Therefore, prospective studies are needed to confirm these findings, enhance our understanding of the predictive value of CSM, and develop strategies for early detection and intervention. Second, the TMEM16A expression analysis was limited to a small subset of specimens, raising potential sampling bias issues and limiting the generalizability of the broader population. Given the small sample size and lack of mechanistic validation, these results should be interpreted as preliminary. A more comprehensive analysis is required to elucidate the role of TMEM16A in different types of adenomas. Third, although this study found correlations between CSM and advanced adenomas, the underlying pathophysiological mechanisms connecting CSM to carcinogenesis are not fully understood. Further studies are needed to explore these mechanisms. Fourth, this study lacked prospective data on patient outcomes with CSM, which limits our understanding of the predictive value of CSM in cancer progression and its impact on patient management. Due to the small number of adenomas exhibiting CSM, this study lacked sufficient power to identify significant clinical, endoscopic, and immunohistochemical differences between type 1 and type 2 CSM. Consequently, future studies with larger cohorts are necessary to evaluate the true significance of these CSM types. Finally, the relationship among inflammation, macrophages, and CSM remains unclear, necessitating further research into these mechanisms.
Our findings indicate that CSM is significantly associated with colorectal adenomas that are larger in size, multiple, protruding, located in the distal colon, and dysplastic histology. Furthermore, our findings indicate that CSM has an independent association with advanced adenomas, potentially driven by TMEM16A. While colonoscopic detection of CSM shows promise as a predictor factor of advanced colorectal adenomas, prospective studies are required to validate these findings.
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