Esophageal Ectopic Sebaceous Gland: A Case Series and Literature Review of Clinical, Endoscopic, and Pathological Features

Abstract

Objectives

Esophageal ectopic sebaceous gland (EESG) is a rare lesion that can be challenging to differentiate from other upper gastrointestinal endoscopic findings. The origin of EESG remains debated, with hypotheses ranging from embryologic misplacement to metaplasia of esophageal epithelium or glands. The aim of our study is to further investigate the clinicopathological features and pathogenesis of EESG.

Materials and Methods

Our study systematically reviewed 87 cases reported in the literature and analyzed an additional 21 cases from our institution. Demographic data (gender, age), lesion location, endoscopic features, and clinical presentations were summarized. Additionally, immunohistochemical staining for androgen receptor (AR), Kiel 67 (Ki-67), and cytokeratin 14 (CK14) was performed on nine cases.

Statistical Analysis

A normality test was conducted to determine whether the age distribution of male and female patients followed a normal distribution. Correlation coefficients and principal component analysis (PCA) were applied to further analyze the characteristics of case onset.

Results

The estimated prevalence of EESG was approximately 0.105‰. Lesions were more frequent in males than in females (nearly 2:1 ratio) and predominantly occurred in middle-aged and elderly individuals (mean age: 56.9 years). Most lesions were located in the middle and/or lower esophagus in both genders (99.6% variance explained by PCA). Endoscopically, EESG presented as distinctive “whitehead acne-like” structures with protrusions corresponding to sebaceous duct openings. Immunohistochemistry showed positive AR expression in all cases (9/9, 100%). Ki-67 and CK14 expression patterns indicated a close association between ectopic lesions and the basal layer of the esophageal squamous epithelium.

Conclusion

EESG typically presents after puberty with a male predominance. Given that sebaceous glands are androgen-responsive, androgens are likely involved in lesion development. The anatomical proximity of ectopic lesions to the basal layer of the squamous epithelium supports the hypothesis that pubertal androgens may drive aberrant differentiation of basal stem cells toward sebaceous gland lineage.

Keywords

ectopic sebaceous glands - endoscopy - esophagus - metaplasia

Introduction

Esophageal ectopic sebaceous gland (EESG) represents a relatively rare clinical finding, typically discovered incidentally during endoscopic evaluation of upper gastrointestinal symptoms or routine physical examinations. Since its initial description in autopsy specimens by De La Pava and Pickren in 1962,[1] EESG has been considered a rare entity, with reported incidence rates varying significantly across studies, ranging from 0.0465‰ to 2%.[1] [2] To date, approximately 80 cases have been documented in the literature ([Supplementary Table S1], available in online version only). Comprehensive epidemiological data on EESG remain scarce, and large-scale clinicopathological analyses with detailed endoscopic characterization are lacking. Owing to limited awareness among endoscopists, EESG may be misdiagnosed as other esophageal lesions, including esophageal xanthoma, candidiasis, squamous papilloma, glycogenic acanthosis, carcinoid tumor, and granular cell tumor, among others.[3]

The histogenesis of EESG remains controversial. Two predominant theories have been proposed[4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14]: the embryologic misplacement theory, which posits that EESG arises from aberrant displacement of ectoderm-derived sebaceous gland precursors during embryonic development, and the metaplasia theory, which suggests that EESG results from the transdifferentiation of esophageal squamous epithelium or submucosal glandular epithelium. The embryologic misplacement theory fails to adequately explain why EESG is predominantly diagnosed in adulthood rather than early life, as one would expect the lesions to be present from birth. In contrast, the metaplasia theory offers a more compelling explanation. However, between the two proposed cell origins within this theory, the submucosal glands are located relatively distant from the mucosal surface compared with the squamous epithelium, making the latter a more likely candidate. To evaluate these competing hypotheses, we analyzed the clinicopathological features of EESG and performed immunohistochemical staining.

Materials and Methods

This retrospective study analyzed 108 cases of EESG. Among them, 87 cases were collected from PubMed literature published between 1978 and 2021 ([Supplementary Table S1], available in online version only),[2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] and 21 cases were obtained from our institution between 2008 and 2025 ([Table 1]). Specimen types included four from endoscopic mucosal resection (EMR),[4] [21] two from esophagectomy specimens resected for esophageal squamous cell carcinoma,[6] [15] and the remainder from endoscopic biopsies. All cases were pathologically confirmed by the identification of sebaceous glands within the esophageal mucosa following standard histological processing—including tissue sampling, fixation, dehydration, clearing, paraffin embedding, sectioning, and hematoxylin and eosin staining (H&E staining).

Table 1 Demographic, endoscopic, clinical, and immunohistochemical findings in 21 cases

Year	Case	Age/sex	Location	Lesion number	Lesion appearance	Lesion size (mm)	Symptoms	Comorbidities	AR	Ki-67	CK14
2008	1	50/M	No data	No data	No data	No data	No data	No data
2015	2	55/M	L	Focal	Yellowish plaque	6	Digestive discomfort	Colonic polyp
2017	3	41/M	M	Focal	Yellowish plaque	5	No data	No data
2017	4	56/M	M	Multiple	Yellowish plaque	5	Digestive discomfort	Colonic polyp
2017	5	45/F	M	Multiple	Yellowish bulge	3–4	Digestive discomfort	Colonic polyp
2017	6	61/M	L	Multiple	Yellowish bulge	1–3	Digestive discomfort	Gastritis
2017	7	40/M	M	Multiple	Yellowish plaque	1–12	Digestive discomfort	Colonic polyp; hyperlipidemia	+	< 5%	+
2017	8	61/F	M	Multiple	Yellowish bulge	2–5	Digestive discomfort	Gastritis	+	< 5%	+
2018	9	63/M	M	One	Yellowish plaque	4	Digestive discomfort	Colonic polyp
2019	10	55/M	L	One	Yellowish plaque	5	Digestive discomfort	Colonic polyp	+	< 5%	+
2020	11	48/M	M + L	Multiple	Yellowish plaque	2–10	Heartburn, dysphagia	GERD; esophagitis	+	< 5%	+
2021	12	68/M	U	Multiple	Yellowish plaque	2–20	Digestive discomfort	Gastritis	+	< 5%	+
2021	13	49/M	M + L	Multiple	Yellowish bulge	1–5	Heartburn, regurgitation	Gastritis; GERD	+	< 5%	+
2022	14	61/F	L	One	Inapparent		Digestive discomfort	Autoimmune gastritis
2022	15	47/M	L	Multiple	Yellowish bulge	1–5	Asymptomatic	Gastritis
2022	16	59/M	U + M	Multiple	Yellowish plaque	5	Digestive discomfort	Gastritis; hyperuricemia	+	< 5%	+
2023	17	39/F	U	Multiple	Yellowish bulge	2–3	Asymptomatic	Gastritis
2024	18	67/M	M + L	Multiple	Yellowish plaque	2–6	Digestive discomfort	Gastritis; gastric polyp	+	< 5%	+
2024	19	59/M	M + L	Multiple	Yellowish bulge	1–3	Digestive discomfort	Gastric polyp
2025	20	32/M	U	One	Yellowish plaque	5	Digestive discomfort	Gastritis	+	< 5%	+
2025	21	60/M	L	Multiple	White patch	20	Digestive discomfort	Esophageal carcinoma in situ

Abbreviations: AR, androgen receptor; CK14, cytokeratin 14; GERD, gastroesophageal reflux disease; Ki-67, Kiel 67; L, lower esophagus; M, middle esophagus; U, upper esophagus; +, positive immunohistochemical staining; <5%, proportion of immunohistochemistry-positive cells less than 5%.

Immunohistochemical staining was performed on nine institutional cases using the following antibodies: androgen receptor (AR; mouse monoclonal, clone AR441, Abcam), cytokeratin 14 (CK14; mouse monoclonal, clone LL002, Abcam), and Kiel 67 (Ki-67; mouse monoclonal, clone MIB-1, Santa Cruz). Positive controls included prostate, tonsil, and lymph node tissues, while negative controls comprised thyroid, smooth muscle, and lung tissues. All immunohistochemical assays were performed on a Roche Ventana BenchMark ULTRA automated staining system and evaluated by an experienced pathologist using an Olympus BX43 microscope.

This study was approved by the hospital ethics committee in accordance with the Declaration of Helsinki and relevant national regulations. Based on the included cases, the following statistical analyses were performed: Information such as patient gender, age, and lesion location was collected. First, a normality test was conducted using the normplot function in Matlab to determine whether the ages of males and females followed a normal distribution. Subsequently, the mean age for each group was calculated. For gender and lesion location, statistical methods, including correlation coefficients and principal component analysis (PCA), were applied to further analyze the characteristics of case onset.

Results

Clinical Features

In our hospital, 21 cases of EESG were identified between January 1, 2008, and June 30, 2025. During this period, a total of 199,442 upper gastrointestinal endoscopy biopsies were performed, yielding an EESG prevalence of 21/199,442 (0.105‰). Among the 21 cases, females accounted for 19.0% (4/21) and males for 81.0% (17/21), with a mean age of 53.1 years. In the 87 literature-reported cases, females accounted for 37.9% (33/87) and males for 62.1% (54/87), with a mean age of 57.9 years. To enhance the statistical power, we pooled the two datasets for analysis. The analysis revealed that the age of onset in the combined cohort of 108 patients approximately followed a normal distribution ([Fig. 1]). Furthermore, the ages of both the female patients (37/108, 34.3%) and the male patients (71/108, 65.7%) separately followed a normal distribution. The study cohort had a mean age of 56.9 years (range: 30–85 years) with a male predominance (ratio close to 2:1). The average age was 57.6 years for males and 55.7 years for females, indicating that the condition predominantly affects middle-aged and elderly individuals.

Fig. 1 Normal probability plot of age distribution (n = 108).

Among the 108 cases, 23 cases were asymptomatic and were incidentally detected during routine examination. The remaining cases with available symptom records underwent endoscopy for indications such as heartburn, dysphagia, epigastric pain, abdominal fullness, belching, and acid regurgitation. 17 cases (15.7%) were complicated by reflux disease. Other documented comorbidities included gastritis, gastrointestinal polyps, peptic ulcer, hiatal hernia, Barrett's esophagus, hyperlipidemia, hyperuricemia, and hypertension. Eight patients had concurrent malignancies: esophageal cancer (3 cases), gastric cancer (2 cases), and nondigestive tract cancers (3 cases).

Endoscopic and Pathological Findings

Endoscopy demonstrated characteristic pale yellow, lobulated or petaloid, protuberant lesions within the esophageal mucosa ([Fig. 2A]). Lesions were solitary in 19 cases (17.9%) and multiple in 87 cases (82.1%; the proportion was 80.0% in our cases and 82.6% in literature-reported cases), with 2 cases lacking documentation. The lesions were predominantly multiple, with 6 cases exhibiting more than 100 lesions. Lesion diameters ranged from 0.5 to 20 mm, manifesting as small punctate protrusions to confluent plaque-like lesions ([Fig. 2]). Lesion distribution included the following: upper esophagus (9 cases), middle esophagus (31 cases), lower esophagus (15 cases), both upper and middle esophagus (5 cases), both middle and lower esophagus (22 cases), whole esophagus (15 cases), and the gastroesophageal junction (1 case), with 10 cases lacking documentation. Although lesions were found throughout the esophagus, they predominantly localized to the middle and/or lower segments (89/98 cases, 90.8%). Statistical analysis revealed that the correlation coefficient for the distribution of affected segments between males and females was 0.990, indicating identical distribution patterns and suggesting no association between affected segment and gender. PCA of the affected segment distribution in males and females showed that the first principal component (explaining 99.6% of the variance) revealed middle and middle with lower segments as the most frequently affected segments in both genders.

Fig. 2 Endoscopic features of esophageal ectopic sebaceous gland (EESG). (A) Case 7 demonstrates the typical morphology of EESG, showing pale yellow lobulated protuberant lesions with a “petal-like” appearance and central “whitehead acne-like” protrusions (endoscope model: GIF-H260). (B, C) Case 8 shows the long-term stability of lesions over 40 months (B: initial examination in 2017, endoscope model: EG-530WR; C: follow-up after 40 months, endoscope model: GIF-H260Z). (D) Case 11 exhibits multiple lesions ranging from small punctate protrusions to confluent plaques (endoscope model: GIF-H260Z). (E, F) The characteristic “whitehead acne-like” appearance is particularly evident under narrowband imaging (NBI) endoscopy. The turquoise narrowband light waves provide enhanced visualization of the mucosal vascular network and improve the contrast of shadows created by the protrusions at sebaceous gland openings (E: case 11, endoscope model: GIF-H260Z; F: case 20, endoscope model: GIF-290J).

Repeated endoscopic follow-up was available for nine patients. Three had no recurrence after lesion resection, while four showed no significant changes over 20 months to 3 years.[14] [16] One case exhibited disease progression from the mid to the upper esophagus over a 2-year period.[16] Another patient, who underwent endoscopy 6 and 7 years ago, showed an initial decrease in lesion number, followed by progression on comparative analysis, though the overall morphology was stable (potential variations due to differences in photographic position, angle, and lighting were considered).[21] In Case 8, in our study, endoscopic morphology remained largely unchanged after 40 months of follow-up ([Fig. 2B, C]). Notably, most lesions exhibited central punctate protrusions, creating a “whitehead acne-like” appearance endoscopically ([Fig. 2]); this feature was more pronounced under narrowband imaging (NBI; [Fig. 2E, F]). These protrusions have been confirmed to represent the openings of ectopic sebaceous gland ducts.[5] [6]

Pathological examination revealed sebaceous glands in all cases. Microscopically, lobulated cell nests were observed beneath the nonkeratinized squamous epithelium, exhibiting round and mild nuclei with abundant foamy cytoplasm. These morphological features were identical to normal sebaceous glands. The lesions were localized between the squamous epithelium and mucosal lamina propria, with the peripheral portions of sebaceous glands connecting to the basal layer of the squamous epithelium ([Fig. 3A]). Histological examination demonstrated the following: intra-acinar ducts within sebaceous glands ([Fig. 3A], red arrow in the upper right corner) and accumulated sebaceous secretions in downstream ducts, showing pink coloration on H&E staining ([Fig. 3A], yellow arrows). In several cases, we could see the direct opening of sebaceous ducts onto the squamous epithelial surface with retained secretions.[6] [13] [15] Notably, none of the cases showed evidence of hair follicle differentiation or hair shaft formation.

Fig. 3 Histopathological and immunohistochemical features of esophageal ectopic sebaceous gland (case 7, images at ×100 magnification). (A) Hematoxylin and eosin (H&E) staining demonstrates the following: peripheral sebaceous glands connecting with the basal layer of the squamous epithelium; visible intra-acinar duct of sebaceous glands (red arrow; inset shows ×200 magnification); pink-stained sebaceous gland secretions accumulated in downstream ducts (yellow arrows). Immunohistochemical staining reveals the following: (B) androgen receptor (AR) expression in peripheral nuclei of sebaceous glands; (C) Kiel 67 (Ki-67) positivity in both basal layer nuclei of the squamous epithelium and peripheral nuclei of sebaceous glands; (D) cytokeratin 14 (CK14) expression predominantly in peripheral cytoplasm of sebaceous glands and basal layer cytoplasm of the squamous epithelium. Note the continuous positivity extending from the squamous epithelium basal layer to the sebaceous gland periphery.

Immunohistochemical Characteristics

Immunohistochemical staining for AR, Ki-67, and CK14 was performed on nine cases with adequate tissue samples ([Table 1]). Both AR and CK14 exhibited positive staining in all cases (9/9, 100% positivity rate), whereas Ki-67 demonstrated a low proliferation index of less than 5% in all cases ([Fig. 3B–D]). The following expression patterns were observed: AR expression was nuclear in peripheral sebaceous gland cells ([Fig. 3B]) and Ki-67 positivity was limited to the peripheral nuclei of sebaceous glands and the basal layer nuclei of the squamous epithelium ([Fig. 3C]). This limited proliferative activity, particularly at the sebaceous gland periphery, confirms an indolent biological nature without malignant potential. CK14 showed strong cytoplasmic expression in the peripheral sebaceous gland cells and the basal layer of the squamous epithelium ([Fig. 3D]). The co-expression of Ki-67 and CK14 in the sebaceous gland periphery and the squamous epithelial basal layer defined a continuous cell population, revealing a developmental relationship between sebaceous germinative cells and epithelial basal cells.

Discussion

Sebaceous glands primarily originate from the pilosebaceous unit (PSU), although a subset is found independently without association with hair follicles. These glands are widely distributed across the body surface, with the highest density observed on the face and scalp. Their prevalence decreases on the chest and abdomen and is lowest on the limbs.[14] Ectopic sebaceous glands have been documented in diverse anatomical sites, predominantly in organs of ectodermal origin. They rarely occur in endoderm-derived tissues. Given that the esophageal mucosa arises from the endoderm, reports of ectopic sebaceous glands in this location remain limited to sporadic cases and small-scale studies. To date, robust epidemiological data on this condition have yet to be established.

In this study, we analyzed 87 cases of EESG from PubMed with relatively complete data and included 21 additional cases from our institution. Cases have been reported in Asian, European, and African populations. Statistical analysis showed that the age of the cases followed a normal distribution. Our analysis revealed the following characteristics: EESG occurs more frequently in males than in females (with a nearly 2:1 ratio) and is more common in middle-aged and elderly individuals than in younger populations (mean age: 56.9 years). Most lesions are located in the middle and/or lower esophagus in both genders, and the majority present as multiple lesions, with some cases exhibiting over 100 lesions. As EESG is commonly confused with other lesions endoscopically, we identified its pathognomonic features: sebaceous glands exhibit a lobular architecture distributed around a central duct, accounting for their characteristic “petal-like” endoscopic appearance. Each lobule (“petal”) represents an acinar unit arranged centripetally around the duct opening ([Fig. 2A]), a structural adaptation that facilitates efficient secretion collection and discharge. Accumulated secretions at the duct orifices elevate the mucosal surface, producing characteristic umbilicated protrusions that resemble cutaneous whitehead acne under white-light endoscopy. Unlike the petal-like and acneiform features of EESG, common mimics such as xanthoma (composed of foamy macrophages), candidiasis (characterized by fungal hyphae), papilloma (showing fibrovascular cores), glycogenic acanthosis (featuring glycogen-rich cells), carcinoid (comprising neuroendocrine nests), and granular cell tumors (of Schwann cell origin) each exhibit unique histopathological signatures reflecting their divergent origins.

As previously mentioned, the embryonic misplacement theory suggests that EESG arises from the aberrant migration of ectoderm-derived sebaceous gland precursors into the esophageal endoderm during embryonic development. This theory explains the ectopic presence of sebaceous glands within the endoderm-derived esophageal epithelium, with these lesions remaining relatively stable over time. However, the embryologic misplacement theory remains controversial. A key counterargument is the disease's predominant occurrence in middle-aged and elderly populations, with no reported pediatric cases. This discrepancy is supported by Rector and Connerley's large-scale study,[22] which examined the esophageal mucosa in infants and young children, yet identified no EESG cases. Collectively, these findings suggest that the theory lacks robust empirical support. Perhaps we should consider this from a different perspective. Among the entire digestive tract, why do ectopic sebaceous glands occur exclusively in the esophagus? Furthermore, why are they not typically observed in organs lined with mucinous columnar epithelium (e.g., the stomach and intestines)? These observations suggest that the squamous epithelium of the esophagus may provide the necessary histological microenvironment for sebaceous gland ectopia.

As noted earlier, the metaplasia theory posits that EESG lesions originate from metaplasia of either the squamous epithelium or the mucous glands. This theory provides a plausible mechanism for the exclusive occurrence of EESG in adults and its consistent absence in children. While we consider the squamous metaplasia hypothesis plausible, the theory of mucous gland metaplasia appears untenable based on histological evidence.[23] Anatomically, esophageal glands are classified into two distinct types: submucosal glands located in the submucosal layer and cardiac glands within the lamina propria. Our observations demonstrate that ectopic sebaceous glands reside in the lamina propria, with their peripheral portions continuous with the surface squamous epithelium. In contrast, submucosal glands are separated from the squamous epithelium by the lamina propria and multiple layers of the muscularis mucosae, an anatomical barrier that prevents metaplastic transformation. Notably, cardiac glands are found in only 1 to 16% of the population, with their distribution predominantly limited to the proximal and distal ends of the esophagus.[23] In contrast, our study demonstrated that EESG primarily occurs in the middle and/or lower esophageal segments. The distinct spatial distribution and low occurrence rate of cardiac glands make their metaplastic transformation into sebaceous glands statistically improbable. Moreover, even if such metaplasia were to occur, the anatomical constraints would preclude its manifestation in the mid-esophageal region, where EESG is frequently observed. Collectively, these findings suggest that cardiac glands are unlikely to be the precursor tissue for esophageal sebaceous glands.

Several studies have proposed that EESG most likely originates from metaplasia of the esophageal squamous epithelium.[4] [11] This hypothesis is strongly supported by our histological observations demonstrating a close anatomical relationship between the ectopic sebaceous glands and the squamous epithelium. Specifically, we identified a direct cellular continuity between the peripheral basal cells of the sebaceous glands and the basal cells of the squamous epithelium ([Fig. 3A]). Immunohistochemical analysis further reinforced this connection, revealing that both cell populations expressed Ki-67 (a proliferation marker) and CK14 (a marker of basal epithelial cells with proliferative and differentiation potential[24]; [Fig. 3C, D]). The co-expression of these markers in cells surrounding the sebaceous glands suggests that the two cell populations may share a common origin. Additionally, we detected AR expression in a subset of sebaceous gland cells ([Fig. 3B]), implying that the function of sebaceous glands in this ectopic location may be regulated by androgen signaling in vivo. Indeed, as target organs of androgens, the secretory function of sebaceous glands is known to be regulated by androgen levels.[25]

Histological evidence indicates that sebaceous glands originate from the differentiation of hair follicle epithelial stem cells located in the basal layer of the epidermal squamous epithelium.[23] The peripheral basal cells of sebaceous glands function as germinative cells, undergoing continuous differentiation and maturation toward the gland center, where they acquire secretory capabilities. Based on these observations, we propose a new hypothesis: multipotent stem cells in the basal layer of the esophageal squamous epithelium may differentiate into sebaceous glands under pubertal androgenic stimulation. Both the activity and volume of these glands are expected to increase with rising androgen levels, leading to the development of structurally mature sebaceous gland lesions. This hypothesis provides a plausible explanation for two key clinical observations: the postpubertal onset of esophageal sebaceous glands and their male predominance.

For endoscopists, recognizing EESG is crucial primarily to avoid misdiagnosis. This rare condition can be easily mistaken for various common esophageal lesions, including candidiasis, leukoplakia, papilloma, xanthoma, glycogenic acanthosis, inflammatory nodular hyperplasia, or even relatively uncommon tumors such as carcinoids and granular cell tumors. To date, no studies have demonstrated any malignant transformation potential in EESG, and the present study also revealed a Ki-67 proliferation index in these lesions comparable to that of normal tissue. Although some individual cases have undergone EMR due to endoscopic suspicion of neoplasia, no research has established EMR as a necessary approach for diagnosing or treating EESG. Therefore, when lesions with characteristic features of EESG are identified, an initial mucosal biopsy may be performed for diagnostic confirmation. Although these ectopic sebaceous glands retain secretory function, no associated clinical symptoms have been reported. Current evidence does not support a correlation between EESG and conditions such as gastroesophageal reflux disease or hyperlipidemia, nor has any definitive relationship been established with smoking, alcohol consumption, or lifestyle factors. Importantly, once a definitive pathological diagnosis is obtained, EESG typically requires no therapeutic intervention as it is asymptomatic.

Conflict of Interest

None declared.

Acknowledgments

The authors thank their colleagues in the Department of Gastroenterology at Guangdong Provincial People's Hospital for providing the endoscopic images.

Ethical Approval

This study has been reviewed and approved by the Ethics Review Committee of Guangdong Provincial People's Hospital (Ethics No: KY-Q-2022–113–01; dated: March 9, 2022).

• References

• 1 De La Pava S, Pickren JW. Ectopic sebaceous glands in the esophagus. Arch Pathol 1962; 73: 397-399
• 2 Chiu KW, Wu CK, Lu LS, Eng HL, Chiou SS. Diagnostic pitfall of sebaceous gland metaplasia of the esophagus. World J Clin Cases 2014; 2 (07) 311-315
• 3 Le A, Amin M, Cappell MS. Case report of a proposed, novel, endoscopic “whitehead pimple” sign of ectopic esophageal sebaceous glands based on their mimicking the dermatologic and histopathologic characteristics of cutaneous whitehead pimples/closed comedones. Dig Dis Sci 2019; 64 (07) 2049-2053
• 4 Yeom DH, Ryu HS. Ectopic sebaceous gland in esophagus presenting as subepithelial tumor. Chonnam Med J 2019; 55 (03) 168-169
• 5 Jeon MS, Kim GH, Jeong DY. et al. Magnifying endoscopy for esophageal ectopic sebaceous glands. Clin Endosc 2018; 51 (05) 495-497
• 6 Nakanishi Y, Ochiai A, Shimoda T. et al. Heterotopic sebaceous glands in the esophagus: histopathological and immunohistochemical study of a resected esophagus. Pathol Int 1999; 49 (04) 364-368
• 7 Bhat RV, Ramaswamy RR, Yelagondahally LK. Ectopic sebaceous glands in the esophagus: a case report and review of literature. Saudi J Gastroenterol 2008; 14 (02) 83-84
• 8 Ramakrishnan T, Brinker JE. Ectopic sebaceous glands in the esophagus. Gastrointest Endosc 1978; 24 (06) 293-294
• 9 Hoshika K, Inoue S, Mizuno M, Iida M, Shimizu M. Endoscopic detection of ectopic multiple minute sebaceous glands in the esophagus. Report of a case and review of the literature. Dig Dis Sci 1995; 40 (02) 287-290
• 10 Kushima R, von Hinüber G, Lessel W, Stolte M, Borchard F. Sebaceous gland metaplasia in cardiac-type mucosa of the oesophago-gastric junction. Virchows Arch 1996; 428 (4–5): 297-299
• 11 Wei IF, Chang CC, Fang CL. et al. Education and imaging. Gastrointestinal: ectopic sebaceous glands in the esophagus. J Gastroenterol Hepatol 2008; 23 (02) 338
• 12 Marín-Serrano E, Jaquotot-Herranz M, Casanova-Martínez L, Tur-González R, Segura-Cabral JM. Ectopic sebaceous glands in the esophagus. Rev Esp Enferm Dig 2010; 102 (02) 141-142
• 13 Grube-Pagola P, Vicuña-González RM, Rivera-Salgado I, Alderete-Vázquez G, Remes-Troche JM, Valencia-Romero AM. Ectopic sebaceous glands in the esophagus. Report of three cases. Gastroenterol Hepatol 2011; 34 (02) 75-78
• 14 Fukuchi M, Tsukagoshi R, Sakurai S. et al. Ectopic sebaceous glands in the esophagus: endoscopic findings over three years. Case Rep Gastroenterol 2012; 6 (01) 217-222
• 15 Csanyi M, Arnaud M, Le Pessot F, Huet E, Piton N, Sabourin JC. About 2 cases of ectopic sebaceous glands in esophagus: endoscopic and histological correlations from biopsies and resected specimens. Ann Pathol 2016; 36 (02) 134-138
• 16 Chen HF, Lee HC, Liao MK. The clinical and endoscopic features of esophageal ectopic sebaceous glands. Adv Dig Med 2020; 7: 179-187
• 17 Marcial MA, Villafaña M. Esophageal ectopic sebaceous glands: endoscopic and histologic findings. Gastrointest Endosc 1994; 40 (05) 630-632
• 18 Kim YS, Jin SY, Shim CS. Esophageal ectopic sebaceous glands. Clin Gastroenterol Hepatol 2007; 5 (01) A23
• 19 Saint-Blancard P, Hervouet M. Ectopic sebaceous glands in the esophagus. Gastroenterol Clin Biol 2008; 32 (02) 192-194
• 20 Humes RJ, Sadowksi BW, Long JO, Damiano MN. An odd place for acne: ectopic esophageal sebaceous glands. ACG Case Rep J 2020; 7 (11) e00465
• 21 Hashimoto H, Horiuchi H, Miura S, Takayanagi S, Gunji T, Morikawa T. Clinicopathologic characteristics of esophageal ectopic sebaceous glands: chronological changes and immunohistochemical analysis. Int J Surg Pathol 2021; 29 (04) 378-384
• 22 Rector LE, Connerley ML. Aberrant mucosa in the esophagus in infants and in children. Arch Pathol (Chic) 1941; 31: 285-294
• 23 Mills SE. Histology for Pathologists. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins/Wolters Kluwer Health; 2012
• 24 Alam H, Sehgal L, Kundu ST, Dalal SN, Vaidya MM. Novel function of keratins 5 and 14 in proliferation and differentiation of stratified epithelial cells. Mol Biol Cell 2011; 22 (21) 4068-4078
• 25 Azmahani A, Nakamura Y, McNamara KM, Sasano H. The role of androgen under normal and pathological conditions in sebaceous glands: the possibility of target therapy. Curr Mol Pharmacol 2016; 9 (04) 311-319
• 26 Wang WP, Wang WS, Tsai YC. Multiple tiny ectopic sebaceous glands discovered throughout entire esophageal tract. Dig Dis Sci 2009; 54 (12) 2754-2757
• 27 Jhang LS, Hung CY, Shieh TY. et al. Ectopic sebaceous gland in the esophagus—Case reports and review of the literature. Adv Dig Med 2016; 3 (03) 118-122
• 28 Park A, Lee JH, Park A. et al. Prevalence rate and clinical characteristics of esophageal ectopic sebaceous glands in asymptomatic health screen examinees. Dis Esophagus 2017; 30 (01) 1-5
• 29 Peixoto A, Rodriques S, Silva M, Maia T, Rios E, Macedo G. Esophageal ectopic sebaceous glands. Acta Gastroenterol Belg 2017; 80 (02) 321
• 30 Auld RM, Lukash WM, Bordin GM. Heterotopic sebaceous glands in the esophagus. Gastrointest Endosc 1987; 33 (04) 332-333
• 31 Bertoni G, Sassatelli R, Nigrisoli E, Conigliaro R, Bedogni G. Ectopic sebaceous glands in the esophagus: Report of three new cases and review of the literature. Am J Gastroenterol 1994; 89 (10) 1844-1847
• 32 Nakada T, Inoue F, Iwasaki M, Nagayama K, Tanaka T. Ectopic sebaceous glands in the esophagus. Am J Gastroenterol 1995; 90: 501-503
• 33 Tsukui M, Yamaguchi H, Shirao K. Ten cases with ectopic sebaceous glands in the esophagus. Prog Dig Endosc 1995; 46: 65-68
• 34 Bae JY, Chon CY, Kim H. Sebaceous glands in the esophagus. J Korean Med Sci 1996; 11 (03) 271-274
• 35 Nishisaki H, Yasutake K, Nakashima T. et al. Five cases with ectopic esophageal sebaceous glands. Dig Endosc 1997; 9 (03) 207-212
• 36 Tak AM, Scott RD, Khan NA. Sebaceous glands in esophagus in gastroesophageal reflux disease. Indian J Gastroenterol 2007; 26 (01) 36
• 37 Thalheimer U, Wright JL, Maxwell P, Firth J, Millar A. Sebaceous glands in the esophagus. Endoscopy 2008; 40 (Suppl. 02) E57
• 38 John F, Raghuraman VU, Taylor JR. Ectopic sebacious glands in the esophageal mucosa. Clin Gastroenterol Hepatol 2012; 10: xxxii
• 39 Yen HH, Chen YY, Chen CJ. Unusual endoscopic finding. Gastroenterology 2013; 145 (05) e1-e2
• 40 Lee SH, Lee DJ, Kim KM, Kim KN, Kang JK. Ectopic sebaceous glands in the esophagus: A case report and review of literature. Scott Med J 2014; 59 (03) e1-e5
• 41 Montalvo N, Tapia V, Padilla H, Redroban L. Heterotopic sebaceous glands in the esophagus, a very rare histopathological diagnosis: A case report and review of the literature. Clin Case Rep 2017; 5 (02) 89-92

Publication History

Article published online:
09 January 2026