Bilateral granulomatous mastitis associated with ductoscopy

Introduction

Background

Granulomatous mastitis (GLM) is a chronic, inflammatory, benign breast disease that typically occurs in one breast women of childbearing age. It was first described in 1972 (1). The current incidence rate is not well defined, and the cause of the disease remains unclear. Clinical features and imaging often make it difficult to distinguish it from breast cancer; therefore, the final diagnosis requires pathological confirmation (2). GLM histologically presents as non-caseating granulomatous lesions. The lesions are located in the central lobular areas and contain epithelioid and multinucleated giant cells, with possible infiltration by neutrophils, lymphocytes, plasma cells, and a small number of eosinophils. These lesions are usually multifocal and may form microabscesses of varying sizes (3).

Rationale and knowledge gap

Recently, GLM has attracted increasing attention. Based on its accompanying clinical features (4,5), such as nipple discharge, nipple deformities, erythema nodosum (EN) and potential clinical causes including trauma, oral contraceptives (6), lactation and pregnancy (7-10), bacterial infection (11), hyperprolactinemia (12), etc., experts have conducted many discussions on the etiology of this disease. The main viewpoints include infectious diseases (13,14), hormonal imbalance (such as hyperprolactinemia), chemical irritation responses, trauma (15), and autoimmune diseases (6,16). Some scholars (11) have described the mechanism of ductal epithelial injury in GLM; however, the triggering factors remain unknown. It is speculated that it may be related to the extravasation of luminal deposits during lactation. However, few studies have attempted to find evidence of an association between ductal epithelial injury, chemical stimulation, and inflammation.

Objective

Based on this, we found that some patients with GLM presented with nipple discharge from the contralateral breast. Doctors performed ductoscopy, and some patients developed masses and pain in the contralateral breast within a short period after ductoscopy. A pathological biopsy confirmed bilateral GLM. This study retrospectively analyzed 40 patients with GLM and nipple discharge from a healthy contralateral breast who underwent ductoscopy. We aimed to find evidence of a possible association between ductal epithelial injury, inflammation, and chemical stimulation. We present this article in accordance with the STROBE reporting checklist (available at https://gs.amegroups.com/article/view/10.21037/gs-2025-77/rc).

Methods

Ethical considerations

This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The research protocol was approved by the Institutional Review Board of Chongqing Traditional Chinese Medicine Hospital (No. 2023-KY-YJS-PT). The requirement for individual consent was waived for this retrospective study.

Research design

This study was a retrospective cross-sectional study. Patients pathologically diagnosed with GLM at the Department of Breast Diseases, Chongqing Traditional Chinese Medicine Hospital, China, between January 2023 and December 2023 were enrolled.

Inclusion and exclusion criteria

Among the 1,360 patients pathologically diagnosed with GLM by core needle biopsy at our center, 92 had nipple discharge. Of these, 49 had discharge only from the affected side, and 43 had discharge from the healthy contralateral side. Among the 43 patients, 1 who had undergone ductoscopy at an outside hospital and 2 with incomplete medical records were excluded. Finally, 40 patients were included in this study (Figure 1).

Figure 1 Flowchart of the study. GLM, granulomatous mastitis.

Ductoscopy

Cytological examination of exfoliated cells

Under aseptic conditions, the patient’s breast was gently massaged and squeezed along the direction of the nipple discharge duct toward the nipple. The initial discharge was discarded, fresh fluid was collected for smearing, dropped onto a glass slide, and two smears of nipple discharge were prepared using the blade-spreading method. The slides were placed in a cell fixation bottle, and the specimens were immediately transported to the pathology department. Cytological smears were stained with hematoxylin-eosin (H&E). Two experienced pathologists at or above the attending physician’s level independently evaluated and analyzed the slides. In the case of assessment discrepancies, the final result was determined through a consensus discussion.

Ductoscopy operation

• Instrument: the ductoscopy system was the FDS-3000 produced by Mitsubishi in Japan, with endoscope diameters of 0.72, 0.55, and 0.45 mm.
• Examination method: based on the condition of the duct, the appropriate endoscope for examination was selected. First, a 1–2 sized dilator was inserted into the duct from the nipple discharge opening and it was expanded. A mixture of lidocaine and 0.9% sodium chloride solution (1:1) was administered for anesthesia. Dilators of sizes 3–5 were sequentially used to expand the duct, while simultaneously inserting a ductoscope. Gradually, the duct shape, direction, wall color, deposits within the lumen, and expansion conditions were examined. Experienced breast specialists carefully observed any narrowing or obstruction and checked for any protruding lesions within the lumen.
• Before withdrawing the endoscope, intraductal irrigation was performed with dexamethasone (5 mg) and chymotrypsin (4,000 IU) to inhibit local inflammation and prevent the accumulation of proteinaceous debris. After the procedure, it was ensured that the nipple would avoid contact with water for 24 h. Experienced breast surgeons performed all ductoscopy procedures. All patients were informed of the risks of ductoscopy and signed informed consent forms.

Study cohorts

All patients were pathologically diagnosed with a GLM of a unilateral breast mass. Ductoscopy was performed on the contralateral breast with the nipple discharge. The patients were divided into the following groups:

• Group A (bilateral GLM group): new-onset GLM after contralateral ductoscopy, defined as patients who developed a mass in the contralateral breast post-ductoscopy, with core needle biopsy confirming GLM in the new mass;
• Group B (unilateral GLM group): patients with nipple discharge in the contralateral breast who underwent ductoscopy but did not develop new masses in the contralateral breast.

Clinical data collection

Patients were recruited from the outpatient and inpatient departments of the Chongqing Traditional Chinese Medicine Hospital, China. Before the initial treatment, all patients had their individual medical records established, and signed an informed consent form for the establishment and application of the GLM-specific disease database. We recorded their age, name, number of pregnancies and deliveries, time from the last delivery to the onset of the mass, history of hyperprolactinemia or mental disorders, or mental disorders, size of the mass measured at the first visit (Figure 2), number of quadrant involved, color of nipple discharge, number of discharge orifices, erythema on both lower limbs (Figure 3), other complications, pus culture results, descriptions of ductoscopy findings, and cytological smear results of nipple discharge (Figure 4). New masses in the contralateral breast were recorded (Figure 5), along with the pathological results of the biopsy (Figure 6) and prolactin (PRL) levels. All patients underwent physical examinations, laboratory tests, and ultrasound follow-up during treatment (Figure 7). Through group-wise data differences and regression analysis, we attempted to identify risk factors for mass formation after ductoscopy. The receiver operating characteristic (ROC) curves were plotted to analyze the predictive value of the predictive value of the new contralateral mass (bilateral GLM group), for related factors after ductoscopy (Figure 8).

Figure 2 Initial mass presented by the patient during the consultation, with noticeable redness, swelling, and marked tenderness in the local area.

Figure 3 Nodular erythema in the patient’s bilateral lower limbs.

Figure 4 The cytological smear of nipple discharge from patients with new-onset masses after ductoscopy. Neutrophils (blue arrow), lymphocytes (green arrow), and histiocytes (red arrow) can be seen (H&E staining, original magnification ×200). H&E, hematoxylin-eosin.

Figure 5 A mass lesion developed on the contralateral side after the patient underwent ductoscopy.

Figure 6 Pathological comparison of bilateral granulomatous mastitis in the same patient. (A) Pathological confirmation via core needle biopsy of the initial mass (granulomatous mastitis). (B) Pathological confirmation via core needle biopsy post-ductoscopy in the contralateral breast (granulomatous mastitis). The arrow indicates the area of ductal injury in the breast mass after ductoscopy. (H&E staining, original magnification ×200). H&E, hematoxylin-eosin.

Figure 7 In color Doppler ultrasound of granulomatous mastitis, irregular hypoechoic or mixed echo areas can be observed, with intraparenchymal anechoic fluid areas (red arrow), rich peripheral blood supply (green arrow), and sinus tract formation.

Figure 8 ROC curve of bilateral GLM group against bilateral lower limb erythema. GLM, granulomatous mastitis; ROC, receiver operating characteristic.

Statistical analysis

The data were processed and analyzed using SPSS 26.0 statistical software. For measurement data conforming to normal distribution, they were expressed as mean ± standard deviation. Paired sample t-test was used for intra-group comparison, and independent two-sample t-test was used for inter-group comparison. If data did not conform to a normal distribution, they were expressed as median (interquartile range). The Wilcoxon signed-rank test was used for intragroup comparisons, and the Mann-Whitney U test was used for intergroup comparisons. Enumeration data were expressed as frequency (percentages), and the Chi-squared test or Fisher’s exact test was used for intergroup comparisons. P<0.05 was considered as statistically significant difference. The following analyses were used to control confounding bias and identify independent risk factors: univariate analysis: variables were preliminarily screened (those with P<0.05 were included in the multivariate model); multivariate logistic regression: backward stepwise method (likelihood ratio test) was adopted to construct the model, and adjusted odds ratio (aOR) and its 95% confidence interval (95% CI) were calculated; model covariates: potential confounding variables such as age were included. Bias control measures: in the research design stage, strict inclusion/exclusion criteria were formulated; in the data collection stage, double independent entry and random sampling verification were implemented; in the statistical analysis stage, analysts were blinded to grouping information (variables were coded by independent personnel). The test level was α=0.05 (two-sided). The sample size was estimated by PASS 15.0 software (test power ≥80%, α=0.05).

Results

This study included 40 patients, all of whom were women of childbearing age. The general patient data are presented in Table 1. The onset time of masses after ductoscopy was 13±7 days. All patients were diagnosed with GLM in one breast. Ductoscopy was performed for the contralateral breast, which had nipple discharge. Patients who developed new masses in the contralateral breast after ductoscopy were classified to the bilateral GLM group (n=10). Patients who did not develop masses after ductoscopy were classified into the unilateral GLM group (n=30). Independent two-sample t-tests, Mann-Whitney U tests, and Fisher’s exact tests revealed the following: the ages of the two groups (z=−0.83, P=0.40), number of pregnancies (z=−1.77, P=0.08), number of deliveries (z=−0.04, P=0.97), time from the last delivery to the onset of the mass (z=−0.37, P=0.71), number of quadrants affected (z=−0.18, P=0.86), largest dimension of the mass (t=−1.66, P=0.11), RRL levels (z=−0.25, P=0.80), nipple discharge orifice (χ²<0.001, P>0.99), and discharge color (χ²=0.03, P=0.85) were not significantly different between the two groups. Comparison of ductoscopy findings, namely floccule (χ²=0.06, P=0.81), fibrous network structure (χ²=0.52, P=0.47), fatty-like discharge (χ²<0.001, P>0.99), bacterial culture of purulent fluid (χ²=1.38, P=0.50), and other complications (P=0.09) showed no statistically significant differences. From the independent two-sample t-test, the short diameter of the mass in the bilateral GLM group compared to that in the unilateral GLM group had a t-value of −2.14 and P=0.04, indicating a statistically significant difference. Although there was no statistical difference in the long diameter of the masses between the two groups, it can be concluded that the initial mass in the bilateral GLM group is larger than that in the unilateral GLM group, suggesting a greater area of breast involvement and more severe condition. In the bilateral GLM group, the ductoscopy cytological smears showed higher occurrences of “neutrophils and lymphocytes” compared to the unilateral GLM group, with a Chi-squared value of 5.21 and P=0.02, indicating statistical significance. This suggests that patients in the bilateral GLM group have a higher incidence of neutrophils and lymphocytes in their ductoscopy cytological smears. The incidence of erythema in both lower limbs in the bilateral GLM group is significantly higher than in the unilateral GLM group (P=0.01), indicating statistical significance (Table 1).

Multivariate analysis of contralateral breast masses after ductoscopy

Using the occurrence of a contralateral breast lump after ductoscopy as the dependent variable (positive assigned value =1, negative assigned value =0), binary logistic regression analysis was performed using the cytological smear from ductoscopy (neutrophils and lymphocytes were assigned a value of 1, other non-inflammatory cells were assigned a value of 0) and the short diameter of the mass was used as independent variables. The results showed that the cytological smear from the ductoscope indicated that “neutrophils and lymphocytes” (OR, 7.356; 95% CI: 1.185–45.658; P=0.03) is an independent risk factor affecting the occurrence of masses after ductoscopy (Table 2). A short diameter of the primary mass (P=0.13) was not a risk factor for the development of a new mass on the opposite side.

Bilateral GLM group ROC analysis of bilateral lower limb erythema

Using the presence of bilateral lower limb erythema as a state variable (assigned a value of 1 for presence and 0 for absence), a ROC curve analysis was conducted with the occurrence of contralateral breast mass after ductoscopy (bilateral GLM group) as the test variable. The results showed that in the bilateral GLM group, the development of contralateral breast masses after ductoscopy had an AUC of 0.843 (0.655–1.000) for predicting erythema in both lower limbs (P=0.008), with a specificity of 0.853, a sensitivity of 0.833, and a Youden index of 0.686 (Table 3 and Figure 2).

Comparison of the number of quadrants of original masses in bilateral GLM groups and newly developed masses on the opposite side, as well as the long diameter, short diameter, pus bacterial culture, and PRL levels

In the bilateral GLM group, a paired sample t-test and Wilcoxon signed-rank test were performed to analyze the quadrant count, long diameter, short diameter, bacterial culture of pus, PRL values after the two occurrences of lesions, and the time of onset between the original and newly developed masses on the opposite side. The results showed that there were no statistically significant differences in the number of quadrants (z=−0.38, P=0.71), long diameter (t=0.39, P=0.71), short diameter (t=0.77, P=0.46), pus bacterial culture (z=−0.82, P=0.41), and PRL levels (z=−1.01, P=0.31) between the original and newly developed masses in the bilateral GLM group (Table 4).

Discussion

GLM, a low-incidence benign inflammatory disease, typically occurs in women 3–5 years childbirth (17). Currently, there are no unified or clear etiologies. Only one case report (18) has previously described ductoscopy-induced GLM. To our knowledge, the present study by our team involves the largest case series to date. Nipple discharge is a common clinical feature of GLM, with a reported incidence of approximately 7.5% in previous literature (14).

At our center, 92 patients (6.8%) were identified, which is consistent with the previously reported clinical incidence. Among these, 40 had nipple discharge from the healthy contralateral breast without mass formation. Ductoscopy was performed in these patients, and 10 developed new masses in the contralateral breast, which were finally confirmed as GLM by pathological biopsy. These patients constituted the bilateral GLM group, with an incidence of approximately 25%. A previous study has reported the incidence of bilateral GLM to be approximately 5.8% (19), which is far lower than that in our study.

During this process, we wondered why some patients developed new masses in the contralateral breast after ductoscopy while others did not. Through retrospective analysis of this series of cases, we were surprised to find that the incidence of EN on both lower limbs and the detection rate of inflammatory cells such as “neutrophils and lymphocytes” in cytological smears of nipple discharge were significantly higher in the bilateral GLM group than in the unilateral GLM group.

This led us to hypothesize that during ductoscopy, some breast ducts with underlying risks (i.e., deposition of lactation secretions in the lumen observed during ductoscopy) may suffer structural damage to the ductal epithelium (20) due to external physical injury from ductoscopy (e.g., excessive irrigation pressure or endoscope-induced ductal injury). This damage allows the lactation secretions deposited in the lumen to escape into the lobular connective tissue outside the lumen. Lactation secretions in the breast ducts are chemically irritating and can induce local foreign body reactions and granulomatous inflammation.

The pathological features of GLM consistently show varying degrees of ductal dilatation, intraductal inflammatory cell infiltration, and involvement of extra-ductal glands (21). Previous studies have revealed that the histological characteristics of GLM include obvious ductal injury, intraductal epithelial ulcers, and polymorphic substances in the lumen (22). Experts have also observed ductal epithelial cell damage in GLM via H&E staining and cellular injury using transmission electron microscopy (23). In our study, pathological H&E-stained sections demonstrated breast ductal injury with inflammatory cell infiltration in the walls of the dilated ducts (Figure 8). Our results indicate that the detection of neutrophils and lymphocytes in ductoscopic cytological smears is an independent risk factor for post-ductoscopic mass formation. This mechanism may be related to secretory extravasation caused by ductal injury. Extravasated lactation secretions can trigger inflammatory responses, even in the absence of bacteria. Previous studies (11,22) have shown that inflammatory masses form around secretions, strongly suggesting that milk components (such as lipids, proteins, and crystals) that leak into the breast tissue interstitium are chemically irritative and may directly induce local foreign body reactions and granulomatous inflammation. The ductal injury observed in our pathological H&E staining indirectly confirms the extravasation of intraductal secretions, which is highly consistent with Taylor’s “chemical inflammation” hypothesis (11). Thus, clinically, for patients with inflammatory cell infiltration (e.g., neutrophils and lymphocytes) detected by ductoscopy, the risk of GLM post-ductoscopy should be monitored and an optimized strategy combining antibiotics (targeting lipophilic bacteria) should be considered.

Inflammation induced by infection, trauma, or chemical irritation is the proposed pathogenesis of GLM advocated by Fletcher et al. (22). Extravasated intraductal secretions accompanied by lymphocyte and macrophage migration to the periductal area can trigger local granulomatous reactions. In our study, cytological smears from ductoscopy of the contralateral GLM showed abundant lymphocytes and neutrophils, which may have resulted from local trauma, leading to ductal epithelial injury (8,24,25). Some scholars argue against an autoimmune etiology (11,12,23), which aligns with our histological findings of ductal injury observed in tissue sections (Figure 6B) and inflammatory cell infiltration around the dilated duct walls. These suggest a potential association between ductal injury and this histological pattern. Clinically, breast trauma patients often develop rapid-onset breast masses, a process mimicked by GLM cases after ductoscopy. This similarity implies that ductoscopy-induced GLM may replicate the pathogenic pathways of trauma-induced ductal injury.

Previous studies have reported the incidence of EN in GLM to be 6.6–7.05% (11,26-28). In our study, 5 out of 10 patients (50%) with bilateral GLM presented with EN in both lower limbs, which was significantly higher than that in the unilateral GLM group (1 case, 3.3%). A recently published study (5) found that patients with bilateral GLM had a higher probability of developing erythema, reporting that four out of seven bilateral GLM cases were GLM-EN patients, which is roughly consistent with our observations. Therefore, they suggested that the presence of EN indicates a more severe disease and longer treatment duration; however, the underlying mechanism for the higher incidence of EN in patients with bilateral GLM remains unclear. Taylor et al. (11) speculated that the coincidental association between EN and GLM provides further evidence of a type IV hypersensitivity reaction induced by bacteria. However, based on our findings, only 3 out of 5 EN cases in the bilateral GLM group tested positive for bacteria, whereas the other two cases showed negative results in both ductoscopic cytology and pus culture. Such evidence seems insufficient to confirm the hypothesis of a type IV hypersensitivity reaction. Our study observed that the development of contralateral GLM masses after ductoscopy can predict the occurrence of EN on both lower limbs, but the underlying mechanism requires further investigation in future studies.

Recent studies (28-30) demonstrated that PRL acts as a cytokine-like factor. When released into the immune system, PRL can regulate lymphocyte responses through paracrine and autocrine mechanisms. High serum PRL levels may increase mammary ductal permeability by acting on breast cells or the mammary immune system and activating downstream proinflammatory pathways. This allows immunogenic substances to enter the lobular interstitium, thereby triggering T cell-mediated immune responses (31). Interestingly, the PRL levels were not elevated, further confirming the multifactorial etiology of GLM. However, both the GLM subtype associated with hyperprolactinemia and the subtype induced by ductoscopy (physical injury) seem to share similarities; under certain conditions, luminal substances enter the breast lobules, leading to the formation of lobular granulomas.

Despite the encouraging results, this study has several limitations. The small sample size and single-center retrospective design may limit the generalizability of the findings. Due to the limitations of retrospective research, in patients with GLM with contralateral nipple discharge, no control group was set up for patients with nipple discharge who did not undergo ductoscopy. Future studies should prioritize multicenter trials with larger sample sizes, while setting up control groups of patients with GLM with contralateral nipple discharge who did not receive ductoscopy. These efforts will help establish a more solid evidence-based medical foundation and provide more clues and insights for exploring the etiology of GLM.

Conclusions

In summary, we reported the largest case series of bilateral GLM associated with ductoscopy to date. The initial primary mass in the bilateral GLM group was larger than that in the unilateral GLM group, indicating that the affected area of the primary mass in the index breast was more extensive and the condition was more severe at disease onset in the bilateral GLM group. The incidence of EN in both lower limbs was significantly higher in bilateral GLM, and the development of contralateral breast masses after ductoscopy showed high sensitivity, specificity, and accuracy in predicting EN.

The detection rates of “neutrophils and lymphocytes” in ductoscopic cytological smears were significantly higher in the bilateral GLM group than in the unilateral GLM group, serving as independent risk factor for post-ductoscopy mass formation.

We speculate that ductal injury with extravasation of static inflammatory substances from the lumen into the breast lobules, which causes chemical irritation, is potentially associated with GLM pathogenesis. Ductoscopy may simulate the pathogenic process of the GLM subtypes induced by breast trauma, leading to ductal injury.

However, this study has limitations due to the absence of a control group of GLM patients with contralateral nipple discharge who did not undergo ductoscopy, and its single-center design. Larger multicenter prospective trials are required to explore the etiology of GLM. Additionally, the development of risk stratification tools in the future could provide preventive intervention support for patients at high risk of GLM after ductoscopy.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://gs.amegroups.com/article/view/10.21037/gs-2025-77/rc

Data Sharing Statement: Available at https://gs.amegroups.com/article/view/10.21037/gs-2025-77/dss

Peer Review File: Available at https://gs.amegroups.com/article/view/10.21037/gs-2025-77/prf

Funding: This study was supported by the Chongqing Municipal Research Institution Performance Incentive and Guidance Special Project (No. jxyn-2021-1-19).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://gs.amegroups.com/article/view/10.21037/gs-2025-77/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The research protocol was approved by the Institutional Review Board of Chongqing Traditional Chinese Medicine Hospital (No. 2023-KY-YJS-PT). The requirement for individual consent was waived for this retrospective study.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Kessler E, Wolloch Y. Granulomatous mastitis: a lesion clinically simulating carcinoma. Am J Clin Pathol 1972;58:642-6. [Crossref] [PubMed]
2. Yin Y, Liu X, Meng Q, et al. Idiopathic Granulomatous Mastitis: Etiology, Clinical Manifestation, Diagnosis and Treatment. J Invest Surg 2022;35:709-20. [Crossref] [PubMed]
3. Cui L, Sun C, Guo J, et al. Pathological manifestations of granulomatous lobular mastitis. Front Med (Lausanne) 2024;11:1326587. [Crossref] [PubMed]
4. Barreto DS, Sedgwick EL, Nagi CS, et al. Granulomatous mastitis: etiology, imaging, pathology, treatment, and clinical findings. Breast Cancer Res Treat 2018;171:527-34. [Crossref] [PubMed]
5. Zeng Y, Zhang D, Fu N, et al. Risk Factors for Granulomatous Mastitis and Establishment and Validation of a Clinical Prediction Model (Nomogram). Risk Manag Healthc Policy 2023;16:2209-22. [Crossref] [PubMed]
6. Saydam M, Yilmaz KB, Sahin M, et al. New Findings on Autoimmune Etiology of Idiopathic Granulomatous Mastitis: Serum IL-17, IL-22 and IL-23 Levels of Patients. J Invest Surg 2021;34:993-7. [Crossref] [PubMed]
7. Hur SM, Cho DH, Lee SK, et al. Experience of treatment of patients with granulomatous lobular mastitis. J Korean Surg Soc 2013;85:1-6. [Crossref] [PubMed]
8. Akcan A, Akyildiz H, Deneme MA, et al. Granulomatous lobular mastitis: a complex diagnostic and therapeutic problem. World J Surg 2006;30:1403-9. [Crossref] [PubMed]
9. Krawczyk N, Kühn T, Ditsch N, et al. Idiopathic Granulomatous Mastitis as a Benign Condition Mimicking Inflammatory Breast Cancer: Current Status, Knowledge Gaps and Rationale for the GRAMAREG Study (EUBREAST-15). Cancers (Basel) 2024;16:3387. [Crossref] [PubMed]
10. Yaghan L, Mohamed AI, Yaghan R. Idiopathic Granulomatous Mastitis: Is It Still a Mysterious Entity? Cureus 2025;17:e81817. [Crossref] [PubMed]
11. Taylor GB, Paviour SD, Musaad S, et al. A clinicopathological review of 34 cases of inflammatory breast disease showing an association between corynebacteria infection and granulomatous mastitis. Pathology 2003;35:109-19.
12. Li J, McGregor HP. Idiopathic granulomatous mastitis associated with hyperprolactinemia: A nonoperative approach. Breast J 2017;23:742-4. [Crossref] [PubMed]
13. Tabaja H, Comba IY, Pritt BS, et al. Granulomatous mastitis secondary to Corynebacterium kroppenstedtii. IDCases 2022;28:e01489. [Crossref] [PubMed]
14. Li S, Huang Q, Song P, et al. Clinical characteristics and therapeutic strategy of granulomatous mastitis accompanied by Corynebacterium kroppenstedtii: a retrospective cohort study. BMC Womens Health 2023;23:388. [Crossref] [PubMed]
15. Zeng Y, Zhang D, Zhao W, et al. Predisposing Factors for Granulomatous Lobular Mastitis: A Case-Control Study. Int J Womens Health 2023;15:1063-75. [Crossref] [PubMed]
16. Wang X, He X, Liu J, et al. Immune pathogenesis of idiopathic granulomatous mastitis: from etiology toward therapeutic approaches. Front Immunol 2024;15:1295759. [Crossref] [PubMed]
17. Fattahi AS, Amini G, Sajedi F, et al. Factors Affecting Recurrence of Idiopathic Granulomatous Mastitis: A Systematic Review. Breast J 2023;2023:9947797. [Crossref] [PubMed]
18. Makineli S, van Diest PJ, Fernandez MA, et al. Idiopathic granulomatous mastitis after ductoscopy: A case report. Int J Surg Case Rep 2021;88:106540. [Crossref] [PubMed]
19. Feng J, Gao Q, Qu W, et al. Clinical Characteristics of Non-Puerperal Mastitis: A Retrospective Analysis of 724 Patients. Int J Womens Health 2024;16:2113-22. [Crossref] [PubMed]
20. Sheybani F, Naderi HR, Gharib M, et al. Idiopathic granulomatous mastitis: Long-discussed but yet-to-be-known. Autoimmunity 2016;49:236-9. [Crossref] [PubMed]
21. Cheng L, Reddy V, Solmos G, et al. Mastitis, a Radiographic, Clinical, and Histopathologic Review. Breast J 2015;21:403-9. [Crossref] [PubMed]
22. Fletcher A, Magrath IM, Riddell RH, et al. Granulomatous mastitis: a report of seven cases. J Clin Pathol 1982;35:941-5. [Crossref] [PubMed]
23. Zhang HJ, Ding PP, Zhang XS, et al. MAC mediates mammary duct epithelial cell injury in plasma cell mastitis and granulomatous mastitis. Int Immunopharmacol 2022;113:109303. [Crossref] [PubMed]
24. Asoglu O, Ozmen V, Karanlik H, et al. Feasibility of surgical management in patients with granulomatous mastitis. Breast J 2005;11:108-14. [Crossref] [PubMed]
25. Diesing D, Axt-Fliedner R, Hornung D, et al. Granulomatous mastitis. Arch Gynecol Obstet 2004;269:233-6. [Crossref] [PubMed]
26. Çetin K, Sıkar HE, Güllüoğlu BM. Idiopathic granulomatous mastitis with erythema nodosum: Is it a variant of clinical presentation indicating treatment resistance? A retrospective cohort study. Breast J 2020;26:1645-51. [Crossref] [PubMed]
27. Velidedeoğlu M, Papila Kundaktepe B, Mete B, et al. Idiopathic granulomatous mastitis associated with erythema nodosum may indicate a worse prognosis. Int J Rheum Dis 2021;24:1370-7. [Crossref] [PubMed]
28. Abuhammad A, Albandak M, Ayyad M, et al. Sarcoidosis Presenting as Granulomatous Mastitis, Erythema Nodosum, and Arthritis Syndrome: A Case Report and Comprehensive Review of the Literature. J Investig Med High Impact Case Rep 2024;12:23247096241267146. [Crossref] [PubMed]
29. Matera L. Endocrine, paracrine and autocrine actions of prolactin on immune cells. Life Sci 1996;59:599-614. [Crossref] [PubMed]
30. Alkaissi H, Kim EJ, Salahi N, et al. Granulomatous Mastitis: An Initial Presentation of Undiagnosed Prolactinoma. Cureus 2024;16:e65639. [Crossref] [PubMed]
31. Nikolaev A, Blake CN, Carlson DL. Association between Hyperprolactinemia and Granulomatous Mastitis. Breast J 2016;22:224-31. [Crossref] [PubMed]