Submitted:
23 August 2026
Posted:
28 August 2026
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Abstract
Background: Idiopathic granulomatous mastitis (IGM) is a rare benign inflammatory breast disease with variable response to corticosteroid therapy. This study aimed to identify predictive factors for steroid responsiveness in IGM patients. Methods: A retrospective analysis of 176 patients with IGM treated at Çukurova University Faculty of Medicine, Department of General Surgery between 2011 and 2019 was conducted. Patients were divided into steroid-responsive (Group 1, n=100) and non-responsive (Group 2, n=76) groups. Demographic characteristics, clinical features, and treatment history were compared using the chi-square test, Mann-Whitney U test, and multivariate logistic regression analysis. Results: Mean age was 39.1 ± 7.6 years. Factors associated with steroid non-responsiveness included extramammary symptoms (40.8% vs. 26.0%, p = 0.038), recurrent disease (21.1% vs. 8.0%, p = 0.012), a higher number of previous attacks (median 2 vs. 1, p < 0.001), previous abscess drainage (31.6% vs. 14.0%, p = 0.005), previous surgical treatment (30.3% vs. 7.0%, p < 0.001), and longer steroid treatment duration (median 6 vs. 4 months, p = 0.006). Multivariate analysis identified recurrent disease (OR = 0.283, p = 0.015), abscess drainage (OR = 0.307, p = 0.007), previous surgery (OR = 0.170, p = 0.001), and steroid treatment duration (OR = 0.880, p = 0.008) as independent predictors of poor steroid response. Conclusions: Steroid non-responsiveness in IGM is associated with disease recurrence, previous abscess drainage, previous surgical intervention, and prolonged steroid therapy. Alternative treatment modalities should be considered in patients with these characteristics.
Keywords:
idiopathic granulomatous mastitis
; corticosteroid therapy
; treatment response
; predictive factors
; breast disease
Introduction
Idiopathic granulomatous mastitis (IGM), first described by Kessler and Wolloch in 1972, is a rare, benign, chronic inflammatory disease of the breast [1]. Its etiology remains uncertain, although autoimmune processes, hormonal factors, and infectious agents have been proposed as potential contributing factors [2,3]. The efficacy of corticosteroid therapy in IGM has been widely interpreted as supporting an autoimmune-mediated pathophysiological process [3]. IGM predominantly affects women of reproductive age and poses both diagnostic and therapeutic challenges, particularly because of its clinical and radiological resemblance to inflammatory breast carcinoma [4]. For this reason, the definitive diagnosis of IGM still relies on needle biopsy and histopathological examination. Its distinguishing features include the absence of malignant cells on biopsy and the presence of non-caseating granulomatous inflammatory changes [4].
The optimal treatment strategy for IGM remains controversial. The uncertain etiology of the disease complicates management strategies [5]. A variety of therapeutic approaches have been used, including observation, antibiotics, corticosteroids, immunosuppressive agents, and surgical excision [6,7]. Corticosteroid therapy has emerged as the first-line treatment option, achieving clinical remission in 50–87% of patients [8,9]. However, a substantial proportion of patients either fail to respond to steroid therapy or experience disease recurrence, highlighting the need for alternative treatment strategies [10].
Despite the widespread use of corticosteroids in the management of IGM, factors predicting treatment response remain poorly defined. Identifying patients who are likely to respond to steroid therapy could help optimize treatment selection, minimize unnecessary adverse effects, and improve clinical outcomes. The present study aimed to identify clinical and demographic factors associated with corticosteroid response in a large cohort of IGM patients.
Materials and Methods
Study Design and Patient Selection
This retrospective cohort study was conducted at the Department of General Surgery, Çukurova University Faculty of Medicine. The medical records of all patients diagnosed with IGM between January 2011 and December 2025 were reviewed retrospectively. The study protocol was approved by the institutional ethics committee.
Inclusion criteria were: (1) histopathologically confirmed diagnosis of IGM, (2) treatment with oral corticosteroids, (3) a minimum follow-up period of 6 months, and (4) complete medical records. Exclusion criteria were: (1) specific granulomatous mastitis (tuberculosis, sarcoidosis, fungal infections), (2) concomitant malignancy, (3) incomplete treatment, and (4) loss to follow-up.
Treatment Protocol
All patients received oral prednisolone as initial therapy. The starting dose was 32 mg/day (n=90) or 64 mg/day (n=86), depending on disease severity and clinician preference. The dose was gradually tapered according to clinical response, typically by 5–10 mg every 2–4 weeks.
Definition of Treatment Response
Patients were classified into two groups according to their response to corticosteroid therapy:
- Group 1 (Steroid-responsive): complete clinical and radiological resolution of the disease with corticosteroid therapy alone.
- Group 2 (Steroid non-responsive): failure to achieve complete remission, disease progression during treatment, or the need for additional intervention (surgery, immunosuppressants).
Data Collection
The following variables were extracted from the medical records:
- Demographic data: age, body mass index (BMI).
- Reproductive history: menopausal status, parity, duration of breastfeeding, history of oral contraceptive use.
- Clinical presentation: presenting symptoms, extramammary findings, laterality, localization.
- Disease characteristics: recurrent disease, number of previous attacks, time from symptom onset to treatment.
- Treatment history: previous antibiotics, steroids, surgical interventions, abscess drainage.
- Treatment details: steroid dose, treatment duration, adverse effects.
Statistical Analysis
Statistical analysis was performed using SPSS version 25.0 (IBM Corp., Armonk, NY). Continuous variables were expressed as mean ± standard deviation or median (interquartile range), depending on the normality of distribution. Categorical variables were presented as frequencies and percentages.
Between-group comparisons were performed using the Student's t-test or the Mann-Whitney U test for continuous variables, and the chi-square test or Fisher's exact test for categorical variables. Variables with p < 0.1 in univariate analysis were included in a multivariate logistic regression model to identify independent predictors of steroid non-responsiveness. Odds ratios (OR) with 95% confidence intervals (CI) were calculated. A p-value < 0.05 was considered statistically significant.
Results
Table 1. Demographic and Clinical Characteristics
A total of 176 patients were included in the study, comprising 100 patients in Group 1 and 76 patients in Group 2. The mean age of the overall cohort was 39.1 ± 7.6 years, with no significant difference between Group 1 and Group 2 (39.15 ± 8.06 vs. 39.02 ± 6.97 years, p = 0.456). Similarly, the mean body mass index (BMI) was comparable between the groups (27.65 ± 2.71 vs. 27.87 ± 2.87 kg/m², p = 0.302).
The majority of patients were premenopausal in both groups (86.0% in Group 1 vs. 78.9% in Group 2), with no statistically significant difference in menopausal status (p = 0.218). Smoking rates were higher in Group 1 compared to Group 2 (38.0% vs. 26.3%); however, this difference did not reach statistical significance (p = 0.102).
The prevalence of rheumatologic diseases was low and similar between the groups (3.0% vs. 1.3%, p = 0.458). Likewise, there were no significant differences in family history of IGM (10.0% vs. 7.9%, p = 0.630) or breast malignancy (15.0% vs. 15.8%, p = 0.886).
Table 1.
Demographic and Clinical Characteristics.
| Characteristic | Group 1 (n=100) | Group 2 (n=76) | Total (n=176) | P-value |
|---|---|---|---|---|
| Age (years) | 39.15 ± 8.06 | 39.02 ± 6.97 | 39.1 ± 7.6 | 0.456 |
| BMI (kg/m²) | 27.65 ± 2.71 | 27.87 ± 2.87 | 27.74 ± 2.77 | 0.302 |
| Menopausal status | 0.218 | |||
| Premenopausal | 86 (86.0%) | 60 (78.9%) | 146 (83.0%) | |
| Postmenopausal | 14 (14.0%) | 16 (21.1%) | 30 (17.0%) | |
| Smoking | 38 (38.0%) | 20 (26.3%) | 58 (33.0%) | 0.102 |
| Rheumatologic disease | 3 (3.0%) | 1 (1.3%) | 4 (2.3%) | 0.458 |
| Family history of IGM | 10 (10.0%) | 6 (7.9%) | 16 (9.1%) | 0.630 |
| Family history of breast malignancy | 15 (15.0%) | 12 (15.8%) | 27 (15.3%) | 0.886 |
Table 2. Reproductive History
Reproductive history parameters were comparable between the two groups. There was no significant difference in the history of oral contraceptive use (17.0% in Group 1 vs. 13.2% in Group 2, p = 0.484). The median number of pregnancies was similar between the groups [2.0 (2.0–3.75) vs. 2.5 (2.0–3.0), p = 0.794], as were the median number of abortions [0.00 (0.00–1.00) in both groups, p = 0.705] and live births [2.00 (1.00–3.00) vs. 2.00 (2.00–3.00), p = 0.747]. A history of breastfeeding was highly prevalent in both groups (93.0% vs. 94.7%, p = 0.637), with a similar median duration of breastfeeding [24.00 (12.00–48.00) vs. 24.00 (15.25–48.00) months, p = 0.832]. Additionally, the rate of puerperal mastitis history did not differ significantly between Group 1 and Group 2 (27.0% vs. 34.2%, p = 0.302).
Table 2.
Reproductive History.
| Variable | Group 1 (n=100) | Group 2 (n=76) | Total (n=176) | P-value |
|---|---|---|---|---|
| OCP use history | 17 (17.0%) | 10 (13.2%) | 27 (15.3%) | 0.484 |
| Number of pregnancies* | 2.0 (2.0–3.75) | 2.5 (2.0–3.0) | 2.0 (2.0–3.0) | 0.794 |
| Number of abortions* | 0.00 (0.00–1.00) | 0.00 (0.00–1.00) | 0.00 (0.00–1.00) | 0.705 |
| Number of live births* | 2.00 (1.00–3.00) | 2.00 (2.00–3.00) | 2.00 (1.25–3.00) | 0.747 |
| Breastfeeding history | 93 (93.0%) | 72 (94.7%) | 165 (93.8%) | 0.637 |
| Breastfeeding duration (months)* | 24.00 (12.00–48.00) | 24.00 (15.25–48.00) | 24.00 (12.00–48.00) | 0.832 |
| Puerperal mastitis history | 27 (27.0%) | 26 (34.2%) | 53 (30.1%) | 0.302 |
*Data presented as median (IQR).
Table 3. Clinical Presentation and Disease Characteristics
The distribution of presenting symptoms was similar between the two groups (p = 0.397). The most common presenting complaint was a breast mass (48.0% in Group 1 vs. 52.6% in Group 2), followed by mastalgia (23.0% vs. 11.8%) and erythema (15.0% vs. 17.1%). An abscess at presentation was observed in 9.0% of patients in Group 1 and 14.5% in Group 2.
Extramammary manifestations were significantly more frequent in Group 2 compared to Group 1 (40.8% vs. 26.0%, p = 0.038). Similarly, recurrent disease was significantly more common in Group 2 (21.1% vs. 8.0%, p = 0.012). In line with this finding, the median number of previous attacks was significantly higher in Group 2 [2.00 (1.00–3.00) vs. 1.00 (1.00–2.00), p < 0.001]. There was no significant difference between the groups in terms of disease laterality (p = 0.864). However, a history of abscess drainage was significantly more frequent in Group 2 compared to Group 1 (31.6% vs. 14.0%, p = 0.005).
Table 3.
Clinical Presentation and Disease Characteristics.
| Variable | Group 1 (n=100) | Group 2 (n=76) | P-value |
|---|---|---|---|
| Presenting symptom | 0.397 | ||
| Abscess | 9 (9.0%) | 11 (14.5%) | |
| Mastalgia | 23 (23.0%) | 9 (11.8%) | |
| Mass | 48 (48.0%) | 40 (52.6%) | |
| Erythema | 15 (15.0%) | 13 (17.1%) | |
| Nipple discharge | 4 (4.0%) | 3 (3.9%) | |
| Nipple retraction | 1 (1.0%) | 0 (0.0%) | |
| Extramammary symptoms | 26 (26.0%) | 31 (40.8%) | 0.038 |
| Recurrent disease | 8 (8.0%) | 16 (21.1%) | 0.012 |
| Number of previous attacks* | 1.00 (1.00–2.00) | 2.00 (1.00–3.00) | <0.001 |
| Laterality | 0.864 | ||
| Right | 36 (36.0%) | 29 (38.2%) | |
| Left | 60 (60.0%) | 43 (56.6%) | |
| Bilateral | 4 (4.0%) | 4 (5.3%) | |
| Previous abscess drainage | 14 (14.0%) | 24 (31.6%) | 0.005 |
*Data presented as median (IQR).
Table 4. Previous Treatment History
Previous treatment modalities differed significantly between the two groups. The use of antibiotics was more frequent in Group 2 compared to Group 1 (64.5% vs. 51.0%); however, this difference did not reach statistical significance (p = 0.074). In contrast, corticosteroid use was significantly higher in Group 2 (55.3% vs. 38.0%, p = 0.023). Similarly, a history of surgical intervention was markedly more common in Group 2 than in Group 1 (30.3% vs. 7.0%, p < 0.001). Conversely, patients without any prior treatment were significantly more frequent in Group 1 compared to Group 2 (36.0% vs. 19.7%, p = 0.018).
Table 4.
Previous Treatment History.
| Treatment | Group 1 (n=100) | Group 2 (n=76) | P-value |
|---|---|---|---|
| Antibiotics | 51 (51.0%) | 49 (64.5%) | 0.074 |
| Corticosteroids | 38 (38.0%) | 42 (55.3%) | 0.023 |
| Surgery | 7 (7.0%) | 23 (30.3%) | <0.001 |
| No previous treatment | 36 (36.0%) | 15 (19.7%) | 0.018 |
Table 5. Current Treatment Characteristics and Outcomes
The initial corticosteroid doses were comparable between the two groups, with no significant difference observed in the distribution of patients receiving 32 mg/day or 64 mg/day (p = 0.570). However, the duration of steroid therapy was significantly longer in Group 2 compared to Group 1. The median treatment duration was 6.00 (3.00–10.00) months in Group 2, whereas it was 4.00 (2.50–6.00) months in Group 1 (p = 0.006).
Table 5.
Current Treatment Characteristics and Outcomes.
| Variable | Group 1 (n=100) | Group 2 (n=76) | P-value |
|---|---|---|---|
| Steroid dose | 0.570 | ||
| 32 mg/day | 53 (53.0%) | 37 (48.7%) | |
| 64 mg/day | 47 (47.0%) | 39 (51.3%) | |
| Steroid duration (months)* | 4.00 (2.50–6.00) | 6.00 (3.00–10.00) | 0.006 |
*Data presented as median (IQR).
Table 6. Multivariate Logistic Regression Analysis for Predictors of Steroid Non-responsiveness
Multivariate logistic regression analysis was performed to identify independent predictors of steroid non-responsiveness. Recurrent disease emerged as a significant independent predictor, associated with a markedly lower likelihood of steroid responsiveness (OR = 0.283, 95% CI: 0.102–0.785, p = 0.015). Similarly, a history of abscess drainage was independently associated with a reduced steroid response (OR = 0.307, 95% CI: 0.130–0.724, p = 0.007). Previous surgical intervention was identified as the strongest predictor of steroid non-responsiveness, with a significantly decreased likelihood of treatment response (OR = 0.170, 95% CI: 0.058–0.499, p = 0.001). In addition, longer steroid treatment duration was significantly associated with lower responsiveness (OR = 0.880, 95% CI: 0.802–0.967, p = 0.008). Extramammary symptoms, number of previous attacks, prior corticosteroid use, and absence of previous treatment were not found to be significant predictors of steroid response (p > 0.05 for all).
Table 6.
Multivariate Logistic Regression Analysis for Predictors of Steroid Non-responsiveness.
| Variable | B | SE | OR | 95% CI | P-value |
|---|---|---|---|---|---|
| Extramammary symptoms | -0.197 | 0.421 | 0.821 | 0.360–1.872 | 0.639 |
| Recurrent disease | -1.263 | 0.521 | 0.283 | 0.102–0.785 | 0.015 |
| Number of previous attacks | -0.307 | 0.242 | 0.735 | 0.458–1.182 | 0.204 |
| Previous abscess drainage | -1.180 | 0.437 | 0.307 | 0.130–0.724 | 0.007 |
| Previous surgery | -1.772 | 0.550 | 0.170 | 0.058–0.499 | 0.001 |
| Previous steroids | -0.303 | 0.447 | 0.739 | 0.308–1.774 | 0.498 |
| No previous treatment | 0.018 | 0.515 | 1.018 | 0.371–2.791 | 0.972 |
| Steroid duration | -0.127 | 0.048 | 0.880 | 0.802–0.967 | 0.008 |
| Constant | 2.452 | 0.595 | 11.612 | — | <0.001 |
Model statistics: -2 Log likelihood = 191.929; Cox & Snell R² = 0.242; Nagelkerke R² = 0.325; Hosmer-Lemeshow test p = 0.524.
Discussion
IGM is a disease with an unpredictable clinical course and heterogeneous response to treatment, and its optimal management remains controversial. The present study represents one of the largest single-center analyses examining the predictors of corticosteroid response in IGM. Our findings show that approximately 57% of patients achieved complete remission with corticosteroid therapy alone, which is consistent with the 50–87% rates reported in previous studies [8,9]. However, a considerable proportion of patients (43%) did not respond adequately to treatment, highlighting the need for reliable markers to guide initial treatment selection.
Although corticosteroids are widely accepted as first-line therapy for IGM, response rates are highly variable and recurrence rates may be substantial [11,12]. This variability has been attributed to factors such as disease severity, extent of inflammation, and underlying immunological mechanisms [13]. Demographic factors and reproductive history characteristics did not differ between groups in terms of steroid treatment response. The absence of an association between these features and treatment response suggests that clinical characteristics of the disease may be more important than demographic and reproductive factors in predicting outcomes. Some previous studies have reported associations between IGM and recent pregnancy, lactation, oral contraceptive use, and smoking [14]. In our study, these factors did not influence response to steroid therapy. This may be interpreted as indicating that although such features may contribute to the emergence of the disease, they do not appear to affect its clinical severity.
In its early stages, IGM typically presents as a rapidly growing breast mass accompanied by breast swelling, erythema, and pain. As the disease progresses, most patients enter an abscess phase, during which abscess rupture may occur [15]. Wang et al. reported that initiating corticosteroid therapy in the early phase of the disease, particularly during the mass stage, was more effective than initiating it in later stages [15]. In our study, no significant association was found between presenting breast symptoms and treatment response. Although steroid non-responsiveness was more frequent among patients with extramammary symptoms in comparative analysis, this factor was not retained as a significant predictor in multivariate logistic regression analysis.
Multivariate analysis identified four independent predictors of steroid non-responsiveness: recurrent disease, the need for abscess drainage, a history of previous surgical intervention, and prolonged steroid treatment duration. These findings have important clinical implications for patient counseling and treatment planning.
Recurrent disease emerged as the strongest predictor of poor steroid response (OR = 0.283). This suggests that patients with a history of IGM recurrence may harbor a more aggressive disease phenotype or have underlying factors that render them less responsive to anti-inflammatory therapy. Previous studies have reported recurrence rates ranging from 5% to 67% in IGM, with some suggesting that inadequate initial treatment may contribute to recurrence [16]. Our findings support the consideration of alternative or combination therapies in patients presenting with recurrent disease.
Another notable finding of our study was the association between a history of abscess drainage and non-response to steroid therapy (OR = 0.307). Abscess formation likely represents a more severe inflammatory process or secondary bacterial infection, both of which may complicate the disease and reduce the efficacy of corticosteroids. This observation is consistent with previous studies suggesting that complicated IGM cases require multimodal treatment [17].
A history of previous surgical intervention emerged as the strongest predictor in our model (OR = 0.170). This may reflect a selection bias, as patients who required surgery likely had more severe or refractory disease. Alternatively, surgical intervention may alter local tissue integrity and inflammatory patterns, or post-surgical fibrosis may impair subsequent response to steroid therapy. In such patients, the early use of immunosuppressive agents or reoperation may be considered.
Interestingly, longer steroid treatment duration was associated with worse outcomes in our study. This most likely reflects reverse causality: non-responsive patients were treated for longer periods before treatment failure was acknowledged. This finding underscores the importance of early response assessment and timely transition to alternative therapies in non-responsive patients. The optimal duration of steroid therapy is not clearly established in the literature, and no consensus exists. The general tendency is to continue therapy for 3–6 months [11,15]. In our study, the treatment duration of 4–6 months is consistent with current recommendations for IGM management.
Comparison of steroid doses showed no difference in efficacy between 32 mg/day and 64 mg/day of prednisolone; however, significantly more adverse effects were observed with the higher dose. This finding supports initiating treatment with lower doses and reserving dose escalation for non-responsive patients.
Taken together, these findings clearly indicate that corticosteroid response in IGM is multifactorial. Disease chronicity, previous treatments, and complications such as abscess formation play important roles in determining treatment outcomes. This highlights the need for patient-tailored, individualized treatment strategies rather than a uniform approach applied to all patients. Closer follow-up, early response assessment, and planning of combination therapies when necessary are particularly important in patients who carry risk factors for steroid non-responsiveness.
Study Limitations
This study has several limitations. The retrospective design may introduce selection and information bias. Treatment protocols varied over the study period, and although the definition of treatment response was clinically meaningful, it may not fully capture patients with partial response. The limited availability of long-term follow-up data precluded evaluation of late recurrences. Additionally, standardized imaging protocols and inflammatory markers that could provide further prognostic information were not available.
Clinical Implications
Based on our findings, we propose a risk-stratified approach to the management of IGM. Patients without risk factors (first presentation, no abscess, no previous surgery) are suitable candidates for corticosteroid monotherapy. Patients with one or more risk factors should be informed about the increased likelihood of treatment failure and may benefit from closer monitoring, earlier response assessment, or initial combination therapy.
Future prospective studies should validate these predictive factors and investigate whether risk-adapted treatment strategies improve outcomes. Further investigation of biomarkers, standardized imaging criteria, and optimal treatment duration will enhance the personalized management of IGM.
Conclusions
Non-responsiveness to corticosteroid therapy in IGM is associated with recurrent disease, abscess formation, previous surgical intervention, and prolonged treatment duration. These factors may help identify patients who are unlikely to respond to steroid monotherapy, thereby facilitating the earlier implementation of alternative treatment strategies. A risk-stratified approach may optimize treatment selection and improve clinical outcomes in this challenging clinical setting.
References
- Kessler, E.; Wolloch, Y. Granulomatous mastitis: a lesion clinically simulating carcinoma. Am. J. Clin. Pathol. 1972, 58(6), 642–646. [Google Scholar] [CrossRef]
- Altintoprak, F.; Kivilcim, T.; Ozkan, O.V. Aetiology of idiopathic granulomatous mastitis. World J. Clin. Cases 2014, 2(12), 852–858. [Google Scholar] [CrossRef]
- Benson, J.R.; Dumitru, D. Idiopathic granulomatous mastitis: presentation, investigation and management. Future Oncol. 2016, 12(11), 1381–1394. [Google Scholar] [CrossRef]
- Azizi, A.; Prasath, V.; Canner, J.; et al. Idiopathic granulomatous mastitis: management and predictors of recurrence in 474 patients. Breast J. 2020, 26(7), 1358–1362. [Google Scholar] [CrossRef]
- Akbulut, S.; Sahin, T.T. Comment on idiopathic granulomatous mastitis with skin rupture: a retrospective cohort study of 200 patients who underwent surgical and nonsurgical treatment. J. Invest Surg. 2021, 34(11), 1246–1247. [Google Scholar] [CrossRef]
- Pandey, T.S.; Mackinnon, J.C.; Bressler, L.; et al. Idiopathic granulomatous mastitis—a prospective study of 49 women and treatment outcomes with steroid therapy. Breast J. 2014, 20(3), 258–266. [Google Scholar] [CrossRef]
- Akbulut, S.; Arikanoglu, Z.; Senol, A.; et al. Is methotrexate an acceptable treatment in the management of idiopathic granulomatous mastitis? Arch. Gynecol. Obstet. 2011, 284(5), 1189–1195. [Google Scholar] [CrossRef]
- Lai, E.C.; Chan, W.C.; Ma, T.K.; et al. The role of conservative treatment in idiopathic granulomatous mastitis. Breast J. 2005, 11(6), 454–456. [Google Scholar] [CrossRef]
- Hovanessian Larsen, L.J.; Peyvandi, B.; Klipfel, N.; et al. Granulomatous lobular mastitis: imaging, diagnosis, and treatment. AJR Am. J. Roentgenol. 2009, 193(2), 574–581. [Google Scholar] [CrossRef]
- Oran, E.Ş.; Gürdal, S.Ö.; Yankol, Y.; et al. Management of idiopathic granulomatous mastitis diagnosed by core biopsy: a retrospective multicenter study. Breast J. 2013, 19(4), 411–418. [Google Scholar] [CrossRef]
- Tan, Q.W.; Zhang, Y.N.; Jia, Y.P.; Gou, J.; Lv, Q.; Yang, X.Q. Methylprednisolone for idiopathic granulomatous mastitis: a prospective observational cohort study. Gland Surg. 2022, 11(9), 1538–1545. [Google Scholar] [CrossRef]
- Lei, X.; Chen, K.; Zhu, L.; Song, E. Treatments for idiopathic granulomatous mastitis: a systematic review and meta-analysis. Breast Care 2017, 12(6), 415–421. [Google Scholar] [CrossRef]
- Azzam, M.I.; et al. Idiopathic granulomatous mastitis: clinical and immunological characteristics and management approaches. Rheumatol. Int. 2023, 43, 1661–1670. [Google Scholar] [CrossRef]
- Al-Khaffaf, B.; Knox, F.; Bundred, N.J. Idiopathic granulomatous mastitis: a 25-year experience. J. Am. Coll. Surg. 2008, 206(2), 269–273. [Google Scholar] [CrossRef]
- Wang, P.; Sun, J.Z.; Fang, H.Y.; Yang, D.J.; Ren, G.S. Optimal timing for corticosteroid therapy in idiopathic granulomatous mastitis: a retrospective analysis highlighting early intervention efficacy. J. Inflamm. Res. 2024, 17, 9617–9624. [Google Scholar] [CrossRef]
- Gautier, N.; Lalonde, L.; Tran-Thanh, D.; et al. Chronic granulomatous mastitis: imaging, pathology and management. Eur. J. Radiol. 2013, 82(4), e165–e175. [Google Scholar] [CrossRef]
- Ong, S.S.; et al. A meta-analysis of idiopathic granulomatous mastitis treatments for remission and recurrence prevention. Front Med. 2024, 11, 1346790. [Google Scholar] [CrossRef]
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