Plasma cell mastitis (PCM) is an aseptic inflammatory reaction that is thought to be caused by ductal dilation due to obstruction of the breast ducts, stimulation of the duct wall by aggregates, inflammatory cell infiltration and proliferation of fibrous tissue in the duct wall, resulting in epithelial detachment and destruction of the milk ducts, overflow of lipid-like material in the duct lumen, triggering an autoimmune response, resulting in plasma cell infiltration and fibrous tissue proliferation around the ducts. PCM accounts for 0.3% to 2.0% of breast diseases abroad and 1.9% to 5.0% of breast diseases in China. It accounts for 3.2% of benign breast diseases [1] [2]. The incidence of PCM has been increasing year by year in recent years. The causes of PCM are not well understood, but the causes of ductal occlusion may include: 1, congenital nipple entropion or dysplasia; 2, breastfeeding disorders, milk retention or breastfeeding difficulties, poor lactation hygiene and ductal injury; 3, bacterial infections, especially anaerobic bacteria, trauma and surgery in the areola area, etc. involving the milk ducts; 4, ductal degeneration to myoepithelial cell degeneration and Contraction weakness, glandular atrophy and degeneration leading to secretion retention, etc.; 5, autoimmune diseases; 6, smoking, breast binding damage to breast ducts, etc.; 7, VitA deficiency and related hormone level imbalance. 2, clinical manifestations Symptoms [6, 7] are mainly breast lumps and nipple overflow. Accompanying symptoms include pain, breast erythema, nipple depression, and adhesion of the lump to the skin. Chronic fistulas, sinus tracts, inflammatory abscesses and enlarged axillary lymph nodes. The four most common clinical manifestations are breast lumps, redness and swelling, pain, and nipple overflow. The nature of the overflow is transparent, white, bloody, etc. Type I: dilated milk ducts with abundant capillaries, white flocculent material in the lumen, and fibrous mesh structure; Type II: dilated milk ducts with abundant capillaries, white flocculent material in the lumen, Type I and II are considered benign and do not require surgical treatment; Type III is also considered benign, but should be followed up and reviewed regularly; Type IV does not exclude the possibility of malignancy, and lobectomy is feasible if necessary to clarify the diagnosis. The diagnosis was made. The results showed that among 95 patients with PCM, 21 patients with type I accounted for 22.1%, 43 patients with type II accounted for 45.3%, 18 patients with type III accounted for 18.9%, and 13 patients with type IV accounted for 13.7%. Zhao Hongmei et al [9] found that duct ectasia (DE) and PCM have different clinical manifestations, differential diagnosis, and pathological changes, and these differences mark two stages of the development of the same disease, each with its own independence, and thus should be treated with different clinical approaches. The authors divided the disease into 3 stages: (1) chronic inflammatory stage: ductal dilatation with inflammatory reactions in and around the ducts; (2) subacute inflammatory stage: increasing inflammation in and around the ducts with mild pain, resembling a mammary stasis cyst or chronic small abscess without obvious pus; (3) acute inflammatory stage: breast lumps with pain, swelling, redness of the skin, and mild generalized fever. The first stage is DE, the third stage is PCM, and the second stage is the transition between the two stages. 4, pathology The main pathological changes of DE are: ① simple ductal dilatation with chronic inflammatory reaction, chronic purulent reaction, foreign body plasma cell reaction, etc. (2) Dilation of breast ducts secondary to rupture and formation of foreign body granulation and cholesterol crystals. ③Focal ductal dilatation with lymphocytic and plasma cell-based chronic inflammation with foreign body giant cell reaction. (iv) Chronic inflammation and fibrosis around the epithelium of the milk ducts. The main pathological changes of PCM are: (1) massive plasma cell infiltration with focal histolytic necrosis and focal neutrophil infiltration on the basis of ductal dilatation. Although no mycobacteria were detected by special staining, it cannot be ruled out that such lesions are caused by mycobacteria or specific infections; (3) non-specific purulent inflammatory lesions of the breast are seen with relatively obvious fat necrosis and small oily cysts and small purulent granuloma formation due to fat necrosis Occasionally, atypical phlebitis is seen, with some areas of plasma cell infiltration. In a small number of cases, the cause was difficult to find and may be related to vasculitis. The ducts were clearly dilated and filled with gray-yellow mucous secretions, with thick gray-white fibrous walls around the ducts, but there were also those without obvious dilatation. On microscopic examination, the epithelium of the dilated mammary ducts was seen to be atrophied, and the lumen contained cellular debris, lipids and fatty acid crystals, with inflammatory cell infiltration, fibrous tissue hyperplasia and hyaline degeneration in the duct wall. The duct wall is commonly necrotic where the inflammatory response is significant, and the surrounding tissue is infiltrated by a large number of plasma cells and a small number of monocytes and lymphocytes. Tuberculosis-like granulomas composed of multinucleated giant cells and epithelioid cells are also seen, often accompanied by abscess formation. 5. Bacteriology PCM bacteriological examination is often negative, presumably with Mycobacterium bovis [11]. The main non-tuberculous branching mycobacteria causing skin and soft tissue lesions are: Mycobacterium maritimus, Mycobacterium incidentalis, Mycobacterium tortuosum, Mycobacterium abscessum, and Mycobacterium ulcerans. Further studies to identify branching mycobacteria such as Mycobacterium abscessus strains have been carried out abroad [12]. Xu Tao et al [13, 14] performed re-slides of pathological specimens from patients originally diagnosed with PCM and applied IK antacid staining and immunohistochemical staining for bovine BCG antibodies, which revealed a detection rate of 60.7% and 73.2% for Mycobacterium tuberculosis type L, suggesting that these PCM cases may be closely related to Mycobacterium tuberculosis type L tuberculosis infection or may be a specific subtype of breast tuberculosis. With the widespread use of antibiotics, non-specific chronic inflammation formed by atypical tuberculosis infection caused by Mycobacterium tuberculosis type L is increasingly common, often making treatment difficult if the diagnosis is not clear. The current methods for detecting Mycobacterium bovis include [15] PCR methods for gene sequences, DNA probe techniques, hybridization techniques, polymerase chain reaction PCR fluorescence quantitative detection, high-resolution melting line method PCR detection, DNA microarray, PCR-DNA sequencing, etc., but they are not carried out on a large scale due to uncertainties in sensitivity and specificity. 6. imaging By retrospectively analyzing the mammographic data of 47 cases of surgically or pathologically confirmed PCM, Ouyang Yu [16] et al. concluded that the mammographic manifestations of PCM were not significantly specific and showed mass shadow, mass shadow, nodular shadow, subareolar ductal dilatation, or only negative manifestations, respectively. The more valuable signs [17] are asymmetric hyperdensity along the long axis of the duct, flame-like appearance, uneven density with hypodense tubular structures, and scattered rod-shaped or hollow small round calcifications. Most of the PCM changes on X-ray are located near the areola and in the central region of the breast, and the areola skin may be thickened, mostly in the form of lamellar faint dense shadows with irregular borders and visible striated changes, which are very different from the infiltrative burr shadows of breast cancer roots with thick and thin tips [18]. MSCT [19] images can show the location, extent, infiltration and relationship with surrounding tissues of PCM lesions, and it is important to explore the imaging staging to guide the clinical selection of reasonable treatment plan. 7. Differential diagnosis PCM needs to be differentiated from the following diseases [20]: ①invasive breast cancer: in clinical practice, PCM is often misdiagnosed as breast cancer, especially in frozen sections, because mononuclear cells and plasma cells appear in patches in the lesion, arranged closely, and separated by fibrous cords in a cord-like arrangement, so it is easy to be misdiagnosed; ②mammary tuberculosis: PCM can appear with multinucleated giant cells and epithelioid cells, forming tuberculosis-like granuloma, but without caseous necrosis. (2) Breast tuberculosis: PCM can involve multinucleated giant cells and epithelioid cells, forming tuberculosis-like granulomas, but there is no caseous necrosis, and no antacid bacilli can be detected; (3) Breast fibrocystic disease: breast fibrocystic disease is a kind of breast hyperplasia, although PCM can involve interlobular ducts, but there is generally no epithelial hyperplasia, sweat gland hyperplasia and lobular hyperplasia. PCM and granulomatous mastitis (GM) both have similar clinical manifestations, and the preoperative misdiagnosis rate can be as high as 89%. The pathology of PCM is characterized by periductal inflammation with plasma cell infiltration. It is thought to be a hypersensitivity reaction to breast milk and often occurs in menstruating mothers with a history of milk stasis. The patient’s nipples and ducts are often normal, and most of the breast lumps are located peripherally, with the onset associated with the peripheral ducts and lobules. The lobe is infiltrated by a variety of inflammatory cells, mainly neutrophils, but also lymphocytes, epithelial macrophages, giant cells, etc. Microabscesses are often seen. 8, treatment For the timing of treatment of PCM, Kong Lingwei et al [21] reported treating 95 patients with PCM, with a cure rate of 92.2% (47/51) and a remission rate of 7.8% (4/51) in the acute mass phase. The overall efficiency rate was 100%, and the recurrence rate was 9.8% (5/51); the cure rate of chronic mass stage was 81.3% (13/16), and the recurrence rate was 18.7% (3/16); the cure rate of abscess stage: 71.4% (15/21); the cure rate of fistula stage was 71.4% (5/7), thus confirming that the acute inflammatory stage of PCM is the best time for drug treatment, and the quiescent stage of mass is the the best entry point for surgical treatment. Elagili [22] used a minimally invasive treatment method to treat PCM with unruptured skin, thin pus, and a single abscess with abscess puncture and irrigation under color ultrasound guidance. Ma Xiangjun et al [23] used a combination of oral dexamethasone and metronidazole in its acute phase based on the understanding of the causes and pathogenesis of PCM, and achieved remarkable results. Dexamethasone exerts its therapeutic effect mainly by suppressing the cellular immune response and reducing capillary dilation, exudation and edema in the acute inflammatory phase; metronidazole exerts its therapeutic effect by fighting against anaerobic bacteria. Su Li et al [24] used a mixture of 2% lidocaine 2ml, acamipexin 0.2g, and tretinoin 40mg to treat 30 cases of PCM in the mass stage with an efficiency of 93.33% by local closed injection at multiple points around the mass and at the base. Kamal [25] concluded that there is a lack of ideal treatment for PCM and that extensive local excision with or without steroid hormone therapy is still the main therapy. The limited excision of the lesion alone may lead to prolonged disease and a high risk of recurrence, while oral hormones and other antibiotics may reduce the size of the breast mass. However, the use of hormones is limited by the “infection” theory of pathogenesis. He believes that hormone therapy is only appropriate for recurrent cases. However, successful treatment of PCM with a combination of antibiotics and hormones has been reported [26, 27], and the combination of the two can control the disease and reduce complications. Due to the possible association of PCM with nontuberculous mycobacterial infections mentioned earlier, first-line agents are recommended [28-31] acamipexin, fluoroquinolones, cefoxitin, sulfonamides, linezolid, epi-mycoplasmin, and doxycycline and clarithromycin in combination to obtain higher sensitivity. We have tried to treat PCM with 3 combinations of anti-mycobacterial drugs (isoniazid 0.3/day + rifampicin 0.45/day + ethambutol 0.75/day) for 6-12 months, and have treated 22 patients with multiple abscesses and sinus tract type with satisfactory therapeutic results, and more intensive clinical studies are currently underway.