In most cases, FM patients are more likely to present with symptoms associated with compression of mediastinal structures. The common manifestation of FM includes the head fullness and facial swelling caused by compression of the superior vena cava and dyspnoea caused by compression of airways and pulmonary veins [
1]. In chest imaging, calcification can be found in 86% of patients. Mediastinal structures including the superior vena cava, central airways, and pulmonary veins can be compressed, which leads to vascular stenoses and pulmonary atelectasis, and the soft tissue mass compressing the mediastinal structure [
10]. In our case, asymptomatic FM was found unexpectedly and there were no overt imaging abnormalities in chest CT. We surmised that the oral immunosuppressive agent used to treat the MG could suppress thymic inflammation, and thus repress the development of FM.
Flieder et al. and other have previously subdivided the idiopathic fibroinflammatory lesions of the mediastinum into three groups based on the histologic pattern of this type of lesion [
8,
9]. According to this staging system, as the lesion stage increases, the dense collagen component also increases but the infiltration of inflammatory cells is reduced. In our case, dense collagen was distributed in a haphazard pattern and was infiltrated with minimal numbers of inflammatory cells. There was no obvious oedematous fibromyxoid tissue. Thus, the pathological pattern found in our case is consistent with the features of stage II fibrosing mediastinitis.
The pathogenesis of FM is largely obscure. However, previous research has shown that FM is associated with several autoimmune diseases [
2]. In a case series of nine idiopathic FM (IFM) patients by Rossi et al. [
2], seven patients were associated with autoimmune or fibro-inflammatory disorders including antineutrophil cytoplasmic antibody-associated vasculitis and aortitis. Further research has shown that several immune cells including monocytes and B cells, and in particular, CD20-plasma cells, were infiltrated in the peripheral region of fibrosing proliferation [
1,
2,
11]. In our case, lymphocyte infiltration was also identified around the fibrosing tissue. Because of the thymic inflammation and overactive immune responses in development of FM, anti-inflammatory therapy such as that involving administration of oral prednisone was applied to treat the FM [
1]. Recently, rituximab targeting CD20
+ B cells was proven to be effective in treating FM [
11]. In consideration of the close association and similar treatment between FM and autoimmune disease, Rossi et al. classified the “IFM associated with systemic autoimmune diseases” as one of the three forms of IFM [
2]. In our case, while the patient had been diagnosed with MG, she denied a history of previous bacterial infection. However, due to the unexpectedness of this case, testing for tuberculosis and histoplasma was not undertaken before surgery. The postoperative T-SPOT test for tuberculosis was negative. Despite this shortcoming, this rare case of asymptomatic FM found in a patient with extended our knowledge on autoimmune disease-associated FM.