The exact etiology of the DIP is uncertain but 58-91% of DIP cases are linked with cigarette smoking[4, 5]. In addition, the DIP may be associated with harmful irritating substances from environmental/occupational (such as asbestos, talc, graphite, silica and aluminum), systemic disease virus infection and drugs [6, 7]. The main histopathological feature of DIP is a large number of macrophages in alveoli, which were usually diffusely distributed throughout the pulmonary acini within alveoli, and proliferation of pneumocytes over the course of alveolar septa . Although there may be mild infiltration of inflammatory cells in the alveolar septum, the alveolar structure generally remained normal. The infiltrating inflammatory cells include a small number of eosinophils, accompanied by fibroblast proliferation. The rare changes are mild fibrosis, but severe fibrosis and honeycomb like lesions are very rare.
Pathological diagnosis is the "gold standard" for the diagnosis of DIP. Methods of lung biopsy included transbronchial lung biopsy (TBLB), CT-guided percutaneous needle biopsy, transbronchial cryobiopsy and surgical lung biopsy. Lung specimens from TBLB are too small, which can't fully reflect the scope and degree of lung lesions and satisfy the diagnosis of interstitial lung disease. The specimens from surgical lung biopsy can meet the diagnostic requirements of interstitial lung disease, but the surgical lung biopsy is costly and traumatic, which is not easy for patients to accept. Transbronchial cryobiopsy or CT-guided percutaneous lung biopsies have fewer healthcare costs, fewer traumatic, and the specimens can meet the diagnostic requirements of interstitial lung disease, which is easy for patients to accept. This patient underwent percutaneous lung biopsy and the result showed that there were a large number of macrophages in the alveolar cavity and chronic inflammation was noted in the interstitium, so it could be diagnosed as DIP. At the same time, the patient had no history of smoking or second-hand smoke, which was rare in the literature. The patient was a sculptor. Because the environmental or occupational exposure may be one of an etiological risk factors, it is speculated that dust inhalation may be one of the inducing factors in this case. However, because the specimens were relatively small, it was impossible to know whether there was dust deposition in other lesions regions.
The special feature of this case was lung CT, which showed a single solid mass in the right lower lung, and then rapidly progressed with peripheral infection. However, the typical imaging manifestation of DIP is diffuse ground glass shadow in both lungs, which is located under the pleura. The lower lung is more than the upper lung, and some are accompanied by linear opacities and reticulation in the base . Honeycomb appearance is uncommon. Therefore, the imaging findings of this case were different from the typical imaging findings of DIP, which were rarely reported in the literature. These imaging findings were often misdiagnosed as pulmonary malignant tumor because of PETCT demonstrated hypermetabolism and the patients were usually treated by surgery. Therefore, for the pulmonary mass, even if PETCT indicates hypermetabolic lesions and highly suspected tumor, the pathological diagnosis of preoperative mass is still very important to avoid irreversible damage to patients.
The main treatment is to quit smoking and glucocorticoid therapy and some cases become spontaneous remission after quitting smoking. Glucocorticoids have been reported to be beneficial in case series, although improvement may be temporary . Environmental/occupational factors are also suspicious etiology of DIP [6, 7]. That DIP improved in two cases after leaving the workplace without steroid treatment was reported by Lougheed et al . Therefore, It is reasonable to terminate any possible environmental risk factors. Initial glucocorticoid therapy consists of 40-60 mg/day for 6 weeks, then decreased gradually and stopped within 6-9 months. Glucocorticoid therapy of this case: intravenous methylprednisolone 40mg for 2 weeks, oral prednisone 40mg for 3 weeks, and then decrease 5 mg weekly until to 20 mg. Then the dose was reduced by 5 mg monthly until to 10 mg and maintained for three months. The total course of treatment was half a year. The case clinical symptoms and radiology were significant improvement after steroid treatment.