Abstract
BackgroundThe working environment of stone miners has been believed to cause their susceptibility to respiratory diseases. Silicosis is an occupational disease caused by exposure to crystalline silica dust which is marked by inflammation and scarring in the lung. The immune system boosted after the silica invasion led to self-damage and lay the foundation of silicosis pathogenesis. Silicosis coexisting with other diseases in one patient has been reported, however, was not reported to coexist with constrictive pericarditis. We, for the first time, reported a patient with silicosis and constrictive pericarditis and thought the immune response was probably the link between the two.Case presentationA 59-year-old Chinese stone miner complained of chest distress was found to have lung nodules which were found to be silica deposits by biopsy. This patient was also found to have constrictive pericarditis at the same time. Later surgical decortication cured his symptoms.ConclusionWe provided the first case having constrictive pericarditis concomitant with silicosis. A probable link between the two diseases was the immune response boosted by the silica deposits.
Highlights
The working environment of stone miners has been believed to cause their susceptibility to respiratory diseases
A probable link between the two diseases was the immune response boosted by the silica deposits
Some believed the silica deposits could cause immune response which was responsible for silicosis progression [4,5] while some others believed the trace metals found on silica dusts played the major role in silicosis pathogenesis [6,7]
Summary
Stone mining is a profession with high risks to occupational lung disease due to its harmful working environment [1,2]. Among all the notorious pathogens present at stone miner’s working site, silica dust is believed to be the responsible agent causing the disease silicosis, a worldwide occupational lung disease. CT guided biopsy of the 25×33 cm lung nodule was performed and pathology demonstrated fibrous tissue hyperplasia and hyaline changes with carbon deposits and chronic inflammatory cell infiltration (Figure 1), which were definite pathologic evidences of silicosis. No tuberculosis bacilli were found in the tissues We had this patient screened for TB (tuberculosis) antibodies, T-spot.TB and PPD skin test. Patient was well recovered from previous dyspnea and chest distress and discharged afterwards. He remained very well and reported no similar symptoms during our follow-ups. Follow-up chest X-rays did not show any enlargement of the 25×33 mm nodule in the right upper lung
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