recently , sandblasting with purpose of abrasion and in preparing metal surfaces for painting , cleansing foundry castings and cleaning building exteriors has become an important etiology for silicosis ( 1 - 3 ) . acute silicosis is usually a progressive disease and despite treatment with corticosteroids it leads to death due to cardio - pulmonary causes and respiratory distress . one of the acute presentations of silicosis is alveolar silicoproteinosis which develops due to pulmonary exposure to silica dust and consequent filling of lungs with proteinaceous material . silicotuberculosis is seen in 25% of patients with acute and classic silicosis and presents in chest radiography as irregular nodules or opacities and cavitations with rapid progression of disease ( 3 ) . the prevalence of silicotuberculosis in south african gold - miners who were also human immunodeficiency virus ( hiv ) positive is considerable ( 4,5 ) . the latter condition which results from excessive accumulation of surfactant lipoprotein is caused by defect in the cleansing properties of alveolar macrophages and in 5 to 10 percent of cases is secondary and mainly occurs in association with other underlying medical conditions specially blood cancers or defects in the immune system such as severe combined immunodeficiency syndrome ( scid ) or hypogammaglobulinemias and is seen after transplantation as well ( 6 ) . patients with alveolar proteinosis are at risk for secondary infections with opportunist pathogens such as aspergillosis , nocardia and mycobacterium avium ( 6 , 7 , 8) . the presented patient in this article was a case of acute silicosis accompanied by tuberculosis which clinically did not respond to first line treatment . the patient is a 29 year old sandblaster from tehran with history of acute silicosis , pulmonary tuberculosis and secondary alveolar proteinosis on anti tb medications for a month and lung transplant candidate who presents with acute respiratory distress to our hospital . his respiratory symptoms have worsened in 10 days and in the past two days later was bed - bound . he also denied hemoptysis , and lost weight of 8 kg in the two months with decreased appetite in few days . two months prior to this admission , he was hospitalized in the tb ward with complaint of weakness , shortness of breath , cough and fever and chills . he had undergone bronchoscopy and transbronchial biopsy and was diagnosed with silicosis and secondary alveolar proteinosis with an inflammatory necrotic lesion consistent with tuberculosis . bronchoalveolar fluid lavage smear and biopsy showed numerous dust laden macrophages , squamous and columnar epithelial cells and was negative for malignancy . at this time , he was diagnosed with acutely exacerbated silicosis and secondary alveolar proteinosis . after evaluation , he received anti tb medications and intravenous hydrocortisone . at presentation , his medications were isoniazid , ethambutol , rifampin , pyrazinamide and prednisolone . blood oxygen saturation on arrival was 55 - 60% and oxygenation with a reserve bag mask eventually improved oxygen measurement upto 90 to 95% . the patient had a temperature of 38.3 c , pulse rate 160 , respiratory rate 22 and blood pressure 120/80 . abdominal exam was soft , nontender with no organomegally . clubbing and edema was not present . high resolution computed tomography ( hrct ) of the lungs showed bilateral alveolar ground glass opacities and consolidations prominently in mid upper zones with inter lobular septal thickening . the patterns were noted to be characteristic but not diagnostic for pulmonary alveolar proteinosis with silicoproteinosis . in comparison with previous ct scan ( two months prior ) disease progression patient 's chest ct scans , 2 month before last admission ( a - c ) and last admission ( d ) . laboratory values are shown in table 1   and the report for radiology and pathology shown at the end of the report . sputum cultures , from previous hospitalization was negative for mycobacteria , bal smear and polymerase chain reaction ( pcr ) . multiple arterial blood gases ( abg 's ) showed hypoxemia so oxygenation with reserve bag mask was administered . he was continued with tb medications and started on broad spectrum antibiotics clindamycin , ceftazidime . furthermore , the aggressive nature of the disease caused concern about pneumocystis carinii ( pcp ) and cotrimoxazole was administered . bronchoalveolar lavage ( bal ) microscopic study showed many dust laden alveolar macrophages and was negative for malignancy and diagnosis of accelerated ( cellular ) phase of silicosis associated with secondary alveolar proteinosis was made . 
 
 upon negative sputum and bal smear and cultures on discharge and according to previous positive pathology , he was discharged from hospital with an oxygen mask , tb medications and prednisolone 40mg / day . resistant tuberculosis and acute silicosis was in the differential diagnosis for this patient with sudden progression of disease ( 1 ) . shortly in a few days , the patient returned to the hospital emergency department with respiratory failure and hypoxemia . spo2 on arrival was 55 - 60% with reserve bag mask . in attempt to intubate the patient acute silicosis is usually an advance disease . despite treatment with corticosteroids , it leads to cardio - respiratory failure and death . alveolar silicoproteinosis is one of the presentations of acute silicosis due to exposure to silica dust and lungs filled with proteinaceous material ( 3 ) . 
 
 pulmonary alveolar proteinosis ( pap ) the authors note extreme rareness of the association of pap and tb in patients without a comprised immune status . they cite four cases reported , one of which was hiv positive and one who was a diabetic ( 9 ) . another article cites eight cases , whose primary diagnosis was tb and co - illness with pap was diagnosed at autopsy in four of them . in one case where pap was the primary diagnosis , antitubercular drugs were ineffective until pulmonary lavage was done ( 10 ) . our patient presented with a rapidly progressive picture of pulmonary disease , with acute silicoproteinosis and pulmonary ( tb ) . pertinent findings from this patient s previous and first hospitalization were a transbronchial lung biopsy specimen showing caseating granulomatous lesion with findings consistent with silicosis accompanied by alveolar proteinosis . additionally , in a patient with rapid progression of disease , multi - drug resistant tuberculosis accompanied with acute silicosis in the differential diagnosis . furthermore , infection with other mycobacteria needed to be in the differential diagnosis although culture results were not positive . also , in this patient , persistent infection with tuberculosis could have exacerbated the pulmonary alveolar proteinosis ( 8,10 ) . symptoms of progressive dyspnea during one month to a year are evidence of exposure to abundant amounts of silica dust . the classic form involves the interstitium of the lung in the forms of nodules or reticulations and is itself considered to have two main forms . one is simple or alveolar and presents as small round or irregular opacities on chest imaging . the other is complicated which involves massive fibrosis with large joining lesions evident on radiology ( 3,11 ) . first is excessive accumulation of surfactant lipoprotein in the alveoli and resultant abnormal gas exchange and is considered the cause of primary acquired cases . pathogenesis in the acquired form is by inhibition of the action of gm - csf by blocking antibodies and resultant impairment of surfactant clearance by alveolar macrophages . treatment with gm - csf is promising in the acquired but not other forms ( 6 ) . second which involves congenital cases ( 2% of all cases ) results from several genetic defects in the surfactant protein ( sp)-b gene or the c molecule of the gm - csf receptor ? third are secondary cases ( 5 - 10% of total cases ) which are associated with other underlying diseases especially hematopoietic and other malignancies ( 7,12 ) . 
 
 on histology , deposits of periodic acid schiff ( pas)-positive proteinaceous material in the alveoli with absence of cellular infiltrate and normal intraalveolar septa are evident . coexisting autoimmune disorders ( in 1.7% according to one study ) including rheumatoid arthritis , positive smooth muscle antibodies , immunoglobulin . elevated cholesterol level has also been found.the disease resembles goodpasture s clinically , hla associations and future therapeutic modalities such as plasmapheresis and immunosuppressive therapies targeting antibody production are among the considerations ( 6 ) . a key step in the pathogenesis of mycobacterium tuberculosis is its first interaction with the host macrophage . this interaction is mediated by several receptors on the macrophage and in association with ligands on the bacterium including the complement receptors of cr1 , cr3 , and cr4 , fcrs , mannose and glucan receptors , scavenger receptors and surfactant protein receptors a and d. also cd43 may be important in providing stable interaction of mycobacteria with macrophages . surfactant protein d binds to tb agent via the cell wall lipoglycan lipo - arabino - mannan ( lam ) and reduces adherence and therefore opsonization of the mycobacteria ( 14 ) . pap involves accumulation of surfactant , defects in surfactant and gm - csf genes , and antibodies made against the latter which is detrimental to macrophage activity and their processing of surfactant . our case was one with rapidly progressive disease which in a sandblaster agrees with the diagnosis of acute silicosis . yet , response to corticosteroid treatment was not seen and the patient s condition continued to deteriorate . in this situation , patient was also diagnosed with tuberculosis , resistant tuberculosis should be considered as well as infection with other mycobacteria ( 8,10 ) . finally , whole lung lavage was the only useful treatment for secondary pap , and our patient was in an unstable condition to undergo this procedure . 
 
 in the modern era , whole lung lavage is performed using general anesthesia and single lung ventilation via a double - lumen endotracheal tube which is the treatment of choice for pap . a total of 20l to 40l of saline is required for initially milky or turbid bal fluid to clear fluid . venoarterial extracorporeal membrane oxygenation ( ecmo ) has been used to avoid dangerous hypoxemia during lavage ( 15 ) . our first experience gained in our center national research institute for tuberculosis and lung diseases ( nritld ) occurred in 2003 about an 11 year old child with idiopathic pap where univent tracheal tube was used under general anesthesia . 
 
 in this patient , preparation for whole lung lavage was made but unfortunately due to irreversible respiratory distress and dismal condition , the procedure was not performed . 
 
 if the patient had probably shown up for follow up between his first and second hospitalizations , earlier whole - lung lavage could have been performed and he could have had better result . finally , a few experiences in cases where tb has complicated alveolar silicoproteinosis to have mostly a poor outcome for the patient .
silicosis is considered to be among the occupational lung diseases and associated with sandblasting , mining , quarrying and tunneling . 
 acute silicosis is usually progressive diseaseand despite treatment with corticosteroids it leads to cardio - respiratory failure and death . 
 alveolar silicoproteinosis is one of it s acute presentations due to exposure to silica dust and lungs filling with proteinaceous material . here 
 , we have presented a 29 year old male sandblaster with the three conditions of acute silicosis , secondary alveolar proteinosis and pulmonary tuberculosis on four anti tuberculous medications who presented with respiratory distress .