Silicosis natural history, complications and prognosis
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Please help WikiDoc by adding content here. It's easy! Click here to learn about editing. complications Tuberculosis: association between silicosis and TB has been known for a long time, but more recent findings show that exposure to silica, without silicosis, may also predispose individuals to TB [1]The increased risk of both pulmonary and extra-pulmonary TB is lifelong even if exposure ceases[2]. the risk increases with severity of silicosis . acute and accelerated silicosis . Pulmonary TB rates can be extremely high in silica-exposed groups with high background population TB and HIV rates. In many instances, it is the chest radiograph rather than clinical features that gives the first indication of TB in the presence of silicosis. Treatment for latent TB infection in people with silicosis (especially those with HIV infection) is recommended.[3] Screening for latent TB , tuberculin skin tests are used to diagnose latent TB, after which a 9-month course of INH is recommended, for active tuberculosis : Direct impairment of macrophage function by crystalline silica and poor drug penetration into silicotic lung nodules have resulted in high (>20%) treatment failure and relapse rates for patients with silicosis who are receiving chemotherapy for tuberculosis (6). This finding has prompted prolonged and more aggressive treatment of tuberculosis for such persons
Mycosis:
Insofar as silica dust impairs cellular defense, silica-exposed workers (without silicosis) may be at increased risk for fungal infections, as they are for mycobacterial infections
Aspergillosis was the most common mycosis among persons with pneumoconiosis. Aspergillosis is a known complication in patients with underlying pulmonary disease, such as pulmonary tuberculosis and pneumoconiosis [4], in which silica-impaired macrophages are incapable of targeting inhaled conidia [5] Measures to protect silica-exposed workers with coexposure to fungi include reducing silica exposure; wetting soil and bird droppings to suppress fungal-contaminated dust; maintaining good personal hygiene; and, in areas with endemic inhaled fungi, using enclosed operator cabs with high-effi ciency particulate air fi ltration or personal respiratory protection for particulates
Pleural involvement in silicosis is rare. Spontaneous pneumothorax is a pleural complication that can develop in such patients. Usually in silicosis pneumothorax is unilateral and rarely bilateral. [6] this wasn to be associated with the presence of bullae [7] Due to direct toxic injury by silica, products of inflammatory response affect the elastic fibres of the alveolar wall leading to formation of bleb [8]
Lung cancer[9]
silica-induced nephropathy has been associated with both glomerular and tubular dysfunction. The hypotheses for the pathophysiology of silica’s effect on the kidney include either a direct toxic effect on the kidney or as an adjuvant to enhance an immunologic mechanism[10]
Rheumatic disease:
Silica exposure effects are not just limited to the lungs; it also has a relationship with some rheumatic diseases, such as rheumatoid arthritis (RA) , scleroderma , systemic lupus erythematosus , Wegener’s granulomatosis and polyarteritis nodosa
The association with scleroderma and silicosis is known as Erasmus syndrome and that with rheumatoid arthritis is known as Caplan’s syndrome[11]
References
- ↑ Cowie RL (1994). "The epidemiology of tuberculosis in gold miners with silicosis". Am J Respir Crit Care Med. 150 (5 Pt 1): 1460–2. doi:10.1164/ajrccm.150.5.7952577. PMID 7952577.
- ↑ Hnizdo E, Murray J (1998). "Risk of pulmonary tuberculosis relative to silicosis and exposure to silica dust in South African gold miners". Occup Environ Med. 55 (7): 496–502. PMC 1757613. PMID 9816385.
- ↑ "Adverse effects of crystalline silica exposure. American Thoracic Society Committee of the Scientific Assembly on Environmental and Occupational Health". Am J Respir Crit Care Med. 155 (2): 761–8. 1997. doi:10.1164/ajrccm.155.2.9032226. PMID 9032226.
- ↑ Kato T, Usami I, Morita H, Goto M, Hosoda M, Nakamura A; et al. (2002). "Chronic necrotizing pulmonary aspergillosis in pneumoconiosis: clinical and radiologic findings in 10 patients". Chest. 121 (1): 118–27. PMID 11796440.
- ↑ Segal BH (2007). "Role of macrophages in host defense against aspergillosis and strategies for immune augmentation". Oncologist. 12 Suppl 2: 7–13. doi:10.1634/theoncologist.12-S2-7. PMID 18039634.
- ↑ Mishra P, Jacob SE, Basu D, Panigrahi MK, Govindaraj V (2014). "Bilateral spontaneous pneumothorax in chronic silicosis: a case report". Case Rep Pathol. 2014: 561861. doi:10.1155/2014/561861. PMC 3976776. PMID 24744938.
- ↑ Mohebbi I, Hassani E, Salarilak S, Bahrami AR (2007). "Do bullae and emphysema increase risk of pneumothorax in silicosis?". J Occup Med Toxicol. 2: 8. doi:10.1186/1745-6673-2-8. PMC 2071907. PMID 17868470.
- ↑ Gupta KB, Manchanda M, Kaur P (2006). "Bilateral spontaneous pneumothorax in silicosis". Indian J Chest Dis Allied Sci. 48 (3): 201–3. PMID 18610678.
- ↑ Brown T (2009). "Silica exposure, smoking, silicosis and lung cancer--complex interactions". Occup Med (Lond). 59 (2): 89–95. doi:10.1093/occmed/kqn171. PMID 19233828.
- ↑ Millerick-May ML, Schrauben S, Reilly MJ, Rosenman KD (2015). "Silicosis and chronic renal disease". Am J Ind Med. 58 (7): 730–6. doi:10.1002/ajim.22465. PMID [ 25940153 [ Check
|pmid=value (help). - ↑ De Vuyst P, Camus P (2000). "The past and present of pneumoconioses". Curr Opin Pulm Med. 6 (2): 151–6. PMID 10741776.