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My name is Alan Taylor and I am and Occupational Medicine resident in an occupational epidemiology course. As part of this course I will be working on Berylliosis page. I am planning on adding and claryifying to the signs and symptoms section and diagnosis. I will add an epidemiology and screening section and possibly a section on pathophisiology

Berylliosis, or chronic beryllium disease (CBD), is a chronic allergic-type lung response and chronic lung disease caused by exposure to beryllium and its compounds, a form of beryllium poisoning. As an occupational lung disease, it is most classically associated with aerospace manufacturing, beryllium mining or manufacturing of fluorescent light bulbs (which once contained beryllium compounds in their internal phosphor coating).[1][2]

The condition is incurable, but symptoms can be treated.[3]

Signs and symptoms

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With single or prolonged exposure by inhalation the lungs may become sensitized to beryllium. Continued exposure causes the development of small inflammatory nodules, called granulomas. Of note, the authors of a 2006 study suggested that beryllium inhalation was not the only form of exposure and perhaps skin exposure was also a cause, as they found that a reduction in beryllium inhalation did not result in a reduction in CBD or beryllium sensitization.[4]

Granulomas are seen in other chronic diseases, such as tuberculosis and sarcoidosis, and it can occasionally be hard to distinguish berylliosis from these disorders. Note, however, that the granulomas of CBD will typically be non-caseating, i.e. not characterized by necrosis and therefore not exhibiting a cheese-like appearance grossly.[5]

Ultimately, this process leads to restrictive lung disease (a decrease in diffusion capacity).

Clinically, patients experience cough and shortness of breath. Other symptoms include chest pain, joint aches, weight loss, and fever.

Rarely, one can get granulomas in other organs including the liver.

The onset of symptoms can range from weeks up to tens of years from the initial exposure. In some individuals a single exposure can cause berylliosis.

Pathogenesis[6]

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In susceptible persons, beryllium exposure can lead to a cell-mediated immune response. The T-cells become sensitized to the beryllium. Each subsequent exposure leads to an immune response involving CD4+ helper T-lymphocytes and macrophages accumulating in the lungs. As this response continues macrophages, CD+4 T-lymphocytes and plasma cells aggregate together to form the noncaseating granulomas.[7][8] Eventually, the final outcome is fibrosis of the lung.[9]

Several studies have shown that there is a genetic component to beryllium sensitivity. Specifically, those beryllium exposed workers with a mutation at the the HLA-DPB1 Glu69 position have increased prevelance of beryllium sensitization and CBD.[10][11] The HLA-DPB1 gene is important for MCH class II molecule function on antigen presenting cells.[12]

Epidemiology

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The number of workers in the United States exposed to beryllium vary but has been estimated to be as high as 800,000 during the 1960s and 1970s.[13] A more recent study estimated the number of exposed workers in the United States from in 1996 to be around 134,000.[14]

The rate of workers becoming sensitized to Beryllium varies based on genetics and exposure levels. In one study they found the prevalence of beryllium sensitization to range from 9 - 19% depending on the industry.[15] Many workers who are found to be sensitive to beryllium also meet the diagnostic criteria for CBD.[15] In one study of nuclear workers, among those who were sensitized to beryllium, 66% were found to have CBD as well.[16] The rate of progression from beryllium sensitization to CBD has been estimated yo be approximately 6-8% per year.[17][6]Stopping exposure to beryllium in those sensitized has not been definitively shown to stop the progression to CBD.

The overall prevalence of CBD among workers exposed to beryllium has ranged from 1 - 5% depending on industy and time period of study.[15][16][18]

Diagnosis

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The differential diagnosis for berylliosis includes:[19]

Of these possibilities, berylliosis presents most similarly to sarcoidosis. Some studies suggest that up to 6% of all cases of sarcoidosis are actually berylliosis.[20]

Definitive diagnosis of berylliosis is based on history of beryllium exposures, documented beryllium sensitivity and granulomatous inflammation on lung biopsy. Given the invasive nature of a lung biopsy diagnosis can also be based on clinical history consistent with berylliosis, abnormal chest x-ray or CT scan findings, an abnormalities in pulmonary function tests.[21]

Establishing beryllium sensitivity is the first step in diagnosis. The beryllium lymphocyte proliferation test (BeLPT) is the standard way of determining sensitivity to beryllium.[21] The test is performed by acquiring either, peripheral blood or fluid from a bronchial alveolar lavage, and lymphocytes are cultured with beryllium sulfate. Cells are then counted and those with elevated number of cells are considered abnormal.[22] Those exposed persons with two abnormal BeLPT tested with peripheral blood, or one abnormal and one borderline result, are considered beryllium sensitized. Also, those with with one abnormal BeLPT tested with fluid from a bronchial alveolar lavage are considered sensitized.[21]

Chest radiography findings of berylliosis are non-specific. Early in the disease radiography findings are usually normal. In later stages interstitial fibrosis, pleural irregularities, hilar lymphadenopathy and ground-glass opacities have been reported.[23][24] Findings on CT are also not specific to berylliosis. Findings that are common in CT scans of people with berylliosis include parenchymal nodules in early stages. One study found that ground-glass opacities were more commonly seen on CT scan in berylliosis than in sarcoidosis. In later stages hilar lymphadenopathy, intersitial pulmonary fibrosis and plueral thickening.[24]

Treatment

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Although the evidence that stopping exposure to beryllium decreases progression of the disease[17], it is still considered to be the an accepted approach to treatment in any stage of disease.[25] In those with early stages of disease, without lung function abnormalities or clinical symptoms, periodic monitoring with physical exam, pulmonary function testing and radiography is the mainstay of treatment.[26] Once clinical symptoms or significant abnormalities in pulmonary function testing appear the first choice of treatment are oral corticosteriods.[21] Individuals are started at higher doses for 3 to 6 months, and the tapered down to the lowest effective dose.[26]

Other treatment modalities include methotrexate and azathioprine but niether have been studied extensively.[26][27]

There is no cure for berylliosis the goals of treatment or to reduce symptoms and slow the progression of disease.[26]

History

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Cases of bronchitis and pneumonia-like symptoms were reported in Germany and Russia in the 1930s, among workers mining and refining beryllium. By 1946, a cluster of cases associated with fluorescent lamp manufacturers were apparent in the United States, and the lamp industry stopped using beryllium in 1949. The level of reaction of individuals varies greatly, with some not developing symptoms until years after exposure within industrial plants, but other workers only exposed to traces of dust became affected as well. A study found 1% of people living within 3/4 of a mile of a beryllium plant in Lorain, Ohio, had berylliosis after exposure to concentrations estimated to be less than 1 milligram per cubic metre of air. In the United States the Beryllium Case Registry contained 900 records, early cases relating to extraction and fluorescent lamp manufacture, later ones coming from the aerospace, ceramics and metallurgical industries.[28][29]

References

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  1. ^ U.S. Army Center for Health Promotion and Preventive Medicine. "USACHPPM: Just the Facts: Beryllium Exposure & Berylliosis". Retrieved 2013-11-10.
  2. ^ General Electric Fluorescent Lamps TP 111R, Dec. 1978, says on pg. 23 that since 1949 GE lamps used relatively inert phosphates found to be safe in ordinary handling of either the intact or broken lamp.
  3. ^ Dweik, Raed A (2008-11-19). "Berylliosis: Treatment & Medication". Medscape. Retrieved 2009-08-21.
  4. ^ Day, GA; Stefaniak, AB; Weston, A; Tinkle, SS (February 2006). "Beryllium exposure: dermal and immunological considerations". International Archives of Occupational and Environmental Health. 79 (2): 161–4. doi:10.1007/s00420-005-0024-0. PMID 16231190. S2CID 41564437.
  5. ^ Sawyer, Richard T.; Abraham, Jerrold L.; Daniloff, Elaine; Newman, Lee S. (2005). "Secondary Ion Mass Spectroscopy Demonstrates Retention of Beryllium in Chronic Beryllium Disease Granulomas". Journal of Occupational and Environmental Medicine. 47 (12): 1218–1226. doi:10.1097/01.jom.0000184884.85325.36. PMID 16340702. S2CID 36725637.
  6. ^ a b Newman, Lee S.; Mroz, Margaret M.; Balkissoon, Ronald; Maier, Lisa A. (2005-01-01). "Beryllium Sensitization Progresses to Chronic Beryllium Disease". American Journal of Respiratory and Critical Care Medicine. 171 (1): 54–60. doi:10.1164/rccm.200402-190OC. ISSN 1073-449X. PMID 15374840.
  7. ^ Falta, Michael T.; Pinilla, Clemencia; Mack, Douglas G.; Tinega, Alex N.; Crawford, Frances; Giulianotti, Marc; Santos, Radleigh; Clayton, Gina M.; Wang, Yuxiao (2013-07-01). "Identification of beryllium-dependent peptides recognized by CD4+ T cells in chronic beryllium disease". The Journal of Experimental Medicine. 210 (7): 1403–1418. doi:10.1084/jem.20122426. ISSN 0022-1007. PMC 3698527. PMID 23797096.
  8. ^ Freiman, D. G.; Hardy, H. L. (1970-03-01). "Beryllium disease. The relation of pulmonary pathology to clinical course and prognosis based on a study of 130 cases from the U.S. beryllium case registry". Human Pathology. 1 (1): 25–44. doi:10.1016/s0046-8177(70)80003-x. ISSN 0046-8177. PMID 5521721.
  9. ^ Saltini, C.; Amicosante, M.; Franchi, A.; Lombardi, G.; Richeldi, L. (1998-12-01). "Immunogenetic basis of environmental lung disease: lessons from the berylliosis model". European Respiratory Journal. 12 (6): 1463–1475. doi:10.1183/09031936.98.12061463. ISSN 0903-1936. PMID 9877510.
  10. ^ Richeldi, L.; Sorrentino, R.; Saltini, C. (1993-10-08). "HLA-DPB1 glutamate 69: a genetic marker of beryllium disease". Science (New York, N.Y.). 262 (5131): 242–244. doi:10.1126/science.8105536. ISSN 0036-8075. PMID 8105536.
  11. ^ Maier, Lisa A.; McGrath, Dierdre S.; Sato, Hiroe; Lympany, Penny; Welsh, Ken; Du Bois, Roland; Silveira, Lori; Fontenot, Andrew P.; Sawyer, Richard T. (2003-12-15). "Influence of MHC class II in susceptibility to beryllium sensitization and chronic beryllium disease". Journal of Immunology (Baltimore, Md.: 1950). 171 (12): 6910–6918. doi:10.4049/jimmunol.171.12.6910. ISSN 0022-1767. PMID 14662898. S2CID 9123749.
  12. ^ Maier, Lisa A.; McGrath, Dierdre S.; Sato, Hiroe; Lympany, Penny; Welsh, Ken; Bois, Roland du; Silveira, Lori; Fontenot, Andrew P.; Sawyer, Richard T. (2003-12-15). "Influence of MHC CLASS II in Susceptibility to Beryllium Sensitization and Chronic Beryllium Disease". The Journal of Immunology. 171 (12): 6910–6918. doi:10.4049/jimmunol.171.12.6910. ISSN 0022-1767. PMID 14662898. S2CID 9123749.
  13. ^ Cullen, Mark; Cherniack, Martin; Kominsky, John (1986-01-01). "Chronic Beryllium Disease in the United States". Seminars in Respiratory and Critical Care Medicine. 7 (3): 203–209. doi:10.1055/s-2007-1012616.
  14. ^ Henneberger, Paul K.; Goe, Sandra K.; Miller, William E.; Doney, Brent; Groce, Dennis W. (2004-10-01). "Industries in the United States with Airborne Beryllium Exposure and Estimates of the Number of Current Workers Potentially Exposed". Journal of Occupational and Environmental Hygiene. 1 (10): 648–659. doi:10.1080/15459620490502233. ISSN 1545-9624. PMID 15631056. S2CID 19773286.
  15. ^ a b c Kreiss, K.; Mroz, M. M.; Zhen, B.; Wiedemann, H.; Barna, B. (1997-08-01). "Risks of beryllium disease related to work processes at a metal, alloy, and oxide production plant". Occupational and Environmental Medicine. 54 (8): 605–612. doi:10.1136/oem.54.8.605. ISSN 1470-7926. PMC 1128986. PMID 9326165.
  16. ^ a b Kreiss, K.; Mroz, M. M.; Zhen, B.; Martyny, J. W.; Newman, L. S. (1993-10-01). "Epidemiology of beryllium sensitization and disease in nuclear workers". The American Review of Respiratory Disease. 148 (4 Pt 1): 985–991. doi:10.1164/ajrccm/148.4_Pt_1.985. ISSN 0003-0805. PMID 8214955.
  17. ^ a b Seidler, A.; Euler, U.; Müller-Quernheim, J.; Gaede, K. I.; Latza, U.; Groneberg, D.; Letzel, S. (2012-10-01). "Systematic review: progression of beryllium sensitization to chronic beryllium disease". Occupational Medicine. 62 (7): 506–513. doi:10.1093/occmed/kqs069. ISSN 0962-7480. PMID 22705916.
  18. ^ Henneberger, P. K.; Cumro, D.; Deubner, D. D.; Kent, M. S.; McCawley, M.; Kreiss, K. (2001-04-01). "Beryllium sensitization and disease among long-term and short-term workers in a beryllium ceramics plant". International Archives of Occupational and Environmental Health. 74 (3): 167–176. doi:10.1007/s004200100237. ISSN 0340-0131. PMID 11355290. S2CID 39949745.
  19. ^ Newman, LS (March 1995). "Beryllium disease and sarcoidosis: clinical and laboratory links". Sarcoidosis. 12 (1): 7–19. PMID 7617981.
  20. ^ Rossman, MD; Kreider, ME (June 2003). "Is chronic beryllium disease sarcoidosis of known etiology?". Sarcoidosis, Vasculitis, and Diffuse Lung Diseases : Official Journal of WASOG / World Association of Sarcoidosis and Other Granulomatous Disorders. 20 (2): 104–9. PMID 12870719.
  21. ^ a b c d Balmes, John R.; Abraham, Jerrold L.; Dweik, Raed A.; Fireman, Elizabeth; Fontenot, Andrew P.; Maier, Lisa A.; Muller-Quernheim, Joachim; Ostiguy, Gaston; Pepper, Lewis D. (2014). "An Official American Thoracic Society Statement: Diagnosis and Management of Beryllium Sensitivity and Chronic Beryllium Disease". American Journal of Respiratory and Critical Care Medicine. 190 (10): e34–e59. doi:10.1164/rccm.201409-1722st. PMID 25398119.
  22. ^ Frome, Edward L; Newman, Lee S; Cragle, Donna L; Colyer, Shirley P; Wambach, Paul F (2003-02-01). "Identification of an abnormal beryllium lymphocyte proliferation test". Toxicology. 183 (1–3): 39–56. doi:10.1016/S0300-483X(02)00439-0. PMID 12504341.
  23. ^ Aronchick, J. M.; Rossman, M. D.; Miller, W. T. (1987-06-01). "Chronic beryllium disease: diagnosis, radiographic findings, and correlation with pulmonary function tests". Radiology. 163 (3): 677–682. doi:10.1148/radiology.163.3.3575713. ISSN 0033-8419. PMID 3575713.
  24. ^ a b Sharma, Nidhi; Patel, Jeet; Mohammed, Tan-Lucien H. (2010). "Chronic Beryllium Disease". Journal of Computer Assisted Tomography. 34 (6): 945–948. doi:10.1097/rct.0b013e3181ef214e. PMID 21084914.
  25. ^ Rossman, M D (1996-10-01). "Chronic beryllium disease: diagnosis and management". Environmental Health Perspectives. 104 (Suppl 5): 945–947. doi:10.1289/ehp.96104s5945. ISSN 0091-6765. PMC 1469698. PMID 8933039.
  26. ^ a b c d Sood, Akshay (2009). "Current Treatment of Chronic Beryllium Disease". Journal of Occupational and Environmental Hygiene. 6 (12): 762–765. doi:10.1080/15459620903158698. PMC 2774897. PMID 19894178.
  27. ^ "Chronic beryllium disease: Don't miss the diagnosis". ResearchGate. Retrieved 2016-03-25.
  28. ^ David Geraint James, Alimuddin Zumla, The granulomatous disorders, Cambridge University Press, 1999, ISBN 0-521-59221-6, pages 336-337
  29. ^ Brown University Medical School. "Berylliosis". Retrieved 2012-08-20.
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