Caplans syndrome pathophysiology: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Caplans syndrome}} | {{Caplans syndrome}} | ||
{{CMG}}; {{AE}} | {{CMG}}; {{AE}} {{SharmiB}} | ||
==Overview== | ==Overview== | ||
[[Caplan's Syndrome|Caplan Syndrome]] is known as Rheumatoid [[pneumoconiosis]]. In patients with [[rheumatoid arthritis]], [[lungs]] show increased [[immune response]] to the foreign materials. In coal miners with RA, exposure to [[silica]] causes the release of different [[cytokines]] as [[interleukin-1]],[[granulocyte colony stimulating factor]] and [[tumor necrosis factor-alpha]] by [[monocytes]] and [[macrophages]]. [[Lymphocytes]] get activated by the [[cytokines]] and leading to hyperactive [[autoimmune]] response. | [[Caplan's Syndrome|Caplan Syndrome]] is known as Rheumatoid [[pneumoconiosis]]. In patients with [[rheumatoid arthritis]], [[lungs]] show increased [[immune response]] to the foreign materials. In coal miners with RA, exposure to [[silica]] causes the release of different [[cytokines]] as [[interleukin-1]],[[granulocyte colony stimulating factor]] and [[tumor necrosis factor-alpha]] by [[monocytes]] and [[macrophages]]. [[Lymphocytes]] get activated by the [[cytokines]] and leading to hyperactive [[autoimmune]] response. | ||
==Pathophysiology== | ==Pathophysiology== | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
*It is understood that [[Caplan's Syndrome|syndrome]] is the result of alteration of [[immune response]] in the patients with [[Rheumatoid arthritis]].<ref name="SchreiberKoschel2010">{{cite journal|last1=Schreiber|first1=J.|last2=Koschel|first2=D.|last3=Kekow|first3=J.|last4=Waldburg|first4=N.|last5=Goette|first5=A.|last6=Merget|first6=R.|title=Rheumatoid pneumoconiosis (Caplan's syndrome)|journal=European Journal of Internal Medicine|volume=21|issue=3|year=2010|pages=168–172|issn=09536205|doi=10.1016/j.ejim.2010.02.004}}</ref> | *It is understood that [[Caplan's Syndrome|syndrome]] is the result of alteration of [[immune response]] in the patients with [[Rheumatoid arthritis]].<ref name="SchreiberKoschel2010">{{cite journal|last1=Schreiber|first1=J.|last2=Koschel|first2=D.|last3=Kekow|first3=J.|last4=Waldburg|first4=N.|last5=Goette|first5=A.|last6=Merget|first6=R.|title=Rheumatoid pneumoconiosis (Caplan's syndrome)|journal=European Journal of Internal Medicine|volume=21|issue=3|year=2010|pages=168–172|issn=09536205|doi=10.1016/j.ejim.2010.02.004}}</ref> | ||
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* [[Macrophages]] engulf [[silica |silica particles]], causing [[inflammation]] which eventually activate the [[fibroblast|firbroblasts]]. | * [[Macrophages]] engulf [[silica |silica particles]], causing [[inflammation]] which eventually activate the [[fibroblast|firbroblasts]]. | ||
*Due to having [[apoptotic]] capacity, engulfed [[silica]] destroy the [[macrophages]] and again get taken up by another [[macrophage]]. This continued process activates [[chronic]] [[immune response]] and [[fibrosis]]. | *Due to having [[apoptotic]] capacity, engulfed [[silica]] destroy the [[macrophages]] and again get taken up by another [[macrophage]]. This continued process activates [[chronic]] [[immune response]] and [[fibrosis]]. | ||
==Genetics== | ==Genetics== | ||
* No [[genetic association]] is found in Caplan Syndrome. | |||
No [[genetic association]] is found in | |||
==Associated Conditions== | ==Associated Conditions== | ||
Conditions associated with [disease name] include: | Conditions associated with [disease name] include: | ||
*[[Rheumatoid Arthritis]] <ref name="SchreiberKoschel2010">{{cite journal|last1=Schreiber|first1=J.|last2=Koschel|first2=D.|last3=Kekow|first3=J.|last4=Waldburg|first4=N.|last5=Goette|first5=A.|last6=Merget|first6=R.|title=Rheumatoid pneumoconiosis (Caplan's syndrome)|journal=European Journal of Internal Medicine|volume=21|issue=3|year=2010|pages=168–172|issn=09536205|doi=10.1016/j.ejim.2010.02.004}}</ref> | *[[Rheumatoid Arthritis]] <ref name="SchreiberKoschel2010">{{cite journal|last1=Schreiber|first1=J.|last2=Koschel|first2=D.|last3=Kekow|first3=J.|last4=Waldburg|first4=N.|last5=Goette|first5=A.|last6=Merget|first6=R.|title=Rheumatoid pneumoconiosis (Caplan's syndrome)|journal=European Journal of Internal Medicine|volume=21|issue=3|year=2010|pages=168–172|issn=09536205|doi=10.1016/j.ejim.2010.02.004}}</ref> | ||
*[[Silicosis]] | *[[Silicosis]] | ||
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[[Microscopic]] features of [[Caplan syndrome]] are | [[Microscopic]] features of [[Caplan syndrome]] are | ||
* [[Central]] [[necrotic]] area with various amounts of [[collagen]] [[tissue]]. <ref name="GoughRivers1955">{{cite journal|last1=Gough|first1=J.|last2=Rivers|first2=D.|last3=Seal|first3=R. M. E.|title=Pathological Studies of Modified Pneumoconiosis in Coal-miners with Rheumatoid Arthritis (Caplan's Syndrome)|journal=Thorax|volume=10|issue=1|year=1955|pages=9–18|issn=0040-6376|doi=10.1136/thx.10.1.9}}</ref> <ref>{{cite journal|doi=10.1164/artpd.1958.78.2.274?journalCode=artpd}}</ref> | * [[Central]] [[necrotic]] area with various amounts of [[collagen]] [[tissue]]. <ref name="GoughRivers1955">{{cite journal|last1=Gough|first1=J.|last2=Rivers|first2=D.|last3=Seal|first3=R. M. E.|title=Pathological Studies of Modified Pneumoconiosis in Coal-miners with Rheumatoid Arthritis (Caplan's Syndrome)|journal=Thorax|volume=10|issue=1|year=1955|pages=9–18|issn=0040-6376|doi=10.1136/thx.10.1.9}}</ref> <ref>{{cite journal|doi=10.1164/artpd.1958.78.2.274?journalCode=artpd}}</ref> | ||
* Few [[nuclei]] might be found in the [[central]] [[necrotic]] area. | * Few [[nuclei]] might be found in the [[central]] [[necrotic]] area. | ||
* Outside of the [[necrotic]] area there are alternate layers of black coal [[dust]] and [[necrotic]] [[tissue]]. | * Outside of the [[necrotic]] area there are alternate layers of black coal [[dust]] and [[necrotic]] [[tissue]]. | ||
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==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
[[Category:Pulmonology]] | [[Category:Pulmonology]] | ||
[[Category:Rheumatology]] | [[Category:Rheumatology]] | ||
Latest revision as of 02:05, 21 June 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sharmi Biswas, M.B.B.S
Overview
Caplan Syndrome is known as Rheumatoid pneumoconiosis. In patients with rheumatoid arthritis, lungs show increased immune response to the foreign materials. In coal miners with RA, exposure to silica causes the release of different cytokines as interleukin-1,granulocyte colony stimulating factor and tumor necrosis factor-alpha by monocytes and macrophages. Lymphocytes get activated by the cytokines and leading to hyperactive autoimmune response.
Pathophysiology
Pathogenesis
- It is understood that syndrome is the result of alteration of immune response in the patients with Rheumatoid arthritis.[1]
- There is an increased immune response to foreign materials in the lungs.Silica initiates hyperactive immune responses in the coal miners with Rheumatoid arthritis
- Macrophages engulf silica particles, causing inflammation which eventually activate the firbroblasts.
- Due to having apoptotic capacity, engulfed silica destroy the macrophages and again get taken up by another macrophage. This continued process activates chronic immune response and fibrosis.
Genetics
- No genetic association is found in Caplan Syndrome.
Associated Conditions
Conditions associated with [disease name] include:
Gross Pathology
Some people who have been exposed to the dust have severe lung scarring that makes it difficult for their lungs to carry oxygen to the bloodstream (called progressive massive fibrosis). People with rheumatoid arthritis do not seem more likely to have this complication of scarring.
Persons with rheumatoid arthritis are more likely to develop larger areas of inflammation and scarring in response to coal dust.
Microscopic Pathology
Microscopic features of Caplan syndrome are
- Central necrotic area with various amounts of collagen tissue. [2] [3]
- Few nuclei might be found in the central necrotic area.
- Outside of the necrotic area there are alternate layers of black coal dust and necrotic tissue.
- Surrounding the dust ring, there is a zone of inflammation containing granulocytes, macrophages, and giant cells. Macrophages might contain some dust particles.
- Outside of the inflammatory zone, there are some palisading cells.
References
- ↑ 1.0 1.1 Schreiber, J.; Koschel, D.; Kekow, J.; Waldburg, N.; Goette, A.; Merget, R. (2010). "Rheumatoid pneumoconiosis (Caplan's syndrome)". European Journal of Internal Medicine. 21 (3): 168–172. doi:10.1016/j.ejim.2010.02.004. ISSN 0953-6205.
- ↑ Gough, J.; Rivers, D.; Seal, R. M. E. (1955). "Pathological Studies of Modified Pneumoconiosis in Coal-miners with Rheumatoid Arthritis (Caplan's Syndrome)". Thorax. 10 (1): 9–18. doi:10.1136/thx.10.1.9. ISSN 0040-6376.
- ↑ . doi:10.1164/artpd.1958.78.2.274?journalCode=artpd. Missing or empty
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