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__NOTOC__
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<br />
{{Caplans syndrome}}
{{Caplans syndrome}}
{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{SharmiB}}
==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
[[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.
 
OR
 
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
 
OR
 
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
 
OR
 
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
 
OR
 
 
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
 
OR
 
The progression to [disease name] usually involves the [molecular pathway].
 
OR
 
The pathophysiology of [disease/malignancy] depends on the histological subtype.
 
==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 [[Caplan's Syndrome|Caplan Syndrome]].
 
==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]]
*[[Silicosis]]
*[[Silicosis]]
*[[Asbestosis]]
*[[Asbestosis]]
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Persons with rheumatoid arthritis are more likely to develop larger areas of [[inflammation]] and scarring in response to coal dust.
Persons with rheumatoid arthritis are more likely to develop larger areas of [[inflammation]] and scarring in response to coal dust.
==Microscopic Pathology==
==Microscopic Pathology==
On [[Microscopic|microscopic histopathological analysis]], rapidly developing [[Nodular|nodular [[pulmonary]] [[lesions]]]] with central necrosis surrounded by [[collagen]] are characteristic findings of [[Caplan's Syndrome|Caplan Syndrome]].
[[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>
* 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|giant cells]]. [[Macrophages]] might contain some [[dust]] particles.
* Outside of the [[inflammatory]] zone, there are some palisading [[cells]].


==References==
==References==
1.<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>
{{WH}}
{{WS}}
[[Category: (name of the system)]]
{{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

Genetics

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

References

  1. ↑ 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.
  2. ↑ 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.
  3. ↑ . doi:10.1164/artpd.1958.78.2.274?journalCode=artpd. Missing or empty |title= (help)
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