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{{Polyarteritis nodosa}}
{{Polyarteritis nodosa}}
{{CMG}};{{APM}} {{AE}} {{OO}} {{CZ}}; [[User:Haritha|Haritha Machavarapu, M.B.B.S.]]
{{CMG}};{{APM}} {{AE}}{{SSW}}


==Overview==
==Overview==
The common causes of PAN are idiopathic, [[Hepatitis B|Hepatitis B infection]], [[Hepatitis C|Hepatitis C infection]], [[hairy cell leukemia]] and drug induced. Less common causes include [[varicella-zoster virus]], [[Parvovirus B19|parvovirus B-19]], [[cytomegalovirus]], human T-cell leukemia virus etc.


=== Hepatitis B and PAN ===
== Causes ==
The pathogenesis of polyarteritis nodosa (PAN) is unknown, and no animal model is available for study. Hepatitis B virus (HBV) infection is strongly linked with PAN. Evidence for immune complex–induced disease is confined to HBV-related PAN; the role of immune complexes in non-HBV-related PAN remains unclear.<sup> [[null 6]]</sup>
 
Impaired function of endothelial cells may be part of idiopathic PAN or a consequence of it; in HBV-PAN, virus replication may directly injure the vessel wall.<sup>[[null 10]] </sup>Endothelial dysfunction can perpetuate the inflammation through cytokine and adhesion molecule production.<sup> [[null 9]]</sup>
 
HBV-associated vasculitis almost always takes the form of PAN. HBV-PAN may occur at any time during the course of acute or chronic hepatitis B infection, although it typically occurs within 6 months of infection.<sup> [[null 10]]</sup>
 
The activity of HBV-PAN does not parallel that of the hepatitis, and symptoms are the same as those of idiopathic PAN. Small studies have found that gastrointestinal manifestations, malignant hypertension, renal infarction, and orchiepididymitis were more common in HBV-PAN.<sup> [[null 10]]</sup>
 
HBV was once the cause of up to 30% of PAN cases.<sup> [[null 11]] </sup>Widespread use of the hepatitis B vaccine has significantly decreased the incidence of HBV-PAN, which is now estimated to account for less than 8% of all PAN cases.<sup> [[null 12]]</sup>
 
=== Genetic associations ===
Loss-of-function mutations in ''CECR1 ''(alsoknown as ''ADA2'')'', ''the gene that encodes adenosine deaminase 2 (ADA2), have been associated with a spectrum of vascular and inflammatory phenotypes that includes polyarteritis nodosa.<sup> [[null 13]] </sup> Navon Elkan and colleagues identified six families with multiple cases of systemic and cutaneous polyarteritis nodosa, most of which had onset during childhood. In all the families, disease was traced to recessive mutations in ''CECR1 ''that resulted in reduced activity of ADA2.<sup> [[null 14]]</sup>
 
Possible roles of ADA2 include regulation of the proliferation of activated T cells and macrophages and the differentiation of monocytes to macrophages. Reduction in ADA2 activity  may affect the adenosine inflammatory-response pathway.<sup> [[null 14]]</sup>
 
Similarly, Gonzalez Santiago et al report two siblings with novel compound heterozygous mutations in ''CECR1 ''who were diagnosed with cutaneous PAN in early childhood.<sup> [[null 15]]</sup>
 
In a study of patients with early-onset livedo reticularis and/or hemorrhagic/ischemic strokes in the context of inflammation or PAN, Caorsi et al detected biallelic homozygous or compound heterozygous ''CECR1'' mutations in 15 of 48 patients from 43 families. In patients with ''CECR1'' mutations, the mean age of onset of disease was 24 months (6 months to 7 years).<sup> [[null 16]]</sup>
 
=== Other disease associations ===
Controversy has surrounded the potential association of hepatitis C virus (HCV) with PAN. HCV may be linked to cutaneous PAN, a benign, limited form of PAN. In a study of 16 patients with cutaneous PAN, 5 tested positive for hepatitis C.<sup> [[null 17]] </sup>HCV-associated PAN has also been described in 31 patients included in a larger 161 patient cohort with HCV-related vasculitis in France.<sup> [[null 18]] </sup>Despite the presence of serum cryoglobulins, these patients were diagnosed with HCV-PAN on the basis of typical histopathologic features of PAN and/or the presence of microaneurysms and/or multiple stenoses on abdominal and/or renal angiography.
 
A number of other infectious organisms have been reported in association with PAN or PAN-like diseases, but causal evidence is inconsistent. These organisms include varicella-zoster virus, parvovirus B-19, cytomegalovirus, human T-cell leukemia virus, streptococcal species, ''Klebsiella'' species, ''Pseudomonas'' species, ''Yersinia'' species, ''Toxoplasma gondii'', Rickettsiae, trichinosis, and sarcosporidiosis.<sup>[[null 19], [null 20]] </sup>Recently, reports of associations with PAN and human immunodeficiency virus<sup> [[null 21]] </sup>and cutaneous PAN and tuberculosis<sup> [[null 22]] </sup>have been published as well.
 
Some syndromes, including rheumatic diseases, malignancies, and infections have been associated with clinical syndromes indistinguishable from idiopathic PAN. Rheumatoid arthritis (RA) and Sjögren syndrome have been associated with PAN. Notably, the incidence of RA-associated vasculitis has decreased greatly since the 1980s, likely attributable to improvements in the management of RA.<sup> [[null 23]] </sup>Cutaneous PAN occurring with HLA-B39 spondyloarthritis,<sup> [[null 24]] </sup>common variable immunodeficiency,<sup> [[null 25]] </sup>and psoriatic arthritis in an 11-year-old boy<sup> [[null 26]] </sup>have also been reported.
 
Hematologic malignancies, such as hairy cell leukemia and, in one case, angioimmunoblastic T cell lymphoma, have been associated with PAN-like vasculitides.<sup> [[null 27], [null 28]]</sup>
 
==Causes==


=== Common Causes ===
=== Common Causes ===
The primary cause of PAN is idiopathic, but secondary causes include [[hepatitis B virus]] [[infection]] <ref name="pmid16148731">{{cite journal| author=Guillevin L, Mahr A, Callard P, Godmer P, Pagnoux C, Leray E et al.| title=Hepatitis B virus-associated polyarteritis nodosa: clinical characteristics, outcome, and impact of treatment in 115 patients. | journal=Medicine (Baltimore) | year= 2005 | volume= 84 | issue= 5 | pages= 313-22 | pmid=16148731 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16148731  }} </ref>, [[hepatitis C virus]] infection, <ref name="pmid19369460">{{cite journal| author=Ramos-Casals M, Muñoz S, Medina F, Jara LJ, Rosas J, Calvo-Alen J et al.| title=Systemic autoimmune diseases in patients with hepatitis C virus infection: characterization of 1020 cases (The HISPAMEC Registry). | journal=J Rheumatol | year= 2009 | volume= 36 | issue= 7 | pages= 1442-8 | pmid=19369460 | doi=10.3899/jrheum.080874 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19369460  }} </ref> and [[hairy cell leukemia]] <ref name="pmid8578313">{{cite journal| author=Hasler P, Kistler H, Gerber H| title=Vasculitides in hairy cell leukemia. | journal=Semin Arthritis Rheum | year= 1995 | volume= 25 | issue= 2 | pages= 134-42 | pmid=8578313 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8578313  }} </ref>. Polyarteritis nodosa is a disease of unknown cause that affects [[arteries]], the [[blood vessels]] that carry [[oxygenated blood]] to [[organs]] and [[tissues]]. It occurs when certain [[immune cells]] attack the affected arteries. More adults than children get this disease. It damages the [[tissues]] supplied by the affected arteries because the tissues are not receiving the [[oxygen]] and nourishment they need. People with active [[Hepatitis B]] and [[Hepatitis C]] may develop this disease.
PAN may be caused by:
* Idiopathic
* [[Hepatitis B infection]]<ref name="pmid12350194">{{cite journal |vauthors=Stone JH |title=Polyarteritis nodosa |journal=JAMA |volume=288 |issue=13 |pages=1632–9 |date=October 2002 |pmid=12350194 |doi= |url=}}</ref> <ref name="pmid16148731">{{cite journal| author=Guillevin L, Mahr A, Callard P, Godmer P, Pagnoux C, Leray E et al.| title=Hepatitis B virus-associated polyarteritis nodosa: clinical characteristics, outcome, and impact of treatment in 115 patients. | journal=Medicine (Baltimore) | year= 2005 | volume= 84 | issue= 5 | pages= 313-22 | pmid=16148731 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16148731  }} </ref>
* [[Hepatitis C infection]].<ref name="pmid19369460">{{cite journal| author=Ramos-Casals M, Muñoz S, Medina F, Jara LJ, Rosas J, Calvo-Alen J et al.| title=Systemic autoimmune diseases in patients with hepatitis C virus infection: characterization of 1020 cases (The HISPAMEC Registry). | journal=J Rheumatol | year= 2009 | volume= 36 | issue= 7 | pages= 1442-8 | pmid=19369460 | doi=10.3899/jrheum.080874 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19369460  }} </ref>
* [[hairy cell leukemia]].<ref name="pmid8578313">{{cite journal| author=Hasler P, Kistler H, Gerber H| title=Vasculitides in hairy cell leukemia. | journal=Semin Arthritis Rheum | year= 1995 | volume= 25 | issue= 2 | pages= 134-42 | pmid=8578313 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8578313  }} </ref>  
* Drug induced
** [[Sulfasalazine]]  


===Drug Side Effect===
=== Less Common Causes ===
*[[Sulfasalazine]]
PAN may be caused by:
* PAN may be caused secondary to infections such as:
** [[Varicella zoster virus|Varicella-zoster virus]]
** [[Parvovirus B19|Parvovirus B-19]]
** [[Cytomegalovirus]]
** [[Human T-cell leukemia virus]]
** [[Streptococcus|Streptococcal]] species
** ''[[Klebsiella]]'' species
** ''[[Pseudomonas]]'' species
** ''[[Yersinia]]'' species
** ''[[Toxoplasma gondii]]''
** [[Rickettsiae]]
** [[Trichinosis]]
** Sarcosporidiosis
** [[Tuberculosis]]<ref name="pmid22035185">{{cite journal |vauthors=Imanishi H, Tsuruta D, Oshimo T, Sowa J, Mizuno N, Nakagawa K, Ishii M |title=Cutaneous polyarteritis nodosa induced by Mycobacterium tuberculosis |journal=J. Dermatol. |volume=39 |issue=8 |pages=738–9 |date=August 2012 |pmid=22035185 |doi=10.1111/j.1346-8138.2011.01398.x |url=}}</ref>
** [[Human Immunodeficiency Virus (HIV)|Human immunodeficiency virus]]<ref name="pmid21989711">{{cite journal |vauthors=Patel N, Patel N, Khan T, Patel N, Espinoza LR |title=HIV infection and clinical spectrum of associated vasculitides |journal=Curr Rheumatol Rep |volume=13 |issue=6 |pages=506–12 |date=December 2011 |pmid=21989711 |doi=10.1007/s11926-011-0214-6 |url=}}</ref>
* PAN be be associated with certain syndromes like:
** [[Rheumatoid arthritis]]<ref name="pmid15126674">{{cite journal |vauthors=Watts RA, Mooney J, Lane SE, Scott DG |title=Rheumatoid vasculitis: becoming extinct? |journal=Rheumatology (Oxford) |volume=43 |issue=7 |pages=920–3 |date=July 2004 |pmid=15126674 |doi=10.1093/rheumatology/keh210 |url=}}</ref>
** [[Sjögren's syndrome|Sjögren syndrome]]
** HLA-B39 spondyloarthritis<ref name="pmid22270344">{{cite journal |vauthors=Nakano H, Ooka S, Shibata T, Ogawa H, Ito H, Takakuwa Y, Tonooka K, Maeda A, Yamasaki Y, Kiyokawa T, Nagafuchi H, Yamada H, Ozaki S |title=Cutaneous polyarteritis nodosa associated with HLA-B39-positive undifferentiated spondyloarthritis in a Japanese patient |journal=Mod Rheumatol |volume=22 |issue=5 |pages=783–6 |date=September 2012 |pmid=22270344 |doi=10.1007/s10165-011-0576-7 |url=}}</ref>
** [[Common variable immunodeficiency]]<ref name="pmid22260879">{{cite journal |vauthors=Pagnini I, Simonini G, Lippi F, Azzari C, Cimaz R |title=Cutaneous polyarteritis nodosa and common variable immunodeficiency: a previously unreported association |journal=Clin. Exp. Rheumatol. |volume=30 |issue=1 Suppl 70 |pages=S169 |date=2012 |pmid=22260879 |doi= |url=}}</ref>
** [[Psoriatic arthritis]]<ref name="pmid21487680">{{cite journal |vauthors=Oulego-Erroz I, Gautreaux-Minaya S, Martinez-Sáenz de Jubera J, Naranjo-Vivas D, Fernéndez-Hernández S, Muñíz-Fontán M |title=Coexistence of polyarteritis nodosa and psoriatic arthritis in a child: an unreported association: Polyarteritis nodosa and Psoriatic arthitritis |journal=Eur. J. Pediatr. |volume=170 |issue=9 |pages=1213–5 |date=September 2011 |pmid=21487680 |doi=10.1007/s00431-011-1459-9 |url=}}</ref>


==References==
==References==

Latest revision as of 19:01, 8 May 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Ali Poyan Mehr, M.D. [2] Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[3]

Overview

The common causes of PAN are idiopathic, Hepatitis B infection, Hepatitis C infection, hairy cell leukemia and drug induced. Less common causes include varicella-zoster virus, parvovirus B-19, cytomegalovirus, human T-cell leukemia virus etc.

Causes

Common Causes

PAN may be caused by:

Less Common Causes

PAN may be caused by:

References

  1. ↑ Stone JH (October 2002). "Polyarteritis nodosa". JAMA. 288 (13): 1632–9. PMID 12350194.
  2. ↑ Guillevin L, Mahr A, Callard P, Godmer P, Pagnoux C, Leray E; et al. (2005). "Hepatitis B virus-associated polyarteritis nodosa: clinical characteristics, outcome, and impact of treatment in 115 patients". Medicine (Baltimore). 84 (5): 313–22. PMID 16148731.
  3. ↑ Ramos-Casals M, Muñoz S, Medina F, Jara LJ, Rosas J, Calvo-Alen J; et al. (2009). "Systemic autoimmune diseases in patients with hepatitis C virus infection: characterization of 1020 cases (The HISPAMEC Registry)". J Rheumatol. 36 (7): 1442–8. doi:10.3899/jrheum.080874. PMID 19369460.
  4. ↑ Hasler P, Kistler H, Gerber H (1995). "Vasculitides in hairy cell leukemia". Semin Arthritis Rheum. 25 (2): 134–42. PMID 8578313.
  5. ↑ Imanishi H, Tsuruta D, Oshimo T, Sowa J, Mizuno N, Nakagawa K, Ishii M (August 2012). "Cutaneous polyarteritis nodosa induced by Mycobacterium tuberculosis". J. Dermatol. 39 (8): 738–9. doi:10.1111/j.1346-8138.2011.01398.x. PMID 22035185.
  6. ↑ Patel N, Patel N, Khan T, Patel N, Espinoza LR (December 2011). "HIV infection and clinical spectrum of associated vasculitides". Curr Rheumatol Rep. 13 (6): 506–12. doi:10.1007/s11926-011-0214-6. PMID 21989711.
  7. ↑ Watts RA, Mooney J, Lane SE, Scott DG (July 2004). "Rheumatoid vasculitis: becoming extinct?". Rheumatology (Oxford). 43 (7): 920–3. doi:10.1093/rheumatology/keh210. PMID 15126674.
  8. ↑ Nakano H, Ooka S, Shibata T, Ogawa H, Ito H, Takakuwa Y, Tonooka K, Maeda A, Yamasaki Y, Kiyokawa T, Nagafuchi H, Yamada H, Ozaki S (September 2012). "Cutaneous polyarteritis nodosa associated with HLA-B39-positive undifferentiated spondyloarthritis in a Japanese patient". Mod Rheumatol. 22 (5): 783–6. doi:10.1007/s10165-011-0576-7. PMID 22270344.
  9. ↑ Pagnini I, Simonini G, Lippi F, Azzari C, Cimaz R (2012). "Cutaneous polyarteritis nodosa and common variable immunodeficiency: a previously unreported association". Clin. Exp. Rheumatol. 30 (1 Suppl 70): S169. PMID 22260879.
  10. ↑ Oulego-Erroz I, Gautreaux-Minaya S, Martinez-Sáenz de Jubera J, Naranjo-Vivas D, Fernéndez-Hernández S, Muñíz-Fontán M (September 2011). "Coexistence of polyarteritis nodosa and psoriatic arthritis in a child: an unreported association: Polyarteritis nodosa and Psoriatic arthitritis". Eur. J. Pediatr. 170 (9): 1213–5. doi:10.1007/s00431-011-1459-9. PMID 21487680.

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