Adult-onset Still's disease classification: Difference between revisions

	Adult-onset Still's disease
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Latest revision as of 04:50, 23 April 2018

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Overview

Adult-onset Stiil's disease (AOSD) may be classified based on the predominant clinical picture with which the patient presents into systemic sub-type and chronic arthritis sub-type. The sub-types differ based on the cytokine profile, clinical course and response to treatment.

Classification

Classification based on clinical presentation

Adult-onset Stiil's disease (AOSD) may be classified based on the predominant clinical picture with which the patient presents. The following are the sub-types:^[1]^[2]

ASOD with pre-dominant systemic symptoms
ASOD with pre-dominant arthritis

Systemic sub-type	Distinguishing features
	Pre-dominant cellular mechanism	Cytokine profile	Clinical presentation	Laboratory findings	Response to treatment	Miscellaneous
	Natural killer (NK) cell dysfunction (marked deficiency) CD8 type (cytotoxic) T cell dysfunction (marked deficiency) Neutrophil, monocyte and macrophage activation	Interleukin 1 beta Interleukin 18 Interferon alpha and beta Interleukin 4	Arthralgia Myalgia Hepatitis Spleenomegaly Spiking fever (evening spike) Orbital inflammation Cardiac dysfunction Pulmonary dysfucntion Weight loss Sore throat Lymphadenopathy	Thrombocytopenia Hyperferritinemia	Strong response to interleukin-1 inhibitors Weak response to interleukin 18 inhibitors and interferon gamma inhibitors	Upregulation of genes involved in granulocyte formation
Arthritis sub-type	Natural killer (NK) cell dysfunction (deficiency) CD8 type (cytotoxic) T cell dysfunction (deficiency) Neutrophil, monocyte and macrophage activation	Interleukin 17 Interleukin 23 Interleukin 6 Tumor necrosis factor alpha (TNF-alpha)	Involvement of wrist, ankle, elbow joints, proximal interphalyngeal joints (PIP) Arthralgia Myalgia Spiking fever Salmon-colored maculopapular rash Less common systemic and organ involvement	Thrombocytosis Arthritis	Strong response to interleukin 6 inhibitors Good response to TNF-alpha inhibitors Weak reponse to interleukin 17 inhibitors

References

↑ Villanueva J, Lee S, Giannini EH, Graham TB, Passo MH, Filipovich A, Grom AA (2005). "Natural killer cell dysfunction is a distinguishing feature of systemic onset juvenile rheumatoid arthritis and macrophage activation syndrome". Arthritis Res. Ther. 7 (1): R30–7. doi:10.1186/ar1453. PMC 1064882. PMID 15642140.
↑ Lee SJ, Cho YN, Kim TJ, Park SC, Park DJ, Jin HM, Lee SS, Kee SJ, Kim N, Yoo DH, Park YW (September 2012). "Natural killer T cell deficiency in active adult-onset Still's Disease: correlation of deficiency of natural killer T cells with dysfunction of natural killer cells". Arthritis Rheum. 64 (9): 2868–77. doi:10.1002/art.34514. PMID 22605480.

[pmid15642140-1] Villanueva J, Lee S, Giannini EH, Graham TB, Passo MH, Filipovich A, Grom AA (2005). "Natural killer cell dysfunction is a distinguishing feature of systemic onset juvenile rheumatoid arthritis and macrophage activation syndrome". Arthritis Res. Ther. 7 (1): R30–7. doi:10.1186/ar1453. PMC 1064882. PMID 15642140.

[pmid22605480-2] Lee SJ, Cho YN, Kim TJ, Park SC, Park DJ, Jin HM, Lee SS, Kee SJ, Kim N, Yoo DH, Park YW (September 2012). "Natural killer T cell deficiency in active adult-onset Still's Disease: correlation of deficiency of natural killer T cells with dysfunction of natural killer cells". Arthritis Rheum. 64 (9): 2868–77. doi:10.1002/art.34514. PMID 22605480.

[1]

[2]

@@ Line 1: / Line 1: @@
 __NOTOC__
+{{Adult-onset Still’s disease}}
-{{Template:Adult-onset Still's disease}}
+{{CMG}}; {{AE}} {{HK}}
-{{CMG}}
 ==Overview==
+Adult-onset Stiil's disease (AOSD) may be classified based on the predominant clinical picture with which the patient presents into [[systemic]] sub-type and chronic [[arthritis]] sub-type. The sub-types differ based on the [[cytokine]] profile, clinical course and response to treatment.
 ==Classification==
 === Classification based on clinical presentation ===
-Adult-onset Stiil's disease (AOSD) may be classified based on the predominant clinical picture with which the patient presents. The following are the sub-types:<ref name="pmid15642140">{{cite journal |vauthors=Villanueva J, Lee S, Giannini EH, Graham TB, Passo MH, Filipovich A, Grom AA |title=Natural killer cell dysfunction is a distinguishing feature of systemic onset juvenile rheumatoid arthritis and macrophage activation syndrome |journal=Arthritis Res. Ther. |volume=7 |issue=1 |pages=R30–7 |date=2005 |pmid=15642140 |pmc=1064882 |doi=10.1186/ar1453 |url=}}</ref>
+Adult-onset Stiil's disease (AOSD) may be classified based on the predominant clinical picture with which the patient presents. The following are the sub-types:<ref name="pmid15642140">{{cite journal |vauthors=Villanueva J, Lee S, Giannini EH, Graham TB, Passo MH, Filipovich A, Grom AA |title=Natural killer cell dysfunction is a distinguishing feature of systemic onset juvenile rheumatoid arthritis and macrophage activation syndrome |journal=Arthritis Res. Ther. |volume=7 |issue=1 |pages=R30–7 |date=2005 |pmid=15642140 |pmc=1064882 |doi=10.1186/ar1453 |url=}}</ref><ref name="pmid22605480">{{cite journal |vauthors=Lee SJ, Cho YN, Kim TJ, Park SC, Park DJ, Jin HM, Lee SS, Kee SJ, Kim N, Yoo DH, Park YW |title=Natural killer T cell deficiency in active adult-onset Still's Disease: correlation of deficiency of natural killer T cells with dysfunction of natural killer cells |journal=Arthritis Rheum. |volume=64 |issue=9 |pages=2868–77 |date=September 2012 |pmid=22605480 |doi=10.1002/art.34514 |url=}}</ref>
-* ASOD with pre-dominant systemic symptoms
+* ASOD with pre-dominant [[systemic]] [[symptoms]]
-* ASOD with pre-dominant arthritis
+* ASOD with pre-dominant [[arthritis]]
 {| class="wikitable"
-! rowspan="5" |Adult-onset Still's disease sub-types
+! rowspan="4" align="center" style="background:#4479BA; color: #FFFFFF;" + |Adult-onset Still's disease sub-types
 ! rowspan="3" |Systemic sub-type
-! colspan="5" |Distinguishing features
+! colspan="6" align="center" style="background:#4479BA; color: #FFFFFF;" + |Distinguishing features
 |-
-!Pre-dominant cellular mechanism
+! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pre-dominant cellular mechanism
-!Clinical presentation
+! align="center" style="background:#4479BA; color: #FFFFFF;" + |Cytokine profile
-!Cytokine profile
+! align="center" style="background:#4479BA; color: #FFFFFF;" + |Clinical presentation
-!Response to treatment
+! align="center" style="background:#4479BA; color: #FFFFFF;" + |Laboratory findings
-!Miscellaneous
+! align="center" style="background:#4479BA; color: #FFFFFF;" + |Response to treatment
+! align="center" style="background:#4479BA; color: #FFFFFF;" + |Miscellaneous
 |-
 |
-* Natural killer (NK) cell dysfunction (deficiency)
+* [[Natural killer cell|Natural killer (NK) cell]] dysfunction (marked deficiency)
-* CD8 type (cytotoxic) T cell dysfunction (deficiency)
+* [[Cytotoxic T cell|CD8 type (cytotoxic) T cell]] dysfunction (marked deficiency)
+* [[Neutrophil]], [[monocyte]] and [[macrophage]] activation
+|
+* [[Interleukin 1 beta]]
+* [[Interleukin 18]]
+* [[Interferon alpha]] and beta
+* [[Interleukin 4]]
 |
+* [[Arthralgia]]
+* [[Myalgia]]
+* [[Hepatitis]]
+* [[Spleenomegaly]]
+* Spiking [[fever]] (evening spike)
+* [[Orbit (anatomy)|Orbital]] [[inflammation]]
+* [[Cardiac]] dysfunction
+* [[Pulmonary]] dysfucntion
+* [[Weight loss]]
+* [[Sore throat]]
+* [[Lymphadenopathy]]
 |
+* [[Thrombocytopenia]]
+* Hyperferritinemia
 |
+* Strong response to [[Interleukin 1|interleukin-1]] inhibitors
+* Weak response to [[interleukin 18]] inhibitors and [[interferon gamma]] inhibitors
 |
+* Upregulation of [[genes]] involved in [[granulocyte]] formation
 |-
-! rowspan="2" |Arthritis sub-type
+!Arthritis sub-type
-|
 |
+* [[Natural killer cells|Natural killer (NK) cell]] dysfunction (deficiency)
+* [[Cytotoxic T cell|CD8 type (cytotoxic) T cell]] dysfunction (deficiency)
+* [[Neutrophil]], [[monocyte]] and [[macrophage]] activation
 |
+* [[Interleukin 17]]
+* [[Interleukin 23]]
+* [[Interleukin 6]]
+* [[Tumor necrosis factor alpha|Tumor necrosis factor alpha (TNF-alpha)]]
 |
+* Involvement of [[wrist]], [[ankle]], [[Elbow-joint|elbow]] joints, [[Proximal interphalangeal joints|proximal interphalyngeal joints]] (PIP)
+* [[Arthralgia]]
+* [[Myalgia]]
+* Spiking [[fever]]
+* Salmon-colored [[maculopapular]] rash
+* Less common [[systemic]] and organ involvement
 |
-|-
+* [[Thrombocytosis]]
-|
+* [[Arthritis]]
-|
-|
 |
+* Strong response to [[interleukin 6]] inhibitors
+* Good response to [[Tumor necrosis factor-alpha|TNF-alpha]] inhibitors
+* Weak reponse to [[interleukin 17]] inhibitors
 |
 |}
@@ Line 47: / Line 83: @@
 ==References==
 {{reflist|2}}
+[[Category: Rheumatology]]