Adult-onset Still's disease pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Adult-onset Still's disease is an automminue inflammatory arthritis that typically affects adolescents and adults ranging from age 16-40 years. Major etiological mechanisms behind cause a dysfunction of the innate and cellular immunity (limited) leading to activation of effector cells of the disease. | |||
=== Putative triggers === | |||
=== Immune dysfunction === | |||
=== Role of interleukin-1 beta === | |||
Interleukin-i beta plays a key role in producing major characteristic features of adult-onset Still's disease. The following processes are affected by an increased production of this key interleukin: | |||
'''Hypothalamic-pituitary axis influence''' | |||
'''Liver synthesis and secretion of acute phase proteins''' | |||
'''Osteoclasts activation and matrix metalloproteinases (MMPs) synthesis''' | |||
'''Innate immune system cells activation''' | |||
'''Increased gene transcription of proinflammatory molecules''' | |||
=== Role of interleukin-18 === | |||
=== Role of interleukin-6 === | |||
=== Role of interleukin-17 === | |||
=== Role of interferon gamma === | |||
=== Role of tumor necrosis factor-alpha (TNF-alpha) === | |||
=== Reactive hemophagocytic lymphohistiocytosis === | |||
==Genetics== | ==Genetics== | ||
Revision as of 00:48, 8 April 2018
Template:Adult-onset Still's disease
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Pathophysiology
Adult-onset Still's disease is an automminue inflammatory arthritis that typically affects adolescents and adults ranging from age 16-40 years. Major etiological mechanisms behind cause a dysfunction of the innate and cellular immunity (limited) leading to activation of effector cells of the disease.
Putative triggers
Immune dysfunction
Role of interleukin-1 beta
Interleukin-i beta plays a key role in producing major characteristic features of adult-onset Still's disease. The following processes are affected by an increased production of this key interleukin:
Hypothalamic-pituitary axis influence
Liver synthesis and secretion of acute phase proteins
Osteoclasts activation and matrix metalloproteinases (MMPs) synthesis
Innate immune system cells activation
Increased gene transcription of proinflammatory molecules