Idiopathic thrombocytopenic purpura pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
In | * In most cases, the cause of ITP is [[autoimmune]] .<ref>{{cite journal |author=Coopamah M, Garvey M, Freedman J, Semple J |title=Cellular immune mechanisms in autoimmune thrombocytopenic purpura: An update |journal=Transfus Med Rev |volume=17 |issue=1 |pages=69–80 |year=2003 |pmid=12522773}}</ref> | ||
* Auto [[antibodies]] against platelets being detected in approximately 60% of cases . | |||
* Most often these antibodies are against platelet membrane [[glycoprotein]]s IIb-IIIa or Ib-IX, and [[IgG]] type.<ref name="pmid18046034">{{cite journal |author=Schwartz RS |title=Immune thrombocytopenic purpura--from agony to agonist |journal=N. Engl. J. Med. |volume=357 |issue=22 |pages=2299–301 |year=2007 |pmid=18046034 |doi=10.1056/NEJMe0707126}}</ref> | |||
* Other cause of ITP is due to chronic infections such as HIV, hepatitis C and H. Pylori. It,s due to molecular mimicry, antibody is formed against the infection and this cross-reacts with platelets. Autoantibodies in ITP react with platelet IIb/IIIa glycoprotein, less commonly with GPIb/IX. Lymphocytes in the spleen make the antiplatelet antibody; that,s why splenectomy works so well. There is a correlation between a platelet's short survival and high turnover rate and the subsequent excellent response to [[splenectomy]]. | |||
* Platelet kinetic studies show that platelet production is normal or reduced rather than increased in about two thirds of ITP patients. | |||
Ultrastructural studies of the bone marrow in ITP show increased signs of megakaryocyte [[apoptosis]] and reduced platelet shedding. | * [[autoantibodies]] from patients with ITP inhibit megakaryocyte growth in vitro. | ||
* [[IgG]] from ITP-plasma inhibits megakaryocyte production. | |||
* Ultrastructural studies of the bone marrow in ITP show increased signs of megakaryocyte [[apoptosis]] and reduced platelet shedding. | |||
* Recent studies suggests that the stimulus for autoantibody production in ITP is due to abnormal [[T helper cell]]s reacting with platelet antigens on the surface of antigen presenting cells.<ref>{{cite journal |author=Semple JW, Freedman J |title=Increased antiplatelet T helper lymphocyte reactivity in patients with autoimmune thrombocytopenia |journal=Blood |volume=78 |issue=10 |pages=2619-25 |year=1991 |pmid=1840468 |doi=}}</ref> This important finding suggests that therapies directed towards T cells may be effective in treating ITP. | |||
Recent | |||
==References== | ==References== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
- In most cases, the cause of ITP is autoimmune .[1]
- Auto antibodies against platelets being detected in approximately 60% of cases .
- Most often these antibodies are against platelet membrane glycoproteins IIb-IIIa or Ib-IX, and IgG type.[2]
- Other cause of ITP is due to chronic infections such as HIV, hepatitis C and H. Pylori. It,s due to molecular mimicry, antibody is formed against the infection and this cross-reacts with platelets. Autoantibodies in ITP react with platelet IIb/IIIa glycoprotein, less commonly with GPIb/IX. Lymphocytes in the spleen make the antiplatelet antibody; that,s why splenectomy works so well. There is a correlation between a platelet's short survival and high turnover rate and the subsequent excellent response to splenectomy.
- Platelet kinetic studies show that platelet production is normal or reduced rather than increased in about two thirds of ITP patients.
- autoantibodies from patients with ITP inhibit megakaryocyte growth in vitro.
- IgG from ITP-plasma inhibits megakaryocyte production.
- Ultrastructural studies of the bone marrow in ITP show increased signs of megakaryocyte apoptosis and reduced platelet shedding.
- Recent studies suggests that the stimulus for autoantibody production in ITP is due to abnormal T helper cells reacting with platelet antigens on the surface of antigen presenting cells.[3] This important finding suggests that therapies directed towards T cells may be effective in treating ITP.
References
- ↑ Coopamah M, Garvey M, Freedman J, Semple J (2003). "Cellular immune mechanisms in autoimmune thrombocytopenic purpura: An update". Transfus Med Rev. 17 (1): 69–80. PMID 12522773.
- ↑ Schwartz RS (2007). "Immune thrombocytopenic purpura--from agony to agonist". N. Engl. J. Med. 357 (22): 2299–301. doi:10.1056/NEJMe0707126. PMID 18046034.
- ↑ Semple JW, Freedman J (1991). "Increased antiplatelet T helper lymphocyte reactivity in patients with autoimmune thrombocytopenia". Blood. 78 (10): 2619–25. PMID 1840468.