Study Identifies Possible Cause of Low Platelet Count in Lupus
Two types of autoantibody-mediated thrombocytopenia in patients with systemic lupus erythematosus, Rheumatology 2006 45(7):851-854, M. Kuwana, J. Kaburaki, Y. Okazaki, et. al.
Having a reduced number of platelets is a serious complication of lupus. A large percentage of cases are due to antibodies that bind to at least one of two proteins on the surface of blood platelets. A group of researchers in Tokyo have studies these two types of antibodies and suggest that antibodies to each of the proteins operate in distinctly different ways.
A low platelet count (also called thrombocytopenia), is a serious blood complication that can affect lupus patients. There are a number of possible causes for low platelets in lupus patients, including side effects from some of the treatments for lupus, but antibodies against proteins on the surface of platelets, which develop as a result of the lupus itself, is the most common cause. The same antibodies are found in people who have low platelets due to a condition called ITP (idiopathic thrombocytopenic purpura). Some patients with ITP will later develop lupus, but others only have the condition of low platelets and never go on to develop the other symptoms of lupus.
In this study, a Japanese research team examined the role of two proteins on the surface of platelets in the immune response that leads to platelet destruction. These proteins are called GPIIb/IIIA and TPOR (thrombopoietin receptor). Blood samples from 32 lupus patients with low platelet levels, 30 lupus patients without low platelet levels, 92 patients with ITP, and 60 healthy people were evaluated. Anti-GPIIb/IIIa and anti-TPOR were more frequent in lupus patients with low platelets than in those without low platelets or in healthy people (but comparable to the levels in those with ITP).
In the bone marrow of patients with the anti-GPIIb/IIIa antibodies, there was a lot of new production of platelets, suggesting that these antibodies were causing destruction of platelets out in the blood stream and the bone marrow was trying to keep up with the diminishing supply. However, anti-TPOR antibodies were associated with a decrease in the production of new platelets in the bone marrow, suggesting that this antibody might be acting to keep new platelets from being made.
That distinction is also reflected in studies of what these antibodies actually bind to. Anti-GPIIB/IIIa antibody seems to bind to circulating platelets and may stimulate their destruction by killer white blood cells. Anti-TPOR antibody blocks signaling that could result in limiting the cells in the bone marrow that give rise to platelets. As is often the case with lupus, one clinical condition, in this case low platelets, can originate in vastly different ways. It may be that different treatments would be optimal for these two types of platelet problems.
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