Tumors of the thymus gland are rare, and usually are accompanied by chest pain and/or myasthenia gravis, an autoimmune neuromuscular disorder which causes facial drooping. There is a long list of autoimmune disorders associated with thymomas. Very rarely, thymomas can cause ITP, sometimes along with myasthenia gravis, and sometimes with no other symptoms present. Removal of a diseased thymus has been known to increase platelets to normal levels, but not always.
journaldatabase.info/articles/itp_early_presentation_thymoma.html
ITP, Early Presentation of Thymoma
I found an interesting web article authored by McMillan Laboratories of The Scripps Research Institute (Robert McMillan, MD is Medical Advisor Emeritus of the PDSA). The article explains that there are two mechanisms by which platelets are destroyed in ITP.
The method of destruction with which we are most familiar involves antibodies erroneously marking platelets as foreign bodies, so that lymphocytes then destroy them in the spleen.
A second method of platelet destruction involves T-cells, a special type of lymphocytes which gain their letter "T" from the thymus, where they are created.
www.scripps.edu/mcmillan/causes.html
Cytotoxic thymic-dependent (T) lymphocytes.
These specialized white blood cells are produced in the bone marrow and then mature in the thymus gland. They have receptors on their surface that are programmed to bind to a specific antigen that, in the case of ITP, is on the surface of platelets and probably megakaryocytes. Cytotoxic T lymphocytes may circulate in the blood but are primarily localized in the spleen and lymph nodes.
Causes of thrombocytopenia in ITP.
Platelet destruction. Platelet destruction in chronic ITP is due to either: (1) antibody binding to a platelet autoantigen(s) followed by phagocytosis of the platelets by white blood cells (neutrophils or monocytes) or (2) binding of cytotoxic T lymphocytes to platelets followed by release of toxins causing platelet death. For platelet destruction by antibody to occur, three things must be present: sufficient antigen (platelets), autoantibody and phagocytic cells. The spleen is an optimal location for this. About one third of the circulating platelets are in the spleen at all times and the production of antiplatelet antibody in the spleen subjects these platelets to high antibody concentrations. The antibody-sensitized platelets circulate slowly through the spleen, which is rich in the phagocytic cells that destroy them. Concurrently, cytotoxic T lymphocytes are reacting with antigens on platelets, adding to the destruction of platelets.
Here is a case study describing an association between thymoma and ITP.
www.sciencedirect.com/science/article/pii/S002252230400902X
Thymoma with idiopathic thrombocytopenic purpura: Report of a case
...however, only rarely is thymoma followed by ITP. We report the case of a patient with thymoma and chronic ITP who was helped by thymectomy.
Clinical summary
A 27-year-old woman with repeated limb petechiae, epistaxis, and menorrhagia was admitted to the hospital. She was treated for 4 months in the department of internal medicine. At first, decreased serum platelet count (13.0 × 109 cells/L) was detected. Erythrocyte count was almost within normal limits. The result of bone marrow examination was consistent with ITP. Prednisone, given orally for 4 months, was effective. Because the patient coincidentally reported discomfort in the chest, thymoma was detected by radiography and computed tomography (Figure 1). Thymectomy was performed. Prednisone was continuously applied in the postoperative period, but the dose was gradually decreased. ITP was improved. Three months later, corticosteroid therapy was no longer used. Platelet counts were normal. During a 1-year follow-up period, ITP did not recur, and the patient appears to be cured.
A different article did not result in platelet count improvement.
My personal interest is that Ellen has a droopy eye, which is now being evaluated for myasthenia gravis. 15% - 20% of cases are caused by thymoma, while the remainder are presumed caused by acetylcholine receptor antibodies. Ellen has a history of benign tumors (adrenal gland, parotid gland and lypoma).
