Thrombocytopenia may be due to 1) a decrease in production, as seen in patients with
marrow aplasia or when the marrow is infiltrated by tumor, 2) disorders in which
platelet destruction exceeds production, or 3) splenomegaly, in which the distribution of
platelets is abnormal. In evaluating the patient with thrombocytopenia, one should look
for splenomegaly on physical examination, which would suggest a syndrome
characterized by platelet sequestration. Second, one should examine a bone marrow
sample to detect aplasia, fibrosis, or infiltration. In patients with a normal spleen and
normal bone marrow function, the underlying disorder must by excess destruction. This
can be due to nonimmune disorders, such as disseminated intravascular coagulation, or
prosthetic cardiac valves, or thrombotic thrombocytopenic purpura, or to the presence of
either immune complexes or specific antiplatelet antibodies. Immune thrombocytopenia
can be induced by a wide range of common drugs, including quinidine, penicillin, gold,
and sulfonamides. Heparin is perhaps the most common drugs in inducing
thrombocytopenia in 1∼10% of patients who receive this anticoagulant. Acute immune
thrombocytopenia seen primarily in children often occurs following a viral infection.
About 90% of these patients recover within 4 to 6 weeks without therapy. In contrast a
chronic form of immune thrombocytopenia is much more common in adults. Antibodies
against specific target antigens, usually against GP Ⅱb/Ⅲa or GP Ⅰb/ⅠⅩ/Ⅴ.
Cognizant of pathogenesis of these various forms of thrombocytopenia will allow the
diagnosis much easier and practical.
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