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Platelet destruction can develop because of immunologic causes (HIV infection, drugs, connective tissue or lymphoproliferative disorders, blood transfusions) or nonimmunologic causes (sepsis, acute respiratory distress syndrome). Manifestations are petechiae, purpura, and mucosal bleeding. Laboratory findings depend on the cause. The history may be the only suggestion of the diagnosis. Treatment is correction of the underlying disorder.
Acute respiratory distress syndrome:
Patients with acute respiratory distress syndrome may develop nonimmunologic thrombocytopenia, possibly secondary to deposition of platelets in the pulmonary capillary bed.
Blood transfusions:
Posttransfusion purpura causes immunologic platelet destruction indistinguishable from immune thrombocytopenic purpura (ITP), except for a history of a blood transfusion within the preceding 7 to 10 days. The patient, usually a woman, lacks a platelet antigen (PLA-1) present in most people. Transfusion with PLA-1–positive platelets stimulates formation of anti–PLA-1 antibodies, which (by an unknown mechanism) can react with the patient's PLA-1–negative platelets. Severe thrombocytopenia results, taking 2 to 6 wk to subside.
Connective tissue and lymphoproliferative disorders:
Connective tissue (eg, SLE) or lymphoproliferative disorders can cause immunologic thrombocytopenia. Corticosteroids and splenectomy are often effective.
Drug-induced immunologic destruction:
Commonly used drugs that occasionally induce thrombocytopenia include
Drug-induced thrombocytopenia occurs typically by causing an immune reaction in which drug bound to the platelet creates a new and “foreign” antigen. This disorder is indistinguishable from ITP except for the history of drug ingestion. When the drug is stopped, the platelet count typically begins to increase within 1 to 2 days and recovers to normal within 7 days. (A table of drugs reported to cause thrombocytopenia, together with analysis of the evidence for a causal relation of the drug to thrombocytopenia, is available at Platelets on the Web.)
Up to 5% of patients receiving unfractionated heparin develop thrombocytopenia, which may occur even with very-low-dose heparin (eg, used in flushes to keep IV or arterial lines open). The mechanism is usually immunologic. Bleeding can occur, but more commonly platelets clump excessively, causing vessel obstruction, leading to paradoxical arterial and venous thromboses, which may be life threatening (eg, thromboembolic occlusion of limb arteries, stroke, acute MI). Heparin should be stopped in any patient who becomes thrombocytopenic or whose platelet count decreases by more than 50%. Because 5 days of heparin is sufficient to treat venous thrombosis and because most patients begin oral anticoagulants simultaneously with heparin, stopping heparin is usually safe. Low mol wt heparin (LMWH) may be less immunogenic than unfractionated heparin. However, LMWH is not useful if heparin-induced thrombocytopenia has already developed, because most antibodies cross-react with LMWH.
Infections:
HIV infection may cause immunologic thrombocytopenia indistinguishable from ITP except for the association with HIV. The platelet count may increase with glucocorticoids, which are often withheld unless the platelet count falls to < 20,000/μL, because these drugs may further depress immune function. The platelet count also usually increases after treatment with antiviral drugs.
Other infections such as systemic viral infections (eg, Epstein-Barr virus, cytomegalovirus), rickettsial infections (eg, Rocky Mountain spotted fever), and bacterial sepsis are typically associated with thrombocytopenia.
Pregnancy:
Mild thrombocytopenia, typically asymptomatic, occurs late in gestation in about 5% of normal pregnancies (gestational thrombocytopenia); it is usually mild (platelet counts < 70,000/μL are rare), requires no treatment, and resolves after delivery. However, severe thrombocytopenia may develop in pregnant women with preeclampsia and the HELLP syndrome (hemolysis, elevated liver function tests, and low platelets—see Abnormalities of Pregnancy: Preeclampsia and Eclampsia); such women typically require immediate delivery, and platelet transfusion is considered if platelet count is < 20,000/μL (or < 50,000/μL if delivery is to be cesarean).
Sepsis:
Sepsis often causes nonimmunologic thrombocytopenia that parallels the severity of the infection. The thrombocytopenia has multiple causes: disseminated intravascular coagulation, formation of immune complexes that can associate with platelets, activation of complement, and deposition of platelets on damaged endothelial surfaces.
Last full review/revision May 2009 by James N. George, MD
Content last modified May 2009
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