Plasma Glycocalicin

• Published in: The New England journal of medicine Vol. 317; no. 17; pp. 1037 - 1042
• Main Authors: Steinberg, Mark H, Kelton, John G, Coller, Barry S
• Format: Journal Article
• Language: English
• Published: Boston Massachusetts Medical Society 22.10.1987
• Subjects: Blood platelets; Bone marrow; Glycoproteins; Plasma
• ISSN: 0028-4793; 1533-4406
• DOI: 10.1056/NEJM198710223171701

In some patients with thrombocytopenia, it is difficult to determine whether the condition is caused by underproduction of platelets (reduced numbers of megakaryocytes) or an increase in the rate of their destruction (normal or increased numbers of megakaryocytes). A noninvasive test to help distinguish between these two categories of thrombocytopenia would be useful. We related the plasma concentration of glycocalicin, a fragment of the platelet-membrane glycoprotein lb, to the mechanism of thrombocytopenia by evaluating bone marrow megakaryocyte content and measuring platelet life span. Plasma glycocalicin was measured with a monoclonal antibody to the glycocalicin component of platelet glycoprotein lb. The mean (±SD) plasma concentration of glycocalicin in 34 healthy controls was 87±20 percent of the level in pooled normal plasma (range, 52 to 127 percent). All of eight patients with aplastic anemia or amegakaryocytic thrombocytopenia confirmed by examining bone marrow (in all patients) and by determining the life span of autologous platelets (in six patients) had glycocalicin levels significantly below the normal range (5 to 27 percent). In contrast, each of 25 patients with thrombocytopenia thought to be caused by a reduction in platelet life span, whose bone marrow contained normal or increased numbers of megakaryocytes, had glycocalicin levels that fell within or above the normal range (48 to 261 percent). There was no overlap of values between the two patient populations. These studies indicate that the measurement of plasma glycocalicin may be a useful adjunct in classifying thrombocytopenic disorders. (N Engl J Med 1987; 317:1037–42.) Thrombocytopenia is a common hematologic abnormality that must be evaluated before the proper therapeutic intervention can be chosen. The mechanism responsible for thrombocytopenia can be separated into three general categories: underproduction, sequestration, and increased destruction of platelets. Abnormal sequestration, which is almost always due to hypersplenism, can usually be determined by physical examination, whereas the differentiation of thrombocytopenia due to underproduction from that due to increased destruction can be more difficult. Initial investigations usually include examination of a stained peripheral-blood film and the bone marrow. The presence of normal or increased numbers of megakaryocytes in the bone marrow essentially excludes . . .