Wang J C, Chen C, Novetsky A D, Lichter S M, Ahmed F, Friedberg N M
Division of Medical Oncology and Hematology, Brookdale University Hospital and Medical Center, Brooklyn, New York 11212, USA.
Am J Med. 1998 May;104(5):451-5. doi: 10.1016/s0002-9343(98)00090-4.
Although the distinction between clonal and reactive thrombocytosis is clinically relevant because clonal thrombocytosis has more thrombohemorragic complications, the differential diagnosis of these two entities can be difficult. Methods such as the detection of unstimulated erythroid or megakaryocyte colony growth are not readily available. Therefore, we measured blood thrombopoietin levels to determine whether these levels can be used to distinguish the two conditions.
Thrombopoietin levels were measured in 73 patients with thrombocytosis (platelet count > 500,000/microL), including 39 patients with clonal thrombocytosis (20 patients with essential thrombocythemia, 15 with agnogenic myeloid metaplasia, 1 patient with polycythemia vera, and 3 with undefined myeloproliferative disorders) and 34 patients with reactive thrombocytosis (17 with malignant tumors, 11 with inflammatory diseases, 4 with sickle cell disease, and 2 with iron deficiency anemia). Seventeen normal volunteers were used as controls.
Thrombopoietin levels were significantly higher (P < 0.05) in patients with clonal thrombocytosis (mean +/- SD of 555 +/- 585 pg/mL), including the subgroup with essential thrombocythemia (505 +/- 459 pg/mL), than in patients with reactive thrombocytosis (290 +/- 133 pg/mL) who had similar levels as controls (201 +/- 112 pg/mL). Thrombopoietin levels in patients with clonal thrombocytosis, including essential thrombocythemia, were not correlated with platelet counts.
Thrombopoietin levels may be helpful in distinguishing between clonal thrombocytosis and reactive thrombocytosis. Thrombopoietin is probably responsible for the elevated platelet counts in clonal thrombocytosis including essential thrombocythemia, but not in reactive thrombocytosis. High thrombopoietin levels in patients with clonal thrombocytosis cannot be explained solely by platelet megakaryocyte mass.
虽然克隆性血小板增多症和反应性血小板增多症的区分在临床上具有重要意义,因为克隆性血小板增多症有更多的血栓出血并发症,但这两种情况的鉴别诊断可能很困难。诸如检测未刺激的红系或巨核细胞集落生长等方法并不容易获得。因此,我们测量了血液中血小板生成素水平,以确定这些水平是否可用于区分这两种情况。
测量了73例血小板增多症患者(血小板计数>500,000/微升)的血小板生成素水平,其中包括39例克隆性血小板增多症患者(20例原发性血小板增多症患者、15例原因不明的骨髓化生患者、1例真性红细胞增多症患者和3例未明确的骨髓增殖性疾病患者)以及34例反应性血小板增多症患者(17例恶性肿瘤患者、11例炎症性疾病患者、4例镰状细胞病患者和2例缺铁性贫血患者)。17名正常志愿者作为对照。
克隆性血小板增多症患者(平均±标准差为555±585皮克/毫升),包括原发性血小板增多症亚组(505±459皮克/毫升),其血小板生成素水平显著高于反应性血小板增多症患者(290±133皮克/毫升),后者与对照组(201±112皮克/毫升)水平相似(P<0.05)。包括原发性血小板增多症在内的克隆性血小板增多症患者的血小板生成素水平与血小板计数无关。
血小板生成素水平可能有助于区分克隆性血小板增多症和反应性血小板增多症。血小板生成素可能是包括原发性血小板增多症在内的克隆性血小板增多症中血小板计数升高的原因,但不是反应性血小板增多症的原因。克隆性血小板增多症患者的高血小板生成素水平不能仅用血小板巨核细胞数量来解释。