ThrombocytosisD75.9

Increased number of platelets in the blood count, see below. Thrombocyt. Thrombocytosis is a very common laboratory abnormality and not a diagnosis in the strict sense. It is recorded in just over one-third of patients requiring intensive care and one-fifth of trauma patients. It has a high clinical value as a possible indication of an underlying solid malignancy or else a primary hematologic neoplasia(paraneoplastic syndrome). Thrombocytosis is defined as a platelet count that exceeds the upper normal value. A uniform numerical definition, however, does not exist, not least because of different analytical instruments and insufficient validation of the standard values. An upper limit value of 500/nl is frequently found in the literature, whereby a hematological stem cell disease cannot be excluded if the value is below this cutoff.

Secondary (reactive) thrombocytosis: The differential diagnosis of thrombocytosis includes primary as well as secondary (reactive) causes, with reactive causes clearly predominating across all age groups. In a series of 732 medical and surgical patients, 88% of thrombocytoses (platelets > 500/nI) were reactive in nature, similarly in a series of 91 patients, in which 70% of thrombocytoses (platelets > 600/nl) could be attributed to a secondary cause.

The most common reactive causes are: tissue trauma including previous surgery, infections and (chronic) inflammation, neoplasia, iron deficiency and hypo-/asplenism. In most patients, clinical signs of a systemic disease underlying thrombocytosis are present. However, subclinical disease can also trigger reactive thrombocytosis. It is important to exclude occult solid neoplasms. In a larger prospective cohort study (primary care patients 40years), solid tumors were detectable in 11.6% and 6.2% of men/women with thrombocytosis in the following year (mainly lung and colorectal carcinomas). It can be assumed that thrombocytosis is not to be regarded as a mere epiphenomenon but promotes tumor growth per se. In ovarian cancer, thrombocytosis is a prognostically unfavorable risk factor.

Primary th rombocytosis: The most common cause of primary thrombocytosis is essential thrombocythemia (ET), which often manifests as isolated thrombocytosis. ET belongs to the myeloproliferative neoplasms (MPN), a group of hematologic stem cell disorders characterized by increased production of mature blood cells. From this group, polycythaemia vera (PV, characterized by polyglobulia), primary myelofibrosis (PMF, characterized by anemia, splenomegaly and detection of immature precursors in peripheral blood) as well as chronic myeloid leukemia (CML, characterized by leukocytosis with left shift to blast) can also be associated with thrombocytosis. Especially in older patients, if thrombocytosis and simultaneous anemia (often macrocytic) are detected, a myelodysplastic syndrome (MDS) or an overlap of myelodysplastic syndrome and myeloproliferative neoplasia (a so-called MDS/MPN) should be considered for differential diagnosis. More rarely, acute myeloid leukemia may also be associated with thrombocytosis. Familial thrombocytoses are very rare, hereditary disorders, which are considered if there is a striking family history.

A significant clinical clue is thromboembolic and hemorrhagic events. Patients with an MPN paradoxically show both a markedly increased risk of thrombosis and bleeding. Furthermore, B-symptomatics, vasomotor symptoms such as flushing, headache or atypical thoracic pain, erythromelalgia (painful, often burning sensations and redness of the acras), pruritus, and splenomegaly represent additional clinical "red hags." Laboratory evidence includes blasts, a leukoerythroblastic blood count (nucleated erythrocytes and myeloid precursors in the peripheral blood), and dysplastic changes in the blood smear.

Therapy of reactive thrombocytosis consists primarily of treatment of the underlying disease. In contrast to its widespread use in patients with MPN, the use of aspirin in reactive thrombocytosis is highly controversial. There are no controlled clinical trials or observational studies demonstrating the benefit of aspirin in this context. Thrombocytosis per se does not seem to relevantly increase the risk of thrombosis, but concomitant prothrombogenic factors do influence the risk of thrombosis. In this context, we clearly recommend against a general use of aspirin in reactive thrombocytosis. A possible treatment decision should only be made on an individualized basis, taking into account the risk of bleeding and thrombosis.