×

This article on Epainassist.com has been reviewed by a medical professional, as well as checked for facts, to assure the readers the best possible accuracy.

We follow a strict editorial policy and we have a zero-tolerance policy regarding any level of plagiarism. Our articles are resourced from reputable online pages. This article may contains scientific references. The numbers in the parentheses (1, 2, 3) are clickable links to peer-reviewed scientific papers.

The feedback link “Was this Article Helpful” on this page can be used to report content that is not accurate, up-to-date or questionable in any manner.

This article does not provide medical advice.

1

What Would Cause An Increase In Blood Platelets?

Platelets, also known as thrombocytes, are small and spherical blood component produced in the bone marrow. They are essential for blood clotting and hemostasis. The normal levels of platelets in blood range from 150,000-450,000 per cubic millimeter of blood. The normal life span of platelet ranges from 7 to 10 days.

The medical term for elevated levels of platelets is thrombocytosis. The higher normal level of platelets is typically 350,000-450,000 per cubic millimeter of blood. Thrombocytosis can be detected in the routine blood test.

What Would Cause An Increase In Blood Platelets?

What Would Cause An Increase In Blood Platelets?

The causes of an increase in blood platelets or thrombocytosis can be grouped as physiological thrombocytosis, primary (clonal) thrombocytosis and secondary (reactive) thrombocytosis.

Physiological Thrombocytosis can result from exercise (workload), increased adrenaline or increased stress.

Primary Thrombocytosis (clonal) is a result of abnormal bone marrow cells, which leads to increased platelets in circulation. Primary thrombocytosis could lead to severe bleeding or clotting complications such as abnormal blood clotting. This is avoided by normalizing platelet count with medications. The different causes include acute megakaryocytic leukemia, myeloproliferative disease, essential thrombocytosis, polycythemia vera, chronic myeloid leukemia, myelodysplastic syndrome and agnogenic myeloid metaplasia.

Secondary Thrombocytosis (reactive) may be a result of any disease or condition that may be affecting an individual. These include acute blood loss, hemolytic anemia, infection, iron deficiency anemia, surgery, inflammatory diseases, post splenectomy, malignant diseases, trauma or due to certain drugs such as vincristine, trans retinoic acid, cytokines and growth factors. Secondary thrombocytosis due to any of the above cause usually subside after the treatment of the underlying cause. The platelet count is elevated for a short period of time after the management of secondary cause, but it does not lead to any clotting complications such as abnormal blood clotting.

Polycythemia Vera: The platelet count in PV may be dramatically increased to as high as 1,000,000 per cubic millimeter of blood. About 66% of patients with this disease have shown increases levels of platelet.

Chronic Myeloid Leukemia: In this disease, about 75% of patients have marked increase in platelet levels.

Agnogenic Myeloid Metaplasia: It is also known as myeloid metaplasia agnogenic or idiopathic myelofibrosis. Thrombocytosis is seen in about 33% of patients suffering from this disease; however, thrombocytopenia is a prominent finding in advanced cases of this disease.

Essential Thrombocytosis: It is also known as primary thrombocythemia. It is a chronic and myeloproliferative disease. Generally, it is an idiopathic disease, but there is a genetic predisposition too.

Infection: Secondary thrombocytosis could be a cause of acute or chronic infection in which there is inhibition of megakaryopoiesis (formation of megakaryocytes, which are precursors to platelets) due to various bacteria and viruses. Few bacterial infections in which there is thrombocytosis include pneumonia, purulent arthritis, tuberculosis, pyelonephritis, osteomyelitis and chronic wound infection.

Iron Deficiency Anemia: The platelet count in iron deficiency anemia, on occasions, may be as high as 1,000,000 per cubic millimeter. The platelet count usually comes back to normal with iron supplements.

Splenectomy: Spleen is responsible for the removal of platelets, so after the splenectomy there is transient increase in the number of platelets, which on times exceed 1,000,000 per cubic millimeter. Generally, the platelet count is back to normal within a few weeks or months. Permanent thrombocytosis after the removal of spleen may be an indication of secondary thrombocytosis such as myeloproliferative disorder.

Inflammatory Diseases: The inflammatory conditions that might cause thrombocytosis include inflammatory bowel disease, liver cirrhosis, rheumatoid arthritis, rheumatic polymyalgia, nephritis and polyarteritis nodosa. The severity of the disease corresponds to the severity of thrombocytosis. The platelet count does return to normal with appropriate treatment of inflammatory diseases.

Malignant Diseases: Thrombocytosis has been associated with many neoplasms such as Hodgkin’s lymphoma, non-Hodgkin’s lymphoma, lung cancer, prostate cancer, pancreatic cancer, ovarian cancer, neoplasm of bladder and mesothelioma. In about 90% of patients suffering from reactive thrombocytosis due to a malignant disease have platelet level in the range of 400,000-1,000,000 per cubic millimeter.

References:

  1. Bussel JB. Immune thrombocytopenia: current treatment options in adults and children. Semin Hematol. 2013;50 Suppl 1:S69-S73. doi: 10.1053/j.seminhematol.2013.06.011. (https://pubmed.ncbi.nlm.nih.gov/24246681/)
  2. Vora AJ, Lilleyman JS. Secondary thrombocytosis. Arch Dis Child. 1993;68(6):745-746. doi: 10.1136/adc.68.6.745. (https://pubmed.ncbi.nlm.nih.gov/8334147/)
  3. Jenkins PV, Rawley O, Smith OP, O’Donnell JS. Elevated factor VIII levels and risk of venous thrombosis. Br J Haematol. 2012;157(6):653-663. doi: 10.1111/j.1365-2141.2012.09085.x. (https://pubmed.ncbi.nlm.nih.gov/22530652/)
  4. Bain BJ. Platelet count and platelet size in males and females. Transfus Apher Sci. 2005;33(3):321-326. doi: 10.1016/j.transci.2004.11.004. (https://pubmed.ncbi.nlm.nih.gov/16126310/)
  5. Johnson DW, Bergstralh EJ, Offord KP, Chu CP, Wilson DM. Beta 2-microglobulin, performance status, and the stage of Hodgkin’s disease. Cancer. 1992;70(8):2066-2071. doi: 10.1002/1097-0142(19921015)70:8<2066::aid-cncr2820700802>3.0.co;2-h. (https://pubmed.ncbi.nlm.nih.gov/1394058/)

Also Read:

Team PainAssist
Team PainAssist
Written, Edited or Reviewed By: Team PainAssist, Pain Assist Inc. This article does not provide medical advice. See disclaimer
Last Modified On:July 25, 2023

Recent Posts

Related Posts