This is due to the presence of structures resembling platelets in the blood such as needle-like cryoglobulin crystals, cytoplasmic fragments of circulating leukemic cells, bacteria, and red blood cell microvesicles. These structures are counted as platelets by the automated machine counter; therefore, causing the platelet number to be falsely elevated. However, such error can be avoided by doing a peripheral blood smear. Diagnosis
Laboratory tests might include: full blood count, liver enzymes, renal function and erythrocyte sedimentation rate.If the cause for the high platelet count remains unclear, bone marrow biopsy is often undertaken, to differentiate whether the high platelet count is reactive or essential. Treatment
Often, no treatment is required or necessary for reactive thrombocytosis. In cases of reactive thrombocytosis of more than 1,000x109/L, it may be considered to administer daily low dose aspirin (such as 65 mg) to minimize the risk of stroke or thrombosis.However, in essential thrombocythemia where platelet counts are over 750x109/L or 1,000x109/L, especially if there are other risk factors for thrombosis, treatment may be needed. Selective use of aspirin at low doses is thought to be protective. Extremely high platelet counts can be treated with hydroxyurea (a cytoreducing agent) or anagrelide (Agrylin).In Janus kinase 2 positive disorders, ruxolitinib (Jakafi) can be effective. References
Schafer AI (March 2004). "Thrombocytosis". N. Engl. J. Med. 350 (12): 1211–9. doi:10.1056/NEJMra035363. PMID 15028825. == External links ==
Major aortopulmonary collateral arteries (or MAPCAs) are arteries that develop to supply blood to the lungs when native pulmonary circulation is underdeveloped. Instead of coming from the pulmonary trunk, supply develops from the aorta and other systemic arteries. Pathogenesis and anatomy
Major aortopulmonary collateral arteries (MAPCAs) develop early in embryonic life but regress as the normal pulmonary arteries (vessels that will supply deoxygenated blood to the lungs) develop. In certain heart conditions the pulmonary arteries do not develop. The collaterals continue to grow, and can become the main supply of blood to the lungs. Though it is usually associated with congenital heart diseases with decreased pulmonary blood flow like tetralogy of Fallot or pulmonary atresia it may be seen sometimes in isolation i.e. not associated with any congenital heart disease in that case it is termed as isolated aortopulmonary collateral artery. In these cases it may be one of the cause of congestive cardiac failure in neonates.Pulmonary arteries come from the right side of the heart, and usually carry deoxygenated blood from the body. These collateral arteries carry blood which has already been oxygenated by the lungs, so are of little use in helping the body to get oxygen. Associated conditions
Pulmonary atresia with ventricular septal defect (or Tetralogy of Fallot with pulmonary atresia) will result in the development of systemic collaterals. Implications of a systemic collateral supply
Major aortopulmonary collateral arteries come from the systemic circulation, because of this they will often have higher pressure than normal found in the lungs, leading to pulmonary hypertension.