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Vol. 42. Issue S1.
Pages 70 (October 2020)
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Vol. 42. Issue S1.
Pages 70 (October 2020)
PP 62
Open Access
The cause of very severe trombocytosis: iron deficiency anemia
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V. Uzel1,*, S. SavaŞ2, M. Soker1
1 Dicle Unıversty Ped. Hematology and Oncology, Diyarbakır, Turkey
2 Dicle Unıversty Pediatrıc Department, Diyarbakır, Turkey
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Objective: Platelet count above 450,000mm3 is defined as thrombocytosis. It is called mild thrombocytosis if the platelet count is between 700,000–900,000mm3, and severe thrombocytosis between 900,000–1,000,000mm3. If the platelet count is over 1,000,000mm3, it is considered as very severe thrombocytosis. In this case report; we have showed that iron deficiency can also lead to very severe thrombocytosis by presenting the case of very severe thrombocytosis developing in an adolescent female patient.

Case report: The 12-year-old girl was referred to our hospital for anemia (Hgb: 5.8g/dL) by an external clinic she applied due to her headache in the morning for the past month. The patient's history and family history were unremarkable. Her physical examination revealed that her general condition was moderate-poor, skin was pale, conjunctiva was extremely pale, peak heart rate: 130–140/min, TA: 90/50mm/Hg. Lymphadenopathy and hepatosplenomegaly were not detected. In the laboratory tests of the patient, the following findings were detected; the leukocytes count was: 14,900/mm3, neutrophil count: 11.9/mm3, Hgb: 4.8g/dL, Hct: 20%, MCV: 53fl, RBC: 3.7milyon/uL, MCH: 12.9pg (27–31), platelet count 2,629,000/mm3. Peripheral smear of the patient was analyzed. In eritrocytes, a high degree of hypochromic microcytes were detected and 80% neutrophils, 2% monocytes, 18% lymphocytes, abundant platelets were seen. Serum iron: 6.7uL/dL (50–120); iron binding capacity: 525uL/dL (155–355); ferritin: 0ng/mL; folate: 10.6ng/mL (0.3–24) and vitamin B12: 437ng/mL. There was no abnormality in other biochemical examinations. Iron replacement was started at a dose of 6mg/kg/day considering iron deficiency anemia and related thrombocytosis. Abdominal ultrasonography was evaluated within normal limits according to age. Since the patient had tachycardia, appropriate cross erythrocyte transfusion was performed. Viral serologies and autoantibodies of the patient were evaluated as normal. The control hgb level was 7.9g/dL and thrombocyte count was 1,875,000/mm3 after transfusion. In the bone marrow aspiration assessment, the myeloid and erythroid series in the normocellular bone marrow were seen as normal, blasts were not seen, megakaryocytes were increased. The patient had hgb: 10.4g/dL, platelet: 732,000/mm3 in the clinical examination performed in the second week. She is under the oral +2 valence iron treatment and had no clinical problem in her follow-up examinations.

Methodology: Information was obtained from the patient file.

Results: In childhood, thrombocytosis usually occurs due to secondary causes and thrombocytosis regresses by controlling the causing disease. Thrombocytosis due to iron deficiency is mostly seen in infancy period.

Conclusion: The cause of thrombocytosis in iron deficiency is not fully understood. The fact that the increase in EPO stimulates TPO receptors (c-mpl) in iron deficiency is known to result in thrombocytosis. However, it is very important that children should be evaluated immediately for infection and iron deficiency before performing further examinations. Keywords: Thrombocytosis; iron deficiency; child.

Idiomas
Hematology, Transfusion and Cell Therapy
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