Demir Eksikliği Anemisi İlişkili Trombositoz; Maskeli Myeloproliferatif Hastalık Olabilir Mi?

Abstract

Amaç: Trombositoz hematoloji bölümünde istenen konsültasyonların sık nedenleri arasındadır. Trombositoz etyolojisi primer ve sekonder olarak sınıflandırılır. Primer trombositoz myeloproliferatif hastalık nedeni ile klonal bir üretim sonucu iken, sekonder trombositoz altta yatan reaktif bir neden sonucunda gelişir ve neden ortadan kalktığı zaman düzelir. Demir eksikliği anemisi(DEA) reaktif trombositozun sık nedenidir. Bu çalışmada amaç DEA ilişkili trombositoz nedeni ile başvuran hastalarda maskelenmiş bir myeloprolif hastalığın varlığını araştırmaktır.
Materyal ve Metot: DEA ve trombositoz nedeni ile hematoloji polikliniğine başvuran 50 hasta çalışmaya dahil edilmiştir. Enfeksiyon, yakın zamanda geçirilmiş cerrahi, malignite, inflamatuvar hastalıklar, aspleni gibi diğer reaktif trombositoz nedenleri ve gebelik çalışma dışı bırakılmıştır. Tüm hastalara DEA tedavsinde oral veya intravenöz yol ile demir replasmanı uygulanmıştır. Tedavi öncesinde ve 1. ayında anemi ve trombosit düzeyleri kontrol edilmiştir. Ayrıca hastalarda myeloproliferatif hastalık araştırmasına yönelik JAK2 V617F (JAK2) mutasyonu taraması yapılmıştır.
Bulgular: Demir tedavisini takiben hemoglobin(Hb) ve ferritin düzeylerinde tedavini 1. ayında anlamlı yükselme izlenmiştir (p<0,001). İntravenöz yol ile tedavi edilenlerde daha yüksek ferritin düzeyine ulaşılmıştır. Kontrollerde hastaların trombosit sayısında belirgin düşüş görülmüştür (p<0,001). İki kadın hastada Hb ve ferritin değerlerinde yükselme olmasına rağmen, trombosit sayısında azalma izlenmemiştir. Bu iki hastada JAK mutasyon pozitifliği tespit edilerek, kronik myeloproliferatif hastalık tanısı konmuştur.
Sonuç: Klinisyenler trombositoz durumlarında reaktif nedenler arasında DEA yanısıra eşlik eden enfeksiyonlar, aspleni, malignite ve inflamatuar hastalıklar da araştırmalıdır. DEA başarı ile tedavi edilmiş olmasına rağmen sebat eden trombositoz durumlarında ise altta yatan KMPH ayırıcı tanıda düşünülmelidir.

Keywords

• Demir eksikliği anemisi (DEA),Trombositoz,JAK mutasyonu

Thrombocytosis Associated with Iron Deficiency Anemia; Is It a Masked Myeloproliferative Disorder?

Abstract

Objectives: Thrombocytosis is a frequent reason for hematological consultation. The etiology of thrombocytosis is classified as primary and secondary. While primary is result of clonal expansion due to myeloproliferative disorders (MPD), secondary thrombocytosis occurs due to a reactive state and regresses when that is resolved. Iron deficiency (IDA) is a frequent cause of reactive thrombocytosis in outpatients. The aim of this study was to investigate whether IDA and thrombocytosis mask a MPD in patients presenting with these complaints.
Materials and Methods: This prospective study included 50 patients who were admitted to our hematology clinic with thrombocytosis and IDA. Causes of reactive thrombocytosis such as infections, surgery, malignancies, inflammatory diseases, asplenia, and pregnancy were excluded. All patients received oral or intravenous(iv) iron replacement as anemia treatment. Anemia and thrombocyte(PLT) count were measured and recorded initially and at the end of first month. JAK2 V617F (JAK2) mutation was also checked due to MPD investigation.
Results: Hemoglobin (Hb) and ferritin levels increased in the first month of treatment (p<0.001). Higher ferritin levels were recorded in patients treated intravenously. A significant decrease was detected in PLT count following iron replacement (p<0.001). In 2 female patients no significant decrease was achieved in PLT count and the level persisted despite increases in Hb and ferritin level. Positive (JAK2) mutation was detected and MPD was diagnosed in these 2 patients.
Conclusion: Clinicians should investigate patients presenting with IDA and thrombocytosis in terms of reactive causes such as infections, asplenia, malignancies, and inflammatory diseases. Furthermore, MPA should be kept in mind as well as other reactive causes if thrombocytosis persists despite successful IDA treatment.

Keywords

• Iron deficiency anemia(IDA),Thrombocytosis,JAK2 mutation

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