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

Year 2019, Volume: 19 Issue: 2, 375 - 380, 28.06.2019

Senem Maral

https://doi.org/10.17098/amj.570912

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

References

• Kasper CK, Whissell YE, Wallerstein RO. Clinical aspects of iron deficiency. JAMA 1965;191:359–63.
• Schloesser LL, Kipp MA, Wenzel FJ. Thrombocytosis in iron deficiency anemia. J Lab Clin Med 1965;66:107–14.
• Griesshammer M, Bangerter M, Sauer T, Wennauer R, Bergmann L, Heimpel H. Aetiology and clinical significance of thrombocytosis: Analysis of 732 patients with an elevated thrombocyte count. J Intern Med 1999;245:295–300.
• Kadikoylu G, Yavasoglu I, Bolaman Z, Senturk T. Thrombocyte parameters in women with iron deficiency anemia. J Natl Med Assoc 2006;98:398–402.
• Dan K. Thrombocytosis in iron deficiency anemia. Intern Med 2005;44:1025–26.
• Aydogan T, Kanbay M, Alici O, Kosar A. Incidence and etiology of thrombocytosis in an adult Turkish population. Thrombocytes 2006;17:328–31.
• 7. McLean E, Cogswell M, Egli I, Wojdyla D, de Benoist B. Worldwide prevalence of anaemia, WHO vitamin and mineral nutrition information system, 1993-2005. Public Health Nutr. 2009;12:444–54.
• Kassebaum NJ, Jasrasaria R, Naghavi M. A systematic analysis of global anemia burden from 1990 to 2010. Blood. 2014;123:615.
• Estadella J, Villamarín L, Feliu A, Perelló J ,Calaf J.Characterization of the population with severe iron deficiency anemia at risk of requiring intravenous iron supplementation. European Journal of Obstetrics & Gynecology and Reproductive Biology, 2018:224;41-4.
• Saydam BK, Genc RE, Sarac F, Turfan EC. Prevalence of anemia and related factors among women in Turkey. Pak J Med Sci. 2017; 33: 433–38.
• Xu X, Zhang Q, Luo J, Xing S, Li Q, Krantz SB. JAK2 (V617F): Prevalence in a large Chinese hospital population. Blood 2007; 109: 339-42.
• Tevet M, Ionescu R, Dragan C, Lupu AR. Influence of the JAK2 V617F mutationand inherited thrombophilia on the thrombotic risk among patients with myeloproliferative disorders. Maedica (Buchar) 2015; 10: 27-32.
• Tefferi A, Ho TC, Ahmann GJ Katzmann JA, Greipp PR. Plasma interleukin-6 and C-reactive protein levels in reactive versus clonal thrombocytosis. Am J Med 1994:97;374–78.
• Alexandrakis MG, Passam FH, Moschandrea IA, Christophoridou AV, Pappa CA, Coulocheri SA et al. Levels of serum cytokines and acute phase proteins in patients with essential and cancer-related thrombocytosis. Am J Clin 2003:26; 135–40.
• Yoshida S, Kohro S, Yamakage M Nakayama M, Namiki A. A case of suspected pulmonary thrombosis in a patient with reactive thrombocytemia who underwent liver subsegmentectomy. Masui.2003;52:1320-22.
• Mishra SB, Bhoyer J, Gurjar M, Muzaffar N, Verma A. Deep vein thrombosis of upper extremities due to reactive thrombocytosis in septic patients. Indian J Crit Care Med. 2014;18:540-42.
• Evstatiev R. Iron deficiency, thrombocytosis and thromboembolism. Wien Med Wochenschr. 2016;166:437-46.
• Hengeveld PJ, Hazenberg MD, Biezeveld MH, Raphael MF. Risk of thrombosis is a reactive thrombocytosis. Ned Tijdschr Geneeskd. 2018;162: 2697.