Can ACIPAYAM, Sadık KAYA, Gönül OKTAY, Gül İLHAN

VASO-OKLUSİV KRİZ ORAK HÜCRELİ ANEMİDE HEMATOLOJİK PARAMETRELERİ NASIL DEĞİŞTİRİR?

Amaç: Vazo-oklüziv kriz ve stabil durumda orak hücre anemili (OHA) çocuklarda hematolojik parametreleri karşılaştırmak. Gereç ve Yöntem: 18 yaş altında 47 hasta (24 vazo-oklüziv krizli ve 23 stabil) bu çalışmaya dahil edildi. Hasta grubu ile aynı yaş grubunda, kronik hastalığı olmayan, 24 çocuk kontrol grubu olarak seçildi. Demografik ve hematolojik parametreler kaydedildi. Tam kan sayımı otomatik analizör ile ölçüldü.Bulgular: Kriz grubunda beyaz küre sayısı(WBC), eritrosit dağılım genişliği (RDW), ortalama eritrosit hemoglobin (MCH), ortalama eritrosit hemoglobin konsantrasyonu (MCHC), trombosit (PLT), nötrofil ve monosit sayıları ortalamaları (17045 /mm3, %21,62, 28,12 pg, 34,96 gr/dl, 432 x 109/L, 10858 /mm3, 1676 /mm3 ) kontrol grubundan (7429 /mm3, %14,66, 26,49 pg, 33,65 gr/dl, 288 x 109/L, 3883 /mm3, 508 /mm3) yüksekti (p<0,05). Krizli grupta eritrosit sayısı (RBC), hemoglobin (HGB), hematokrit (HCT) ve ortalama trombosit hacmi (MPV) ortalamaları (sırasıyla: 2.98 x106/mm3, 8,35 gr/dl, %23,64, 9,46 fL) kontrol grubundan (4.75 x 106/mm3, 12,62 gr /dl, %37,49, 10,16 fL) düşüktü (p <0,05). Stabil grupta RBC, HGB, HCT ve MPV ortalamaları (sırasıyla: 3.19 x 106/mm3, 8,49 gr /dl, %24,77, 10,16 fL) kontrol grubundan (4.75 x 106/mm3, 12,62 gr/dl, %37,49, 10,16 fL) düşüktü (p<0,05). Stabil grupta WBC, RDW, nötrofil, lenfosit ve monosit sayısı ortalamaları (sırasıyla: 12924 /mm3, %21,37, 10150 /mm3, 3985 /mm3, 1240 /mm3) kontrol grubundan (7429 /mm3, %14,66, 3883 /mm3, 2691 /mm3, 508 /mm3) yüksekti (p<0,05). Sonuç: Bu çalışmada MCH, MCHC ve PLT sayımının vazooklüziv kriz için üstün bir tanısal belirteç olabileceği sonucuna varılmıştır.

Anahtar Kelimeler:

Orak hücreli anemili, vazooklüziv kriz, hematolojik parametre

How Does Vaso-occlusive Crisis Alter Hematological Parameters in Sickle Cell Anemia?

Aim: To compare hematological parameters between children with steady-state sickle cell disease (SCD) and those with vaso-occlusive crisis. Materials and methods: Forty-seven patients (under 18 years of age) , 23 in the steady state and 24 in crisis were in this study. Control group included 24 age-matched children without chronic disease. Hematological parameters were recorded. Complete blood counts were measured by automated analyzer. Results: In crisis group, white blood cells (WBC), red cell distribution width (RDW), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), platelet (PLT), neutrophil and monocytes mean values (17045 /mm3, 21.62 %, 28.12 pg, 34.96 gr/dl, 432 x 109/L, 10858 /mm3, 1676 /mm3) were higher than control (7429 /mm3, 14.66 %, 26.49 pg, 33.65 gr/dl, 288 x 109/L, 3883 /mm3, 508 /mm3), (p<0.05). Red blood cell (RBC), hemoglobin (HGB), hematocrit (HCT) and mean platelet volume (MPV) levels (2.98 x106 /mm3, 8.35 gr/dl, 23.64 %, 9.46 fL) in crisis group were lower than control (4.75 x 106/mm3, 12.62 gr /dl, 37.49 %, 10.16 fL), (p <0.05). In steady-state group, RBC, HGB, HCT and MPV levels (3.19 x 106/mm3, 8.49 gr /dl, 24.77 %, 10.16 fL) were lower than control (4.75 x 106/mm3, 12.62 gr/dl, 37.49 %, 10.16 fL) (p<0.05). In steady-state group, WBC, RDW, neutrophils, lymphocytes and monocytes values (12924 /mm3, 21.37%, 10150 /mm3, 3985 /mm3, 1240 /mm) were higher than control (7429/mm3, 14.66%, 3883 /mm3, 2691 /mm3, 508 /mm3), (p<0.05). Conclusion: MCH, MCHC and PLT counts can be superior diagnostic markers for vaso-occlusive crisis

Keywords:

Sickle cell anemia, vasoocclusive crisis, hematological parameter,

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Patel DK, Mohapatra MK, Thomas AG, Patel S, Purohit P. Procalcitonin as a biomarker of
bacterial infection in sickle cell vaso-occlusive crisis. Mediterr J Hematol Infect
Dis. 2014;6(1):e2014018.
Koren A, Wald I, Halevi R, Ben Ami M. Acute chest syndrome in children with sickle cell
anemia. Pediatr Hematol Oncol. 1990;7(1):99-107.
Ahmed SG. The role of infection in the pathogenesis of vaso-occlusive crisis in patients
with sickle cell disease. Mediterr J Hematol Infect Dis. 2011;3(1):e2011028.
Valavi E, Ansari MJ, Zandian K. How to reach rapid diagnosis in sickle cell disease? Iran J
Pediatr. 2010;20(1):69-74.
Antmen B. Orak hücre anemisi. Türk Ped Arş 2009; 44: 39-42.
Akohoue SA, Shankar S, Milne GL, Morrow J, Chen KY, Ajayi WU, Buchowski MS. Energy
expenditure, inflammation, and oxidative stress in steady-state adolescents with sickle cell anemia.
Pediatr Res. 2007;61(2):233-8.
Emmanuelchide O, Charle O, Uchenna O. Hematological parameters in association with
outcomes in sickle cell anemia patients. Indian J Med Sci. 2011;65(9):393-8.
Schimmel M, Nur E, Biemond BJ, van Mierlo GJ, Solati S, Brandjes DP, Otten HM, Schnog
JJ, Zeerleder S; Curama Study Group. Nucleosomes and neutrophil activation in sickle cell
disease painful crisis. Haematologica. 2013;98(11):1797-803.
Akinbami A, Dosunmu A, Adediran A, Oshinaike O, Adebola P, Arogundade O.
Haematological values in homozygous sickle cell disease in steady state and haemoglobin phenotypes
AA controls in Lagos, Nigeria. BMC Res Notes. 2012 1;5:396.
Walke VA, Walde MS. Haematological study in sickle cell homozygous and heterozygous
children in the age group 0-6 years. Indian J Pathol Microbiol. 2007 ;50(4):901-4.
el Sayed HL, Tawfik ZM. Red cell profile in normal and sickle cell diseased children. J Egypt
Soc Parasitol. 1994;24(1):147-54.
Mohan JS, Lip GY, Bareford D, Blann AD. Platelet P-selectin and platelet mass, volume and
component in sickle cell disease: relationship to genotype. Thromb Res. 2006;117(6):623-9.

Mustafa Kemal Üniversitesi Tıp Dergisi-Cover

ISSN: 2149-3103
Yayın Aralığı: Yılda 3 Sayı
Başlangıç: 2010
Yayıncı: Hatay Mustafa Kemal Üniversitesi Tıp Fakültesi Dekanlığı

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