Ankilozan spondilitli hastalarda inflamasyon ve trombosit aktivitesi arasındaki ilişki
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Tarih
2009
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Yayıncı
Trakya Üniversitesi Tıp Fakültesi
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Çalışmamızda, aterosklerotik komplikasyonlara bağlı morbidite ve mortalitenin arttığı ankilozan spondilit gibi kronik inflamasyonla seyreden bir hastalıkta, trombosit ve endotel aktivasyonunun değerlendirilmesi amaçlandı. Trakya Üniversitesi Tıp Fakültesi, İç Hastalıkları Anabilim Dalı, Hematoloji Bilim Dalı'nda yürütülen çalışmaya, ankilozan spondilit tanısıyla izlenen 59 hasta ve kontrol grubu olarak 22 sağlıklı birey alındı. Hastaların klinik özellikleri kaydedilerek, tam kan sayımları ve akut faz parametreleri değerlendirildi. Ankilozan Spondilitli hastalar "Bath Ankylosing Spondylitis Disease Activity Index" kullanılarak aktif ve inaktif hastalık grubu olarak ikiye ayrıldı. Ayrıca 15 hastadan oluşturulan bir altgrupta ise, uygulanacak "tumour necrosis factor-?" blokeri tedavisinden önce ve tedaviden 12 hafta sonra olmak üzere, testler iki kez yapıldı. Tüm hastalarda ve kontrol olgularında, akım sitometrik çalışma ile trombositlerde CD62P ekspresyonu, trombosit-monosit kompleks ve trombosit-nötrofil kompleksleri belirlendi. ELISA yöntemiyle, plazmada E-selektin ve serumda sCD40L düzeyleri çalışıldı. Ankilozan spondilitli grubun sCD40L ve trombosit-monosit kompleks düzeyleri kontrol grubundan anlamlı olarak yüksekti (sırası ile, p=0,016 ve 0,013). sE-selektin düzeyleri ankilozan spondilitli hastalarda kontrol grubuna göre düşük olma eğilimindeydi (p=0,064). CD62P pozitif trombosit ve adenozin difosfat ile uyarı sonrası CD62P pozitif trombosit düzeyleri ankilozan spondilitli grup ve kontrol grubu arasında benzerdi (p>0,05). Endotel ve trombosit aktivasyon parametreleri açısından aktif ve inaktif hastalık grupları arasında anlamlı fark yoktu (p>0,05). Ankilozan spondilitli hastalarda "tumour necrosis factor-?" blokeriyle tedavi sonrasında endotel ve trombosit aktivasyon parametreleri açısından anlamlı değişiklik olmadı (p>0,05). Çalışmamızda, ankilozan spondilitli hastalarda trombosit-monosit ve trombosit-nötrofil kompleksleri ve sCD40L düzeylerinin kontrol grubuna göre artmış olduğunu gözlemledik. Bu sonuç, ankilozan spondilitte kronik inflamasyonla ilişkili olarak artmış olduğu söylenen endotel fonksiyon bozukluğu ve ateroskleroz eğilimine katkıda bulunuyor olabilir. Ancak hastalık aktivitesinin bu parametrelerle ilişkisini saptamadık. Ayrıca, romatoid artrit çalışmalarında trombosit ve endotel aktivasyonu parametrelerinde "tumour necrosis factor-?" blokeriyle genelde gözlenen düzelmenin ankilozan spondilitte olmadığını saptadık. Bu durum, ankilozan spondilitde artmış ateroskleroz eğiliminin romatoid artrit ile birebir aynı mekanizmalarla olmadığını düşündürmektedir.
Abstract
In our study, we evaluated parameters of endothelial and platelet activation in ankylosing spondylitis which is a chronic inflammatory disease in which morbidity and mortality secondary to atherosclerotic complications is increased. The study which was conducted by Trakya University Medical Faculty, Department of Internal Medicine, Division of Hematology included 59 ankylosing spondylitis patients and 22 healthy control subjects. The patients? clinical features were recorded, whole blood counts and acute phase parameters were evaluated. Ankylosing spondylitis patients were divided in two disease groups as active and inactive, by using "Bath Ankylosing Spondylitis Disease Activity Index". In addition, in a subgroup of 15 patients, parameters were evaluated two times as before and 12 weeks after the beginning of "tumour necrosis factor-?" blocker therapy. In all patients and control subjects, platelet P-selectin expression, platelet-monocyte complexes and platelet-neutrophil complexes were determined by flow cytometry. In addition, plasma E-selectin and serum sCD40L levels were determined by ELISA. In ankylosing spondylitis group platelet-monocyte complexes and scD40L levels were significantly higher than the control group (p=0,013 and 0,016, respectively). In ankylosing spondylitis patients, sE-selectin levels tended to be lower than the control group (p=0,064). CD62P-positive platelet levels before and after adenosine diphosphate stimulation were similar between the ankylosing spondylitis and control group (p>0,05). According to the endothelial and platelet activation parameters, there was no significant difference between active and inactive disease groups (p>0,05). In ankylosing spondylitis patients according to endothelial and platelet activation parameters, there was no significant change after "tumour necrosis factor-?" blocker therapy (p>0,05). In our study, we observed that ankylosing spondylitis patients had higher platelet-monocyte and platelet-neutrophil complexes and sCD40L levels than the control group. This result might be contributing to endothelial dysfunction and atherosclerosis which are said to be more frequent in ankylosing spondylitis patients in association with chronic inflammation. However, we didn't find any relationship between disease activity and these parameters. In addition, we observed that the improvement in endothelial and platelet activation parameters obtained with "tumour necrosis factor-?" blocker in rheumatoid arthritis did not occur in ankylosing spondylitis. This condition makes one think that the preposition for increased tendency to atherosclerosis in ankylosing spondylitis is not exactly by the same mechanisms.
Abstract
In our study, we evaluated parameters of endothelial and platelet activation in ankylosing spondylitis which is a chronic inflammatory disease in which morbidity and mortality secondary to atherosclerotic complications is increased. The study which was conducted by Trakya University Medical Faculty, Department of Internal Medicine, Division of Hematology included 59 ankylosing spondylitis patients and 22 healthy control subjects. The patients? clinical features were recorded, whole blood counts and acute phase parameters were evaluated. Ankylosing spondylitis patients were divided in two disease groups as active and inactive, by using "Bath Ankylosing Spondylitis Disease Activity Index". In addition, in a subgroup of 15 patients, parameters were evaluated two times as before and 12 weeks after the beginning of "tumour necrosis factor-?" blocker therapy. In all patients and control subjects, platelet P-selectin expression, platelet-monocyte complexes and platelet-neutrophil complexes were determined by flow cytometry. In addition, plasma E-selectin and serum sCD40L levels were determined by ELISA. In ankylosing spondylitis group platelet-monocyte complexes and scD40L levels were significantly higher than the control group (p=0,013 and 0,016, respectively). In ankylosing spondylitis patients, sE-selectin levels tended to be lower than the control group (p=0,064). CD62P-positive platelet levels before and after adenosine diphosphate stimulation were similar between the ankylosing spondylitis and control group (p>0,05). According to the endothelial and platelet activation parameters, there was no significant difference between active and inactive disease groups (p>0,05). In ankylosing spondylitis patients according to endothelial and platelet activation parameters, there was no significant change after "tumour necrosis factor-?" blocker therapy (p>0,05). In our study, we observed that ankylosing spondylitis patients had higher platelet-monocyte and platelet-neutrophil complexes and sCD40L levels than the control group. This result might be contributing to endothelial dysfunction and atherosclerosis which are said to be more frequent in ankylosing spondylitis patients in association with chronic inflammation. However, we didn't find any relationship between disease activity and these parameters. In addition, we observed that the improvement in endothelial and platelet activation parameters obtained with "tumour necrosis factor-?" blocker in rheumatoid arthritis did not occur in ankylosing spondylitis. This condition makes one think that the preposition for increased tendency to atherosclerosis in ankylosing spondylitis is not exactly by the same mechanisms.
Açıklama
Tıpta Uzmanlık Tezi
Anahtar Kelimeler
Ankilozan Spondilit, Ateroskleroz, CD40L, E-selektin, İnflamasyon, P-selektin, Trombosit-monosit Kompleksi, Trombosit-nötrofil Kompleksi, Ankylosing Spondylitis, Atherosclerosis, CD40L, E-selectin, Inflammation, P-selectin, Platelet-monocyte Complexes, Platelet-neutrophil Complexes
