Hellp sendromu patogenezinde kompleman regulator proteini faktor h'nin rolü
Başlık çevirisi mevcut değil.
- Tez No: 354017
- Danışmanlar: DOÇ. DR. DANIŞMAN YOK
- Tez Türü: Tıpta Uzmanlık
- Konular: Kadın Hastalıkları ve Doğum, Çocuk Sağlığı ve Hastalıkları, Obstetrics and Gynecology, Child Health and Diseases
- Anahtar Kelimeler: Belirtilmemiş.
- Yıl: 2005
- Dil: Türkçe
- Üniversite: Marmara Üniversitesi
- Enstitü: Tıp Fakültesi
- Ana Bilim Dalı: İç Hastalıkları Ana Bilim Dalı
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: Belirtilmemiş.
Özet
Özet yok.
Özet (Çeviri)
The Hellp syndrome is a manifestation of pre-eclampsia that presents as a moderately severe form of thrombotic micro angiopathy occurring approximately %0.6 of all pregnancies, typically during the third trimester or at term. The pathogenesis of the Hellp syndrome remains an enigma. It has been proposed that disorders including the Hellp syndrome, thrombotic thrombocytopenic purpura (TTP) and the hemolytic uremic syndrome (HUS) may all be part of a spectrum of the same disease process. Although the pathogenesis may be similar, these are not the same diseases. The common link appears to be endothelial cell injury with subsequent vasospazm and platelet activation; then microthrombuses occur in the circulation. Shiga toxin is directly responsible for endothelial cell injury in diarrheaassociated HUS. It's proposed a complement-based theory of microangiopathy, based on deficiency or dysfunction of complement regulatory proteins in atypical HUS. Because, atypical HUS has been associated in %15-30 of cases with factor H deficiency or dysfunction, one of the complement regulatory proteins. Also all forms of HUS (diarrhea-associated, otosomal dominant, otosomal recessive, sporadic) has been associated with hypocomplementemia. The aim of the study is to describe the data provided from the patients of Hellp syndrome and to asses factor H deficiency and activation of complement system in the pathogenesis of Hellp syndrome. Twenty-two Hellp syndrome patients (mean age:27.8±6.20), 21 preeclampsia patients (mean age:27.5±6.80), age and gestation time matched 23 healthy pregnant women (mean age:26.04±4.38) and age matched 24 healthy non-pregnant women (mean age:30.2±6.63) were included in the study. The personal data, routine laboratory evaluation, serum factor Hand C3 measurments were provided. Of women with Hellp syndrome, 81.8% of the cases occurred prepartum and 18.2% postpartum. Of women with prepartum Hellp syndrome, 77.7% of cases developed at third trimester and 22.3% at term. At the time of hospital admission, 36.4% patients determined to have class 1, 59.1 % class 2 and 4.5% class 3 Hellp 57 syndrome. Thirteen percent of those patients had acute renal failure during hospitalization, no patient required dialysis in this period. The serum levels of factor H were significantly higher in the groups of pregnant women (Hellp syndrome, pre-eclampsia and healthy pregnant groups) than healthy, non-pregnant group; however no difference was encountered between the pregnant groups (p>O.05), that is thought to be unrelevant with Hellp syndrome pathogenesis. Complement activation is thought to be an etiologic factor behind the Hellp syndrome. Paradoxically we found that serum C3 levels were within the normal range in Hellp syndrome. However no difference was encountered between the pregnant groups (p>O.05), that is thought to be unrelevant with Hellp syndrome pathogenesis. There is conflicting evidence about the complement activation in the pathogenesis of preeclampsia. We found that serum levels of C3 were within the normal range in preeclampsia. However no difference was encountered between the pregnant groups (p>O.05), that is thought to be unrelevant with preeclampsia pathogenesis also. In conclusion, complement activation could not be detected in the pathogenesis of preeclampsia and Hellp syndrome. It's thought that high serum levels of C3 were due to the physiological modifications of pregnancy. Because none of the pregnant women diagnosed with Hellp syndrome had low C3 levels, the finding of C3 deficiency would argue against a diagnosis of Hellp syndrome and for a diagnosis of pregnancy induced HUS. But it must be assesed whole complement components in the group of Hellp syndrome and compared to the group of pregnancy related HUS in further studies
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