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Summary and ConclusionPre-term delivery is probably the most challenging problem in modern obstetrics and remains a leading cause of neonatal mortality and morbidity. The clinical diagnosis of PTL that precedes preterm delivery is inaccurate, and almost half of the patients with pre-term uterine contractions and intact fetal membranes delivered at term (Dizon and Townson: 2001).Increasing Pathophysiologic evidence is emerging that links lower and upper genital tract infection with early spontaneous preterm delivery. Patients who develop warning signs of PTL have reached a critical stage because progression of the symptoms will lead to establishment of PTL and decreased opportunity for effective treatment. Although treatment of lower genital tract infection (ie, BV) has been shown to reduce the occurrence of spontaneous preterm delivery in some high risk populations, it is unclear whether such infections are causal or merely associated with a concurrent occult chronic upper genital tract infection (Goldenberg: 2000b).It is becoming clear that bacterial infection of the chorionic decidual interface incites an intense inflammatory response that leads to disruption of the interface and the eventual onset of PTL. Bacterial invasion of the chorionic decidual interface leads to activation of mononuclear leukocytes with the production of numerous pro inflammatory cytokines, including IL-6, G-CSF, IL-1?, IL-1?, IL-8, and TNF- ?, which promote a cascade of events that culminates in pre-mature ripening of the cervix and the onset of uterine contractions (Goldenberg: 2000 c). These inflammatory proteins represent potential markers for use in identifying patients with occult upper genital tract infections who are at risk for subsequent spontaneous preterm delivery (Patrick-et al: 2002).A number of approaches have been proposed for detection of PTL including biochemical markers, such as estradiol, mediators of inflammation and corticotropin releasing hormone as well as uterine activity monitoring and risk factor scoring systems (Hauth, 2000).Ferritin is produced primarily by the liver, spleen, bone, and placenta. However, it is also released by infiltrating leukocytes in response to acute and chronic infection. (Moroz et al: 1987). Ferritin appears to serve as an important host defense against bacterial invasion by sequestering iron, an essential nutrient for bacterial growth.Increased concentrations of ferritin during pregnancy may be part of an acute phase response, which suggested the increased risk of poor pregnancy outcome. Pathogens (fungi, bacteria and protozoa), and neoplastic cells require iron as an essential nutrient for their growth, the host defends against invasion by withholding and withdrawing iron, iron binding proteins, and production of ferritin to allow intracellular retention of iron and to make it unavailable. For release into serum, intestinal iron absorption also is decreased. Alterations of ferritin levels during infection and inflammation mirror the increased levels observed in association with other acute phase reactants (Haram et al: 1983).In addition, a placental isoform of ferritin (Placental isoferritin) has been identified and has been shown to be expressed in syncytiotrophoblast, and decidual macrophages (Maymon et al: 2000).The aim of this study is to test the value of cervical ferritin in prediction of PTL and its correlation to serum ferritin. Our study included 15 control women with term gestational age and 35 cases, complaining from symptoms and signs of PTL, and all were subjected to history, general and local examination for cervical length, direction and dilatation, the sample of mucous from external os of the cervix or posterior fornix of the vagina was taken before local examination with suction pipette for cervical ferritin, and blood samples were taken from each case to detect serum ferritin.In this study we have divided the patients into two main groups:The control group; which involve (15) pregnant women at full term with gestational age between 37-42 weeks.The study group: which involve (35) pregnant women with signs and symptoms of spontaneous PTL with gestational age between 24-36 weeks.The study group is subdivided into three subgroups:Subgroup (a): involve (16) pregnant women with gestational age £ 29 weeks.Subgroup (b): involve (10) pregnant women with gestational age between 30-33 weeks.Subgroup (c): involve (9) pregnant women with gestational age between 34-36 weeks.Ferritin (serum and cervical) was estimated by Enzyme linked immuno-Sorbent Assay [ELISA] method.The results were statistically analyzed and show that serum & cervical ferritin concentrations are statistically higher in all cases of spontaneous PTL than control term group; and high within all subgroups with no statistical difference between them but with high levels in women with gestational age ? 29 weeks within subgroup (a). And when we made correlation between cervical and serum ferritin we found that they were significant in PTL cases than term ones.So ferritin either cervical or serum may be a useful addition to the current available parameters of antenatal care as a good marker of PTL especially for women at risk of PTL.Conclusion:Elevated cervical and serum ferritin levels are strongly associated with early PTD.Because large percentages of early PTDs are associated with occult upper genital tract infection, ferritin may be an important marker of this process as an acute phase reactant.Recommendation:Ferritin measurement whether in cervical fluid or serum is an easy and economic method that can be used as routine investigation in antenatal care clinics, to detect pregnant women whom will be at risk of PTL, but after the pregnant woman full fill the exclusion criteria that we have mention them before in this study, and that to make sure that ferritin is used as an acute phase reactant of subclinical genital tract infections that thought to be the leading cause of spontaneous PTL.
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