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Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
Calprotectin europaediatrics 2009
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Calprotectin europaediatrics 2009

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  • Many names=Calprotectin is a suitable descriptive name for this multipotent calcium binding protein with protective properties.'
  • Neutrophil granulocytes,Monocytes/macrophages,Epithelial cells,Keratinocytes,Pancreatic cell lines,Tracheal gland cells
    Skin (epidermis/dermis),Lung,Gut,Oral mucosa,Cervix mucosa,Body fluids
    As calprotectin is preformed and ready to be released from activated circulating leucocytes,its concentration in plasma can increase much more rapidly in response to bacteraemia and endotoxaemia than acute phase proteins(CRP) synthesised in the liver.
  • calprotectin is antiproliferative and can induce apoptosis in human and animal cells, both in normal and transformed cells.these activities can be reversed by the addition of zinc.Calprotectin can inhibit several zinc-dependent metalloproteinases,probably by sequestration of zinc
    Calprotectin is a surrogate marker of neutrophil turnover and is elevated in a number of inflammatory conditions
    Neutroplil contain a large number of calprotectin which will be released upon their activation
  • In normal pregnancy there is both a neutrophilia and a mild neutrophil activation. In preeclampsia both direct and indirect evidence supports further marked neutrophil activation. In the pathogenesis of preeclampsia peripheral blood neutrophils may play a vital role in communicating between the preeclamptic placenta and the maternal vascular endothelium and contribute to the endothelial cell dysfunction that characterizesthe maternal syndrome of preeclampsia. Preeclampsia shares many elements with the systemic inflammatory
    response syndrome. Neutrophils, key effectors of the systemic inflammatory response syndrome,
  • Peripheral blood neutrophils are already activated in normal pregnancy..in preeclampsia the neutrophil count is increased relative to pregnancy
    Preeclampsia shares many clinical and laboratory characteristics with the systemic inflammatory response syndrome
    Activation of peripheral blood neutrophils occuring in isolated IUGR In a manner similar to that seen in preeclampsia
    Hypoxia=neutrophils modulate cell adhesion molecule expression when exposed to decreased oxygen tension
    Mediators=Neutrophil activation may result from the presence of soluble mediators of inflammation,such TNFα or IL6,which have been reported in the maternal circulation of patients with preeclampsia and in the amniotic fluid of patients with IUGR
    Lendothelial=eukocyte activation may be related to endothelial stimulation resulting in overexpression of endothelial cell adhesion molecules and their subsequent shedding.
    neutrophil activation is more a consequence of local or systemic inflammatory response than a primary effector of the pathologic hfeatures of the diseases
    THE activation might take place during the uteroplacental passage
  • Calprotectin has apoptosis-inducing activities,and placental apoptosis is augmented in preeclampsia. Matrix metalloproteinases (MMPs) are zinc-dependent enzymes that have reduced activity in the invading cytotrophoblasts of preeclamptic patients, possibly contributing to the reduced trophoblast invasion and subsequent dysfunctional uteroplacental circulation in preeclampsia It has been demonstrated that calprotectin inhibits MMPs by the sequestration of zinc.Theoretically,augmented calprotectin concentrations could play a role in the pathophysiology of preeclampsia, for example,through augmented apoptosis and/or reduced trophoblast invasion
  • A failure of trophoblastic invasionof the spiral arteries which results in placental insufficiency
  • Protasi apo keimano
  • Calprotectin elevated in preeclampsia in maternal not fetal
  • The concentrations of calprotectin in both arterial and venous umbilical plasma were much lower than in maternal plasma in a study AM J OBTSTR GYN BY BRAEKKE(NORWAY)
    REASON=low degree of activated neutrophils, low content of calprotectin,or rapid calprotectin turnover in the fetuses
  • Transcript

    • 1. CORD BLOOD CALPROTECTIN CONCENTRATIONS IN FULLTERM PREGNANCIES WITH NORMAL AND RESTRICTED FETAL GROWTH Sofia Liosi 1 , Despina D. Briana 1 Dimitrios Gourgiotis 2 , , Maria Boutsikou 1 , Stavroula Baka 1 , Antonios Marmarinos , Dimitrios Hassiakos 1 , Ariadne Malamitsi-Puchner 1 . 1.Neonatal Division, 2nd Department of Obstetrics and Gynecology, Athens University Medical School, Athens, Greece 2.Research Laboratories, 2nd Department of Pediatrics, Athens University Medical School, Athens, Greece
    • 2. Calprotectin • a 36-kDa calcium and zinc binding protein • comprises two heavy chains of 14 kDa and one light chain of 8 kDa • constitutes approximately 60% of soluble cytosol proteins in human neutrophil granulocytes
    • 3. Calprotectin • a marker of neutrophil turnover • immunomodulatory and antimicrobial effects • antiproliferative effects (inducing apoptosis)
    • 4. Intrauterine growth restriction (IUGR) • Failure of the fetus to achieve his/her intrinsic growth potential • Consequence of anatomical and/or functional disorders and diseases in the feto-placental-maternal unit • Results to increased morbidity and mortality in intra- and extra-uterine life
    • 5. Neutrophil activation is present in preeclampsia and isolated intrauterine growth restriction • • • Possible mechanisms may be: hypoxia the presence of soluble mediators of inflammation endothelial stimulation
    • 6. IUGR • associated with an increased incidence of apoptosis in IUGR-affected fetal membranes
    • 7. Hypothesis • Umbilical cord blood concentrations of calprotectin in IUGR cases may differ from respective concentrations in appropriate-for-gestational-age (AGA) controls since the former present increased neutrophil activation and excessive apoptosis .
    • 8. Aim • Investigate cord blood calprotectin concentrations in IUGR, and AGA pregnancies at birth • Correlate determined concentrations with gestational age, gender and mode of delivery .
    • 9. Subjects • 160 healthy, singleton full-term pregnancies - 1 10 AGA (placental weight: 480-621 g) - 50 asymmetric IUGR ( placental weight 230 -400g) • Apgar scores: > 8 in 1 st and 5 th minute
    • 10. Gestation Related Optimal Weight (GROW) computergenerated programme www.gestation.net d 6 5 P p E x S c l M n k o G ) h g w r i B y D e a m t s u C ( b : = W
    • 11. Causes of IUGR • • • • Preeclampsia ( n=6 ) Pregnancy induced hypertension (n=5 ) Various diseases : severe type I DM ( n=5),iron deficiency anemia (n=3), hypothyroidism (n=7) Maternal smoking ( n=24 )
    • 12. Demographic data • • • • • • IUGR Gestational age (weeks) 38 .36 ±1 .27 * BW (g) 25 07 ± 264.5 * BW centile 3 .0 (0-5) Gender (male/female) 21/29 Mode of delivery (VD/ECS)** 22/28 Parity (1st /other) 31 / 19 * values are mean ± SD **VD: vaginal delivery/ ECS: elective cesarian section AGA 3 8.98 ± 1.07 * 3 310 ± 310.5* 44.5 (20-99) 66/44 77/33 76/34
    • 13. Methods • • • Blood collected from: Doubly-clamped umbilical cords (m ixed arteriovenous blood ) – reflecting fetal state Determination of plasma calprotectin concentrations by enzyme immunoassay ( Human Calprotectin ELISA, HBT Hycult Biotechnology b.v , Uden, The Netherlands) Statistical analysis (parametric tests)
    • 14. CALPROTECTIN LEVELS (ng/ml) Figure 1. Error bars of the concentrations of Calprotectin in IUGR cases and AGA controls. 320 300 280 260 240 220 0 AGA GROUP (N=110) IUGR GROUP (N=50)
    • 15. Results (1) • No statistically significant differences in cord blood calprotectin concentrations between IUGR and AGA groups .
    • 16. Results (2) • • In a combined group Cord blood calprotectin concentrations were significantly decreased in cases of caesarean section . • The effect of birthweight, customized centile, gestational age, gender and parity on calprotectin concentrations was not significant .
    • 17. Results (3) • In the IUGR group • Calprotectin was significantly elevated for every week increase in gestational age. • Calprotectin was positively correlated with birthweight.
    • 18. Conclusions (1) • Cord blood calprotectin concentrations at term are independent of intrauterine growth and probably do not reflect the increased neutrophil activation and excessive apoptosis expected in IUGR • P arity, gender and maternal age do not seem to have any impact on umbilical cord blood calprotectin concentrations
    • 19. Conclusions (2) • Calprotectin may have a limited role during fetal life, possibly due to the lower degree of neutrophil activation in the fetus. • Neutrophil activation and apoptosis seem to increase with advancing gestational age in the IUGR group, as indicated by the increasing calprotectin concentrations with progressing pregnancy
    • 20. Conclusions (3) • Excessive inflammatory response associated with vaginal delivery may account for the higher calprotectin concentrations in the latter

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