الفهرس 
RECURRENT PREGNANCY LOSS
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Abstract
Recurrent pregnancy loss leaves a bad impact on patient psyche. It
is also not one of the easy tasks to be dealt with in reproductive medicine.
RPL is two to three consecutive miscarriages before 20 weeks’ gestation
(Regan et al., 2010). About 1–3% of women suffer from this medical
condition during their reproductive period (Toth et al., 2010). Until know
up to 50% of RPL cases the definite underlying cause or
pathophysiological mechanisms is still not determined (Karvela et al.,
2008).
Nowadays, obesity is a major health burden on governments and
becoming a global problem across the world (Anonymous, 2001). It is
documented that obese mothers act like a risk factor for adulthood obesity
in their new coming offspring (Parsons et al., 2001). Obesity promotes to
a poor pregnancy outcome, for example spontaneous or unexplained
intrauterine fetal death (Froen et al., 2001)
Poor outcome that affects the mother and the offspring due to pre
pregnancy maternal obesity for example diabetes, hypertension and many
thrombophlic problems. Off spring of many obese mothers are more liable
to face difficulties during birth, macrosomia, and prenatal death
(Nuthalapaty and Rouse, 2004).
Gene mutations can be turned on by any change in the home
environment and also the external environment in which human grow
(Lobo, 2008).Many hormones depend on their mechansime on Jinas Kinas,
JAK-signal transducers and activators of transcription STAT which
greatly affects fat cell function. In Obesity leptin and IL-6 increase in
obese women continually activating intracellular JAK-STA3. Leptin
works mainly on central nervous system, IL-6 works on peripheral organs
and they can switch targets. Continuous JAK-STAT3 activation by leptin
and IL-6 lead to the increased expression of the negative regulator
SOCS3. SOCS3 in then have a negative feedback on leptin and IL-6
signaling regulating it plus antagonizing insulin action which leads to
gaining more weight and insulin resistance (Wunderlich et al., 2013).
JAK2 a tyrosine kinase has main role in signal transduction in
many hematopoietic growth factor receptors. The(V617F) mutation is due
to valine-to-phenylalanine substitution at position 617this mutation
happened due to a gain-of-function mutation in the gene encoding the
Janus kinase2 (JAK2) leading to continues activation tyrosine kinase and
mutation, V617F, in the JH2 pseudo-kinase domain of JAK2 gene is
responsible for offspring loss. This mutation was found in patients
suffering from thrombocythemia. Thrombocythemia during pregnancy
leads to sudden pregnancy loss and decreased percentage in live rates
(Randone et al., 2011; El-magraby and Bedwey, 2012).
Thrmobophilia leads to thrombosis of the utero-placental
circulation due to cascading that ocurrs in haemostatic response.
Disturbance and decrease in placental perfusion may lead to recurrent
pregnancy loss (Lockwood, 2011).This case control study included 250 female patients. The study
group consists of 150 female patients with history of recurrent pregnancy
loss for two consecutive times or more, aged (20-34) and having a body
mass index of >24.9. The control group consists of 100 aged matched
women having normal body mass index and as well as having a minimum
of one live child birth and no past history of previous pregnancy loss or
uncomplicated pregnancy. All participants underwent a standard
diagnostic workup including Systemic Pedigree analysis, serum
progesterone, FSH and LH, anticardiolipin (IgM and IgG), couple
karyotypying and abdominal ultrasound scan. All women were
investigated for the mutations by using the allele-specific multiplex PCR
technique to genotype all participants in the study.
Results
Jak2v617 mutation was found in cases (9.3%) while no jak2 v617f
mutation was found among the control group, p< 0.001). Patients in case
group were obese with a mean BMI of (30.9 ±4.3) vs mean BMI control
group (22.4 ±1.1, p<0.001).History of live birth in case group (42.7%) vs
100 %in control, P< (0.001). consanguineous marriages were positive
(57.4% vs 13 %, p<0.001). Only 13 patients of the case group experienced
pregnancy loss after 12 weeks of gestation while the rest of the case group
(137) including 14 patients who were positive for jak2 v617f mutation
experienced pregnancy loss before 12 weeks of gestation (p <0.06).