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MULTIPLE SCLEROSIS COMPLICATED BY FETAL EARLY ONSET GROWTH RESTRICTION – Possible effect of disease modifying drugs Dr.Muzibunnisa Begam1, Dr.Howaida.

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Presentation on theme: "MULTIPLE SCLEROSIS COMPLICATED BY FETAL EARLY ONSET GROWTH RESTRICTION – Possible effect of disease modifying drugs Dr.Muzibunnisa Begam1, Dr.Howaida."— Presentation transcript:

1 MULTIPLE SCLEROSIS COMPLICATED BY FETAL EARLY ONSET GROWTH RESTRICTION – Possible effect of disease modifying drugs Dr.Muzibunnisa Begam1, Dr.Howaida Khair1, Dr.Farsana Khan1, Dr.Sultan Salahudheen2, Dr.Sabha Shaikh1 1 Tawam Hospital, Al Ain, 2 Sh.Zayed Hospital, AbuDhabi, UAE. Background: Multiple sclerosis (MS) is an autoimmune disease of the central nervous system that commonly presents in childbearing population. The disease severity and rate of progression is highly variable. Patients with relapsing–remitting disease are generally commenced on disease modifying drugs (DMDs) early to reduce the frequency of relapse and to slow disease progression. Interferon- β (IFN-β) and glatiramer acetate are currently considered as first-line therapies. The evidence towards the adverse effects of DMDs on pregnancy has been conflicting and IFN-β exposure has been associated with preterm birth and lower mean birth weight(1). Case: Our patient was a G2P1, with MS diagnosed 5 years ago. Her MS symptoms began with unilateral optic neuritis and became progressive 2 years later with epilepsy and left sided hemiplegic complications. She was initiated on IFN-β, conceived spontaneously and stopped the medication at 3 months of pregnancy. She was continued on Levetiracetam to control her epilepsy. Her disease course was stable during pregnancy. However, her pregnancy was complicated with severe early onset growth restriction (IUGR) at 22 weeks of gestation. Workup for IUGR including detailed anatomic survey, karyotyping by amniocentesis, TORCH screen were normal. Findings of echogenic bowel, high resistance with early diastolic notching in the uterine artery, absent end diastolic flow in the umbilical artery and oligohydramnios suggested placental insufficiency. At 30 wks of gestation, she needed to be delivered by emergency C-section due to severe pre-eclampsia (PET) and HELLP syndrome. She recovered well uneventfully. Baby was admitted to Neonatal unit. Early trophoblast invasion is important for the placental function and the maintenance of fetal growth (Figure)(2). In our patient, continuation of DMDs well into the time of full placental development might have contributed to the IUGR. Conclusion: In summary, we have reported a rare association of severe IUGR complicated by HELLP in woman with MS requiring DMDs. It is difficult to prove if MS or DMDs caused the pregnancy complications as it an isolated report. However, it is advisable that women who continue their DMDs into their pregnancies should be followed for development of fetal and maternal complications during the pregnancy. Reference: 1) Ellen Lu, Bing Wei Wang, Colleen Guimond, Anne Synnes et al. Safety of disease-modifying drugs for multiple sclerosis in pregnancy: current challenges and future considerations for effective pharmacovigilance. Expert Rev. Neurother. 13(3), 251–261 (2013). 2) Peter Parham & Ashley Moffett. Variable NK cell receptors and their MHC class I ligands in immunity, reproduction and human evolution Nature Reviews Immunology 13,


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