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Autoimmune diseases in pregnancy
Abdullah Al-Harthy
• For years, women with potentially serious
systemic autoimmune diseases have been
advised not to get pregnant.
• We now know that, with careful medical and
obstetric management, most of these women
can have successful pregnancies.
Autoimmune disease
•inappropriate immune response of the body
against substances and tissues normally
present in the body
•In other words, the immune system
mistakes some part of the body as a pathogen
and attacks its own cells
•The treatment of autoimmune diseases is
typically with immunosuppression medication
which decreases the immune response.
Objectives:
• Why Rheumatic Diseases Important in
Pregnancy ?
• effect of rheumatic diseases in the mother on
fertility
• discuss the maternal and fetal effects of
pregnancy
Risk of Transmission From Mother to Fetus
Fetal Outcome
 USE OF RHEUMATIC DRUGS DURING PREGNANCY AND
LACTATION
 DVT vs. Back pain
Why Rheumatic Diseases
Important in Pregnancy ?
Rheumatic diseases often affect women
during their childbearing years, when
pregnancy is an expected event.
Careful medical and obstetric prepared to
handle the possible complications.
Effect on Fetal Outcome .
Effect of rheumatic diseases in the mother
on fertility
• SLE, RA, the vasculitides and the
spondyloarthropathies are not known to
directly affect fertility. Although SLE patients
are as fertile as the general population .
• There is a reported reduced fertility rate in
patients with active disease who are treated
with high dose corticosteroid therapy, as
menstrual irregularities and anovulatory
cycles may occur.
Effect of rheumatic diseases in the mother
on fertility
• End-stage renal failure secondary to
lupus nephritis can result in
amenorrhoea.
• Amenorrhoea in renal patients may also
be due to ovarian failure secondary to
cyclophosphamide or it may be of
autoimmune origin.
Discuss the maternal and fetal effects of
pregnancy
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
 (a) Flares :  many patients used to stop all their therapy upon 
discovering that they were pregnant, which may have contributed to an 
increased risk of flare in pregnancy.
 (b) Hypertension : 25% of pregnancies in women with SLE are 
complicated by hypertensive disorders and there is also a higher rate of 
caesarean sections
 (c) Renal Lupus : kidney is one of the major target organs and up 
to 60% of patients experience focal or diffuse renal involvement 
Proteinuria without the presence of red cells or casts in the urine can be 
difficult to distinguish from pre-eclampsia.                    features: 
proteinuria greater than 500 mg/24 h, haematuria, red cell casts and 
hypertension. 
(d) Pre-eclampsia : pre-eclampsia and lupus nephritis
may co-exist in pregnancy, it is essential to differentiate
isolated pre-eclampsia from renal lupus during pregnancy, as
management will be very different depending on the
diagnosis.
 Pre-eclampsia can be defined as blood pressure over 140/90
or the rise of 30 mmHg systolic or 15 mmHg diastolic in
combination with proteinuria (>300 mg/24 h) and oedema at
greater than 20 weeks gestation
 proteinuria is more likely to be due to pre-eclampsia than
lupus nephritis. Lupus nephritis is more likely if there is a
positive urinary sediment
antiphospholipids Syndrome (APLS)
in SLE patient presented with CLOT
coangulation defect
livedo reticularis
obstetric complication - recurrent miscarriage & IUGR
thrombocytopenia
Discuss the maternal and fetal effects of
pregnancy
Anti-phospholipid Syndrome
 (a) Thrombosis : All women are in a prothrombotic state during 
pregnancy and for 6 weeks postpartum and so are at increased 
risk of deep vein thrombosis, pulmonary emboli and stroke , A 
higher pregnancy success rate has been shown in women with 
APS and recurrent miscarriages taking low dose aspirin in 
pregnancy
 (b) Pre-eclampsia : Pre-eclampsia is most common in 
pregnancies where the mother has APS. In patients with APS, it 
often recurs and may present as very early onset pre-eclampsia 
(<20 weeks)
  Patients with APS also have an increased incidence and severity 
of the HELLP syndrome than the general population, 
 with or 
without pre-eclampsia or eclampsia. 
• (c) Thombocytopenia :It should be noted that
thrombocytopenia may occur for a variety of reasons in
pregnancy. Although APS, lupus or HELLP are the best known
associations in patients with rheumatic diseases, it should not
be forgotten that approximately 9% of healthy women
develop mild thrombocytopenia for non-autoimmune
reasons.
• Isolated anti-platelet antibodies can cause an idiopathic
thrombocytopenia. Thrombocytopenia associated with APS
may worsen in pregnancy or due to treatment with heparin.
Discuss the maternal and fetal effects of
pregnancy
• Rheumatoid Arthritis
• RA has been known to improve during pregnancy for many years. 
Several studies have shown significant improvement in 75–95% of 
pregnant women with RA. The improvement By Blood plasma 
Expansion .
• Or If It Get worst mainly by patient when she stoped her 
medications 
DVT vs. Back pain
Wells score or criteria 
• Wells score or criteria: (possible score −2 to 9)
• Active cancer (treatment within last 6 months or palliative): +1
point
• Calf swelling ≥ 3 cm compared to asymptomatic calf (measured
10 cm below tibial tuberosity): +1 point
• Swollen unilateral superficial veins (non-varicose, in
symptomatic leg): +1 point
• Unilateral pitting edema (in symptomatic leg): +1 point
• Previous documented DVT: +1 point
• Swelling of entire leg: +1 point
• Localized tenderness along the deep venous system: +1 point
• Paralysis, paresis, or recent cast immobilization of lower
extremities: +1 point
• Recently bedridden ≥ 3 days, or major surgery requiring regional
or general anesthetic in the past 12 weeks: +1 point
• Alternative diagnosis at least as likely: −2 points
• Those with Wells scores of two or more
have a 28% chance of having DVT, those
with a lower score have 6% odds.
Alternatively, Wells scores can be
categorized as high if greater than two,
moderate if one or two, and low if less
than one, with likelihoods of 53%, 17%,
and 5% respectively
Causes of Back Pain in Pregnant
• Pregnancy back pain typically happens where the pelvis meets
the spine, at the sacroiliac joint.
• Weight gain . During a healthy pregnancy, women typically gain
between 25 and 35 pounds. The spine has to support that
weight. That can cause lower back pain. The weight of the
growing baby and uterus also puts pressure on the blood
vessels and nerves in the pelvis and back.
• Posture changes. Pregnancy shifts The center of gravity.
• Hormone changes. During pregnancy, your body makes a
hormone called relaxin that allows ligaments in the pelvic area
to relax and the joints to become looser in preparation for the
birth process. The same hormone can cause ligaments that
support the spine to loosen, leading to instability and pain.
• Muscle separation.
• Stress
• sciatica is used to describe a symptom rather
than a specific disease. Some use it to mean
any pain starting in the lower back and going
down the leg.
• Spinal disc herniation
• Spinal stenosis
• Pregnancy
sciatica
Risk of Transmission From Mother to
Fetus
SLE and Sjögren's syndrome are the most widely
recognized rheumatic diseases in which
pathogenic antibodies can pass from mother to
infant through the transmission of anti-Ro
and/or anti-La across the placenta during
pregnancy
 The prevalence of these auto-antibodies in SLE patient is about
35% but transmission of IgG antibodies across the placenta
between weeks 16 and 32 gestation occurs in about 5% of
mothers.
 Neonatal transmission usually resolves within the first 6 months
of life, as maternal antibodies are destroyed in the infant.
The most severe complication of neonatal lupus
syndrome is congenital heart block (CHB).
Complete CHB is diagnosed when fetal bradycardia is
identified usually between 18 and 28 weeks.
 It is important to closely monitor these pregnancies
by serial Doppler echocardiography.
 Measurement of AV time intervals is a suggested
surveillance instrument, as incomplete block may
progress in utero or post-delivery and carries a 20%
mortality rate. Permanent pacemakers are required
by 67% of survivors with complete CHB.
Dexamethasone or betamethasone may be given to
try and reverse heart block, as it is able to cross the
placenta unlike prednisolone
Fetal Outcome
• Fetal Loss : The risk is increased in women who have previously
experienced fetal loss, active renal disease at conception, maternal hypertension
and the presence of anti-phospholipid antibodies.
• Recurrent fetal loss is also one of the criteria when diagnosing APS and the
presence of both lupus anticoagulant and anticardiolipin antibodies is associated
with the highest risk of fetal loss.
• Intrauterine Growth Restriction : In SLE patients,
hypertension, active lupus and APS are significant predictive factors for
IUGR.
• Fetal loss in early pregnancy in APS can be due to failure of the placenta to
implant, due to the effect of anti-phospholipid antibodies on anionic
phospholipids and the effect of B2-glycoprotein on trophoblasts. Thrombosis
in APS is also thought to have a role in pregnancy loss due to uteroplacental
insufficiency from multiple placental thromboses and infarcts
• Premature Delivery : is common in patients with lupus,
vasculitis, systemic sclerosis and especially antiphospholipid syndrome .
• There are several complications of prematurity, regardless of underlying
cause, such as breathing difficulties, infection, jaundice, feeding
difficulties, developmental abnormalities and neonatal death.
• Breathing difficulties are usually due to insufficient surfactant, which can
be reduced by a 48-h course of dexamethsone or betamethasone in cases
where there is a high chance of premature delivery, such as active
maternal disease or fetal distress.
USE OF RHEUMATIC DRUGS DURING
PREGNANCY AND LACTATION
  Pregnancy Lactation
NSAID Yes
(avoid after 32 weeks(
Yes
Sulfasalazine Yes Yes
Antimalarials Yes Yes
Corticosteroids Yes Yes
Cyclosporin Yes probably yes
Azathioprine Yes probably yes
Mycophenolate No No
Methotrexate No No
Cyclophosphamide No No
Anti-tumor necrosis
factor (TNF(
No No
Rituximab No No
Warfarin No
(with caution, only after
first trimester(
Yes
Heparin Yes Yes
POINTS TO REMEMBER
All women should undergo counseling before
conception for their specific risk, depending on their
condition and the medications they are taking.
Each woman’s rheumatic disease should be well
under control for a period of at least 3-6 months
before attempting pregnancy.
Women with a low-risk profile can be managed with
usual visits to the rheumatologist as a precaution.
Those with a high-risk profile should be managed by
both the rheumatologist and obstetric team with
experience in high-risk pregnancies.
Summary
• Pregnancies in women with rheumatic diseases require a
multi-disciplinary, carefully monitored, coordinated approach
before, during and after pregnancy to ensure the best
possible success for mother and baby.
• In contrast to SLE, APS, vasculitis and systemic sclerosis there
is little evidence for poor maternal or fetal outcomes in RA or
other forms of inflammatory arthritis such as psoriasis and
seronegative spondyloarthropathies.
• Prior to pregnancy it is important to counsel the mother
concerning potential complications, establish disease activity
control, screen for hypertension and renal involvement,
exclude pulmonary hypertension and make appropriate
changes to the woman's therapy.
During pregnancy it is essential to monitor all
aspects of disease activity such as renal
involvement, as well as pregnancy complications
such as IUGR, thrombo-embolic disease and pre-
eclampsia, particularly in patients with SLE, APS,
vasculitis and systemic sclerosis.
After pregnancy it is essential to counsel the
mother on postpartum issues such as breast-
feeding and contraception, as well as to monitor
for and treat any postpartum flares as these are
common in all the rheumatic diseases.
References
• American college of rheumatology
• http://arthritis-research.com
• Medscape
• Current Diagnosis & Treatment in
Rheumatology, Third Edition
autoimmune diseases in pregnancy

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autoimmune diseases in pregnancy

  • 1. Autoimmune diseases in pregnancy Abdullah Al-Harthy
  • 2. • For years, women with potentially serious systemic autoimmune diseases have been advised not to get pregnant. • We now know that, with careful medical and obstetric management, most of these women can have successful pregnancies.
  • 3. Autoimmune disease •inappropriate immune response of the body against substances and tissues normally present in the body •In other words, the immune system mistakes some part of the body as a pathogen and attacks its own cells •The treatment of autoimmune diseases is typically with immunosuppression medication which decreases the immune response.
  • 4.
  • 5. Objectives: • Why Rheumatic Diseases Important in Pregnancy ? • effect of rheumatic diseases in the mother on fertility • discuss the maternal and fetal effects of pregnancy
  • 6. Risk of Transmission From Mother to Fetus Fetal Outcome  USE OF RHEUMATIC DRUGS DURING PREGNANCY AND LACTATION  DVT vs. Back pain
  • 7. Why Rheumatic Diseases Important in Pregnancy ? Rheumatic diseases often affect women during their childbearing years, when pregnancy is an expected event. Careful medical and obstetric prepared to handle the possible complications. Effect on Fetal Outcome .
  • 8. Effect of rheumatic diseases in the mother on fertility • SLE, RA, the vasculitides and the spondyloarthropathies are not known to directly affect fertility. Although SLE patients are as fertile as the general population . • There is a reported reduced fertility rate in patients with active disease who are treated with high dose corticosteroid therapy, as menstrual irregularities and anovulatory cycles may occur.
  • 9. Effect of rheumatic diseases in the mother on fertility • End-stage renal failure secondary to lupus nephritis can result in amenorrhoea. • Amenorrhoea in renal patients may also be due to ovarian failure secondary to cyclophosphamide or it may be of autoimmune origin.
  • 10.
  • 11. Discuss the maternal and fetal effects of pregnancy SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)  (a) Flares :  many patients used to stop all their therapy upon  discovering that they were pregnant, which may have contributed to an  increased risk of flare in pregnancy.  (b) Hypertension : 25% of pregnancies in women with SLE are  complicated by hypertensive disorders and there is also a higher rate of  caesarean sections  (c) Renal Lupus : kidney is one of the major target organs and up  to 60% of patients experience focal or diffuse renal involvement  Proteinuria without the presence of red cells or casts in the urine can be  difficult to distinguish from pre-eclampsia.                    features:  proteinuria greater than 500 mg/24 h, haematuria, red cell casts and  hypertension. 
  • 12. (d) Pre-eclampsia : pre-eclampsia and lupus nephritis may co-exist in pregnancy, it is essential to differentiate isolated pre-eclampsia from renal lupus during pregnancy, as management will be very different depending on the diagnosis.  Pre-eclampsia can be defined as blood pressure over 140/90 or the rise of 30 mmHg systolic or 15 mmHg diastolic in combination with proteinuria (>300 mg/24 h) and oedema at greater than 20 weeks gestation  proteinuria is more likely to be due to pre-eclampsia than lupus nephritis. Lupus nephritis is more likely if there is a positive urinary sediment
  • 14. Discuss the maternal and fetal effects of pregnancy Anti-phospholipid Syndrome  (a) Thrombosis : All women are in a prothrombotic state during  pregnancy and for 6 weeks postpartum and so are at increased  risk of deep vein thrombosis, pulmonary emboli and stroke , A  higher pregnancy success rate has been shown in women with  APS and recurrent miscarriages taking low dose aspirin in  pregnancy  (b) Pre-eclampsia : Pre-eclampsia is most common in  pregnancies where the mother has APS. In patients with APS, it  often recurs and may present as very early onset pre-eclampsia  (<20 weeks)   Patients with APS also have an increased incidence and severity  of the HELLP syndrome than the general population,   with or  without pre-eclampsia or eclampsia. 
  • 15. • (c) Thombocytopenia :It should be noted that thrombocytopenia may occur for a variety of reasons in pregnancy. Although APS, lupus or HELLP are the best known associations in patients with rheumatic diseases, it should not be forgotten that approximately 9% of healthy women develop mild thrombocytopenia for non-autoimmune reasons. • Isolated anti-platelet antibodies can cause an idiopathic thrombocytopenia. Thrombocytopenia associated with APS may worsen in pregnancy or due to treatment with heparin.
  • 16.
  • 17. Discuss the maternal and fetal effects of pregnancy • Rheumatoid Arthritis • RA has been known to improve during pregnancy for many years.  Several studies have shown significant improvement in 75–95% of  pregnant women with RA. The improvement By Blood plasma  Expansion . • Or If It Get worst mainly by patient when she stoped her  medications 
  • 18. DVT vs. Back pain Wells score or criteria 
  • 19. • Wells score or criteria: (possible score −2 to 9) • Active cancer (treatment within last 6 months or palliative): +1 point • Calf swelling ≥ 3 cm compared to asymptomatic calf (measured 10 cm below tibial tuberosity): +1 point • Swollen unilateral superficial veins (non-varicose, in symptomatic leg): +1 point • Unilateral pitting edema (in symptomatic leg): +1 point • Previous documented DVT: +1 point • Swelling of entire leg: +1 point • Localized tenderness along the deep venous system: +1 point • Paralysis, paresis, or recent cast immobilization of lower extremities: +1 point • Recently bedridden ≥ 3 days, or major surgery requiring regional or general anesthetic in the past 12 weeks: +1 point • Alternative diagnosis at least as likely: −2 points
  • 20. • Those with Wells scores of two or more have a 28% chance of having DVT, those with a lower score have 6% odds. Alternatively, Wells scores can be categorized as high if greater than two, moderate if one or two, and low if less than one, with likelihoods of 53%, 17%, and 5% respectively
  • 21. Causes of Back Pain in Pregnant • Pregnancy back pain typically happens where the pelvis meets the spine, at the sacroiliac joint. • Weight gain . During a healthy pregnancy, women typically gain between 25 and 35 pounds. The spine has to support that weight. That can cause lower back pain. The weight of the growing baby and uterus also puts pressure on the blood vessels and nerves in the pelvis and back. • Posture changes. Pregnancy shifts The center of gravity. • Hormone changes. During pregnancy, your body makes a hormone called relaxin that allows ligaments in the pelvic area to relax and the joints to become looser in preparation for the birth process. The same hormone can cause ligaments that support the spine to loosen, leading to instability and pain. • Muscle separation. • Stress
  • 22. • sciatica is used to describe a symptom rather than a specific disease. Some use it to mean any pain starting in the lower back and going down the leg. • Spinal disc herniation • Spinal stenosis • Pregnancy sciatica
  • 23.
  • 24. Risk of Transmission From Mother to Fetus SLE and Sjögren's syndrome are the most widely recognized rheumatic diseases in which pathogenic antibodies can pass from mother to infant through the transmission of anti-Ro and/or anti-La across the placenta during pregnancy  The prevalence of these auto-antibodies in SLE patient is about 35% but transmission of IgG antibodies across the placenta between weeks 16 and 32 gestation occurs in about 5% of mothers.  Neonatal transmission usually resolves within the first 6 months of life, as maternal antibodies are destroyed in the infant.
  • 25. The most severe complication of neonatal lupus syndrome is congenital heart block (CHB). Complete CHB is diagnosed when fetal bradycardia is identified usually between 18 and 28 weeks.  It is important to closely monitor these pregnancies by serial Doppler echocardiography.  Measurement of AV time intervals is a suggested surveillance instrument, as incomplete block may progress in utero or post-delivery and carries a 20% mortality rate. Permanent pacemakers are required by 67% of survivors with complete CHB. Dexamethasone or betamethasone may be given to try and reverse heart block, as it is able to cross the placenta unlike prednisolone
  • 26. Fetal Outcome • Fetal Loss : The risk is increased in women who have previously experienced fetal loss, active renal disease at conception, maternal hypertension and the presence of anti-phospholipid antibodies. • Recurrent fetal loss is also one of the criteria when diagnosing APS and the presence of both lupus anticoagulant and anticardiolipin antibodies is associated with the highest risk of fetal loss. • Intrauterine Growth Restriction : In SLE patients, hypertension, active lupus and APS are significant predictive factors for IUGR. • Fetal loss in early pregnancy in APS can be due to failure of the placenta to implant, due to the effect of anti-phospholipid antibodies on anionic phospholipids and the effect of B2-glycoprotein on trophoblasts. Thrombosis in APS is also thought to have a role in pregnancy loss due to uteroplacental insufficiency from multiple placental thromboses and infarcts
  • 27. • Premature Delivery : is common in patients with lupus, vasculitis, systemic sclerosis and especially antiphospholipid syndrome . • There are several complications of prematurity, regardless of underlying cause, such as breathing difficulties, infection, jaundice, feeding difficulties, developmental abnormalities and neonatal death. • Breathing difficulties are usually due to insufficient surfactant, which can be reduced by a 48-h course of dexamethsone or betamethasone in cases where there is a high chance of premature delivery, such as active maternal disease or fetal distress.
  • 28. USE OF RHEUMATIC DRUGS DURING PREGNANCY AND LACTATION   Pregnancy Lactation NSAID Yes (avoid after 32 weeks( Yes Sulfasalazine Yes Yes Antimalarials Yes Yes Corticosteroids Yes Yes Cyclosporin Yes probably yes Azathioprine Yes probably yes Mycophenolate No No Methotrexate No No Cyclophosphamide No No Anti-tumor necrosis factor (TNF( No No Rituximab No No Warfarin No (with caution, only after first trimester( Yes Heparin Yes Yes
  • 29. POINTS TO REMEMBER All women should undergo counseling before conception for their specific risk, depending on their condition and the medications they are taking. Each woman’s rheumatic disease should be well under control for a period of at least 3-6 months before attempting pregnancy. Women with a low-risk profile can be managed with usual visits to the rheumatologist as a precaution. Those with a high-risk profile should be managed by both the rheumatologist and obstetric team with experience in high-risk pregnancies.
  • 30. Summary • Pregnancies in women with rheumatic diseases require a multi-disciplinary, carefully monitored, coordinated approach before, during and after pregnancy to ensure the best possible success for mother and baby. • In contrast to SLE, APS, vasculitis and systemic sclerosis there is little evidence for poor maternal or fetal outcomes in RA or other forms of inflammatory arthritis such as psoriasis and seronegative spondyloarthropathies. • Prior to pregnancy it is important to counsel the mother concerning potential complications, establish disease activity control, screen for hypertension and renal involvement, exclude pulmonary hypertension and make appropriate changes to the woman's therapy.
  • 31. During pregnancy it is essential to monitor all aspects of disease activity such as renal involvement, as well as pregnancy complications such as IUGR, thrombo-embolic disease and pre- eclampsia, particularly in patients with SLE, APS, vasculitis and systemic sclerosis. After pregnancy it is essential to counsel the mother on postpartum issues such as breast- feeding and contraception, as well as to monitor for and treat any postpartum flares as these are common in all the rheumatic diseases.
  • 32. References • American college of rheumatology • http://arthritis-research.com • Medscape • Current Diagnosis & Treatment in Rheumatology, Third Edition