anemia is one of important manifestation esp in pregnant SLE female

1. Marwa Abo Elmaaty Besar
Lecturer of Internal Medicine
(Rheumatology Immunology Unit)
(Pediatric Rheumatology)
Management of Anemia in pregnant SLE
patient

3. ANEMIA IN SLE:
Anaemia is the most common haematology
complication among SLE, 59% of SLE.
Anaemia raise morbidity and mortality of SLE:
•Renal failure, serositis, seizure, and several
complication.
•Affect foetal development.
•IDA lead to mental growth retardation in children.
•IDA increase risk of preterm birth.

4. Etiology
:

5. Most common types:
•Iron deficiency anemia (IDA).
•Autoimmune hemolytic anemia (AHA).
•Chronic inflammatory anemia (ACD).
Age: 25-34 years.

6. IRON DEFICIENCY ANEMIA (IDA):
Rise of blood volume during pregnancy, 40-45%.
Angiogenesis of enlarging uterus.
Need of fetal and maternal if venous return disturbance was
occurred
Bleeding was happened during parturition.
Other cause; chronic GIT loss due to long term steroid use.

7. AUTOIMMUNE HEMOLYTIC ANEMIA:
Usually with lupus activity.
Low complement, high titre of anti-dsDNA
antibodies.
IgG and IgM ACL are present frequently in AHA
patients.

8. CHRONIC INFLAMMATORY ANAEMIA
(ACD)
Caused by long term cytokine production; IL1, IL6, (TNF-α),
(IFN-γ).
•Reduction RBCs age.
•Disturbance in erythroid progenitor cell proliferation.
•Rising cellular iron uptake and retention.
•Increase cytokines lead to raise hepcidin, lead decrease
intestinal iron absorption.
•IL1; activate macrophage lead to increase iron uptake
and iron reserve.
•IL6 negatively in iron reserve release to the blood.
ACD is higher among SLE with higher disease activity.
Usually mild 9-11g/dl, more sever in those with autoimmune

10. PURE RED CELL APLASIA:
PRCA is characterized by anaemia, reticulocytopenia, and
erythroblastopenia in the bone marrow.
Types: Congenital or acquired.
Acquired causes of PRCA
o Infections (especially human parvovirus B19)
o Haematological malignancies such as chronic
lymphocytic leukaemia (CLL).
o Chronic haemolytic anaemia.
o Autoimmune diseases.
o Various drugs and chemicals.

11. Pathogenesis: humoral antibody or natural killer (NK) or T cell-
mediated damage to precursors
oHumoral immunity-mediated damage includes
 Complement-mediated lysis,
 Formation of antibody-epo complex,
 EPO receptor blocking antibody,
 Increased production of autoantibodies due to t-cell
dysfunction,
 Blockade of burst-forming units-erythroid (BFU-E)
differentiation.
oNK/T cell-mediated damage includes cytolysis against bone
marrow normoblasts

13. INVESTIGATION:
Ferritin not useful investigation; it increase with SLE
with inflammation.
Reticulocyte index is major step in detect cause of
anemia.
RET-He or Reticulocyte Hemoglobin Equivalent is a
parameter calculating HB in reticulocyte.
 Normal value is 27.2. sufficient for erythropoiesis.
 Lowest level 45-54 years old.
 IDA, RET-He level is decreased.

14. Direct Coomb’s test: positive Coomb s test indicate
AIHA.
Blood film: schistocyte in microangiopathies (TTP).
Serum lactate dehydrogenase, liver function tests,
Immunoglobulins and serum protein electrophoresis
have to be measured in AIHA

15. MANAGEMENT:
ACD
Asymptomatic ACD; don’t require specific treatment.
Symptomatic ACD;
• No indication of steroid or immunosuppression; an
erythropoiesis-promoting agents; epoetin-alfa, darbepoetin
alfa.
• Steroid at high dose; 1 mg/kg/day, with gradual tapering if
response.
• Immunosuppression to maintain remission.
Response rising hemoglobin level >11g/dl in one month after initiating
treatment.
The Open Rheumatology Journal, 2013, 7,
87-95

16. AIHA
Steroid; 1 mg/kg/day.
If no response; pulse steroid (1gm/daily for 3 days).
Azathioprine 2 mg/kg/day.
Cyclophosphamide up to 2 mg/kg.
Splenectomy 60% success.
IVIG, Danazol, Rituximab, Mycophenolate mofetil are other
option for refractory AIHA.
Response assed by haematocrit rise, Reticulocyte
count decrease
The Open Rheumatology Journal, 2013, 7,

17. Article in Indian pediatrics ·

18. Expert Rev. Clin. Immunol. 8(5),
(2012)
MICROANGIOPATHIES IN
PREGNANCY

20. HELLP syndrome; immediate delivery.
Acute fatty liver of pregnancy: delivery as soon as possible,
patient stabilization by fresh frozen plasma, other blood clots,
correction of hypoglycemia and electrolyte abnormalities.
TTP: plasma exchange or plasmapheresis, high dose steroid,
IVIG, aggressive immunosuppression.
CAPS: anticoagulant, prompt delivery.
Expert Rev. Clin. Immunol. 8(5),
(2012)

21. PURE RED CELL APLASIA (PRCA)
Corticosteroid in high dose, first drug used..
Cyclophosphamide and cyclosporine highly effective,
30% -62%.
Azathioprine can be used.
The Open Rheumatology Journal, 2013, 7,
87-95

24. prognosi
s