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Drug trial shows promise for less invasive treatment of rare foetal blood disease

IANS logo Reported By IANS |
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New Delhi, Aug 8 (IANS) A new investigational drug, nipocalimab, has shown promising results in altering the standard treatment for Hemolytic Disease of the Fetus and Newborn (HDFN), potentially delaying or preventing anemia and reducing the need for intrauterine blood transfusions in high-risk pregnancies.

HDFN is a severe condition where the blood types of a mother and her foetus are incompatible, leading to life-threatening anemia in the baby.

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Currently, treatment typically involves multiple ultrasound-guided intrauterine blood transfusions, which carry risks like fetal death, premature rupture of membranes, and pre-term birth.


“If further studies support using nipocalimab to treat HDFN, it will make treating the foetus in these pregnancies safer and easier for pregnant moms,” said Dr. Kenneth Moise Jr. a professor at the Department of Women’s Health at Dell Medical School, University of Texas at Austin.

UNITY study tracked 13 pregnant women with a history of fetal loss or early intrauterine transfusions due to HDFN in previous pregnancies.

DNA tests indicated that their current fetuses were at high risk of HDFN.

The participants received intravenous nipocalimab between 14 and 35 weeks of gestation. Remarkably, 54 per cent of the participants had live births at or after 32 weeks without requiring a transfusion, and some did not need transfusions even after birth.

Additionally, none of the babies developed fetal hydrops, a dangerous condition associated with lower survival rates due to fluid accumulation in the foetus.

Nipocalimab works by preventing the transfer of harmful antibodies across the placenta, thereby protecting the foetus’ red blood cells.

Dr. Moise noted that nipocalimab is the only drug in development with the potential to treat a variety of alloimmune and autoantibody diseases, including fetal/neonatal alloimmune thrombocytopenia and rheumatoid arthritis, a work in progress.

–IANS

ts/rad

(This report is auto-generated from IANS news service. 'Main Media' holds no responsibility for its content.)

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