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En solo 50 años la enfermedad hemolítica perinatal por isoinmunización anti D pasó de ser una enfermedad sin etiología conocida, incurable y no prevenible, a la situación actual en que por las técnicas de prevención, diagnóstico oportuno y tratamiento especializado tiene baja incidencia y altas expectativas de sobrevida, incluso en los casos más severos. Se describe la historia, las técnicas de prevención, diagnóstico, manejo y tratamiento de la enfermedad.

In just 50 years the perinatal hemolytic disease due to RhD isoimmunization went from being a disease without known etiology, untreatable and not preventable to the current situation in which the prevention techniques, opportune diagnosis and specialized treatment has low its incidence and has an expected high survival even in the more severe cases. This article describes the history, prevention techniques, diagnosis, management and treatment of the disease.

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El objetivo de este trabajo fue determinar la presencia del gen RHD en células fetales obtenidas de líquido amniótico por PCR. Se estudiaron 65 muestras de líquido amniótico, 11 de madres RhD negativas sensibilizadas con anti-D. Se confirmó el origen fetal del ADN analizando un locus VNTR y 3 loci STR en las muestras de ADN de líquido amniótico y sangre materna. En las muestras no contaminadas (n = 62) se realizó la genotipificación RHD utilizando una estrategia de PCR multiplex que permite la obtención de tres productos de amplificación en los fenotipos RhD positivos y sólo un fragmento de ADN en los fenotipos RhD negativos. Se genotipificaron 54 fetos RhD positivos (8 de madres RhD negativas sensibilizadas) y 8 fetos RhD negativos (3 de madres RhD negativas sensibilizadas). La genotipificación del ADN fetal permite diagnosticar con una única amniocentesis fetos en riesgo real de enfermedad hemolítica fetoneonatal y evitar la utilización de métodos invasivos en casos de fetos RhD negativos. (AU)

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OBJECTIVE: To review the management strategies and outcome in gravidas with anti-M isoimmunization over the past 26 years at The Ohio State University. METHODS: Data collected from 115 pregnancies found to have anti-M antibody at The Ohio State University from September 1969 through February 1996 were reviewed retrospectively. We analyzed indirect antiglobulin tests, amniotic fluid with spectrophotometric examination, direct antiglobulin tests, M antigen status, antepartum course, and perinatal outcome. RESULTS: Anti-M antibody was found in 90 women who had 115 pregnancies over 26 years. Among those with positive indirect antiglobulin tests, 104 pregnancies had titers at or below 1:4. Only one patient with an initial low titer experienced more than a three-fold increase to 1:64. Two women underwent a total of eight amniocenteses when titers were at or above 1:128. Forty-two (60%) of the 70 infants tested were positive for M antigen. Nine infants required phototherapy. Eight of these infants were delivered preterm. There was an increase in the number of women seen with anti-M antibody in pregnancy at our institution, with nearly 10% of all gravidas with a positive antibody screen having anti-M alloantibodies. There were no cases of hemolytic disease of the newborn, mild or severe. CONCLUSION: The prevalence of anti-M isoimmunization may be increasing. The incidence of severe hemolytic disease of the newborn due to anti-M is extremely low. We found no cases in our review of 115 pregnancies, although there have been several cases of severe hemolytic disease of the newborn reported. If anti-M is detected in pregnancy, the titer is low (no more than 1:4), and there is no history of prior pregnancy complications suggesting a hemolytic disease process, we recommend no further testing other than an indirect antiglobulin test at 28 weeks to look for the emergence of other alloantibodies. However, if the initial titer is elevated or there is a concerning obstetric history, serial titers should be performed and amniocenteses reserved for rising titers.

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A retrospective analysis was made of Rh-sensitized patients delivered of their babies at Duke University Medical Center during a 24 year period. Records of 202 obstetric patients representing 280 sensitized pregnancies from a pool of 39,910 deliveries were analyzed for past obstetric history, blood group information, antibody determinations, amniocentesis data, and details of the pregnancy and delivery. The medical records of the corresponding infants were analyzed for their neonatal course. A severity index (SI) was devised to classify the degree of severity of the erythroblastosis fetalis. A significant correlation between SI and the delta OD450 of amniotic fluid, umbilical cord hematocrit, and bilirubin was noted. The evaluation of amniotic fluid delta OD450 is considered to be the cornerstone of clinical management. Twenty-nine patients had initial Liley zone 1 determinations which decreased to delta OD450 = 0.000; however, only 10 of 29 (34.5%) of the infants were unaffected, and 13 of 29 (44.8%) had mild sensitization, four of 29 (13.8%) had moderate sensitization, and two of 29 (6.9%) had severe sensitization. The previously held concept of "critical titer" as a guide for initiating amniocentesis is challenged, and the recommendation is made that amniocentesis for amniotic fluid determination should be undertaken in any patient with a positive indirect Coombs titer.

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A new cord blood factor has been suggested as a measure of the severity of haemolytic disease of the newborn at birth. One hundred and seventy three cases of Rhesus iso-immunisation have been classified as mild, moderate and severe according to the readings of Optical Density Difference of bilirubin in the liquor amnii and correlated with the cord blood haemoglobin, cord blood serum bilirubin, and the new cord blood factor. The new cord blood factor gave the best correlation.

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