STUDY OBJECTIVE: To examine the chromosome makeup of fragmented human embryos. DESIGN: Prospective. SETTING: Assisted reproductive technology (ART) program. PATIENTS: One hundred twenty-one poor-quality embryos from 58 patients 31 to 40 years of age admitted for an ART program were examined for chromosome makeup. RESULTS: Chromosome anomalies were observed in 31.9% (29/91) of poor-quality embryos, 19.8% (18/91) displayed mosaicism (diploid/haploid, diploid/triploid, diploid/aneuploid), 5.5% (5/91) showed polyploidy, 2.2% (2/91) had pulverized chromosomes, 2.2% (2/91) revealed aneuploidy, 1.1% (1/91) had prematurely condensed chromosomes, and 1.1% (1/91) had structural rearrangements involving chromosome number 2. The mean age of patients showing anomalies (36.5 years) was not significantly higher than the mean for the entire group (35.5 years). CONCLUSIONS: The incidence of chromosome anomalies in fragmented human embryos is high. These anomalies originate either in the gametes or through mitotic nondisjunction within the embryos. It is not advisable to replace such embryos into patients going through in vitro fertilization.
STUDY OBJECTIVE: To examine the chromosome makeup of fragmented human embryos. DESIGN: Prospective. SETTING: Assisted reproductive technology (ART) program. PATIENTS: One hundred twenty-one poor-quality embryos from 58 patients 31 to 40 years of age admitted for an ART program were examined for chromosome makeup. RESULTS:Chromosome anomalies were observed in 31.9% (29/91) of poor-quality embryos, 19.8% (18/91) displayed mosaicism (diploid/haploid, diploid/triploid, diploid/aneuploid), 5.5% (5/91) showed polyploidy, 2.2% (2/91) had pulverized chromosomes, 2.2% (2/91) revealed aneuploidy, 1.1% (1/91) had prematurely condensed chromosomes, and 1.1% (1/91) had structural rearrangements involving chromosome number 2. The mean age of patients showing anomalies (36.5 years) was not significantly higher than the mean for the entire group (35.5 years). CONCLUSIONS: The incidence of chromosome anomalies in fragmented human embryos is high. These anomalies originate either in the gametes or through mitotic nondisjunction within the embryos. It is not advisable to replace such embryos into patients going through in vitro fertilization.