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Failed Fertilization in IVF

The IVF procedure is the only method to determine if there is a fertilization defect as a cause of the infertility problem. We are able to examine the eggs 18 hours after insemination to see if there is evidence of fertilization, that is the presence of the male and female pronucleus. The pronuclei have the chromosomes from the husband and wife. It is very frustrating to find out that a fertilization defect exists. Intra-Cytoplasmic Sperm Injection (ICSI) is a procedure we can do in the IVF lab to literally inject a sperm into the egg and has helped many patients with fertilization defects conceive. This procedure is not without risk to the egg and future embryo, so it is important to have a clear indication for it. Many clinicians question if we should do ICSI on all patients to ‘assure fertilization’ because most will not have a fertilization defect. While beyond the scope of the topic presented herein, we are learning more about the potential risks of ICSI. This will be covered elsewhere on our web site.

Failed fertilization can occur due to problems with the sperm, egg, or both. Environmental contaminants like DDE have been associated with failed fertilization (1). These chemical can be found in seminal plasma and follicular fluid. Several studies have shown that reactive oxygen species may be elevated in the seminal fluid of men with poor semen analyses. These compounds may damage sperm DNA which may lead to failed fertilization (2). Anti-oxidants like vitamin C and vitamin E may be helpful. Anti-Sperm Antibodies (ASA) are accepted causes of failed fertilization. These anti-bodies may bind the sperm head and inhibit fertilization. Men with a prior vasectomy and reversal, congenital absence of the vas deferens, testicular trauma, or mumps orchitis may have these anti-bodies. Not all laboratories do analyses for ASA> A defect in the sperm acrosome, the portion of the sperm that contains enzymes needed to penetrate the granulosa cells surrounding the egg, may also be a cause of fertilization failure. The laboratory test for the acrosome reaction is not well standardized and at present not part of the standard evaluation. The sperm has a receptor for ZP3, which is present in the zona pellucida. The zona pellucida is the shell about the egg to which the sperm binds through interaction with this receptor and this leads to the events of fertilization. If the receptor were lacking or the egg not producing the ZP3 protein, fertilization would fail. Liu and Baker (3) found that defective sperm –zona pellucida interaction was present in 64 % of men with severely abnormal sperm parameters. When a sperm enters the egg the DNA is tightly packed in chromatin. Normally this will decondense and the fertilization process can continue. Defective sperm decondensation has been reported to be a cause of fertilization failure (4).

The egg contributes to fertilization failure as well. Egg quality is very important and may be due to intrinsic unique feature of the patient or to her response to the medications used to stimulate the ovaries. A number of studies have examined several features of eggs that failed to fertilize. Abnormal chromosome numbers were seen in a high percentage of failed fertilizations. One group (5) found that 20 % had an abnormal karyotype (chromosome complement). The also found asynchronous or highly condensed chromosomes as well as pulverized chromosomes in unfertilized eggs. Thus, the chromosomes of unfertilized eggs are often abnormal. Similar data was shown by Zhivkova (6). She used FISH analysis and cytogenetic analysis and found premature sperm condensation and oocytes with high aneuploidy rates (5 % haploid abnormal, 21 % hypohaploid, 36% hyperhaploid, and 7 % diploid). These eggs had abnormal chromosome complements that did not allow further development. It is also possible that the spindle apparatus which allows the chromosomes to split appropriately may be abnormal and be a cause of failed fertilization.

From the above, it is clear that there are many reasons for failed fertilization. Some of them may not be easy to correct, even with ICSI. As we learn more about how follicles and eggs develop, we will likely help patients produce better eggs and therefore decreased the chances for failed fertilization based on eggs factors.

References:

1. Younglai EV, Foster WG, Hughes EG, Trim K, Jarrell JF. Levels of environmental contaminants in human follicular fluid, serum, and seminal plasma of couples undergoing in vitro fertilization. 2002. Arch. Environ. Contam. Toxicol. 43:121-126.

2. Saleh RA, Agarwal A, Nada EA, El-Tonsy MH, Sharma RK, Meyer A, Nelson DR, Thomas AJ. Negative effects of increased sperm DNA damage in relation to seminal oxidative stress in men with idiopathic and male infertility. 2003. Fertil. Steril. 79(3):1597-1605.

3. Liu DY, Baker HWG. Frequency of defective sperm-zona pellucida ineraction in severely teratozoospermic infertile men. 2003. Hum. Reprod. 18(4):802-807.

4. Esterhuizen AD, Franken DR, Becker PJ, Lourens JGH, Muller II, van Rooyen LH. Defective sperm decondensation: a cause for fertilization failure. 2002. Andrologia 34:1-7.

5. Benkhalifa M, Kahraman S, Caserta D, Domez E, Qumsiyeh MB. Morphological and cytogenetic analysis of intact oocytes and blocked zygotes. 2003. Prenatal Diagn. 23:397-404.

6. Zhivkova R. Ploidity and chromatin status of human oocytes after failed in vitro fertilization. 2003. Eur. J. Obstetr. Gynae. Rep. Biol. 109:185-189.

 

 

 

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