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Human Reproduction Update Advance Access first published online on September 28, 2006
This version published online on October 12, 2006
Human Reproduction Update, doi:10.1093/humupd/dml047
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© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received April 24, 2006
Revised August 9, 2006
Accepted August 22, 2006

Article

Globozoospermia revisited

A.H.D.M. Dam 1, I. Feenstra 2, J.R. Westphal 1, L. Ramos 1, R.J.T. van Golde 1, and J.A.M. Kremer 1 *

1 Department of Obstetrics and Gynaecology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
2 Department of Human Genetics, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands

* To whom correspondence should be addressed.
J.A.M. Kremer, E-mail: j.kremer{at}obgyn.umcn.nl


  Abstract

Globozoospermia is a rare (incidence <0.1%) but severe disorder in male infertility. Total globozoospermia is diagnosed by the presence of 100% round-headed spermatozoa lacking an acrosome. It is still unclear whether patients whose ejaculate contains both normal and globozoospermic cells (partial globozoospermia) suffer from a variation of the same syndrome. Apart from the fact that affected males suffer from reduced fertility or even infertility, no other physical characteristics can be associated with the syndrome. ICSI is a treatment option for these patients, although low fertilization rates after ICSI show a reduced ability to activate the oocyte. In globozoospermic cells, the use of acrosome markers has demonstrated an absent or severely malformed acrosome. Chromatin compaction appears to be disturbed but is not consistently over- or undercondensed. In some cases, an increased number of cells with DNA fragmentation have been observed. The analysis of the cytogenetic composition revealed an increased aneuploidy rate in some cases. Nonetheless, no increased number of spontaneous abortions or congenital defects has been reported in pregnancies conceived after ICSI. The pathogenesis of globozoospermia most probably originates in spermiogenesis, more specifically in acrosome formation and sperm head elongation. In several knockout mouse models, a phenotype similar to that in humans was found. Together with the occurrence of affected siblings, these findings indicate a genetic origin, which makes globozoospermia a good candidate for genetic analysis. More research is needed to elucidate the pathogenesis of human globozoospermia to further understand globozoospermia as well as (abnormalities in) spermiogenesis and spermatogenesis in general.

Keywords: acrosome/genetics/globozoospermia/male infertility/round-headed sperm cells.

This is a new version of this article as an error in the referencing of an author has been corrected.


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