The abstract has been presented in the Poster Session of the ASRM/CFAS Conjoint Annual Meeting 2005 at Montreal, Canada, and has been published in Fertility and Sterility 2005; 84;S217–218.
Detection of 90K/MAC-2BP in the Seminal Plasma of Infertile Males With Accessory Gland Infection and the Autoimmune Pathogenetic Hypothesis
Version of Record online: 2 JAN 2013
2006 American Society of Andrology
Journal of Andrology
Volume 27, Issue 6, pages 780–784, November-December 2006
How to Cite
Caroppo, E., Niederberger, C., Iacovazzi, P. A., Correale, M. and D'Amato, G. (2006), Detection of 90K/MAC-2BP in the Seminal Plasma of Infertile Males With Accessory Gland Infection and the Autoimmune Pathogenetic Hypothesis. Journal of Andrology, 27: 780–784. doi: 10.2164/jandrol.106.000034
This research was financially supported by the Italian Ministry of Health, Research Project 105-4-2001.
- Issue online: 2 JAN 2013
- Version of Record online: 2 JAN 2013
- Received for Publication April 2, 2006; accepted for Publication June 21, 2006
- Male infertility;
ABSTRACT: The purpose of the study was to evaluate 90K/MAC-2BP, a glycoprotein member of the Scavenger Receptor Cystein Rich superfamily, in the seminal plasma of infertile male patients with male accessory gland infection in order to investigate a putative autoimmune pathogenesis. 90K seminal concentration and sperm parameters were evaluated in 50 patients with male accessory gland infection at baseline and after cycles of treatment with Levofluoxacin 500 mg daily for 15 days plus serratiopeptidase 10 mg daily for 30 days. Treatment was continued for up to 6 cycles in cases of persistant bacteriospermia and/or clinical and ejaculatory signs of the disease. Patients with persistant male accessory gland infection after 6 cycles were defined as nonresponders. The same parameters were evaluated at baseline and after a 2-month period in 30 healthy controls. Patients with male accessory gland infection showed impaired sperm parameters and had lower seminal 90K concentration compared to controls. After treatment, seminal 90K level significantly increased in patients compared to controls. Twenty-two patients responded to treatment (44%), while 28 were nonresponders (56%). No difference in pretreatment and posttreatment sperm parameters and seminal 90K was observed between the 2 subgroups. Thirteen patients (26%) had identifiable bacteriospermia: significantly less pretreatment seminal 90K was observed compared to patients without bacteriospermia. Seminal 90K is decreased in patients with male accessory gland infection, and may be restored by a treatment with quinolones. However, the clinical utility of a 90K assay in these patients remains uncertain, as its level is not predictive of response to treatment.