American Journal of Epidemiology Advance Access originally published online on August 24, 2005
American Journal of Epidemiology 2005 162(7):705; doi:10.1093/aje/kwi267
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LETTERS TO THE EDITOR |
MACALUSO ET AL. REPLY
1 Division of Reproductive Health, Centers for Disease Control and Prevention, Atlanta, GA 30341-3724
2 Center for Epidemiology and Biostatistics, Children's Hospital Medical Center, Cincinnati, OH 45229-3039
Zaviacic and Ablin (1
) suggest that assessment of semen exposure based on pre- and postcoital measurement of prostate-specific antigen (PSA) in vaginal fluid is not valid for evaluating condom effectiveness (2, 3). We disagree for two reasons: 1) in the absence of semen exposure, the small amount of PSA produced by the female paraurethral glands would yield PSA values below the cutoff point we use to assess semen exposure; and 2) coitally dependent increases in endogenous PSA levels would also be below the threshold of detection and thus could not be misclassified as semen exposure.
Zaviacic and Ablin (1) describe a plausible mechanism by which PSA secreted by the female paraurethral glands might contaminate vaginal fluid. However, they ignore our findings that PSA levels in the eluate of self-collected vaginal swabs are well below 1 ng/ml in the absence of recent exposure to semen, increase sharply immediately after exposure to even minuscule amounts of semen, and return to below 1 ng/ml within 24–48 hours (4, 5). In the sampling and extraction protocol we used, 1 ng/ml in the eluate corresponds to 3 ng/ml in vaginal fluid (3). The urinary levels of endogenous PSA cited by Zaviacic and Ablin could not lead to a false-positive result for semen exposure in our assay system. Thus, we restate that our system yields PSA results of 
1 ng/ml in the absence of semen exposure, and substantially above 1 ng/ml after semen exposure.
Zaviacic and Ablin (1) suggest that endogenous PSA may increase in women during intercourse and may reach high levels in female ejaculate, citing a study by Cabello (line-listed data available at http://drgspot.net/cabello.htm) (6). In that study, 24 women collected urine samples before and after orgasm induced by self-manipulation; only six participants collected fluid that the author referred to as ejaculate. PSA concentrations were near zero in the 24 preorgasmic urine samples and were below 1 ng/ml in 23 of 24 postorgasmic urine samples and in four of six ejaculate samples. The average PSA concentration in the ejaculate samples was 0.82 ng/ml after exclusion of one result of 32 ng/ml, which the author regarded as abnormal (6). Considering that PSA from urine or female ejaculate would be diluted in PSA-free vaginal fluid, as well by an additional factor of three in our laboratory procedures, Cabello's data indicate that coitally dependent increases in endogenous PSA would almost invariably yield PSA values well below 1 ng/ml in our system. This conclusion is also indirectly supported by our condom effectiveness studies (3, 7), which provide substantial evidence that PSA levels are below 1 ng/ml after intercourse in the vast majority of condom-protected acts.
Having concluded that endogenous PSA is unlikely to interfere with our system for detecting semen exposure, we want to reiterate that not all PSA increases detected by our system should be interpreted as condom failures. Our methods enable us to select alternative thresholds for pre- and postcoital PSA levels, which we have used in our analyses to define a lower and upper boundary for the semen exposure rate (2, 3). We have discussed the uncertain biologic significance of small increases in PSA levels, which may reflect sampling error or exposure to small amounts of semen that may not entail increased risk of pregnancy or sexually transmitted diseases (2, 3, 7, 8).
Overall, our research findings support two other statements we have made in previous reports (7, 8): 1) most instances of condom use completely protect women from exposure to semen, and 2) condom failure results in a distribution of semen exposure levels, most of which are low and may not entail significant pregnancy or disease risk. Therefore, we maintain that the methods we have developed provide a scientifically valid framework for the objective assessment of condom effectiveness.
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ACKNOWLEDGMENTS |
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Conflict of interest: none declared.
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References |
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 TOP References |
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- Zaviacic M, Ablin RJ. The use of prostate-specific antigen as a criterion for condom effectiveness. (Letter). Am J Epidemiol 2005;162:704–5.
[Free Full Text] - Lawson ML, Macaluso M, Duerr A, et al. Partner characteristics, intensity of the intercourse, and semen exposure during use of the female condom. Am J Epidemiol 2003;157:282–8.
[Abstract/Free Full Text] - Macaluso M, Lawson ML, Hortin G, et al. Efficacy of the female condom as a barrier to semen during intercourse. Am J Epidemiol 2003;157:289–97.
[Abstract/Free Full Text] - Lawson L, Macaluso M, Bloom A, et al. Objective markers of condom failure. Sex Transm Dis 1998;25:427–32.[Web of Science][Medline]
- Macaluso M, Lawson L, Akers R, et al. Prostate-specific antigen in vaginal fluid as a biological marker of condom failure. Contraception 1999;59:195–201.[CrossRef][Web of Science][Medline]
- Cabello S. Female ejaculation: myth and reality. (http://drgspot.net/cabello.htm).
- Galvao L, Candido-Oliveira L, Diaz J, et al. Effectiveness of the female and male condom in preventing exposure to semen during vaginal intercourse: a randomized trial. Contraception 2005;71:130–6.[CrossRef][Web of Science][Medline]
- Macaluso M, Lawson ML, Duerr A, et al. Macaluso et al. respond to "Condom effectiveness and prostate-specific antigen." Am J Epidemiol 2003;157:301–2.
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