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Male accessory gland infection and subfertility: a diagnostic challenge
Trum, J.W.
Publication date
1999
Link to publication
Citation for published version (APA):
Trum, J. W. (1999). Male accessory gland infection and subfertility: a diagnostic challenge.
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J W Trum, RA Schipper, FM Gubler, P Wertheim, KH Kurth, F van der Veen .
Submitted.
.-Abstract
The purpose of this study was to evaluate whether a previous Chlamydia trachomatis infec-tion leads to ana-tomical changes in the male accessory glands. A group of 147 men atten-ding the infertility clinic underwent a transrectal and scrotal ultrasonography. All men were tested for the presence of Chlamydia trachomatis specific antibodies in serum. A previous C. trachomatis infection was diagnosed in 47.6% of men. Transrectal
ultrasono-graphic abnormalities were observed in 70% of men. Scrotal ultrasonoultrasono-graphic abnormali-ties were observed in 65.3% of men. There was no correlation between any observed ultra-sonographic feature of the prostate, seminal vesicles and scrotal contents and a previous
C. trachomatis infection.
A previous Chlamydia trachomatis infection does not lead to specific anatomical changes of the male accessory glands, which can be observed by transrectal or scrotal ultrasonography.
Introduction
Chlamydia trachomatis is a sexually transmitted disease that may cause severe damage in
the female genital tract, leading to tubal infertility (Mol et al. 1997; Dabekausen et al. 1994; Paavonen et al. 1989; Sellors et al. 1988). Compared to its role in the female nothing is known about a C. trachomatis infection and possible anatomical changes in the male genital tract (Greendale et al. 1993, Purvis and Christiansen 1993).
Transrectal ultrasonography (TRUS) and scrotal ultrasonography (SUS) with color Doppler flow play a role in the investigation of male infertility (Kim and Lipschulz 1996; Trum etal.1996; Poore and Jarow 1995; Honig 1994; Jarow 1993; Meacham et al.1993; Pryor and Hendry 1991). TRUS and SUS are established methods to detect anatomical changes, caused by a microbial infection, in the male genital tract. (Behre et al. 1995; Brown et al. 1995; Holden and List 1994; Ludwig and Weidner 1994; Littrup étal. 1988; Di Trapani et al 1988).
The purpose of this paper is to evaluate whether a previous C. trachomatis infection leads to anatomical changes in the male accessory glands.
Materials and Methods
Between April 1995 and January 1997, we asked a cohort of 147 subfertile men of 18 years and older who presented at the Center for Reproductive Medicine at the Academic Medical Center in Amsterdam to participate in the study. This study was carried out as part of a study in the detection of sexually transmitted disease as a cause of male infertility. The Institutional Review Board of our hospital obtained approval. All patients gave writ-ten informed consent. Prostate specific antigen values in serum were measured, to exclude prostatic carcinoma (hybritech test).
C. trachomatis infection. Antibodies to C. trachomatis were determined by the enzyme
lin-ked assay from Labsystems ( Helsinki, Finland) based on a species specific synthetic pepti-de. This test allows the screening and diagnosis of C. trachomatis infection without interfe-rence of C. pneumoniae antibodies. The presence of an actual C. trachomatis infection was investigated by means of a DNA hybridization assay on an urethral swab specimen
(PACE2, Genprobe Inc, San Diego, CA). All patients had aTRUS to search for ultrasono-graphic abnormalities that could be related to infection of the male accessory glands. In a previous study we have shown that with TRUS, anatomical changes like calcifications, dilatation of the venous plexus and cysts are the only reproducible ultrasonographic criteria that may be caused by genital tract infection (chapter 7). Only reproducible criteria were used. One observer, a skilled urologist trainee, who was unaware of the serologic status of the patient, performed all examinations. TRUS was performed with a 7-5 Mhz probe (Briiel and Kjser, Naerum, Denmark) The prostate was scanned in the transverse planes and sagittal planes. The ultrasound abnormalities, calcifications, dilatation of the peri-prostatic plexus and cysts and the presence of the seminal vesicles were noted. All patients had a SUS with color Doppler flow measurements. One observer, a skilled radiologist, who was also unaware of the serologic status of the patient, performed all examinations. SUS was performed with a 7.5 mHz high resolution linear array transducer (Acuson, Mountain View, Ca) with pulsed and color Doppler capabilities. Ultrasound abnormalities that could be related to a previous epididymo-orchitis, like calcifications, cysts, dilatation of the epidi-dymis (cauda/corpus>3mm, caput>10mm), were noted. Size and volume of the testes were measured. Differences in ultrasonographic findings between patients with and without evi-dence of a previous C. trachomatis infection were assessed using the Chi-squared test. Relative risks of previous infection to develop anatomical changes and their 95% confi-dence intervals were calculated.
Results
Results of all included men (147) could be evaluated. The mean age was 34.2 years (stan-dard deviation 6.7). None of the patients indicated genito-urinary complaints. Only one patient tested positive for the actual presence of C. trachomatis with the PACE2 DNA hybridization assay.
In 70 patients (47.6%), specific IgA and/or IgG antibodies against C. trachomatis indica-ting a previous infection, were found. Mean PSA value was 1.3ng/ml. All values were within normal limits.
TRUS and SUS were well tolerated by all patients. No signs of acute infection, benign prostatic hyperplasia or carcinoma of prostate or testis were found. The observed ultra-sound abnormalities are summarized in table I. In 103 patients (70%) ultrasonographic abnormalities of the prostate and in 96 patients (65.3%) ultrasonographic abnormalities of the scrotal contents were observed.
Table I Prevalences of ultrasonographic features in a male infertility population as seen with transrectal and scrotal ultrasonography. (N=l47)
Ultrasonographic feature N= men with feature (%)
TRUS:
Prostatexalcifications 65 (44.2) Dilatation peri-prostatic plexus 64 (43.5) Prostatexysts 15 (10.2) SUS:
Testis left: calcifications 11 (7.5)
Testis right: calcifications 9 (6.9)
Testis left: cysts 2 (1.4)
Testis right: cysts 0 (0)
Epididymis left: calcifications 3 (2)
Epididymis right: calcifications 3 (2)
Epididymis left: cysts 15 (10.2) Epididymis right: cysts 17 (11.6) Epididymis left: dilatation 71 (48.3) Epididymis right: dilatation 69 (46.9)
The relative risks to develop anatomical changes in the male accessory glands after a previous infection with C. trachomatis are shown in table II. There was no correlation between any observed ultrasound abnormality of the prostate and a previous infection with C. trachomatis. Only 10% of men recorded a treatment for a symptomatic C. trachomatis infection in the past. There was no difference in number of anatomical changes in the male accessory glands of men with a previous symptomatic infection versus men with a subclinical C. trachomatis infection (p=0.16).
The relative risk to develop calcifications in the left testis was 2.75 (95%CI 0.78 to 9.74), No correlation was found between a previous infection with C. trachomatis and other scrotal ultrasonographic features, including the right testis.
Table II A previous C.trachomatis infection and the relative risk of anatomical changes in the male accessory glands as seen with transrectal- and scrotal ultrasonography.
Ultrasonographic feature N = men with a N = men without a Relative risk previous chlamydial previous chlamydial (95%CI) infection (70) infection (77)
TRUS
Prostatexalcifications 36 29 0.75 (0.53 to 1.04) Dilatation peri-prostatic plexus 28 36 1.16 (0.82 to 1.64) Prostate:cysts 6 9 1.21 (0.64 to 2.31) SUS
Testis left: calcifications 2 9 2.75 (0.78 to 9.74) Testis right: calcifications 4 5 1.08 (0.51 to 2.28)
Testis left: cysts 0 2
-Testis right: cysts 0 0
-Epididymis left: calcifications 1 2 1.44 (0.29 to 7.19) Epididymis right: calcifications 1 2 1.44(0.29 to 7.19) Epididymis left: cysts 9 6 0.77 (0.49 to 1.21) Epididymis right: cysts 7 10 1.18 (0.65 to 2.13) Epididymis left: dilatation 34 37 0.99 (0.70 to 1.39) Epididymis right: dilatation 27 42 1.41 (0.98 to 2.01)
Discussion
In this study we have shown that men with serologic evidence of a previous C. trachomatis infection do not have more anatomical changes in the male accessory glands than men wit-hout serologic evidence. Ninety percent of men with antibodies to C. trachomatis could not recall to have suffered from genito-urinary complaints associated with a C. trachomatis infection in the past. The fact that we used an accurate C. trachomatis specific antibody test, means that most of these men were correctly identified by the test (Moss et al. 1993). The relative risk to develop calcifications in the left testis was 2.75 whereas the relative risk in the right testis to develop calcifications was only 1.08. There is no reason to believe that the left testis is more at risk for sequelae after a previous infection than the right testis. Furthermore, the 9 5 % confidence interval was broad and varied from 0.78 to 9.74. In conclusion, a previous C. trachomatis infection in a male infertility population, indica-ted by serologic chlamydial specific antibodies is not associaindica-ted with anatomical changes of the male accessory sex glands. However, the results of this study do not exclude the possi-bility that a C. trachomatis infection might lead to more discrete abnormalities, which can-not be detected with present date ultrasonography.
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