Depuydt CE, Bosnians E, Zalata A, Schoonjans F, Comhaire FH.

The relation between reactive oxygen species and cytokines in andrological patients with or without male accessory gland infection. J Androl 1996; 17: 699-707.

41. Weidner W, Ludwig M, Miller J.

Therapy in male accessory gland infection-what is fact, what is fiction? Andrologia 1998; 30 (Suppl 1): 87-90. 42. ComhaireFH, Rowe PJ, Farley TM.

The effect of doxycycline in infertile couples with male accessory gland infection: a double blind prospective study. Int J Androl 1986; 9: 91-98.

ORCHITIS AND EPIDIDYMITIS

Orchitis

Orchitis is an inflammatory lesion of the testicle associated with a predominantly leukocytic exsudate inside and outside the seminiferous tubules resulting in tubular sclerosis. The inflammation causes pain and swelling. Chronic inflammatory changes in the seminiferous tubules disrupt the normal process of spermatogenesis and cause alterations both in sperm number and quality [1].

It is generally accepted that orchitis may also be an important cause of spermatogenetic arrest [2], which may be reversible. Following orchitis, testicle atrophy occurs [2].

Orchitis is classified according to aetiology (Table 15).

Table 15. Classification of epididymo-orchitis [3]

Diagnosis

Patients with epididymo-orchitis usually present with unilateral scrotal pain [4]. The diagnosis is based on medical history and palpation. Ultrasonography demonstrates a swollen, enlarged testis. The sonographic feature of the tissue does not allow any differential diagnosis [5].

Ejaculate analysis

Ejaculate analysis, including leukocyte analysis, indicates persistent inflammatory activity (see above Androlo-gical investigations and spermatology). In many cases, especially in acute epididymo-orchitis, transiently decreased sperm counts and reduced forward motility are observed [2]. Obstructive azoospermia due to complete obstruction is a rare complication. Mumps orchitis may result in bilateral testicular atrophy [3] and testicular azoospermia. When granulomatous orchitis is suspected, sperm-bound autoantibodies occur (see above Andrological investigations and spermatology).

Therapy

Only the therapy of acute bacterial epididymo-orchitis and of specific granulomatous orchitis is standardized [3] (Table 16).

Several regimens are thought to improve the inflammatory lesion. Therapies with corticoids and non-steroidal antiphlogistic substances, such as diclofenac, indometacin and acetylsalicylic acid, have unfortunately not been evaluated as to their andrological outcome [5]. A further therapeutic trial is based on the idea of preventing deleterious effects of inflammation on spermatogenesis by gonadotrophin-releasing hormone (GnRH) treatment [6].

In mumps orchitis, systemic interferon alpha-2b therapy has been reported to prevent testicular atrophy and azoospermia [7]. In idiopathic granulomatous orchitis, surgical removal of the testis is the therapy of choice.

Date: 2016-06-12; view: 271