Tauber R, Johnsen N.

Antegrade scrotal sclerotherapy for the treatment of varicocele: Technique and late results. J Urol 1994; 151: 386-390.

Thon W F, Sigmund G, Bahren W, Steimann J.

Perkutane Sklerotherapie bei Vena testikularis Insuffiziens. Akt Urol 1986; 17: 240-243.

Seyferth W, Jecht E, Zeitler E.

Percutaneous sclerotherapy of varicocele. Radiology 1981; 139: 335-340.

Sigmund G, Bahren W, Gall H, Lenz M, Thon W.

Idiopathic varicoceles: feasibility of percutaneous sclerotherapy. Radiology 1987; 164: 161-168.

Lenk S, Fahlenkamp D, Gliech V, Lindeke A.

Comparison of different methods of treating varicocele. J Androl 1994; 15 (Suppl): 34S-37S.

Feneley MR, Pal MK, Nockler IB, Hendry WF.

Retrograde embolisation and causes of failure in the primary treatment of varicocele. BrJ Urol 1997; 80:642-646.

Lenz M, Hof N, Kersting-Sommerhoff B, Bautz W.

Anatomic variants of the spermatic vein: importance for percutaneous sclerotherapy of idiopathic varicocele. Radiology 1996; 198: 425-431.

Bassi R, Radice F, Bergami G, De-Grazia F, Papa B.

Surgical treatment of varicocele. Our experience in the last 10 years. Minerva Chir 1996; 51: 533-536.

30. Wallijn E,Desmet R.

Hydrocele: a frequently overlooked complication after high ligation of the spermatic vein for varicocele. Int J Androl 1978; 1:411-415.

31. Goldstein M, Kim FY, Mathews GJ.

Mini-incision microsurgical subinguinal varicocelectomy with delivery of the testis. J Urol 1996; 155 (Suppl) abstract videotape: 305A.

Goldstein M.

Varicocelectomy: General considerations; in Goldstein M (ed): Surgery of Male Infertility. Philadelphia, Saunders, 1995, pp 169-172.

33. McDougall E.

Minimally invasive therapy. J Urol 1995; 153: 712-713.

Miersch WD, Schoeneich G, Winter P, Buszello H.

Laparoscopic varicocelectomy: indication, technique and surgical results. Br J Urol 1995; 76: 636-638.

Tan SM, Ng FC, Ravintharan T, Lim PH, Chng HC.

Laparoscopic varicocelectomy: technique and results. Br J Urol 1995; 75: 523-528.

Tulloch WS.

Varicocele in subfertility: results of treatment. Br Med J 1955; 2: 356-358.

HYPOGONADISM

Introduction

Men with hypogonadism usually present with symptoms of androgen deficiency (see above Andrological investigations and spermatology).

In some cases, hypogonadotrophic hypogonadism may be a cause of infertility [1].

Table 11. Disorders with male hypogonadism. Modified from [2]

Hypothalamic - pituitary origin (hypogonadotrophic = secondary hypogonadism)

? Idiopathic hypogonadotrophic hypogonadism (including Kallmann's syndrome)

? Delay of puberty

? Hyperprolactinaemia

Hypergonadotrophic syndromes = primary hypogonadism (= testicular origin)

? Anorchia (+ acquired)

? Klinefelter's syndrome

? Leydig cell tumours

? General diseases, e.g. liver cirrhosis

Target organ resistance to androgens

? Testicular feminization

? Reifenstein syndrome

6.2.2 Hypogonadotrophic hypogonadism

Aetiology, diagnosis and therapeutic management

Hypogonadotrophic hypogonadism is caused either by hypothalamic or pituitary diseases.

The failure of hormonal regulation can easily be determined [3].

Endocrine deficiency leads to a lack of spermatogenesis and testosterone secretion due to decreased

secretion patterns of LH and FSH. The therapy of choice is human chorionic gonadotrophin (hCG) treatment,

with the later addition of human menopausal globulin (hMG), dependent on initial testicular volume [4].

If hypogonadotrophic hypogonadism is hypothalamic in origin, a 1-year therapy with pulsatile gonadotrophin

releasing hormone (GnRH) is as effective as gonadotrophins in stimulating spermatogenesis [5].

Once pregnancy has been induced, patients will go back to testosterone substitution (see below).

Conclusion

Effective drug therapy is available to achieve fertility in men with hypogonadotrophic hypogonadism.

6.2.3 Hypergonadotrophic hypogonadism

Aetiology, diagnosis and therapeutic management

Common conditions associated with hypergonadotrophic hypogonadism in younger men include injury to and

loss of the testicles (e.g. after bilateral testicular cancer) (Table 11). More recently it has been recognized that

hypogonadism may occur after extensive testicular biopsy to recover sperm for IVF/ICSI [6]. Men with Klinefelter's syndrome are at risk for spontaneous hypogonadism with ageing. Those undergoing extensive testicular biopsy in the context of IVF/ICSI will almost certainly have an exacerbated risk [7]. Hypergonadotrophic hypogonadism may occur spontaneously in the elderly, in patients with erectile dysfunction [8], and after LHRH treatment or surgical castration for prostatic cancer [9]. All these conditions are not clinically significant for infertile men. Hypogonadism may be associated with osteoporosis [10]. The laboratory diagnosis of hypergonadotrophic hypogonadism is based on decreased serum testosterone and increased LH levels [2]. Additional prolactin measurement is suggested.

Testosterone supplementation is only indicated in men with levels consistently lower than normal (< 12 nmol/l = 300 ng/dl).

Injectable, oral and transdermal testosterone preparations are available for clinical use [2]. The best preparation is the one that maintains serum testosterone levels as close to physiological concentrations as possible [11].

Conclusion

There is general agreement that patients with primary or secondary hypogonadism should receive testosterone substitution therapy.

References

Date: 2016-06-12; view: 320