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144

Practical Urology: EssEntial PrinciPlEs and PracticE

even more a1A-selective silodosin. Interestingly,

9.

Motofei IG, Rowland DL. The physiological basis of

34

 

abnormal ejaculation occurs mostly in younger

 

human sexual arousal: neuroendocrine sexual asymme-

patients, and when occurring in the context of

 

try. Int J Androl. 2005;28:78-87.

10.

Behre HM, Heinemann L, Morales A, et al. Rationale,

treatment of lower urinary function suggestive

 

design and methods of the ESPRIT study: energy, sexual

of benign prostatic hyperplasia, it apparently is

 

 

desire and body PropoRtions wIth AndroGel®, testoster-

associated with greater therapeutic efficacy. This

 

one 1% gel therapy, in hypogonadal men. Aging Male.

may also be the reason why abnormal ejacula-

 

2008;11:101-106.

tion rarely has been a cause for premature study

11.

Rochira V, Balestrieri A, Madeo B, et al. Congenital estro-

discontinuation, even with tamsulosin

or

 

gen deficiency in men: a new syndrome with different

 

phenotypes; clinical and therapeutic implications in

silodosin.

 

 

 

 

men. Mol Cell Endocrinol. 2002;193:19-28.

 

 

 

 

 

12.

Wallen K. Sex and context: hormones and primate sex-

Conclusions

 

 

ual motivation. Horm Behav. 2001;40:339-357.

 

13.

Stuckey BG. Female sexual function and dysfunction in the

 

 

 

 

 

reproductive years: the influence of endogenous and exog-

The various aspects of human sexual function

 

enous sex hormones. J Sex Med. 2008;5:2282-2290.

14.

Davis SR, Moreau M, Kroll R, et al. Testosterone for low

are regulated in the central nervous system and

 

libido in postmenopausal women not taking estrogen. N

also in the periphery. This regulation involves a

 

Engl J Med. 2008;359:2005-2017.

complex neural and endocrine network, which

15.

Schover LR. Androgen therapy for loss of desire in

makes extrapolation from animal models

to

 

women: is the benefit worth the breast cancer risk? Fertil

humans difficult. Moreover, sexual dysfunction

 

Steril. 2008;90:129-140.

16.

Bancroft J. The endocrinology of sexual arousal.

is not a life-threatening disorder which implies

 

J Endocrinol. 2005;186:411-427.

very high safety thresholds for drugs used in its

 

17.

Westheide J, Cvetanovska G, Albrecht C, et al. Prolactin,

treatment. Therefore, it is not surprising that

 

subjective well-being and sexual dysfunction: an open

only few drugs have been approved for sexual

 

label observational study comparing quetiapine with

dysfunction treatment. On the other hand, sev-

18.

risperidone. J Sex Med. 2008;5:2816-2826.

eral important drug classes, for example, antide-

Krüger THC, Hartmann U, Schedlowski M. Pro-

 

lactinergic and dopaminergic mechanisms underlying

pressants, may have important adverse effects

 

 

sexual arousal and orgasm in humans. World J Urol.

on sexual function. Disorders of sexual arousal

 

 

2005;23:130-138.

remain difficult to treat.

 

19.

Stimmel GL, Gutierrez MA. Sexual dysfunction and psy-

 

 

 

chotropic medications. CNS Spectr. 2006;11 (8 Suppl 9):

 

 

 

24-30.

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Pharmacology of sExUal fUnction

27.Miner MM, Settel AD. Centrally acting mechanisms for the treatment of male sexual dysfunction. Urol Clin North Am. 2007;34:483-496.

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11

Metabolic Evaluation and Medical

Management of Stone Disease

Dorit E. Zilberman, Michael N. Ferrandino,

and Glenn M. Preminger

Epidemiology

Renal stone disease continues to be considerable medical problem, often causing significant patient morbidity. The lifetime risk for stone formation has been reported to be as high as 12% for men and 6% for women.1 However, the rate of female stone formation is insidiously increasing, probably as a result of diet changes and lifestyle associated risk factors such as obesity.2 Recent studies suggest the current male to female ratio of stone formation is now 1.3:1 (M:F).2,3

Moreover, the overall incidence of stone disease is increasing in the USA as stone disease prevalence increased from 3.8% to 5.2% between 1976 and 1994.2-4 Similar increases have been reported by authors from Japan5 and Germany.6 Again, this upsurge is partly attributed to changes in diet and lifestyle and some have suggested that global warming could be augmenting stone formation risk.7

As of 2000, the estimated annual cost attributed to urolithiasis was $2.1 billion dollars representing a 50% increase since 1994. This cost estimation includes initial diagnosis, emergent and surgical intervention, and metabolic evaluation.3 As a consequence of an increased stone disease burden, it is predicted that the overall expenses related to nephrolithiasis will increase by 25% over current expenditures.7

Stone Types and Associated

Diseases/Metabolic Conditions

Traditionally, stone classification is divided into two main groups: Calcium-based and non- calcium-based stones (Table 11.1). Calciumbased stones, which are the largest group, consist of calcium oxalate monohydrate and calcium oxalate dehydrate, each of which accounts for 40–60%, and less frequently calcium phosphate, which accounts for 2–4% of stones analyzed.8

The second group of non-calcium stones consists of (from most to least common): Struvite (infection) stones, uric acid stones, cystine, urate-contained stones, xanthine, and drug-induced stones (indinavir, ephedrine, triamterene, probenecid, sulfinpyrazole, chemotherapy). Table 11.2 summarizes stone composition and their associated metabolic disorders.

Calcium-Based Urolithiasis

Stones with calcium components develop as a result of the greatest variety of metabolic derangements and oftentimes patients present with a combination of stone forming risk factors. The most prevalent diagnoses in calcium stone formers are absorptive hypercalciuria (type I and II), hypocitraturia, hypomagnesiuria, renal leak hypercalciuria,

C.R. Chapple and W.D. Steers (eds.), Practical Urology: Essential Principles and Practice,

147

DOI: 10.1007/978-1-84882-034-0_11, © Springer-Verlag London Limited 2011