SemOpenAlex |

SemOpenAlex

Matches in SemOpenAlex for { <https://semopenalex.org/work/W105499144> ?p ?o ?g. }

Showing items 1 to 100 of ±164 with 100 items per page.

W105499144 endingPage "95" @default.
W105499144 startingPage "77" @default.
W105499144 abstract "AbbreviationsAACEAmerican Association of Clinical EndocrinologistsAIDSacquired immunodeficiency syndromeCVAcerebrovascular accidentDHTdihydrotestosteroneFDAFood and Drug AdministrationLHluteinizing hormoneNOnitric oxideNOSnitric oxide synthasePBIpenile brachial indexPGE1prostaglandin E1 American Association of Clinical Endocrinologists acquired immunodeficiency syndrome cerebrovascular accident dihydrotestosterone Food and Drug Administration luteinizing hormone nitric oxide nitric oxide synthase penile brachial index prostaglandin E1 The purpose of these guidelines is to present a framework for the evaluation, treatment, and follow-up of the patient—indeed, of the couple—who presents with sexual dysfunction. The conventional focus on male erectile dysfunction is incomplete because whenever a man experiences erectile difficulties, his wife or sexual partner suffers as well. Furthermore, disruption in other aspects of the male sexual response cycle, such as diminished libido and delayed or premature ejaculation, also may impair the couple’s sexual gratification. Thus, these guidelines also discuss the cause and, when possible, the available treatments to recognize and rectify disorders of sexual desire, orgasm, and ejaculation. Erectile dysfunction is often compounded by sexual difficulties in the partner or relationship issues. Male sexual dysfunction is most appropriately viewed as a chronic disease with medical, psychologic, and behavioral components that must not be treated in a mechanical and purely medicinal manner. The patient and his sexual partner must be active participants in the full continuum of care. These guidelines address the complexity involved in diagnosing the various aspects of the disorder and offer an organized system of care for the couple. In this way, the outcome can be a cost-effective improvement. The American Association of Clinical Endocrinologists (AACE) believes that, although a multi-disciplinary approach may be required in many cases, the clinical endocrinologist is the most appropriate specialist to lead and coordinate the evaluation of the problem, to decide on multispecialty consultations, and to provide follow-up care. According to a recent survey, the Massachusetts Male Aging Study, 52% of men beyond 40 years of age may have some degree of erectile failure. For various reasons, only a small percentage of men seek medical help. This situation is unfortunate because advances in the understanding of male sexual chemistry have led to the development of a wide range of options to help men reclaim their inherent sexual capacity. Sexual problems can affect men of any age but seem to become more common as men advance in years. Normal male sexual function requires an integrated response between central and local stimuli. Neural signals originating in the brain are transmitted to a thoracolumbar erection center and trigger the psychogenic erection associated with either fantasy or viewing erotic material. This process works in tandem with a reflex erection involving scrotal or genital stimulation, which activates neural impulses in the pudendal nerve that, when transmitted to S4-5 spinal cord sites, stimulate a reflexogenic erection. Although neural signals are crucial, the vigor of a man’s erection is ultimately determined by vascular events governing the flow of blood into the corpora cavernosa. The force with which blood flows into the corpora cavernosa is mediated by an intriguing intracavernosal chemistry sequence involving the enzyme nitric oxide synthase (NOS), nitric oxide (NO), and a second enzyme (adenylate cyclase), which helps generate the cyclic guanosine monophosphate needed to maximize intracavernosal blood flow and increase the pressure within the corpora cavernosa. The role of testosterone in male sexual function remains complex and controversial. Men acquire full sexual and reproductive competence at adolescence when, in response to pulsatile pituitary luteinizing hormone (LH) secretion, Leydig cell testosterone production surges to adult levels as coincidental pulsatile pituitary follicle-stimulating hormone (FSH) secretion initiates and maintains the orderly process of spermatogenesis in testicular Sertoli cells. Thereafter, the role of testosterone becomes unclear. Some men with below-normal testosterone levels can still have nocturnal erections, but for fully satisfactory sexual and erectile function, a “normal” quotient of testosterone must be present in the bloodstream. As testosterone levels decline, so does a man’s sexual function. Two actions of testosterone—one central and the other peripheral—are thought to be critical. Testosterone is the main hormonal mediator of a man’s libido. As testosterone levels decline, sexual desire decreases. Testosterone also has a critical role in stabilizing the levels of intracavernosal NOS, the enzyme responsible for triggering the NO cascade required to have an erection. Thus, the man with inadequate circulating testosterone will have a dampened libido and suboptimal erectile function. Anything that interferes with hypothalamic pulsatile LH release or reduces the number of Leydig cells available to respond to LH will result in decreased production of testosterone. As men age, the absolute number of Leydig cells decreases by about 40%, and the vigor of pulsatile LH release is dampened. In association with these events, the free testosterone level declines approximately 1.2% per year and may be associated with commensurate increases in serum LH levels. Most aging men with subnormal levels of testosterone, however, have low or inappropriately normal levels of LH. Some clinicians believe that age-appropriate but lowered levels of free testosterone (in comparison with those in young men) are not contributory to sexual dysfunction. Nevertheless, some clinical studies have substantiated positive responses to testosterone therapy in men with borderline low levels of free testosterone. In the absence of comorbid conditions, treatment designed to achieve normal testosterone levels will allow the restoration of completely normal erectile function. Thus, several factors—neural activity, vascular events, intracavernosal NOS, and androgens—must work in harmony to maintain normal male sexual function. When a man’s sexual function falters, some aspect of these various factors may be malfunctioning. In addition, other disruptive influences (psychologic, emotional, or pharmacologic factors, individually or collectively) may impair a man’s sexual function. For example, in depressed men, sexual problems—diminished libido, erectile dysfunction, and premature ejaculation—are common, but the antidepres-sant medications routinely prescribed to counter the manifestations of depression are themselves associated with a range of adverse effects on sexual function (see subsequent section on drug-related causes of erectile dysfunction). Libido problems may be related to hypogonadism, hyperprolactinemia, depression, fear of sexual failure, certain medications, or systemic illness. Ejaculatory difficulties can be attributed to either organic or psychogenic problems and are manifested by retarded ejaculation, an-ejaculation, or premature ejaculation. Medication effects and nerve damage are common organic causes. Relationship difficulties may affect ejaculatory function as well. Therefore, AACE has developed a systematic medical approach for assessment of each couple and all potential risk factors in the sexual relationship (see Appendix). This approach allows formulation of a plan to diagnose and treat the difficulties and achieve long-term correction. This outcome can be accomplished only with the continued cooperative efforts of the endocrinologist and both partners. The aging man’s sexual function is a quality-of-life issue. These guidelines will educate physicians about sexual dysfunction, enhance the care and management of affected patients, and thereby provide an important public service. The endocrinologist is ideally positioned to identify and evaluate the full range of medical, physical, and psychiatric problems responsible for disrupting an individual man’s sexual function. With the full diagnostic array outlined, the endocrinologist can offer a rational and comprehensive treatment tailored to each man’s needs and can maximize opportunities to restore normal sexual function. A man’s sexual function is inextricably linked to his sexual body chemistry. The treatment of erectile dysfunction can best be managed by those who understand man’s body chemistry, particularly his sexual body chemistry. Endocrinologists are body chemistry experts, singularly equipped to understand and cope with the alterations in sexual body chemistry responsible for the diminution of sexual function in previously sexually active men. Furthermore, because endocrinologists are trained in the cognitive sciences, they routinely scan the complete diagnostic horizon in search of specific individual factors, or a coalition of factors, that may impair an individual man’s sexual function. Often, a combined therapeutic approach, with use of resources from several disciplines, is necessary. Although impotence, or erectile dysfunction, may be the consequence of specific vascular, pharmacologic, hormonal, neurologic, or psychiatric contributions, causality is not always unifocal. Indeed, sometimes multiple problems coexist and collectively contribute to cripple a man’s sexual function. For effective treatment, all impediments to normal sexual function must be identified and then managed both individually and collectively. Sexual dysfunction may reflect problems with the following factors:•Libido•Ejaculation•Erectile function•A combination of the above factors Reduced libido can result from organic or psychologic causes. It often accompanies low levels of serum testosterone or increased levels of serum prolactin, and these changes may be either primary or secondary. It can also be associated with psychologic problems, relationship difficulties, medical illnesses, and use of certain drugs. Ejaculatory difficulties can consist of premature, retarded, absent, or retrograde ejaculation. Premature ejaculation is more common in young men than in older men. It can disappear or diminish with increasing age and sexual experience. Men who have erectile dysfunction often complain of premature ejaculation. The exact definition of premature ejaculation is controversial, but ejaculation before or within 2 minutes after vaginal penetration would be a working definition. Psychologic or medical factors (or both) must be considered. Adrenergic agents, especially decongestants, are common causes of premature ejaculation, as is endogenous epinephrine produced by anxiety. Retarded ejaculation or anejaculation also can be due to psychologic, neurologic, or medical causes or some combination of these factors. Retrograde ejaculation often occurs in patients with neurologic disorders, especially diabetic neuropathy, or as a complication of transurethral resection of the prostate. Erectile dysfunction is the most common problem, afflicting 80 to 85% of the patients seeking medical help for sexual dysfunction. Erectile dysfunction is defined as the inability to achieve or maintain an erection of sufficient duration and firmness to complete satisfactory intercourse through vaginal penetration. In their definition of erectile dysfunction, Masters and Johnson included the fact that such failure must occur in more than 25% of sexual attempts. This criterion highlights the fact that any normal man can occasionally have erectile failure. The loss of erectile capacity is important to most men. Sexual function serves deeply felt, personal needs and reinforces the permanence of pair-bonding in couples, which aids in the stability of society in general. Sexual function can also be viewed as a status symbol and a psychologic boost. Sexual dysfunction may cause substantial emotional concerns. With the man demonstrating age-related decreased sexual desire, and possibly function, the partner may have emotional concerns as well, manifested by doubts about attractiveness or questions about the man’s faithfulness. Adrenergic impulses maintain tonic contraction of the smooth muscle of the corpora cavernosa in the flaccid state. Penile erections are the result of enhanced blood flow, caused by arteriolar vasodilatation and cavernosal relaxation attributable to nerve stimulation. Various stimuli trigger the higher centers of the brain, and nerve impulses flow down the spinal cord to the thoracolumbar ganglia (Fig. 1). This process causes nerve impulses (especially from nonadrenergic, noncholinergic nerve fibers) to activate. The main neurotransmitter produced seems to be NO, the endothelium-derived relaxing factor (Fig. 2). This agent causes relaxation of the arterioles and cavernosal smooth muscle of the penis, which allows increased blood flow and increases the intracorporeal pressure to approximate the systolic pressure. The dilated corpora compress the venous outflow channels against the elastic tissue of the tunica albuginea, an action that prevents venous leakage and further increases the intracavernosal pressure to above systolic pressure. Just before ejaculation, the ischio-cavernosal and pubocavernosal muscles contract to increase intracavernosal pressure further; the response is ejaculation. Tactile stimulation of the penile shaft activates parasympathetic fibers, which travel in the pudendal nerve and function through the spinal reflex arc from S2 to S4. This process further enhances relaxation of the cavernous smooth muscle, which increases blood flow to the penis and, subsequently, intracavernosal pressure. Usually, both mechanisms are at work to cause erections, but as men age, they derive less stimulation from the higher centers and need to rely more on direct penile stimulation—hence, the requirement of aging men to practice extended foreplay. The mechanisms involved are complex and may be related to decreased production of or responsiveness to NOS, the enzyme that produces NO.Fig. 2The nitric oxide (NO) cascade, underlying penile erection. cGMP = cyclic guanosine monophosphate; NADPH = reduced form of nicotinamide adenine dinucleotide phosphate; NOS = nitric oxide synthase; PDE = phosphodiesterase. (From Spark RF. Sexual Health in Men: The Complete Guide. Cambridge, MA: Perseus Publishing, 2000:105.)View Large Image Figure ViewerDownload (PPT) Before the causes of erectile dysfunction are discussed, the normal aging-related changes in erectile function should be reviewed. Some men seeking help need only reassurance that their symptoms merely represent the expected age-related physiologic changes in function. In young men, the higher centers of the brain are easily stimulated by fantasizing or thinking about sex, which seems to cause an erection nearly at will. With aging, this ability decreases. Ability to reach arousal with suggestive photographs also becomes less effective, although arousal by viewing a suggestive video may remain longer. Increased interaction of the couple, especially with fore-play, is needed to achieve a satisfactory erection. Another aging-related change is an increase in the refractory period—that is, the time from ejaculation to the next erection. This interval may range from 30 minutes in a young man to several days in an octogenarian, according to the work of Masters and Johnson. Erections, once achieved through fantasy and fore-play, are more fragile as men age. Older men must maintain their focus; if they become distracted by thinking of work or other activities, detumescence may occur. The telephone ringing may be enough to cause detumescence. In addition, men may occasionally experience detumescence without ejaculation for no apparent reason. The two main categories of erectile dysfunction are psychologic and organic. Often the dysfunction is of “mixed” etiologic origin, inasmuch as both factors are important. Every man who has some problem with erectile function develops performance anxiety, and determining whether psychologic factors are the main problem or merely a minor accompaniment may be difficult. Organic causes can be vascular, neurologic, hormonal, medical, or pharmacologic, and some men have multiple etiologic factors. Most of these causes affect the intrapenile vasculogenic mechanisms, whether arterial or venous. Another common finding is a decrease in local NO, which is thought to be the main neurotransmitter in initiating the erectile process. Fibrosis may also be present within the corpora cavernosa, which can limit their expandability, prevent the venules from compressing against the tunica albuginea, and thereby allow venous leakage from the penis. If the corpora cavernosa cannot expand and fill with blood, decreased erectile firmness occurs. Although atherosclerotic plaques, or damage by trauma or irradiation, may decrease blood flow to the penis, vascular causes of erectile dysfunction are more often due to a failure of neural, muscular, or chemical factors. Venous leakage occurs when incomplete filling of the corpora, or intracavernosal fibrosis, causes failure of the veins to be pressed shut against the tunica albuginea. Erectile function can be impaired as a result of a cerebrovascular accident (CVA or stroke), demyelinating diseases, or even seizure disorders. Tumors or trauma to the spinal cord can also be causative factors of erectile dysfunction. Autonomic and peripheral sensory nerves may be damaged by trauma or transurethral resection of the prostate. A common cause of impaired erectile and ejaculatory function is nerve damage attributable to diabetic autonomic neuropathy. The prevalence of this disorder increases with the duration of disease in both type 1 and type 2 diabetes, and it is more likely to develop when the plasma glucose is poorly controlled. Hormonal perturbations may contribute to sexual dysfunction, especially erectile dysfunction. Most such problems revolve around dysfunction of the hypothalamic-pituitary-gonadal axis and are associated with either excess prolactin or decreased testosterone levels. Other endocrine disorders that may be associated with impairment of libido or erectile function include hypothyroidism, hyperthyroidism, adrenal insufficiency, or excessive levels of adrenal corticosteroids. In such cases, patients may experience a generalized fatigue or weakness from the effects of the illness. Tumors of the hypothalamic-pituitary area may cause hypogonadism by mass effect, destruction of normal pituitary tissue, or oversecretion of prolactin, which may suppress gonadotropins and cause secondary hypogonadism. Postreceptor action of increased prolactin levels may also result in erectile problems, even in the presence of a normal testosterone level. Hyperprolactinemia, which can be due to medications, hypothyroidism with increased thyrotropin, chest wall injuries, or compression of the pituitary stalk, can result in sexual problems. Rarely, a patient may demonstrate an excess of a variant large prolactin molecule, macroprolactin, which is biologically inert and therefore incapable of causing sexual dysfunction. Any major medical illness or surgical procedure can suppress the central axis and cause secondary hypogonadism. Primary hypogonadism due to autoimmune destruction of the testicles occurs in some men as they age. A related cause is unilateral mumps orchitis occurring during the early adult years, with later failure of the “good testis.” Congenital causes include Klinefelter’s syndrome, Kallmann’s syndrome, and myotonic dystrophy. The incidence of hypogonadism in patients with acquired immunodeficiency syndrome (AIDS) is quite high. Hypogonadism is defined as a free testosterone level that is below the lower limit of normal for young adult control subjects. Previously, age-related decreases in free testosterone were accepted as “normal,” but this concept has been challenged. Similarly, several clinical conditions that were once accepted as normal age-related disorders are now thought to lead to medical problems—for example, hypertension, osteoporosis, and menopause. No agreement exists on the physiologically appropriate level of testosterone as men age or the serum testosterone level at which a man begins to experience impairment of his sexual function. The definition of relative hypogonadism is also uncertain. Many men have normal sexual function even if their testosterone levels decline into the age-adjusted lower normal range. Patients with borderline testosterone levels warrant a clinical trial of testosterone. The threshold of response to testosterone therapy, and thus the necessary dosage, varies—especially in the younger decades of life. If LH is increased and the testosterone level is low, the patient will have decompensated primary testicular failure. In this setting, testosterone replacement therapy is essential. Men with testicular failure may have the entire spectrum of hypogonadism, which includes osteoporosis, anemia, muscle weakness, depression, and lassitude, as well as sexual dysfunction. The sexual dysfunction, especially decreased libido and decreased erectile capacity, often reverses with testosterone replacement therapy. The variability of response in some patients may be related to comorbid medical illnesses, vascular dysfunction at the penile level, or psychologic factors. Any medical condition that can cause general debility has the potential to decrease sexual desire and performance. Pain, shortness of breath, angina, muscle weakness, or a CVA may be responsible for the dysfunction. The most common medical conditions associated with sexual difficulties are diabetes mellitus and hypertension, possibly because of the microvascular and neurovascular changes that are inherent in these conditions. In patients with diabetes, these factors may lead to a decrease in penile nerve stimulation and in generation of NO. Some investigators have found hypogonadism to be commonly associated with diabetes mellitus. Poorly controlled plasma glucose levels add a separate risk factor, as does the presence of diabetic neuropathy. Not only is hypertension a separate risk factor for sexual problems but hypertension and diabetes often coexist in a patient. Generalized atherosclerosis and peripheral vascular disease may impede blood flow to the penis, as may a damaged vessel attributed to pelvic injury or radiation therapy to the groin. Recently, a cardiologist reported an assessment of 50 men who presented with erectile dysfunction but who had no history of cardiac disease. Most men had multiple cardiac risk factors, and 56% had asymptomatic ischemic changes on a treadmill test, consistent with silent ischemia. Because erectile dysfunction and cardiovascular disease share common risk factors, erectile dysfunction may be a predictor of future cardiovascular disease. A search for cardiovascular risk factors was suggested as part of the evaluation in men with sexual difficulties. Cigarette smoking can cause vascular insufficiency as well as a decrease in intrapenile NO levels. Excessive consumption of alcohol or use of other recreational drugs may cause sexual dysfunction, either by a direct effect on the penile neurovascular system or by causing increased prolactin, decreased testosterone production, or both. In Peyronie’s disease, collagen tissue is converted to fibrous tissue for unknown reasons; hence, a palpable fibrous plaque is created in the tunica albuginea. The usual manifestation is a bending of the penis to one side during erection, which can occasionally be painful. Both prescription and over-the-counter medications have been shown to be the cause of erectile problems in as many as 25% of cases (Table 1). Although single medications can induce erectile dysfunction, the adverse effects of medications are often additive. This situation is particularly frequent in older men who are taking multiple medications, and partial or complete erectile dysfunction often results. A psychologic component can make partial erectile dysfunction progress to complete erectile dysfunction. Some medications can affect libido, whereas others affect erectile function or ejaculation. Nonprescription medications, such as antihistamines or decongestants, may also impair erectile function.Table 1Sexual Side Effects of Common Prescription MedicationsType of drug and generic nameBrand nameSexual side effectsAntihypertensive medicationsDiureticsSpironolactoneAldactoneDecreased libido, breast swelling, impotenceThiazidesDiuril, HydroDIURIL, Naturetin, Naqua, many othersImpotenceFurosemideLasixNoneCentrally acting agentsMethyldopaAldometDecreased libido, impotenceClonidineCatapresImpotenceReserpineSerpasil, Raudixin, Ser-Ap-EsDecreased libido, impotence, depressionα-Adrenergic blockersPrazosinMinipress“Dry” (retrograde) ejaculationTerazosinHytrin“Dry” (retrograde) ejaculationβ-Adrenergic blockersPropranololInderalImpotence, decreased libidoMetoprololLopressorImpotence, decreased libidoCombined α- and β-adrenergic blockersLabetalolNormodyne, TrandateInhibited ejaculationNonadrenergic vasodilatorHydralazineApresolineNoneSympathetic nerve blockerGuanethidineIsmelinImpotence, “dry” (retrograde) ejaculationAngiotensin-converting enzyme inhibitorsCaptoprilCapotenNoneEnalaprilVasotecNoneLisinoprilZestrilImpotence in a small percentage (1%) of casesPsychiatric medicationsAntidepressantsTricyclics:AmitriptylineElavilInhibited ejaculation, impotenceAmoxapineAsendinDecreased libido, impotenceDesipramineNorpraminInhibited ejaculationDoxepinSinequanInhibited ejaculation, impotenceImipramineTofranilInhibited ejaculation, impotenceMaprotilineLudiomilInhibited ejaculationNortriptylineAventyl, PamelorInhibited ejaculationProtriptylineVivactilInhibited ejaculation, impotenceAtypical agent:TrazodoneDesyrelPriapismMonoamine oxidase inhibitors:IsocarboxazidMarplanInhibited ejaculationPhenelzineNardilInhibited ejaculation, decreased libidoTranylcypromineParnateInhibited ejaculationAntipsychotic medicationsPhenothiazine group:ThioridazineMellarilInhibited ejaculation, priapism, decreased libidoChlorpromazineThorazineInhibited ejaculationMesoridazineSerentilInhibited ejaculation, decreased libidoFluphenazineProlixinInhibited ejaculation, decreased libidoSerotonin reuptake inhibitors:Fluoxetine (and others in this class)ProzacAnorgasmy (8%)PerphenazineTrilafonInhibited ejaculationTrifluoperazineStelazineInhibited ejaculationThioxanthene group:ChlorprothixeneTaractanInhibited ejaculationThiothixeneNavaneInhibited ejaculation, impotenceButyrophenone:HaloperidolHaldolAntimania medicationEskalith, LithobidInhibited ejaculationLithium carbonateAntiulcer medicationsCimetidineTagametDecreased libido, impotence, gynecomastiaRanitidineZantacNoneFamotidinePepcidNoneFrom Spark RF. Male Sexual Health: A Couple’s Guide. Yonkers, NY: Consumer Reports Books, 1991: 117-118. Open table in a new tab From Spark RF. Male Sexual Health: A Couple’s Guide. Yonkers, NY: Consumer Reports Books, 1991: 117-118. Most psychotropic drugs can affect libido or erectile function, either through a direct action or by increasing prolactin or decreasing testosterone levels. Although anti-depressants may cause erectile dysfunction in susceptible patients, they may also be beneficial in improving libido in depressed men. Antihypertensive medications may cause erectile dysfunction either by drug-specific effects or by decreasing the systolic blood pressure and thereby decreasing the intracavernosal penile pressure. This effect is especially prevalent in patients with diabetes or hypertension who have underlying microvascular disease. Ketoconazole, aminoglutethimide, and similar drugs actually decrease the production of testosterone. Most of the earlier antihypertensive agents—such as reserpine, guanethidine, and hydralazine—caused sexual dysfunction. Some β-adrenergic blocking agents may cause sexual problems, but dysfunction with angiotensin-converting enzyme inhibitors or calcium channel blockers is less common. Some drugs (spironolactone, cimetidine, flutamide, or cyproterone acetate) may block the peripheral androgen receptors. Cimetidine may assume a greater importance because it can now be purchased without a prescription. Drugs such as α-methyldopa, spironolactone, digoxin, and metoclopramide may raise prolactin levels. Thiazide diuretics, finasteride, anticholinergic agents, and pain medications can cause erectile dysfunction. An algorithm for suggested evaluation of erectile dysfunction is shown in Figure 3. The initial assessment of a male patient with sexual dysfunction and his partner is best performed by a physician who has the training, experience, and interest to conduct an extensive evaluation of the relevant medical, psychologic, and hormonal factors. Accordingly, the clinical endocrinologist is the physician best suited to direct the evaluation and treatment of this problem by a multidisciplinary team. Ideally, the couple should undergo assessment together at the first visit or soon thereafter. A discussion about the partner is important. Is the patient married, single, divorced, or widowed? Because newer relationships may have adjustment problems, the duration of the relationship is important, as is the age disparity between the partners. The health of the partner is very important; 15% of men report a decreased sexual frequency or ability because of health problems that their partners are experiencing, and the men are infrequently aware of this connection. The question of whether a couple is still sexually active in other ways is more revealing: do they practice alternative sexual techniques even if intravaginal penetration is not possible? This adjustment highl" @default.
W105499144 created "2016-06-24" @default.
W105499144 creator A5004379748 @default.
W105499144 creator A5012241174 @default.
W105499144 creator A5012744169 @default.
W105499144 creator A5027421431 @default.
W105499144 creator A5082470792 @default.
W105499144 creator A5082889558 @default.
W105499144 creator A5089993010 @default.
W105499144 creator A5091573455 @default.
W105499144 date "2003-01-01" @default.
W105499144 modified "2023-10-16" @default.
W105499144 title "American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for The Evaluation and Treatment of Male Sexual Dysfunction: a Couple’s Problem–2003 Update" @default.
W105499144 cites W1010041877 @default.
W105499144 cites W119971457 @default.
W105499144 cites W1217396828 @default.
W105499144 cites W1486595651 @default.
W105499144 cites W16935447 @default.
W105499144 cites W1709062265 @default.
W105499144 cites W1963505659 @default.
W105499144 cites W1968109225 @default.
W105499144 cites W1971029030 @default.
W105499144 cites W1973221149 @default.
W105499144 cites W1975653633 @default.
W105499144 cites W1981571351 @default.
W105499144 cites W1985592735 @default.
W105499144 cites W1987204652 @default.
W105499144 cites W1987790218 @default.
W105499144 cites W1993142467 @default.
W105499144 cites W1998032693 @default.
W105499144 cites W2002789928 @default.
W105499144 cites W2006168368 @default.
W105499144 cites W200666033 @default.
W105499144 cites W2007506740 @default.
W105499144 cites W2008160250 @default.
W105499144 cites W2008386128 @default.
W105499144 cites W2009870466 @default.
W105499144 cites W2012615408 @default.
W105499144 cites W2013444727 @default.
W105499144 cites W2030572594 @default.
W105499144 cites W2030615837 @default.
W105499144 cites W2031261194 @default.
W105499144 cites W2038162032 @default.
W105499144 cites W2038429708 @default.
W105499144 cites W2043085884 @default.
W105499144 cites W2044591543 @default.
W105499144 cites W2047038182 @default.
W105499144 cites W2052135387 @default.
W105499144 cites W2056147576 @default.
W105499144 cites W2057133744 @default.
W105499144 cites W2057233158 @default.
W105499144 cites W2057264359 @default.
W105499144 cites W2061122425 @default.
W105499144 cites W2067814588 @default.
W105499144 cites W2070200767 @default.
W105499144 cites W2070848494 @default.
W105499144 cites W2072524643 @default.
W105499144 cites W2075661590 @default.
W105499144 cites W2077972461 @default.
W105499144 cites W2081975982 @default.
W105499144 cites W2088906358 @default.
W105499144 cites W2089269000 @default.
W105499144 cites W2091178888 @default.
W105499144 cites W2092749062 @default.
W105499144 cites W2092920855 @default.
W105499144 cites W2095316737 @default.
W105499144 cites W2096736777 @default.
W105499144 cites W2096932013 @default.
W105499144 cites W2105830583 @default.
W105499144 cites W2109676316 @default.
W105499144 cites W21141216 @default.
W105499144 cites W2133927893 @default.
W105499144 cites W2141925633 @default.
W105499144 cites W2148030225 @default.
W105499144 cites W2150052163 @default.
W105499144 cites W2153768594 @default.
W105499144 cites W2248357131 @default.
W105499144 cites W22857079 @default.
W105499144 cites W2297358297 @default.
W105499144 cites W2312845168 @default.
W105499144 cites W2314125128 @default.
W105499144 cites W2330186243 @default.
W105499144 cites W2396087373 @default.
W105499144 cites W2401073401 @default.
W105499144 cites W2405299563 @default.
W105499144 cites W2412734941 @default.
W105499144 cites W2415708956 @default.
W105499144 cites W2419464538 @default.
W105499144 cites W2441133196 @default.
W105499144 cites W2463675698 @default.
W105499144 cites W2468332851 @default.
W105499144 cites W2731265298 @default.
W105499144 cites W4237190129 @default.
W105499144 cites W4249523014 @default.
W105499144 cites W4249934572 @default.
W105499144 cites W4255795935 @default.
W105499144 cites W4296586706 @default.
W105499144 cites W4322545 @default.