Printer Friendly

Erectile dysfunction in men with HIV-1: effect of hypogonadism and antiretroviral therapy.


Erectile dysfunction (ED) is the inability to attain or maintain an erection sufficient for sexual intercourse. It is more common amongst men with HIV-1 (receiving antiretroviral therapy or not) than HIV-1-negative men [1,2]: 74% of HIV-1-positive men report ED [3]. However, the overall prevalence of ED in HIV-1-positive men is unknown. This is due to differences in studies, such as ED case definitions, sample sizes, and study designs. Moreover, whilst age and CD4+ count are usually considered, co-morbid conditions such as AIDS-defining illnesses, cardiovascular disease and psychological conditions, are more difficult to adjust for. HIV-1-positive men with ED rate their quality of life as lower than men with normal erectile function [4]. Diagnosing and treating ED has benefits at two levels: the individual, by strengthening sexual relationships and self-esteem, and the population, by potentially facilitating more consistent condom usage ('safer sex culture') in men who might otherwise not use condoms because of ED. The causes of ED affect all men regardless of HIV-1 serostatus; however, hypogonadism and antiretroviral therapy (ART) are associated with ED in HIV-1-positive men and these are the subject of this review.


Hypogonadism is not a common cause of erectile dysfunction (>95% patients have normal testosterone levels) [5], but is the commonest endocrinopathy and cause of sexual dysfunction in HIV-1-positive men [6]. Serum testosterone levels decrease with progressive HIV-1 disease [7, 8]. Before ART, up to 50% of men with AIDS were affected, 33% of whom reported impotence and 67% low libido [8]. In the ART era, 20-25% of HIV-1-positive men are hypogonadic--still higher than the prevalence in the general male population [9]. The reduction in prevalence is largely due to the reduction in morbidity and mortality associated with ART.

Hypogonadism in HIV-1 patients is probably caused by chronic pyrexia, stress, malnutrition and weight loss [10]. HIV-1 wasting syndrome is associated with low total and free testosterone levels compared to men with similar CD4+ counts but no wasting [11]. Hypothalamic-pituitary dysfunction, prolactinaemia [11] and increased sex hormone binding globulin (SHBG) [12] may also be associated with hypogonadism in HIV-1 wasting [8]. Drugs to treat HIV-1-related diseases may be implicated, for example ketaconazole [13]. The testes themselves are targeted by HIV-1: testicular destruction by HIV-1-associated infections (e.g. toxoplasmosis, Mycobacterium avium intracellulare, cytomegalovirus) [14], cytokine-induced Leydig cell impairment [15], and rarely testicular carcinoma [16] occur.


The diagnosis of hypogonadism relies on clinical features of androgen deficiency and subnormal serum testosterone levels. Symptoms include fatigue, weight loss, low libido and depression. Signs include gynaecomastia, alopecia, wasting and testicular atrophy. Symptoms are difficult to differentiate from HIV-1 infection per se and the laboratory diagnosis of hypogonadism is complex. Testosterone is 98-99% bound to serum proteins (-58% bound to SHBG and -40% bound to albumin) but only the free fraction (1-2%) is pharmacologically active. Total testosterone (i.e. bound and free fractions) displays diurnal secretion, being highest at 8-9am and decreasing during the day. Total testosterone, measured in the morning, is a cheap assay but does not account for relative changes in protein binding, for example in patients with hypoalbuminaemia. Also, the concentration of SHBG is higher in HIV-1 infection [17]: total testosterone level may fall but the free fraction may remain constant in some men. There are also physiological changes in testosterone production that may complicate the diagnosis. Testosterone decreases with age, with 40% of men over 60 years of age having < 12nmol/1 and 20% <10.4 nmol/1. SHBG, however, decreases with age, and therefore it is not clear if older men are really hypogonadal. In order to overcome the limitations of using total testosterone alone, it is recommended that the free androgen index and SHBG level be measured in clinically compatible cases where total testosterone levels are normal or borderline [18]. Free testosterone is preferable, but equilibrium dialysis is expensive and not a routine test.

The definition of a subnormal total testosterone level is controversial: <300ng/dl (two standard deviations from the mean testosterone level in young men) is frequently used [5]; but this cannot be applied to older men (in whom total testosterone is known to fall) and HIV-1-infected men. Moreover, a total testosterone level should not be interpreted separately from clinical features of androgen deficiency. A low level should be repeated, and if it persists, an endocrinologist should be consulted to exclude primary (testicular) or secondary (hypothalamus-pituitary) hypogonadism. Follicle-stimulating hormone and luteinising hormone will be high in primary disease and low-normal in secondary disease. Prolactin, thyroid-stimulating hormone and cortisol may be abnormal in secondary disease and an MRI scan of the pituitary fossa is indicated.


Testosterone supplementation should be considered for symptomatic hypogonadism with documented laboratory evidence of androgen deficiency. Testosterone supplementation increases libido and sexual function [19], nocturnal penile tumescence and sleep-related erections in men without HIV-1 [20]. The effect on sexual function in HIV-1-positive men is not widely studied. Testosterone has been used for the treatment of AIDS-related cachexia on the basis of low serum testosterone [11] and dehydroepiandrosterone [21] in HIV-1-positive men with wasting syndrome. Whilst low libido is frequently improved by adequate dosage [22-25], testosterone supplementation appears to be less effective in correcting ED in HIV-1-infected men [23], although a trial of testosterone supplementation may be clinically beneficial in some men. Testosterone may be given by oral, intramuscular and transdermal routes (reviewed elsewhere) [5,17]. Oral preparations are less effective than intramuscular and transdermal formulations [26,27] and are potentially hepatotoxic (e.g. hepatitis, hepatoma, carcinoma) [28]. Intramuscular injections do not mirror the diurnal variation of testosterone levels and result in an initial surge of hormone. Transdermal preparations mirror diurnal variations of testosterone [29] and are convenient for patients.

Adverse effects of testosterone supplementation include salt and water retention, gynaecomastia, prostatic neoplasia, poyycythaemia, sleep apnoea, testicular atrophy and acne. Oral formulations are associated with hepatotoxicity [30], for example increased alkaline phosphatase and conjugated bilirubin. Oxandrolone appears to be the least hepatotoxic oral form [31]. The effect of testosterone on the immune system is ill-defined. Natural killer cell activity is augmented by testosterone supplementation but serum immunoglobulin levels are decreased [32]; other data suggest that testosterone has no effect on viral load or CD4 count [33]. There is one case report of Kaposi's sarcoma (KS) in an HIV-1-negative patient being treated with exogenous testosterone for aplastic anaemia [34]. The tumour regressed when the androgen was stopped. In HIV-1 infection, testosterone levels may be higher [35] or lower [36] in men with KS than in men without KS. There are no large prospective studies to clarify any association between testosterone and KS.

The dosage of testosterone required to reverse the clinical features of androgen deficiency varies between individuals. Patients with a clinical response to testosterone supplementation can be maintained on the current dosage without the need for a testosterone assay [17]. For patients with minimal or no response, a serum testosterone level is indicated and an increased dose considered [37]. All patients should be monitored for the development of poylcythaemia, hepatotoxicity and changes in digital rectal examination and prostate-specific antigen for prostatic carcinoma.


Before ART, the prevalence of ED amongst HIV-1-positive men was estimated to be 53-67% [1, 4, 38, 39]. In a case-control study comparing HIV-1-positive and -negative gay men [1], 75% of seropositive subjects reported low libido compared with 31% of seronegative men (P<0.05). In the same study, 30% of HIV-1-positive haemophiliacs reported premature ejaculation compared with 4% of seronegative controls (P<0.05). Age was excluded as a confounder because most subjects were aged in the mid-30s. Pre-ART studies, however, had limitations. No large-scale prevalence studies were conducted. CD4+ cell count and viral load were inconsistently reported, the instruments for self-assessment and case definitions for ED differed between studies, and co morbid conditions were frequently neglected.

ART has decreased the morbidity and mortality from HIV-1/AIDS and, consequently, improved sexual health. ART per se, however, is associated with ED. Studies of ED during ART have been improved by using the validated Index of Erectile Function Questionnaire, a multi-dimensional self-report instrument for the evaluation of male sexual function [40,41] developed approximately when protease inhibitors (PIs) became available. None the less, differences in study type and size, adjustment for confounders and ART regimens remain (Table 1). How does one differentiate androgen deficiency (being common in HIV-1 infection) from ART as the primary cause of ED? Patients on ART may have normal serum testosterone [2,42] but subnormal levels of luteinising and follicle-stimulating hormones [42]. This at least suggests that ED in men taking ART is not due to disturbances at the hypothalamo-pituitary level.

In a study of non PI-based ART [2], the prevalence of ED in men receiving ART cf. no ART is 26% and 25%, respectively. ED is more prevalent with PI-based regimens (27.5%) cf. non-PI regimens (19.5%) in a study of 189 asymptomatic HIV-1 seropositive men [42]. Data indicate that Pis--particularly indinavir [44, 45], ritonavir [45, 46] and saquinavir [46]--are associated with ED. There was no association between PI use and ED in one study [47], but the duration of ART is not stated here and might bias the results if patients receive ART for only a short time. The mechanism by which PIs cause ED is unknown; however, raised oestradiol levels may result from the altered hepatic metabolism of oestrogens by PIs [46, 47]. Increased oestradiol directly opposes androgenic effects [2].

ED becomes more common as patients advance to AIDS [39], with up to 62% of sufferers compared with 42% of HIV-1-positive men (P=0.02) in one study [4]. Difficulty in maintaining an erection and achieving ejaculation are the most frequent self-reported problems in AIDS sufferers [4]. In a study of 78 HIV-1 seropositive men an association was noted between CD4 <200 cells/[micro]l, ED and low libido (P=0.02) [48]. Of 60 men receiving ART, half had undetectable viral load. It is not specified which patients with viral suppression had low CD4 counts--which would better define any association between viral load, CD4 count and ED. The results are also limited because no details of ART regimens and physical health (including hypogonadism and AIDS-defining illness) are given. The study highlights why there is no easily discernible relationship between plasma HIV-1 load, CD4 count and ED in the literature [49].


ED is becoming a more acceptable and potentially better managed health issue, particularly with the advent of the phosphodiesterase-5 inhibitors and more open dialogue about men's health. Specific guidelines for the management of ED [50] apply to all men. However, HIV-1 per se, HIV-1-related chronic illness, drug interactions with ART and side effects from ART are associated with ED and require attention. In the pre-ART era when patients were ill and dying, sexual function was overshadowed. Now that ART has given patients better health, prognosis and treatment optimism, sexual health has also improved. At the same time, there appears to have been a parallel increase in unprotected anal intercourse and STI rates amongst homosexually active men in large Western cities. With this in mind, should HIV-1-positive men be treated for ED?

There is a fear that restoring sexual function may facilitate more unprotected anal intercourse; this has been borne out to some degree in a study of 429 HIV-1-seropositive men [51]. The prevalence of unprotected anal intercourse with any partners in the previous 3 months was significantly higher in users of sildenafil (60%) when compared with non-users (29%) (P<0.001). Sildenafil users (38%) were also more likely to have unprotected sex with men of unknown HIV-1 status or known seronegative men, than men not using sildenafil (17%) (P<0.01). Another study suggests that the high incidence of HIV-1 and STIs emerging in men aged 50 years and over may be due to sildenafil use in combination with a general lack of HIV-1/STI knowledge [52].

Most people would find it unacceptable and draconian to suggest that HIV-1-positive men abstain from sex altogether. Similarly, withholding treatment for ED on the presumption that the patient might have unprotected intercourse seems unreasonable. Clinicians should pay particular attention to the following issues when counselling HIV-1-positive patients with (or without) ED [53, 54]:

(1) Uphold the principles of medical ethics, that is respect for autonomy (self-determination and freedom), justice (rights and responsibilities, both personal and public health) and beneficence (doing well by the patient);

(2) Recognise 'the physician's confidence in his or her own ability to judge whether particular patients are likely to be responsible with a newly erect penis';

(3) Impart safer sex information to maximise a patient's sexual health (e.g. prevent STIs, HIV-1 superinfection) and that of his sexual partner(s); and

(4) Understand and reinforce the jurisdiction-specific legalities around the duty to disclose serostatus (e.g. public health acts).

The discussion should be documented carefully in the case notes. A thorough sexual history may identify sexual partners who may be at risk of infection and appropriate contact tracing should be undertaken. Safer sex and disclosure of serostatus should be covered during pre-test counselling for HIV-1 and again following an HIV-1 diagnosis. It seems, however, that these issues are rarely mentioned during subsequent consultations with HIV-1 positive patients. In a multicentre study, 29% of 389 HIV-1 infected patients reported that no clinician had ever talked with them about safer sex [53]. Clinicians are even less likely to discuss disclosure of serostatus than safer sex practices because they may feel ill-equipped to tackle the topic [55]. Referral to a counsellor or sex therapist may be appropriate.


Hypogonadism is a significant factor associated with ED in men with HIV-1. Where possible a clinical diagnosis should be supplemented by laboratory evidence of subnormal testosterone. Primary and secondary causes should be excluded before using testosterone supplementation. The patient should be carefully monitored for adverse effects. PIs are strongly associated with ED. Any adverse effect of ART on ED would also appear to be determined by duration of therapy. Prospective studies are needed to exclude CD4 count as a confounding factor. Apart from addressing the concerns of the patient, identifying and managing ED, with appropriate counselling, may facilitate more consistent condom use amongst HIV-1-positive men and their sexual partners.


[1.] Jones M, Klimes I, Catalan J. Psychosexual problems in people with HIV infection: controlled study of gay men and men with haemophilia. AIDS Care, 1994, 6, 587-593.

[2.] Lamba H, Goldmeier D, Mackie NE, Scullard G. Antiretroviral therapy is associated with sexual dysfunction and with increased serum oestradiol levels in men. Int J STD AIDS, 2004, 15, 234-237.

[3.] Ende AR, Lo Re V 3rd, DiNubile MJ, Mounzer K. Erectile dysfunction in an urban HIV-positive population. AIDS Patient Care STD, 2006, 20, 75-78.

[4.] Tindall B, Forde S, Goldstein D et al. Sexual dysfunction in advanced HIV disease. AIDS Care, 1994, 6, 105-107.

[5.] Crum NF, Furtek KJ, Olson PE et al. A review of hypogonadism and erectile dysfunction among HIV-infected men during the pre- and post-HAART eras: Diagnosis, pathogenesis, and management. AIDS Patient Care STD, 2005, 19, 869-885.

[6.] Hofbauer LC, Heufelder AE. Endocrine implications of human immunodeficiency virus infection. Medicine (Baltimore), 1996, 75, 262-278.

[7.] Christeff N, Gharakhanian S, Thobie N et al. Evidence for changes in adrenal and testicular steroids during HIV infection. J Acquir Immune Defic Syndr, 1992, 5, 841-846.

[8.] Dobs AS, Dempsey MA, Ladenson PW, Polk BE. Endocrine disorders in men infected with human immunodeficiency virus. Am J Med 1988,84,611-616.

[9.] Rietschel P, Corcoran C, Stanley T et al. Prevalence of hypogonadism among men with weight loss related to human immunodeficiency virus infection who were receiving highly active antiretroviral therapy. Clin Infect Dis, 2000, 31, 1240-1244.

[10.] Grinspoon SK, Bilezikian JP. HIV disease and the endocrine system. N Engl J Med 1992,327,1360-1365.

[11.] Coodley GO, Loveless MO, Nelson HD, Coodley MK. Endocrine function in the HIV wasting syndrome. J Acquir Immune Defic Syndr, 1994,7,46-51.

[12.] Martin ME, Benassayag C, Amiel C et al. Alterations in the concentrations and binding properties of sex steroid binding protein and corticosteroid-binding globulin in HIV+patients. J Endocrinol Invest; 1992, 15, 597-603.

[13.] Sonino N. The use of ketoconazole as an inhibitor of steroid production. N Engl J Med, 1987, 317, 812-818.

[14.] De Paepe ME, Guerrieri C, Waxman M. Opportunistic infections of the testis in the acquired immunodeficiency syndrome. Mt Sinai J Med, 1990,57,25-29.

[15.] Chabon AB, Stenger RJ, Grabstald H. Histopathology of testis in acquired immune deficiency syndrome. Urology, 1987, 29, 658-663.

[16.] Logothetis CJ, Newell GR, Samuels ML. Testicular cancer in homosexual men with cellular immune deficiency: report of 2 cases. J Urol 1985, 133, 484-486.

[17.] Cofrancesco J Jr, Whalen JJ 3rd, Dobs AS. Testosterone replacement treatment options for HIV-infected men. JAcquir Immune Defic Syndr Hum Retrovirol 1997, 16, 254-265.

[18.] Morris PD, Malkin CJ, Charmer KS, Jones TH. A mathematical comparison of techniques to predict biologically available testosterone in a cohort of 1072 men. EurJ Endocrinol 2004, 151, 241-249.

[19.] Burris AS, Banks SM, Carter CS et al. A long-term, prospective study of the physiologic and behavioral effects of hormone replacement in untreated hypogonadal men. J Androl, 1992, 13, 297-304.

[20.] Cunningham GR, Hirshkowitz M, Koremman SG, Karacan I. Testosterone replacement therapy and sleep-related erections in hypogonadal men. J Clin Endocrinol Metab 1990, 70, 792-797.

[21.] Mulder JW, Frissen PH, Krijnen P et al. Dehydroepiandrosterone as predictor for progression to AIDS in asymptomatic human immunodeficiency virus-infected men. J Infect Dis, 1992, 165,413-418.

[22.] Rabkin JG, Rabkin R, Wagner G. Testosterone replacement therapy in HIV illness. Gen Hosp Psychiatry, 1995, 17, 37-42.

[23.] Rabkin JG, Rabkin R, Wagner GJ. Testosterone treatment of clinical hypogonadism in patients with HIV/AIDS. Int J STD AIDS, 1997, 8, 537-545.

[24.] Rabkin JG, Wagner GJ, Rabkin R. Testosterone therapy for human immunodeficiency virus-positive men with and without hypogonadism. J Clin Psychopharmacol 1999, 19,19-27.

[25.] Rabkin JG, Wagner GJ, Rabkin R. A double-blind, placebo-controlled trial of testosterone therapy for HIV-positive men with hypogonadal symptoms. Arch Gen Psychiatry, 2000, 57, 141-147; discussion 155-156.

[26.] Arver S, Dobs AS, Meikle AW et al. Improvement of sexual function in testosterone deficient men treated for 1 year with a permeation enhanced testosterone transdermal system. J Urol, 1996, 155, 1604-1608.

[27.] Morales A, Johnston B, Heaton JW, Clark A. Oral androgens in the treatment of hypogonadal impotent men. J Urol 1994, 152, 1115-1118.

[28.] Lue TF, Lee KL. Pharmacotherapy for erectile dysfunction. Chin Med J (Engl), 2000, 113, 291-298.

[29.] Matsumoto AM, Bremner WJ. Serum testosterone assays--accuracy matters. J Clin Endocrinol Metah, 2004, 89, 520-524.

[30.] Salehian B, Wang C, Alexander G et al. Pharmacokinetics, bioefficacy, and safety of sublingual testosterone cyclodextrin in hypogonadal men: comparison to testosterone enanthate--a clinical research center study. J Clin Endocrinol Metah, 1995, 80, 3567-3575.

[31.] Bonkovsky HL, Singh RH, Jafri IH et al. A randomized, controlled trial of treatment of alcoholic hepatitis with parenteral nutrition and oxandrolone. II. Short-term effects on nitrogen metabolism, metabolic balance, and nutrition. Am J Gastroenterol 1991, 86, 1209-1218.

[32.] Calabrese LH, Kleiner SM, Barna BP et al. The effects of anabolic steroids and strength training on the human immune response. Med Sci Sports Exerc, 1989, 21, 386-392.

[33.] Mylonakis E, Koutkia P, Grinspoon S. Diagnosis and treatment of androgen deficiency in human immunodeficiency virus-infected men and women. Clin Infect Dis, 2001, 33, 857-864.

[34.] Rosenthal E, Dor JF, Pesce A et al. [Kaposi disease and sex hormones: apropos of a case, review of the literature]. Rev Med Interne, 1994, 15, 186-189.

[35.] Christeff N, Gharakhanian S, Thobie N et al. Effect of interferon alpha on high serum androgen concentrations in HIV positive men with Kaposi s sarcoma. J Clin Pathol, 1997, 50, 341-345.

[36.] Klauke S, Schoefer H, Althoff PH et al. Sex hormones as a cofactor in the pathogenesis of epidemic Kaposi's sarcoma. AIDS, 1995, 9, 1295-1296.

[37.] Rhoden EL, Morgentaler A. Risks of testosterone-replacement therapy and recommendations for monitoring. N Engl J Med 2004, 350, 482-492.

[38.] Colson AE, Sax PE. Sexual dysfunction and HIV infection. AIDS Clin Care, 2000, 12, 39-41; 43, 45-6.

[39.] Newshan G, Taylor B, Gold R. Sexual functioning in ambulatory men with HIV/AIDS. Int J STD AIDS, 1998, 9, 672-676.

[40.] Rosen RC, Cappelleri JC, Smith MD et al. Development and evaluation of an abridged, 5-item version of the International Index of Erectile Function (IIEF-5) as a diagnostic tool for erectile dysfunction. Int J Impot Res, 1999, 11, 319-26.

[41.] Rosen RC, Riley A, Wagner G et al. The international index of erectile function (IIEF): a multidimensional scale for assessment of erectile dysfunction. Urology, 1997, 49, 822-830.

[42.] Collazos J, Martinez E, Mayo J, Ibarra S. Sexual dysfunction in HIV infected patients treated with highly active antiretroviral therapy. J Acquir Immune Defic Syndr, 2002, 31, 322-326.

[43.] Lallemand F, Salhi Y, Linard F et al. Sexual dysfunction in 156 ambulatory HIV-infected men receiving highly active antiretroviral therapy combinations with and without protease inhibitors. J Acquir Immune Defic Syndr, 2002, 30, 187-190.

[44.] Sollima S, Osio M, Muscia F et al. Protease inhibitors and erectile dysfunction. AIDS, 2001, 15, 2331-2333.

[45.] Schrooten W, Colebunders R, Youle M et al. Sexual dysfunction associated with protease inhibitor containing highly active antiretroviral treatment. AIDS, 2001, 15, 1019-1023.

[46.] Colson AE, Keller MJ, Sax PE et al Male sexual dysfunction associated with antiretroviral therapy. J Acquir Immune Defic Syndr, 2002, 30, 27-32.

[47.] Martinez E, Collazos J, Mayo J, Blanco MS. Sexual dysfunction with protease inhibitors. Lancet, 1999, 353, 810-811.

[48.] Cove J, Petrak J. Factors associated with sexual problems in HIV positive gay men. Int J STD AIDS, 2004, 15, 732-736.

[49.] Hijazi L, Nandwani R, Kell P. Medical management of sexual difficulties in HIV-positive individuals. Int J STD AIDS, 2002, 13, 587-592.

[50.] Ralph D, McNicholas T. UK management guidelines for erectile dysfunction. Br Med J, 2000, 321, 499-503.

[51.] Marks G, Richardson JL, Milam J et al. Use of erectile dysfunction medication and unsafe sex among HIV+ men who have sex with men in care. Int J STD AIDS, 2005,16, 271-272.

[52.] Karlovsky M, Lebed B, Mydlo JH. Increasing incidence and importance of HIV/AIDS and gonorrhea among men aged >/= 50 years in the US in the era of erectile dysfunction therapy. Scand J Urol Nephrol, 2004, 38, 247-252.

[53.] Marks G, Richardson JL, Crepaz N et al. Are HIV care providers talking with patients about safer sex and disclosure?: A multi-clinic assessment. AIDS, 2002, 16, 1953-1957.

[54.] Richardson JL, Milam J, McCutchan et al. Effect of brief safer-sex counseling by medical providers to HIV-1 seropositive patients: a multi-clinic assessment. AIDS, 2004, 18, 1179-1186.

[55.] Marks G, Crepaz N. HIV-positive men's sexual practices in the context of self-disclosure of HIV status. JAcquir Immune Defic Syndr, 2001, 27,79-85.

Correspondence to: Derek J Chan, Head of Division, Sexual Health Medicine, Albion Street Centre, 150-154 Albion Street, Surry Hills, NSW2010, Australia. Email:
Table 1. Studies of ED prevalence in the ART era

Reference Study Sample Age CD4+
 type size (years) count
 (n) (cells/

[42] Cross 189 36.80 450
 sectional (mean) (mean)

[43] Cross 156 40.50 415
 sectional (median) (median)

[44] Cross 334 36 431
 sectional (median) (median)

[2] Case HIV+: 73 HIV+: 40.5 N/S
 control HIV-: 100 HIV-: 35.2

(45] Cross 904 39 Most 200
 sectional (mean) to 500

[46] Retrospective 254 37 Most 20
 (median) to 199

[47] Cross 14 37.40 374
 sectional (mean) (mean)

[48] Cross 78 N/S Most 301
 sectional to 500+

Reference ART class ED prevalence
 (or commonest drug)

[42] 86% on ART 27.5% in PI users
 N/S 19.5% overall
 3.5% in untreated
 All on ART 111/156(71%)
 * 58% using Pis (N/S) suffered sexual
 * 42% using non-Pis dysfunction
 (N/S) 91/111 (86%)
 suffered ED

[44] 95% on ART 80% in PI users
 * 75% using Pis 10% overall
 * 25% using NRTls
 (ZDV, 3TC, d4T)
 [+ or -] NNRTI

[2] 64% on ART 26% in ART users
 * NRTls (N/5) 25% in HlV+
 * NNRTls (NVP) (no ART)
 10% in HIV--

(45] All on ART 31% in PI users, cf
 * 75% using Pis 12% PI-na<ve
 (IDV, NFV) (OR=2.56, 95%
 * NRTls and NNRTls (N/S) CI, 1.33-5.03)

[46] All on ART 44% in PI users, cf
 * 62% using IDV 27% in non-PI users
 (and SOV,NFV) (P<0.05)
 * NRTls (ZDV, 3TC, d4T)
 * NNRTls (N/S)

[47] All on ART 100%
 * 92% using Pis (IDV)
 * NRTls (d4T, 3TC)

[48] 78% on ART (regimen 51% lost erection
 N/S) with condom
 38% had difficulty
 keeping erection
 33% had difficulty
 attaining erection

N/S, not specified; PI, protease inhibitor; NRTI, nucleoside reverse
transcriptase inhibitor; NNRTI, non-nucleoside reverse transcriptase
inhibitor; IDV, indinavir; NFV, nelfinavir; SOV, saquinavir;
ZDV, zidovudine; 3TC, lamivudine; d4T, stavudine; NVP, nevirapine.
COPYRIGHT 2007 Mediscript Ltd.
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2007 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:LEADING ARTICLE
Author:Chan, Derek J.
Publication:Journal of HIV Therapy
Geographic Code:1USA
Date:Jun 1, 2007
Previous Article:Risk of HIV transmission in discordant partners.
Next Article:Differences between HIV positive gay men who 'frequently,' 'sometimes' or 'never' engage in unprotected anal intercourse with serononconcordant...

Related Articles
"Shy" study suggests new treatment mechanism.
Involuntary weight loss: interview with Lisa Capaldini, M.D.
Reversible right ventricular dysfunction in HIV-infected patients.
Living with HIV: how to make it easier.
Sex after HIV: sexual function/dysfunction in men with HIV infection.
How does hormonal contraception affect HIV therapy?
Antisocial personality disorder blunts HIV treatment benefits.
Psychiatric issues can loom large in HIV.
The intimate link between erectile dysfunction and heart disease.
Erectile dysfunction can have a devastating effect on a relationship. Safe and effective treatment is available.

Terms of use | Copyright © 2017 Farlex, Inc. | Feedback | For webmasters