To our knowledge this is the first large scale epidemiologic study to investigate the association between HIV and LUTS. We also provide insight into voiding function in MSM, a minority group that has been frequently ignored in urological research. Older case series have highlighted the effect of HIV/AIDS on voiding based on urodynamic findings.8,9
Kane et al studied 18 HIV infected patients who presented for urodynamic testing.9
Detrusor hyper-reflexia, detrusor-sphincter dyssynergia and detrusor areflexia were present in 5, 5 and 1 patient, respectively. Hermieu et al studied 39 HIV infected patients with voiding symptoms during a 3-year period and 87% had urodynamic abnormalities.8
A neurological cause was identified in 61.5% of these cases with the most common disorders arising from AIDS defining illnesses (ie cerebral toxoplasmosis and HIV encephalitis). While the urodynamic specifics of these cases is of interest for understanding the pathophysiology of LUTS in HIV infected patients, it is not clear from these studies that HIV in and of itself confers a greater risk of LUTS.
It has been demonstrated that HIV infection alone produces an increased risk of nonHIV related chronic medical conditions such as cardiovascular, liver, renal and bone disease.4–6
These conditions may be the result of a weakened immune system, chronic inflammation, toxicity of HAART and/or direct effects of HIV on cells.16
Interestingly cohort studies examining the appropriate time to initiate antiretroviral therapy have shown that renal, hepatic and cardiovascular function may be adversely affected by sustained HIV replication and/or immunodeficiency.3
Theoretical risk factors for LUTS in HIV infected persons include chronic urinary tract inflammation, toxicity of HAART, sequelae of opportunistic infections, and direct effects of the virus on the central and peripheral nervous systems.16,17
In our analysis UTI, prostatitis, and gonorrhea were independent risk factors for moderate (but not severe) LUTS. It is implied that infection is unlikely to be the sole underlying cause of bothersome urinary symptoms in HIV infected men. Therefore, it is likely that a direct toxic effect of the virus and/or HAART may be contributing to the burden of LUTS in HIV infected men.
Several important limitations warrant mention. The cross-sectional nature of the data set prohibits statements regarding causality. However, that does not decrease the usefulness of these results in drawing attention to HIV infected individuals as a population at increased risk for LUTS. The cohort is limited to self-identified MSM. Given that sexual practices may have influenced the self-report of LUTS in the study population, our findings may not necessarily be generalizable to HIV infected men who have sex exclusively with women. The use of a web based survey may have introduced selection bias. There could be undercoverage of people who do not read or use computers. In addition, the survey was available only in English. Nonresponse bias and volunteer bias may also diminish the generalizability of our results to the general HIV infected population. It is also important to note that we did find positive associations where we expected them (eg age and depression) in keeping with established risk factors of LUTS. Unfortunately we did not obtain information regarding the use of HAART and the role it may have in the development of LUTS.
Despite these limitations, the current report suggests an important area of directed clinical inquiry and further research for the HIV infected population. Providers should be aware that HIV infected men are at increased risk for reporting LUTS. These men should be screened accordingly and treated appropriately. Future studies should confirm these findings in population based samples and focus on the pathophysiology that underlies our observations so as to better tailor treatments. Future studies should also investigate the role of HAART in LUTS in HIV infected people.