A new study finds that symptomatic Covid-19 infection is associated with the risk of developing or exacerbating overactive bladder symptoms.

As an overlooked area of study, only a handful of investigations have focused on the impact of Covid-19 infection on the urinary system. Previous studies have found increased urinary tract symptoms, including the frequency, urgency, and waking up to urinate, post Covid-19 infection; they attributed the symptoms to inflammation and described the condition as Covid-Associated Cystitis (CAC).

Overactive bladder is characterized by a frequent and sudden urge to urinate that can be difficult to control. A person with an overactive bladder may experience urgent incontinence or unintentional loss of urine immediately after feeling an urgent need to urinate, as well as the need to urinate more than typical throughout the day and night.

Roberts and colleagues at the Oakland University William Beaumont School of Medicine investigated the incidence of developing or worsening CAC/Covid-related lower urinary tract symptoms between symptomatic and asymptomatic individuals with Covid-19. They additionally measured the change in the International Consultation on Incontinence Questionnaire-overactive bladder (ICIQ-OB) score for individuals with other health conditions and infected with Covid-19. Here, I provide an overview of their study’s findings and discuss some primary implications.

Roberts et al retrospectively asked participants to score their overactive bladder symptoms at three different points in time using the International Consultation on Incontinence Questionnaire: pre-pandemic, two months following their Covid-19 infection (if they had a documented positive Covid-19 test result), and at the time of the study.  The questionnaire helped evaluate the severity and “bothersome” characteristics of symptoms.

Symptomatic individuals with Covid-19 have notably higher rates of worsening or developing overactive bladder symptoms compared to asymptomatic participants and those who tested negative for Covid-19. Following systematic analysis, Roberts and colleagues found that participants previously symptomatic with Covid-19 infection had a 36.6% incidence of developing covid-associated cystitis, with 22% of the group developing overactive bladder. Symptomatic Covid-infection was associated with a two-fold increased risk of worsening overactive bladder symptoms in comparison to asymptomatic Covid infection and a three-fold increased risk to those who tested Covid-negative.

From pre-pandemic to the time of study, Roberts et al found a 6.5 average point increase on the International Consultation on Incontinence Questionnaire-Overactive bladder among individuals who reported a positive Covid-19 test. The greatest changes regarding individual overactive bladder symptoms were the average increases in urgency (0.8 +/- 0.8) and frequency (0.8 +/- 0.9), followed by the average score increases for urge urinary incontinence (0.7 +/- 0.8) and nocturia (0.6 +/- 0.8) right after. Among participants with reported a positive Covid-19 test and other comorbidities, those with diabetes mellitus, chronic steroid, or immunosuppressed were more likely to experience to have increased average score differences compared to participants who tested negative for Covid-19 and without co-morbidities.

As Roberts et al noted in their publication, some possible physiological explanations behind the association include inflammation and direct infection to urogenital organs. When SARS-CoV-2 invades the body, various immune cells activate and cause systemic inflammation. Moreover, individuals who were Covid-positive may develop bladder inflammation and thereby felt greater “bothersome” urinary symptoms. Alternatively, the release of proinflammatory cells, including cytokines, can trigger afferent nerves and detrusor muscle contractions that cause urinary discomfort symptoms. One additional biological explanation is the possibility that SARS-CoV-2 directly infects urogenital organs. Similar to the heart and lungs, bladder urothelial cells are rich with ACE2 receptors, which is one of the primary entryways for SARS-CoV-2. Further, urothelial cells can be directly infected with Covid-19, leading to inflammation and increasing the likelihood of bothersome urinary symptoms.

Albeit interesting, we must heed Robert et al’s findings with caution. 31.9% of participants were Covid-positive, which is much higher than the rates reported in the literature. The difference in percentage suggests that selective bias is a confounder, as participants were invited to join the study because of past participation with the BLAST study and indicated a willingness to later join future research. Moreover, those who had symptomatic Covid infection or had tested positive for Covid were more likely to accept the study’s invitation. External stress from the pandemic was also likely experienced among participants, which can also be a factor in overactive bladder symptoms. Recall bias may have also confounded the study’s findings. Roberts et al. did not conduct a urinalysis, so symptoms may also be influenced by other infectious or inflammatory causes that may have been present.

According to the most recent report by the Centers for Disease Control and Prevention, 1 in 13  adults in the United States have Long Covid symptoms. Such symptoms, like an overactive bladder, can severely disrupt a person’s daily life and well-being; additional research must be done to determine the pathophysiology between such symptoms and SARS-CoV-2 and help construct effective treatments.

 

Read the original article on Forbes.