Post-COVID-19 interstitial cystitis and bladder dysfunction: a growing concern for public health

Dear Editor, Interstitial cystitis (IC), also known as bladder pain syndrome (BPS), is an ongoing condition of the bladder marked by inflammation of the bladder, constant pelvic or bladder pain, urinary urgency, urinary frequency, and nocturia as well. Unlike other urinary tract infections (UTIs), interstitial cystitis is an idiopathic and nonbacterial condition[1,2]. Bladder dysfunction simply means the bladder is not able to store or empty urine normally. The causative agent of bladder dysfunction may be neurogenic, psychogenic, infectious agents, and hormonal and metabolic conditions as well. COVID-19 is induced by the SARS-CoV-2 virus, which gains entry into host cells via the receptor angiotensin-converting enzyme 2 (ACE2), a homolog of ACE that plays a significant role in the renin–angiotensin system. While SARS-CoV-2 primarily contaminates the respiratory tract, its ability to influence multiple organs is due to the widespread presence of ACE2 in the human body, leading to damage in various organs[3]. SARS-CoV-2, the virus responsible for COVID-19, may also cause local inflammation of the bladder, which hyper-activates the body’s immune response, resulting in the overproduction of inflammatory cytokines, including interleukin 6. These pro-inflammatory molecules have been detected in the urine and serum of patients with COVID-19. The presence of these mediators in urine can damage the bladder mucosa, and due to this damage, increased urinary frequency and nocturia can be observed in such patients[2]. These pro-inflammatory mediators associated with the SARS-CoV-2 virus may also affect the central and peripheral nervous systems by causing neuronal demyelination, which ultimately results in nerve damage. One of these nerves may be the pudendal nerve, which plays a key role in bladder function. Demyelination and damage to the pudendal nerve can cause bladder incontinence, further complicating the urinary symptoms experienced by patients with COVID-19[4]. Recent observations suggest that COVID-19 can impact the genitourinary system. Specifically, “COVID-19-associated cystitis” has been identified in adult patients who have had COVID-19 and experience symptoms such as urinary frequency and nocturia[4]. Mumm et al first observed increased urinary frequency in 7 males out of 57 patients admitted to their COVID-19 wards. In other observations, all the COVID-19 positive patients (7 females and 32 males; all African American) developed de novo urinary symptoms without urinary tract infection by urine culture[2]. In recent years, there has been an increased burden in managing post-COVID pain symptoms, which are attributed to immunological abnormalities and inflammatory damage. Chronic pain has a positive relationship with viral infections, often leading to peripheral or central neurological complications through either direct invasion of the nervous system or immune-mediated reactions. The leading mechanisms underlying post-COVID pain symptoms include nerve damage resulting from direct viral entry into cells of the nervous system and overactivation of the inflammatory cascade[5]. Further research is needed to better understand the emerging phenomenon of post-COVID-19 cystitis and associated urinary dysfunctions. Comprehensive studies are still required to explain the root causes, risk factors, and long-term consequences. Moreover, increased attention and awareness are essential for healthcare providers to effectively manage post-COVID symptoms. By prioritizing research and clinical care, we can improve symptoms and quality of life for individuals affected by these consequences associated with COVID-19.