Virus World

COVID can worsen lower urinary tract symptoms in men Stephanie Soucheray, MA COVID-19 ArLawKa AungTun/ iStock Share Research in the Journal of Internal Medicine indicates that SARS-CoV-2 infections may worsen lower urinary tract symptoms (LUTS) in men, based on 18,000 men treated for LUTS in Hong in 2021 and 2022. This study, the authors say, is the largest to show COVID-19 can result in increased rates of benign prostate hyperplasia (BPH), or enlargement of the prostate, resulting in a number of urinary symptoms. The study suggests the male reproductive tract is a site for COVID-19-related inflammation and pathophysiology. The study included outcomes among 17,986 men seeking treatment for LUTS. All patient records were gathered from Hong Kong Hospital Authority, the sole healthcare provider in Hong Kong. All patients were on monotherapy for LUTS, in the form of long-acting alpha-1 adrenoreceptor blockers, and seen between January 1, 2021, and December 31, 2022. Case patients had a positive PCR test for COVID-19 while seeking treatment for LUTS, and controls were negative. A total of 10,651 patients had a positive PCR test for SARS-CoV-2.

COVID-19 patients had much higher rates of urine retention

The authors found striking differences between urinary symptoms in cases and controls. The group with SARS-CoV-2 had significantly higher rates of retention of urine (4.55% versus 0.86%), bacteria in the urine (9.02% versus 1.97%), and blood in the urine (1.36% versus 0.41%). "Subgroup analysis stratified by age showed that the statistically significant higher incidence of BPH complications and outcomes in SARS-CoV-2 patients can be consistently observed across the majority of the age groups, with the exception of younger age groups," the authors said. Urinary symptoms were not associated with COVID-19 severity, except in the case of urinary tract infections. Patients with asymptomatic COVID-19 were less likely to suffer infections. "The lower incidence of UTI and bacteriuria observed in patients with low severity COVID-19 is postulated to be related to a relatively higher risk of UTI in patients with more severe disease due to immunocompromised state as well as possible catheterization,” the authors said. "We are excited to be the first to report the effects of COVID-19 on complications of benign prostatic hyperplasia—or enlarged prostate—and also demonstrate the alarming extent of its urological effects," said corresponding author Alex Qinyang Liu, MD, of Hong Kong's Prince of Wales Hospital, in a press release on the study.

Research published in J. Internal Medicine (Oct. 18, 2023):

https://doi.org/10.1111/joim.13719

A slew of detailed studies has now quantified the increased risk the virus poses to older people, men, and other groups. For every 1,000 people infected with the coronavirus who are under the age of 50, almost none will die. For people in their fifties and early sixties, about five will die — more men than women. The risk then climbs steeply as the years accrue. For every 1,000 people in their mid-seventies or older who are infected, around 116 will die. These are the stark statistics obtained by some of the first detailed studies into the mortality risk for COVID-19. Trends in coronavirus deaths by age have been clear since early in the pandemic. Research teams looking at the presence of antibodies against SARS-CoV-2 in people in the general population — in Spain, England, Italy and Geneva in Switzerland — have now quantified that risk, says Marm Kilpatrick, an infectious-disease researcher at the University of California, Santa Cruz. “It gives us a much sharper tool when asking what the impact might be on a certain population that has a certain demographic,” says Kilpatrick. The studies reveal that age is by far the strongest predictor of an infected person’s risk of dying — a metric known as the infection fatality ratio (IFR), which is the proportion of people infected with the virus, including those who didn’t get tested or show symptoms, who will die as a result. “COVID-19 is not just hazardous for elderly people, it is extremely dangerous for people in their mid-fifties, sixties and seventies,” says Andrew Levin, an economist at Dartmouth College in Hanover, New Hampshire, who has estimated that getting COVID-19 is more than 50 times more likely to be fatal for a 60-year-old than is driving a car.

But “age cannot explain everything”, says Henrik Salje, an infectious-disease epidemiologist at the University of Cambridge, UK. Gender is also a strong risk factor, with men almost twice more likely to die from the coronavirus than women. And differences between countries in the fatality estimates for older age groups suggest that the risk of dying from coronavirus is also linked to underlying health conditions, the capacity of health-care systems, and whether the virus has spread among people living in elderly-care facilities.

To estimate the mortality risk by age, researchers used data from antibody-prevalence studies. In June and July, thousands of people across England received a pinprick antibody test in the post. Of the 109,000 randomly selected teenagers and adults who took the test, some 6% harboured antibodies against SARS-CoV-2. This result was used to calculate an overall IFR for England of 0.9% — or 9 deaths in every 1,000 cases. The IFR was close to zero for people between the ages of 15 and 44, increasing to 3.1% for 65–74-year-olds and to 11.6% for anyone older. The results of the study have been posted to the medRxiv preprint server.

Another study from Spain that started in April, and tested for antibodies in more than 61,000 residents in randomly selected households, observed a similar trend. The overall IFR for the population was about 0.8%, but it remained close to zero for people under 50, before rising swiftly to 11.6% for men 80 years old and over; it was 4.6% for women in that age group. The results also revealed that men are more likely to die of the infection than are women — the gap increasing with age. “Men face twice the risk of women,” says Beatriz Pérez-Gómez, an epidemiologist at the Carlos III Institute of Health in Madrid, who was involved in the Spanish study. The results have also been posted to the medRxiv server.Differences in the male and female immune-system response could explain the divergent risks, says Jessica Metcalf, a demographer at Princeton University, New Jersey. “The female immune system might have an edge by detecting pathogens just a bit earlier,” she says...

The virus was found within the sperm of some 13% of screened male COVID-19 patients. Males who suffer from moderate or severe cases of COVID-19 could experience reduced fertility, according to a new study conducted by Dr. Dan Aderka of Sheba Medical Center. Aderka reported that not only was the virus found within the sperm of some 13% of screened male COVID-19 patients, but that there was a 50% decrease in the sperm volume, concentration and motility in patients with moderate disease even 30 days post diagnosis. Finally, post-mortem tests of 12 COVID-19 patients demonstrated moderate to severe changes in the testicular cells supporting sperm development and those producing testosterone, the hormone that induces sperm division and multiplication.

Aderka, whose research has not yet been published, told The Jerusalem Post that the cause for this phenomenon seems to be the presence of the ACE2 receptor on the surface the cell of the Sertoli and Leydig cells of the testis, the same receptors on the cells of lungs, kidneys and hearts. The Sertoli cells support sperm maturation. The Leydig cells produce testosterone. He said the coronavirus binds to the ACE2 receptors and destroys the cells, which causes infertility. “As normal sperm maturation takes 70 to 75 days, it is possible that if we are doing a sperm examination two and a half months after recovery, we may see even more reduced fertility,” Aderka said. “It could be even more detrimental.”

He added that it is also still unclear if the effects on the quality and quantity of the sperm are reversible or persistent. He said doctors will need to examine these same patients six months and a year after recovery to see if the damage “stands the test of time.” This is something his team is planning to do. Aderka said that there is another hypothesis that can now be explored, also as a result of his research: “Interestingly, an enzyme called TMPRSS2 assists the virus in binding to the ACE receptor, facilitating its internalization into the cells.” TMPRSS2 is activated by testosterone. “This phenomenon may explain the higher COVID-10 morbidity and mortality of men compared to women,” he told the Post, adding that it also may explain the lower morbidity and mortality of children, whose testosterone levels are low.