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Association between COVID-19 status and Leydig cell functional capacity among men in hospitalized cohorts
Ravinder Anand-Ivell1, Xinyuan Yang1, Alexander W Tarr2,3
1School of Biosciences, University of Nottingham, Sutton Bonington, UK.
Insights
COVID-19 infection in men can cause Leydig cell dysfunction, leading to hypogonadism. This study measured the INSL3 biomarker in hospitalized patients, finding reduced levels in severe cases that recovered with treatment.
Area of Science:
- Endocrinology
- Virology
- Men's Health
Background:
- COVID-19 pandemic caused significant illness and death, especially in elderly men.
- SARS-CoV-2 infection is linked to reduced testosterone and increased LH, suggesting Leydig cell impact.
- Leydig cells are crucial for testosterone production in the testes.
Purpose of the Study:
- To investigate Leydig cell function in men hospitalized with COVID-19 using the INSL3 biomarker.
- To determine if COVID-19 directly impacts Leydig cells and causes hypogonadism.
Main Methods:
- Measured serum insulin-like peptide 3 (INSL3) levels in two cohorts of hospitalized men with COVID-19.
- Analyzed INSL3 in relation to disease severity and treatment response.
Main Results:
- Reduced INSL3 levels, indicating primary hypogonadism, were observed in severely ill men from Nottingham.
- Less severely affected men in London showed normal INSL3 initially, with a slight decline that recovered with treatment.
- Leydig cell deficiency and hypogonadism were associated with COVID-19 symptoms, particularly in severe cases.
Conclusions:
- COVID-19 is associated with Leydig cell deficiency and hypogonadism, especially in severely ill patients.
- Leydig cell function appears to recover with treatment in most cases.
- Direct viral impact or indirect systemic inflammation likely contributes to Leydig cell dysfunction in COVID-19.
Background:
The first wave of the COVID-19 pandemic in the UK in 2020 led to significant morbidity, hospitalization, and death, particularly amongst elderly men. Recent meta-analyses confirmed that SARS-CoV-2 infection led to reduced testosterone and increased LH, suggestive of testicular Leydig cell involvement.
Methods:
The unique Leydig cell biomarker insulin-like peptide 3 (INSL3) was measured in two cohorts of hospitalized men in Nottingham and London with moderate to severe COVID-19 symptoms.
Results:
For Nottingham men, circulating INSL3 was reduced at entry (0.36 0.34 ng/ml; n = 143), indicative of primary hypogonadism, but appeared to recover to normal values after treatment. For the less severely affected London men, INSL3 at entry was within the normal range (0.89 + 0.30 ng/ml; n = 43), though sequential blood sampling suggested a small decline thereafter, which recovered with treatment.
Conclusion:
In this first study of the biomarker INSL3 in hospitalized men with COVID-19, the results identify a Leydig cell deficiency and consequent hypogonadism as integral to the symptoms of the illness, which was most marked in severely ill patients. In most cases, Leydig cells appeared to recover with treatment. Whether Leydig cells are directly affected by SARS-CoV-2 virus or indirectly via systemic inflammation is unclear, though both are likely.
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