Endocrine Abstracts

A 48-year-old gentleman, father of 3 children, was referred to our endocrinology clinic, with sexual dysfunction and hypergonadotrophic hypogonadism. He had a history of severe Coronovirus-Disease-2019(COVID-19) pneumonitis for which he received prolonged ventilatory support. Post extubation, he experienced testicular pain and swelling. A testicular ultrasound showed a left-sided hydrocele, multiloculated epididymal-cyst and a right testicular cyst. He also described new symptoms of lethargy and poor sexual function, since discharged from hospital. He had a past medical history of Type-2 Diabetes on oral agents, Polycystic-Kidney-Disease, a post-COVID-19 occipital haemorrhagic infarct and class-1 obesity. Endocrine testing revealed total testosterone:4.7nmol/l, FSH:11.7u/l, LH:6.1u/l, SHBG:8nmol/l, Free-Androgen-Index:58.7, prolactin:187mU/l, cortisol:431nmol/l, ferritin:161ug/l, PSA:0.26ug/l, HbA1c:82mmol/mol. This biochemical picture was consistent with primary hypogonadism, contrary to the profile that might have been expected in an obese man with metabolic syndrome, who had survived critical illness. Magnetic-Resonance-Imaging (MRI) of the head did not show any pituitary pathology. Transdermal testosterone was initiated and on follow-up, testosterone levels as well sexual function had improved. A number of case-reports and small studies have demonstrated the presence of male-hypogonadism in the acute phase and during recovery from COVID-19. The male reproductive system can be affected by the Severe-Acute-Respiratory-Syndrome-Coronovirus-2(SARS-CoV-2), causing COVID-19, in numerous ways. SARS-CoV-2 uses the Angiotensin-Converting-Enzyme-2(ACE-2)-receptor and Trans-Membrane-Serine protease-2(TMPRSS-2) to infect host cells. ACE-2 and TMPRSS-2 are co-expressed in the testes. The development of hypogonadism can also be attributed to increased pro-inflammatory cytokines. Severe inflammation can disrupt the Blood-Testicular-Barrier (BTB), allowing direct damage of the seminiferous epithelium and spermatogonial stem cells. Possible effects of COVID-19 on the Hypothalamic-Pituitary-Gonadal (HPG) axis have also been proposed, with a declined testosterone:LH ratio. Small studies of patients with moderate to severe COVID-19 reported that epididymo-orchitis can be present in 10-25% of this cohort. Although this seems to be more common at the moderate to severe spectrum of Covid-19, recent studies have demonstrated that this might also be the case for patients at the milder end of the spectrum too. Virus-induced endocrine disorders, including male-hypogonadism, have been implicated in the pathogenesis, of the "post-COVID condition’, as defined by the World-Health-Organisation (WHO), which can affect up to 1/3 of patients having contracted COVID-19. In the post pandemic era, concerns over the long-term sequelae of COVID-19 on the male reproductive health have been raised by a number of fertility societies, something that could also been reflected on the male-hypogonadism workload of our endocrine practice.