Sepsis continues to produce widespread inflammation, illness, and death, prompting intensive research aimed at uncovering causes and therapies. In this article, we focus on ghrelin, an endogenous peptide with promise as a potent anti-inflammatory agent. Ghrelin was discovered, tracked, and isolated from stomach cells based on its ability to stimulate release of growth hormone. It also stimulates appetite and is shown to be anti-inflammatory in a wide range of tissues. The anti-inflammatory effects mediated by ghrelin are a result of both the stimulation of anti-inflammatory processes and an inhibition of pro-inflammatory forces. Anti-inflammatory processes are promoted in a broad range of tissues including the hypothalamus and vagus nerve as well as in a broad range of immune cells. Aged rodents have reduced levels of growth hormone (GH) and diminished immune responses; ghrelin administration boosts GH levels and immune response. The anti-inflammatory functions of ghrelin, well displayed in preclinical animal models of sepsis, are just being charted in patients, with expectations that ghrelin and growth hormone might improve outcomes in patients with sepsis.

Sepsis continues to be a major cause of morbidity, mortality, and post-recovery disability in patients with a wide range of non-infectious and infectious inflammatory disorders, including COVID-19. The clinical onset of sepsis is often marked by the explosive release into the extracellular fluids of a multiplicity of host-derived cytokines and other pro-inflammatory hormone-like messengers from endogenous sources (“cytokine storm”). In patients with sepsis, therapies to counter the pro-inflammatory torrent, even when administered early, typically fall short. The major focus of our proposed essay is to promote pre-clinical studies with hCG (human chorionic gonadotropin) as a potential anti-inflammatory therapy for sepsis.

Coronavirus disease-2019 is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 virus). Coronavirus disease-2019 (COVID-19) was declared a pandemic in March 2020 and has changed our lives in many ways. This infection induces a hypercoagulable state leading to arterial and venous thrombosis, but the exact pathophysiology of thrombosis is unknown. However, various theories have been postulated including excessive cytokine release, endothelial activation, and disseminated intravascular coagulation (DIC). We present a patient diagnosed with cerebral venous sinus thrombosis (CVST) with COVID-19 infection. A 66-year-old man presented to a hospital for evaluation of persistent headaches. He tested positive for COVID-19, and MRI of the brain and CT venogram revealed CVST. He was started on heparin drip in the hospital and transitioned to oral anticoagulants at the time of discharge. His headaches improved with treatment. Even though headache is the most frequent and initial symptom of cerebral venous thrombosis, it is rarely the only symptom. A high index of suspicion is therefore required to diagnose CVST especially if the patient presents with a simple complaint like a headache. Common complaints can delay the diagnosis leading to disease progression. Considering the high mortality rates in patients diagnosed with CVST, we suggest the importance of knowing the association between COVID-19 infection and CVST, especially in susceptible patients.