Abstract
Obesity is a risk factor for SARS-CoV-2 infected patients to develop respiratory failure. Leptin produced in visceral fat might play a role in the deterioration to mechanical ventilation. A cross sectional study was performed. The mean BMI was 31 kg/m2 (range 24.8–48.4) for the 31 SARS-CoV-2 ventilated patients and 26 kg/m2 (range 22.4–33.5) for 8 critically ill non-infected control patients. SARS-CoV-2 infected patients with a similar BMI as control patients appear to have significantly higher levels of serum leptin. The mean leptin level was 21.2 (6.0–85.2) vs 5.6 (2.4–8.2) ug/L for SARS-CoV-2 and controls respectively (p = 0.0007). With these findings we describe a clinical and biological framework that may explain these clinical observations. The ACE2 utilization by the virus leads to local pulmonary inflammation due to ACE2-ATII disbalance. This might be enhanced by an increase in leptin production induced by SARS-CoV-2 infection of visceral fat. Leptin receptors in the lungs are now more activated to enhance local pulmonary inflammation. This adds to the pre-existent chronic inflammation in obese patients. Visceral fat, lung tissue and leptin production play an interconnecting role. This insight can lead the way to further research and treatment.
Highlights
The spread of 2019 novel coronavirus SARS-CoV-2 throughout the world is a massive provocation of Critical Care facilities worldwide
All other extraordinary findings within this syndrome such as gastric retention, arterial and venous thrombosis, loss of smell, disproportional weight loss, relatively high C-reactive protein (CRP), hemodynamic stability and the limited need for insulin might be explained by hyperleptinemia
We found significantly higher levels of leptin in our SARS-CoV-2 ventilated patients compared to control patients
Summary
The spread of 2019 novel coronavirus SARS-CoV-2 throughout the world is a massive provocation of Critical Care facilities worldwide. The clinical course of SARS-CoV-2 infected individuals with fever, fatigue, cough, and dyspnea typically shows a deterioration in health 7–9 days after disease onset [1, 2]. Symptoms of fever and dyspnea resolve around day 10–12 post onset, yet some patients go on to develop respiratory failure and become ventilator dependent [1, 2, 3]. It has been shown that 70–90% of the SARS-CoV-2 infected patients that are admitted to the intensive care with respiratory failure are overweight [4]. In our ICU 90% of all SARS-CoV-2 positive patients with respiratory failure had a Body Mass Index (BMI) of 25 kg/m2 or higher
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