Impact of pneumothorax on mortality, morbidity, and hospital resource utilization in COVID-19 patients: a propensity matched analysis of nationwide inpatient sample database.

BACKGROUND: Spontaneous pneumothorax (PTX) is more prevalent among COVID-19 patients than other critically ill patients, but studies on this are limited. This study compared clinical characteristics and in-hospital outcomes among COVID-19 patients with concomitant PTX to provide insight into how PTX affects health care utilization and complications, which informs clinical decisions and healthcare resource allocation. METHODS: The 2020 Nationwide Inpatient Sample was used analyze patient demographics and outcomes, including age, race, sex, insurance status, median income, length of hospital stay, mortality rate, hospitalization costs, comorbidities, mechanical ventilation, and vasopressor support. Propensity score matching was employed for additional analysis. RESULTS: Among 1,572,815 COVID-19 patients, 1.41% had PTX. These patients incurred significantly higher hospitalization costs ($435,508 vs. $96,668, p < 0.001) and longer stays (23.6 days vs. 8.6 days, p < 0.001). In-hospital mortality was substantially elevated for PTX patients (65.8% vs. 14.4%, p < 0.001), with an adjusted odds ratio of 14.3 (95% CI 12.7-16.2). Additionally, these patients were more likely to require vasopressors (16.6% vs. 3.3%), mechanical circulatory support (3.5% vs. 0.3%), hemodialysis (16.6% vs. 5.6%), invasive mechanical ventilation (76.9% vs. 15.1%), non-invasive mechanical ventilation (19.1% vs. 5.8%), tracheostomy (13.3% vs. 1.1%), and chest tube placement (59.8% vs. 0.8%). CONCLUSIONS: Our findings highlight the severe impact of PTX on COVID-19 patients, characterized by higher mortality, more complications, and increased resource utilization. Also, being Hispanic, male, or obese increased the risk of developing concomitant PTX with COVID-19.

Uncoupling hepatic insulin resistance - hepatic inflammation to improve insulin sensitivity and to prevent impaired metabolism-associated fatty liver disease in type 2 diabetes.

Diabetes mellitus is a metabolic disease clinically-characterized as acute and chronic hyperglycemia. It is emerging as one of the common conditions associated with incident liver disease in the US. The mechanism by which diabetes drives liver disease has become an intense topic of discussion and a highly sought-after therapeutic target. Insulin resistance (IR) appears early in the progression of type 2 diabetes (T2D), particularly in obese individuals. One of the co-morbid conditions of obesity-associated diabetes that is on the rise globally is referred to as non-alcoholic fatty liver disease (NAFLD). IR is one of a number of known and suspected mechanism that underlie the progression of NAFLD which concurrently exhibits hepatic inflammation, particularly enriched in cells of the innate arm of the immune system. In this review we focus on the known mechanisms that are suspected to play a role in the cause-effect relationship between hepatic IR and hepatic inflammation and its role in the progression of T2D-associated NAFLD. Uncoupling hepatic IR/hepatic inflammation may break an intra-hepatic vicious cycle, facilitating the attenuation or prevention of NAFLD with a concurrent restoration of physiologic glycemic control. As part of this review, we therefore also assess the potential of a number of existing and emerging therapeutic interventions that can target both conditions simultaneously as treatment options to break this cycle.