Methemoglobinemia in the Setting of G6PD Deficiency and SARS-CoV-2 Infection.

catalyzes the pentose phosphate shunt. It is required to maintain the level of nicotinamide adenine dinucleotide We report a case of a 58 year old African American male patient with Coronavirus Disease-2019 (COVID-19) in the setting of multiple concomitant hematologic disorders, including Glucose-6-phosphate dehydrogenase deficiency (G6PD deficiency) and sickle cell trait. Typically, G6PD deficiency remains clinically silent, and only a minority of patients will show signs of chronic hemolytic anemia. However, all G6PD deficient patients are at risk of non-immune hemolysis after exposure to a variety of infectious pathogens, including COVID-19. Our patient displayed evidence of methemoglobinemia and subsequent tissue anoxia. We review the theories and mechanisms behind the increased risk of complications and severity of illness in the context of COVID-19 and hematologic disorders. These patients may require alternative treatment pathways due to their comorbidities. This case emphasizes the complications that can arise in this setting, and highlights important considerations for patient treatment.

Stearic acid methyl ester affords neuroprotection and improves functional outcomes after cardiac arrest.

Cardiac arrest causes neuronal damage and functional impairments that can result in learning/memory dysfunction after ischemia. We previously identified a saturated fatty acid (stearic acid methyl ester, SAME) that was released from the superior cervical ganglion (sympathetic ganglion). The function of stearic acid methyl ester is currently unknown. Here, we show that SAME can inhibit the detrimental effects of global cerebral ischemia (i.e. cardiac arrest). Treatment with SAME in the presence of asphyxial cardiac arrest (ACA) revived learning and working memory deficits. Similarly, SAME-treated hippocampal slices after oxygen-glucose deprivation inhibited neuronal cell death. Moreover, SAME afforded neuroprotection against ACA in the CA1 region of the hippocampus, reduced ionized calcium-binding adapter molecule 1 expression and inflammatory cytokines/chemokines, with restoration in mitochondria respiration. Altogether, we describe a unique and uncharted role of saturated fatty acids in the brain that may have important implications against cerebral ischemia.

Palmitic acid methyl ester is a novel neuroprotective agent against cardiac arrest.

We previously discovered that palmitic acid methyl ester (PAME) is a potent vasodilator first identified and released from the superior cervical ganglion and remain understudied. Thus, we investigated PAME's role in modulating cerebral blood flow (CBF) and neuroprotection after 6 min of cardiac arrest (model of global cerebral ischemia). Our results suggest that PAME can enhance CBF under normal physiological conditions, while administration of PAME (0.02 mg/kg) immediately after cardiopulmonary resuscitation can also enhance CBF in vivo. Additionally, functional learning and spatial memory assessments (via T-maze) 3 days after asphyxial cardiac arrest (ACA) suggest that PAME-treated rats have improved learning and memory recovery versus ACA alone. Furthermore, improved neuronal survival in the CA1 region of the hippocampus were observed in PAME-treated, ACA-induced rats. Altogether, our findings suggest that PAME can enhance CBF, alleviate neuronal cell death, and promote functional outcomes in the presence of ACA.