Importance of Insulin Resistance in the COVID-19 Era: A Retrospective Analysis of a Single Center in Mexico.

Introduction and objectives Type 2 diabetes mellitus (T2DM) has been one of the main risk factors associated with mortality from the coronavirus disease 2019 (COVID-19). Insulin resistance (IR) is a preceding and underlying condition of T2DM, which has been thought that it could increase mortality from COVID-19 since it favors the entry of severe acute respiratory syndrome coronavirus type 2 in the host cell. This article reports a biochemical study that estimated the prevalence of IR in COVID-19 patients and non-diabetic patients without COVID-19 history. It also assesses the prognostic role of IR in the evolution of patients with COVID-19. Materials and methods In this single-center, retrospective and cross-sectional design, we included patients with severe and critical COVID-19 and non-diabetic patients without COVID-19 history. We calculated the Homeostatic Model Assessment Insulin Resistance (HOMA-IR) and defined IR with a HOMA-IR >2.6. We estimated the prevalence of IR in both groups and used x 2 to assess the association between IR and mortality from severe and critical COVID-19. Results One hundred and twenty-three COVID-19 patients were included with a mean age of 53±15 years: 77 (62.6%) were men and 46 (37.4%) were women. Eighty (65%) patients were critical while the rest were severe. Forty-three (35%) patients died. Seventy-one (57.7%) patients had IR; there was no evidence of an association between IR and mortality from severe or critical COVID-19. Fifty-five non-diabetic patients without COVID-19 history were included with a median age of 40 (26-60) years; 35 (63.6%) were men and 20 (36.4%) were women. Nineteen (34.5%) people had IR. Conclusion IR was more prevalent in patients with severe and critical COVID-19 than in non-diabetic patients without COVID-19 history. Our results showed no evidence of the association between IR and mortality from severe and critical COVID-19.

Nitric oxide determines the development of actinomycetoma by Nocardia brasiliensis in eNOS knockout C57BL/6 mice.

Mycetoma is a chronic human infectious disease that produces severe deformation frequently in the lower extremities. Etiological agents include fungi (eumycetoma) and bacteria (actinomycetoma) that produce similar clinical and microscopic changes. The clinical appearance includes swelling, abscesses, ulcers, scars and sinuses that drain purulent material with microbe microcolonies. The pathogenesis of actinomycetoma has been studied mainly in rodents. Using this approach, it was found that Nocardia brasiliensis produces proteases that may play a role in tissue damage, as well as immunosuppressive molecules, such as brasilicardin A. Nitric oxide (NO) is a molecule with biological activities depending on its local concentration. Its effect on killing intracellular bacteria such as Mycobacterium tuberculosis has been known for decades. NO plays an important role in innate and adaptive immunity. It can promote or suppress some biological activities despite its short half-ife. NO is produced by three different nitric oxide synthases (NOS). We used the genetic blockade of eNOS in C57BL/6 mice to demonstrate the role of NO in actinomycetoma development. Inflammation and actinomycetoma were prevented in genetically modified mice infected with N. brasiliensis. T cell proliferation was increased in these rodents, and antibody production, IL-6 and IL-10 expression were similar and TNF-α was lower.