ABSTRACT
Background: Several studies have suggested that HIF-1α regulates eosinophil activity and induces epithelial inflammation via NF-κB activation in the pathophysiology of asthma. The purpose of this study was to examine the expression of the transcription factors HIF-1α and nuclear HIF in mononuclear cells obtained from peripheral blood samples of healthy pediatric patients, asthmatic patients, and asthmatic exacerbations, regardless of disease severity. Methods: HIF-1 levels were measured using immunocytochemistry in 133 patients aged 6 to 17 years in this crosssectional and comparative study. A microscope was used to examine glass slides, and positive cells were counted in four fields per slide using an image analyzer. Results: HIF-1α and nuclear HIF levels were significantly higher in asthma patients and even higher in patients experiencing asthma attacks (p<0.0001, 95% CI). There was no significant difference in the percentage of HIF-1α expression between groups with intermittent asthma and those with mild persistent asthma, nor between patients with asthma and those experiencing asthma exacerbations. Conclusions: When compared to healthy individuals, the expression of nuclear HIF and HIF-1α is increased in peripheral mononuclear cells in asthma patients and even more so in asthma exacerbations. This suggests that HIF-1α is important in the pathogenesis of this disease.
ABSTRACT
BACKGROUND Subacute thyroiditis, myocarditis, and hepatitis are inflammatory disorders that may develop after viral infections, including SARS-CoV-2. These entities may appear after resolution of the respiratory syndrome. CASE REPORT A previously healthy 64-year-old male patient came to the hospital reporting severe chest pain. He had a history of a COVID-19 pneumonia with PCR confirmation 4 weeks before. On admission to the Coronary Care Unit (CCU), the patient had a negative PCR for SARS-CoV-2; the following tests were performed: total T3 643.4 ng/dl (reference 35-193 ng/dl), total thyroxine 12.0 µg/dl (reference 4.8-11.7 µg/dl), free T4 1.85 ng/dl (reference 0.7-1.48 ng/dl), TSH 0.01 µIU/ml (reference 0.35-4.94 µIU/ml); total bilirubin 0.76 mg/dl (reference 0.0-1.5 mg/dl), alkaline phosphatase 185 U/L (reference 40-150 U/L), alanine aminotransferase 194.6 U/L (reference 6-66 U/L), aspartate aminotransferase 93.4 U/L (reference 9-55 U/L); on admission to the CCU high-sensitivity troponin I 548.3 pg/ml (reference 0.0-34.2 pg/ml), after 24 h in the CCU 801 pg/ml, and after 11 days (as an outpatient) 4.5 pg/ml. A thyroid gammagram revealed absent uptake of the radionuclide. Normal cardiac gammagraphy and cardiac enzymes ruled out myocardial ischemia and infarction. The following diagnoses were made: myocarditis, subacute thyroiditis, and reactive hepatitis due to SARS-CoV-2 infection. CONCLUSIONS COVID-19 has been demonstrated to be a multisystemic inflammatory disorder. The serious illness that developed in our patient after relief of his pulmonary disease underlines this nature. We suggest close follow-up of patients even after apparent clinical resolution, and performing thyroid, myocardial, and liver tests if clinically indicated.
