Corticosteroids for COVID-19 patients requiring oxygen support? Yes, but not for everyone: Effect of corticosteroids on mortality and intensive care unit admission in patients with COVID-19 according to patients' oxygen requirements.

Corticosteroids reduce mortality in hospitalized patients with coronavirus disease 2019 (COVID-19), but the response seems to vary according to the level of respiratory support needed. This retrospective cohort study included COVID-19 patients with oxygen saturation (SatO2 ) in room air <92% admitted between March 3 and April 30, 2020. Following the interim protocol, patients could receive dexamethasone or methylprednisolone, and were classified according to oxygen requirements. The primary endpoint was admission to the intensive care unit (ICU) or mortality. Kaplan-Meier and Cox hazards analyses were used. Of the 115 patients included, 38 received corticosteroids. Among requiring high-flow, noninvasive ventilation (NIV) or fraction of inspired oxygen (FiO2 ) > 0.40, the hazard ratio (HR) for death or ICU admission, between the corticosteroids and non-corticosteroids group, was 0.07 (95% CI 0.01-0.4), p = .002, and for patients requiring low-flow oxygen, the HR was 0.70 (95% CI 0.13-3.8), p = .68. Significant differences were also observed when all patients were analyzed together. A significant reduction in mortality and ICU admission frequency was observed among patients requiring high-flow oxygen or NIV, but not among those requiring low-flow oxygen. Better targeting of COVID-19 patients is needed for the beneficial use of corticosteroids.

A study on the TNF-alpha system in Caucasian Spanish patients with alcoholic liver disease.

BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) is thought to be a critical driving force of inflammatory damage in alcoholic liver disease (ALD). We aimed to establish whether there is a correlation between plasma levels of the soluble TNF-alpha receptors 1 and 2 (sTNFR1 and sTNFR2) and the severity of liver damage in patients with ALD. We also aimed to elucidate whether functionally active polymorphisms in the promoter region of the TNF-alpha gene modulate the development of ALD. DESIGN: We studied 614 Spaniards. Of these, 278 were alcoholics (103 without liver histologic abnormalities, 89 with non-cirrhotic liver disease and 86 with cirrhosis) and 336 were non-alcoholics (115 healthy controls, 114 with non-alcoholic non-cirrhotic liver disease and 107 with cirrhosis unrelated to alcohol). Plasma levels of sTNFR1 and sTNFR2 were determined by ELISA and results were expressed in ng/mL and subsequently converted in log(10). TNF-alpha gene promoter region polymorphisms at the positions -238, -308 and -863 were assessed by restriction fragment length polymorphisms (RFLPs) on white cell DNA. Differences in plasma sTNFR1 and sTNFR2 levels between groups were compared with the one-way and two-factor analysis of variance test, and Student's t-test. Genotype distribution and allele frequencies in the different groups were compared using the chi(2) test or Fisher's exact test. RESULTS: sTNFR1 and sTNFR2 plasma levels were significantly higher in patients with cirrhosis than in those with non-cirrhotic liver disease (p<0.001) and individuals without liver disease (p<0.001), both in the alcoholic and the non-alcoholic group. Among cirrhotics, sTNFR1 and sTNFR2 levels had a significant positive correlation with the severity of the liver disease, graded with the Child-Pugh's score (p=0.003 and p<0.001, respectively). TNF-alpha genotype distribution and allele frequencies of the three loci assessed were similar in the groups studied, hence no particular genotype or haplotype could be linked to ALD. CONCLUSIONS: The TNF-alpha system is activated in patients with cirrhosis of the liver irrespective of aetiology. TNF-alpha polymorphisms at positions -238, -308 and -863 are not linked to ALD.

Cardiovascular abnormalities in hyperthyroidism: a prospective Doppler echocardiographic study.

PURPOSE: We investigated the prevalence and clinical importance of cardiovascular abnormalities in patients with hyperthyroidism. METHODS: All consecutive patients diagnosed with hyperthyroidism during a period of 24 months were included in the study. Medical history, complete physical examination results, electrocardiographic findings, laboratory determinations, and Doppler echocardiographic findings were obtained for all patients within 24 hours of diagnosis, and after euthyroidism had been achieved. Age- and sex-matched controls also were studied. RESULTS: Thirty-nine patients (mean [+/-SD] age, 52 +/- 20 years; range, 25 to 86 years; 72% women), and 39 age- and sex-matched controls, were included. Atrial fibrillation was present in 7 patients (18%). Moderate or severe mitral or tricuspid regurgitation, or both, were present in 9 patients (23%) and in only 1 control (3%; P= 0.01). Mean pulmonary arterial systolic pressure was 38 +/- 12 mm Hg (range, 17 to 64 mm Hg) in patients and 27 +/- 4 mm Hg (range, 19 to 37 mm Hg) in controls (P= 0.001). Sixteen patients (41%) and 1 control (3%) had pulmonary arterial systolic pressure >or=35 mm Hg. Left ventricular systolic dysfunction was detected in 1 patient. After correction of hyperthyroidism, a significant decrease in pulmonary arterial systolic pressure was observed, and the levels became similar to those of controls. CONCLUSION: In patients with hyperthyroidism, there is a high prevalence of pulmonary hypertension and atrioventricular valve regurgitation. These abnormalities usually correct after treatment for hyperthyroidism.