Importance. COVID-19 is caused by SARS-CoV-2, a betacoronavirus that uses the angiotensin-converting enzyme-related carboxypeptidase (ACE2) receptor to gain entry into cells. ACE2 receptor is widely expressed in multiple organs, including the retina, an extension of the central nervous system. The ACE2 receptor is involved in the diabetic and hypertensive retinopathy. Additionally, coronaviruses cause ocular infections in animals, including retinitis, and optic neuritis. Objective. To assess whether there is any retinal disease associated with COVID-19. Design. We have evaluated 27 asymptomatic subjects, with retinal fundoscopic, optical coherence tomography (OCT) and OCT angiography fourteen days after hospital discharge due to COVID-19 bilateral pneumonia. Results. Cotton wool exudates were evident in six out of 27 patients evaluated, a 22%. Cotton wool exudates are a marker vascular disease severity in other medical context, that is diabetes and hypertension, and are associated with increased risk for acute vascular events. Whether antiaggregation therapy may play a role on fundoscopicselected patients with COVID-19 requires prospective trials.
Antiphospholipid antibodies are a type of autoantibodies that have been implicated in the occurrence of thrombocytopenia and thrombotic events and have been described in autoimmune disorders and diverse viral diseases. In this study anticardiolipin antibodies (immunoglobulin G [IgG] isotype) were determined in serum from 100 patients with chronic hepatitis C and 52 healthy controls. In addition, hepatitis C virus (HCV) markers (anti-HCV and HCV RNA) were investigated in 73 patients with thrombotic disorders and no clinical evidence of liver disease; of these patients 37 cases tested negatively for anticardiolipin antibodies and 36 positively. Anticardiolipin test was positive more frequently (22%) in the group of patients with chronic hepatitis C than in healthy controls (1.9%; P < .001). Using conditional logistic-regression analysis we found that in hepatitis C patients the presence of thrombocytopenia, portal hypertension and the existence of prior thrombotic episodes were significantly related to positivity for anticardiolipin antibodies (P < .05 in all cases). In patients with no evidence of liver disease and a history of thrombotic events, hepatitis C markers were absent in all cases who tested negatively for anticardiolipin antibodies (n = 37), but were present in 16.7% of those positive for anticardiolipin (n = 36) (P = .01). In conclusion, anticardiolipin antibodies are frequently found in patients with chronic hepatitis C and in these patients they may be implicated in the occurrence of thrombosis and in the development of thrombocytopenia. Occult HCV infection is present in a significant proportion of patients with thrombotic disorders and positive for anticardiolipin (the antiphospholipid syndrome).
The purpose of this investigation was to compare the genotypic profiles of Staphylococcus aureus isolated from atopic dermatitis (AD) patients and from control subjects, and to study the relationship between clinical severity, immune response, and genomic pattern of S. aureus isolated from AD patients. We selected 32 patients with AD and S. aureus skin colonization and 31 atopic controls with no history of AD who where asymptomatic carriers of S. aureus. Microarray-based genotyping was performed on S. aureus isolates. In AD patients, clinical severity was assessed using the Scoring Atopic Dermatitis index and total IgE levels and staphylococcal superantigen-specific IgE levels (SEA, SEB, SEC, TSST1) were determined. The genes lukE, lukD, splA, splB, ssl8, and sasG were more frequent in isolates from AD patients. CC30 was more common in isolates from atopic controls than in AD patients. There was a correlation between total IgE and clinical severity, but an association between clinical severity, immune response, and the presence of S. aureus superantigen genes, including enterotoxin genes, could not be demonstrated. Finally, a correlation was found between AD severity and other S. aureus genes, such as sasG and scn. S. aureus factors besides superantigens could be related to the worsening and onset of AD.
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