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Vasculitides
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Ivy M. Obonyo, Virginia A. Jones, Kayla A. Clark, Maria M. Tsoukas
Overview: COVID-19-associated vasculitis/vasculopathy is a group of vasculitides caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The etiology of COVID-19 vasculitis is not well elucidated and continues to evolve. Studies to date show that SARS-CoV-2 infects its host via the angiotensin-converting-enzyme 2 receptor on endothelial cells. These same findings have proposed that SARS-CoV-2 infection and subsequent host inflammatory response enable the initiation of endotheliitis. Ultimately, the outcome of this response may lead to widespread endothelial dysfunction and apoptosis.
Herpes Simplex Virus Ocular Disease
Published in Marie Studahl, Paola Cinque, Tomas Bergström, Herpes Simplex Viruses, 2017
Three forms of HSV endotheliitis are seen clinically: disciform, diffuse, and linear. Disciform endotheliitis is by far the most common form of endotheliitis. It is typically a round area of stromal edema overlying KP in the central or paracentral cornea (Fig. 11). Elevated intraocular pressure may occur from inflammatory cells blocking the aqueous outflow or because of a primary inflammation of the trabecular meshwork. Severe cases may progress to immune interstitial stromal keratitis with permanent edema, scarring, and neovascularization.
Clinical Manifestations and Long-term Outcomes of Endothelial Keratoplasty in Patients with Proven VZV-related Endothelial Decompensation
Published in Ocular Immunology and Inflammation, 2023
Lin-Hui He, Jing-Hao Qu, Rong-Mei Peng, Yun-Xiao Zang, Ge-Ge Xiao, Jing Hong
At the 12-month follow-up, the mean BSCVA improved from 1.12 ± 0.47 logMAR to 0.39 ± 0.43 logMAR (p = .002). The antiviral treatment regimens administered and postoperative complications are summarized in Table 3. Preoperative antiviral treatment was provided to 3 patients, and 5 patients started prophylactic topical and systemic antiviral therapy immediately after surgery. During the follow-up, recurrence of endotheliitis occurred in 3 patients at 6, 6 and 3 months respectively (Figure 3c,d) and scleritis occurred in 1 patient at 6 months. Two patients with endotheliitis were successfully treated by topical and systemic antiviral treatment and one patient with scleritis was successfully treated by topical antiviral treatment. Neurotrophic ulcers occurred in one patient despite receiving sustaining topical and systemic antiviral treatment immediately after surgery. (Figure 3e,f) The other one patient with endotheliitis eventually underwent a second surgery because of graft failure despite receiving sustaining topical and systemic antiviral treatment for 8 months. (Figure 3g,h) There were 5 patients left who didn’t receiving any kind of antiviral treatment. There was no new-onset glaucoma, but 4 patients needed an increased number of antiglaucomatous drugs, and one needed surgery. There were 2 cases of graft detachment, and both were successfully controlled by rebubbling at 3 days and 10 days after surgery, respectively.
Noninvasive Diagnosis of Viral Keratouveitis with Retro-corneal Endothelial Plaques: A Case Series
Published in Ocular Immunology and Inflammation, 2022
Shuo Yu, Debo You, Rupesh Agrawal, Yun Feng
In vivo confocal microscopy plays an important role in the clinical assessment of viral keratitis. Dendritic cells, which appear at the basal epithelial cell level, initiate and control the transition of local innate to adaptive immune responses.18 They migrate to the site of tissue damage during viral infection.19 In our study, the influx of dendritic cells was in accordance with the inflammatory responses during keratitis. We found that the dendritic cells dissipated with clinical improvement from the stromal infiltration. A clear view of the endothelium was difficult to attain at presentation because of the opacification and edema of the stroma. However, morphological alterations characteristic of corneal endotheliitis could be observed after a few days of treatment. The absence or reduction in the responses of the subbasal nerve was probably related to virus invasion and thus led to a decrease in corneal sensitivity. The rapid loss of corneal endothelial cells may lead to decompensation and poor prognosis.
A 22-year-old COVID-19 positive male with no prior medical history presented to the emergency department with pulmonary infarction
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Islam Younes, Ramez Alyacoub, Onyeka Nwachukwu, Anuraag Sah, Remolina Carlos
The pathophysiology of thrombosis in COVID-19 Patients is still unclear. Endotheliitis, hypercoagulability, and hyperviscosity are described in different studies. Endotheliitis is caused by direct viral infection, facilitated by the overexpression of angiotensin-converting enzyme receptor 2, to the endothelial cells with inflammatory cell infiltration was described in Ackermann et al. study. Angiogenesis was also an unexpected finding that was found in this study distinguishing COVID-19 histopathology from Influenza A (H1N1) [6]. Zhang et al. found that hypercoagulability markers as D-dimers, fibrinogen, and factor VIII were found to be elevated in most participants. Protein c, protein S, and antithrombin deficiency were detected in all participants [7]. Systemic extrapulmonary hyper-inflammation and hypercytokinemia are thought to be a cause of hyperviscosity [5,8]. Microthrombi in the lung arteries were described in a case series of autopsy reports from patients with severe acute respiratory syndrome due to COVID-19 [9]. This finding of in situ thrombosis supports the arterial thrombosis and the unusual high prevalence of PE in COVID-19 patients without evidence of DVT [10]. Our 22 year old patient with no known risk factor developed pulmonary embolism with pulmonary infarction without evidence of DVT, supports the possibility of in situ venous and arterial thrombosis.