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Purpose: To report a case of Epstein-Barr virus (EBV) keratouveitis-induced malignant glaucoma after repeat penetrating keratoplasty (PK). Methods: Retrospective review of the patient's medical records and review of literature on EBV corneal endotheliitis and/or anterior uveitis. Results: A 78-year-old Thai female patient presented with a markedly edematous corneal graft, dense pigmented keratic precipitates, fibrinous anterior chamber reaction, uniformly flat anterior chamber, and ocular hypertension of 55 mmHg in the left eye on the first day after the third PK. An aqueous tap for polymerase chain reaction analysis was positive for EBV DNA but negative for other herpesviruses. The patient was diagnosed with EBV endotheliitis and anterior uveitis-induced malignant glaucoma; and successfully treated with oral valacyclovir and topical 2% ganciclovir eye drops. Conclusions: EBV endotheliitis and anterior uveitis can induce malignant glaucoma following PK. A high index of suspicion is required when a patient has a history of unexplained multiple graft rejections. [ABSTRACT FROM AUTHOR]

Despite the end of the pandemic, coronavirus disease 2019 (COVID-19) remains a major public health concern. The first waves of the virus led to a better understanding of its pathogenesis, highlighting the fact that there is a specific pulmonary vascular disorder. Indeed, COVID-19 may predispose patients to thrombotic disease in both venous and arterial circulation, and many cases of severe acute pulmonary embolism have been reported. The demonstrated presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) within the endothelial cells suggests that direct viral effects, in addition to indirect effects of perivascular inflammation and coagulopathy, may contribute to pulmonary vasculopathy in COVID-19. In this review, we discuss the pathological mechanisms leading to pulmonary vascular damage during acute infection, which appear to be mainly related to thromboembolic events, an impaired coagulation cascade, micro- and macrovascular thrombosis, endotheliitis and hypoxic pulmonary vasoconstriction. As many patients develop post-COVID symptoms, including dyspnea, we also discuss the hypothesis of pulmonary vascular damage and pulmonary hypertension as a sequela of the infection, which may be involved in the pathophysiology of long COVID. [ABSTRACT FROM AUTHOR]

Introduction: Trochlear nerve palsy (TNP) is a common cause of vertical diplopia resulting from superior oblique muscle weakness. While herpes zoster is a well-documented cause of cranial neuropathies, reports of TNP associated with herpes zoster infection remain limited. Case Presentation: We report a case of a 65-year-old patient with typical herpes zoster ophthalmicus on the left side of his face with subsequent corneal endotheliitis and isolated TNP. The MRI revealed a faint enhancement at the cavernous sinus on the same side as the TNP. Cerebrospinal fluid detected human herpesvirus 3, confirming the diagnosis. An intravenous antiviral was administered for 14 days with prolonged maintenance to prevent recurrence. Oral corticosteroids were also used as an adjuvant to reduce inflammation. After treatment, the uveitis subsided, and the vertical diplopia recovered partially. TNP from herpes zoster is a rare presentation. The underlying pathogenic mechanisms, including potential direct viral invasion, inflammatory responses, and possible vasculopathy affecting the trochlear nerve, are explored. Conclusion: TNP can be a rare neuro-ophthalmic complication of herpes zoster infection. Clinicians should maintain a high index of suspicion when assessing patients with cranial neuropathies in the context of herpes zoster. Prompt antiviral therapy and supportive measures can aid in the resolution of symptoms and alleviate potential long-term sequelae.

Introduction: Trochlear nerve palsy (TNP) is a common cause of vertical diplopia resulting from superior oblique muscle weakness. While herpes zoster is a well-documented cause of cranial neuropathies, reports of TNP associated with herpes zoster infection remain limited. Case Presentation: We report a case of a 65-year-old patient with typical herpes zoster ophthalmicus on the left side of his face with subsequent corneal endotheliitis and isolated TNP. The MRI revealed a faint enhancement at the cavernous sinus on the same side as the TNP. Cerebrospinal fluid detected human herpesvirus 3, confirming the diagnosis. An intravenous antiviral was administered for 14 days with prolonged maintenance to prevent recurrence. Oral corticosteroids were also used as an adjuvant to reduce inflammation. After treatment, the uveitis subsided, and the vertical diplopia recovered partially. TNP from herpes zoster is a rare presentation. The underlying pathogenic mechanisms, including potential direct viral invasion, inflammatory responses, and possible vasculopathy affecting the trochlear nerve, are explored. Conclusion: TNP can be a rare neuro-ophthalmic complication of herpes zoster infection. Clinicians should maintain a high index of suspicion when assessing patients with cranial neuropathies in the context of herpes zoster. Prompt antiviral therapy and supportive measures can aid in the resolution of symptoms and alleviate potential long-term sequelae. [ABSTRACT FROM AUTHOR]

ObjectiveTo describe the clinical findings, multimodal corneal imaging features and treatment in canine patients diagnosed with endotheliitis.Animals studiedFour canine patients met inclusion criteria for bilateral corneal disease with endothelial inflammation and secondary corneal edema that responded to topical anti-inflammatory treatment.MethodsThe patients selected underwent a complete ophthalmic examination with emphasis on the cornea including ultrasound pachymetry (USP), Fourier-domain optical coherence tomography (FD-OCT), in vivo confocal microscopy (IVCM), and digital slit lamp photography.ResultsAll patients in this study demonstrated thickened corneas due to edema with USP and FD-OCT. With IVCM, mild to severe polymegathism and pleomorphism of corneal endothelial cells, reduced endothelial cell density, hyperreflective keratic precipitates (KPs), and extracellular debris as well as hyporeflective pseudoguttata were observed. With FD-OCT, hyperreflective KPs were commonly observed on the inferior cornea. Clinical examination and advanced imaging results were consistent with a diagnosis of endotheliitis. All patients initially responded to topical anti-inflammatory treatment and required continued therapy; two patients also received topical netarsudil, a rho-associated coiled-coil kinase inhibitor.ConclusionEndotheliitis should be considered for canine patients with bilateral edema that is most severe in the inferior cornea. Careful inspection of Descemet's membrane-endothelial complex should be performed for KPs or inflammatory debris. Chronic administration of topical anti-inflammatories may be necessary to prevent flare-ups of endotheliitis.

Purpose: To examine the clinical outcomes in chronic or recurrent anterior uveitis in the presence or absence of cytomegalovirus (CMV) and investigate the predictive factors for uveitic activity and recurrence. Methods: Polymerase chain reaction (PCR) was performed in a prospective cohort of immunocompetent adults with recurrent or chronic anterior uveitis to detect CMV in aqueous humor. The clinical outcomes were compared between eyes with and without CMV DNA. Logistic regression was performed to evaluate associations between iris depigmentation, CMV-PCR status, uveitic activity, and recurrence. Results: Thirty-eight eyes of 38 subjects with a mean age of 61.1 ± 11.2 years old were analyzed. Fifteen eyes were positive for CMV. More eyes with CMV developed recurrences and remained actively inflamed at 6, 12, and 24 weeks though the differences were insignificant. The presence of iris depigmentation was predictive of a greater odd of uveitic recurrences by 12 and 24 weeks (Odds ratio (OR) = 9.17 and 5.72, P = 0.007 and 0.034 respectively), whereas positive CMV-PCR predicts a greater odd of uveitic activity at postoperative 12 and 24 weeks (OR = 13.08, 34.30; P = 0.027, 0.007). Conclusion: Eye with and without detectable CMV behaved similarly in their clinical course. Our findings suggested that iris depigmentation was predictive of more frequent uveitic recurrence, regardless of the PCR status, whereas the presence of CMV in aqueous humor was associated with persistent uveitic activity. Iris changes may be present during the earlier phase of the disease and precede the detection of virus from the aqueous humor at a later stage of CMV infection. [ABSTRACT FROM AUTHOR]

Abstract Purpose To describe unusual clinical features and therapeutic management of a case of cytomegalovirus (CMV) ocular disease in a patient on immunomodulatory therapy. Setting/venue Moorfields Eye Hospital NHS Foundation Trust, London, UK. Methods Medical history, clinical findings, investigation results, and multimodal imaging were retrospectively collected. Results A 61-year-old, South-East Asian man, developed CMV-related endotheliitis and occlusive retinal vasculitis, diagnosed by wide-angle fluorescein angiography. No retinitis was present on the fundus examination. Suspicion of CMV etiology was based on anterior segment findings, especially the presence of coin-shaped endothelial lesions. The diagnosis was confirmed by aqueous polymerase chain reaction (PCR) analysis which was positive for CMV DNA. The combined use of topical and systemic valganciclovir resulted in significant improvement of the picture. Conclusions CMV can manifest in the eye as occlusive retinal vasculitis without the presence of typical retinitis.

Despite the end of the pandemic, coronavirus disease 2019 (COVID-19) remains a major public health concern. The first waves of the virus led to a better understanding of its pathogenesis, highlighting the fact that there is a specific pulmonary vascular disorder. Indeed, COVID-19 may predispose patients to thrombotic disease in both venous and arterial circulation, and many cases of severe acute pulmonary embolism have been reported. The demonstrated presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) within the endothelial cells suggests that direct viral effects, in addition to indirect effects of perivascular inflammation and coagulopathy, may contribute to pulmonary vasculopathy in COVID-19. In this review, we discuss the pathological mechanisms leading to pulmonary vascular damage during acute infection, which appear to be mainly related to thromboembolic events, an impaired coagulation cascade, micro- and macrovascular thrombosis, endotheliitis and hypoxic pulmonary vasoconstriction. As many patients develop post-COVID symptoms, including dyspnea, we also discuss the hypothesis of pulmonary vascular damage and pulmonary hypertension as a sequela of the infection, which may be involved in the pathophysiology of long COVID.

Severe acute respiratory syndrome coronavirus-2 causes hyperinflammation and activation of coagulation cascade and, as a result, aggravates endothelial cell dysfunction. N-acetylcysteine and Sulodexide have been found to mitigate endothelial damage. The influence on coronary artery endothelial cells of serum collected after 4 ± 1 months from coronavirus infection was studied. The concentrations of serum samples of interleukin 6, von Willebrand Factor, tissue Plasminogen Activator, and Plasminogen Activator Inhibitor-1 were studied. The cultures with serum of patients after coronavirus infection were incubated with N-acetylcysteine and Sulodexide to estimate their potential protective role. The blood inflammatory parameters were increased in the group of cultures incubated with serum from patients after coronavirus infection. Supplementation of the serum from patients after coronavirus infection with N-acetylcysteine or Sulodexide reduced the synthesis of interleukin 6 and von Willebrand Factor. No changes in the synthesis of tissue Plasminogen Activator were observed. N-acetylcysteine reduced the synthesis of Plasminogen Activator Inhibitor-1. N-acetylcysteine and Sulodexide increased the tPA/PAI-1 ratio. N-acetylcysteine may have a role in reducing the myocardial injury occurring in the post-COVID-19 syndrome. Sulodexide can also play a protective role in post-COVID-19 patients.

Purpose: To describe unusual clinical features and therapeutic management of a case of cytomegalovirus (CMV) ocular disease in a patient on immunomodulatory therapy. Setting/venue: Moorfields Eye Hospital NHS Foundation Trust, London, UK. Methods: Medical history, clinical findings, investigation results, and multimodal imaging were retrospectively collected. Results: A 61-year-old, South-East Asian man, developed CMV-related endotheliitis and occlusive retinal vasculitis, diagnosed by wide-angle fluorescein angiography. No retinitis was present on the fundus examination. Suspicion of CMV etiology was based on anterior segment findings, especially the presence of coin-shaped endothelial lesions. The diagnosis was confirmed by aqueous polymerase chain reaction (PCR) analysis which was positive for CMV DNA. The combined use of topical and systemic valganciclovir resulted in significant improvement of the picture. Conclusions: CMV can manifest in the eye as occlusive retinal vasculitis without the presence of typical retinitis. [ABSTRACT FROM AUTHOR]

In the early months of the outbreak (2020–2022), COVID-19 was responsible for acute respiratory distress syndrome (ARDS) and an exceptional number of intensive care unit (ICU) admissions. Weaning difficulties from invasive mechanical ventilation (IMV) and many deaths related to COVID-19 were associated with persistent pulmonary hyperinflammation leading to pulmonary fibrosis and sometimes, in the first wave of the pandemic and before the use of dexamethasone was introduced, pulmonary cystic necrosis. A 72-year-old man hospitalized with severe COVID-19 required IMV and died on day 31 of refractory ARDS. Postmortem examination of the lungs found obliterative endotheliitis proximal to pulmonary cystic necrosis. The presence of SARS-CoV-2 envelope and complement/lectin (MASP-2) deposits near the endotheliitis lesions suggested that the virus acted directly on vascular involvement by a complement-mediated mechanism. Together with classic features of ARDS (epithelial lesions and diffuse alveolar damage), endothelial involvement with endotheliitis was the hallmark of severe COVID-19. Corticosteroids and complement blockade were sometimes beneficial for treating severe COVID-19, perhaps by preventing microvascular damage.

Here, we report the case of a patient with multiple parallel-line endotheliitis with myopic shift, which has not been previously reported. A 36-year-old man visited our clinic with blurred vision in his left eye. A slit lamp examination revealed an interesting pattern of multiple parallel lines of keratic precipitates, along with subtle corneal edema. The spherical equivalents measured in the right and left eyes were −9.25 and −11.875 diopter, respectively, with the left eye showing more myopic progression. On specular microscopy, endothelial cell loss was found in the left eye. After administration of a weak topical steroid, keratic precipitates and corneal edema resolved completely within 2 days. The myopic shift in his left eye recovered to −10.0 diopters. Multiple parallel-line endotheliitis can be easily treated with a weak topical steroid in a short period. A temporary myopic shift may occur, which in this case resolved upon disease recovery. However, corneal endothelial cell loss is inevitable; therefore, careful monitoring is needed.

Purpose: To examine the clinical outcomes in chronic or recurrent anterior uveitis in the presence or absence of cytomegalovirus (CMV) and investigate the predictive factors for uveitic activity and recurrence. Methods: Polymerase chain reaction (PCR) was performed in a prospective cohort of immunocompetent adults with recurrent or chronic anterior uveitis to detect CMV in aqueous humor. The clinical outcomes were compared between eyes with and without CMV DNA. Logistic regression was performed to evaluate associations between iris depigmentation, CMV-PCR status, uveitic activity, and recurrence. Results: Thirty-eight eyes of 38 subjects with a mean age of 61.1 ± 11.2 years old were analyzed. Fifteen eyes were positive for CMV. More eyes with CMV developed recurrences and remained actively inflamed at 6, 12, and 24 weeks though the differences were insignificant. The presence of iris depigmentation was predictive of a greater odd of uveitic recurrences by 12 and 24 weeks (Odds ratio (OR) = 9.17 and 5.72, P = 0.007 and 0.034 respectively), whereas positive CMV-PCR predicts a greater odd of uveitic activity at postoperative 12 and 24 weeks (OR = 13.08, 34.30; P = 0.027, 0.007). Conclusion: Eye with and without detectable CMV behaved similarly in their clinical course. Our findings suggested that iris depigmentation was predictive of more frequent uveitic recurrence, regardless of the PCR status, whereas the presence of CMV in aqueous humor was associated with persistent uveitic activity. Iris changes may be present during the earlier phase of the disease and precede the detection of virus from the aqueous humor at a later stage of CMV infection.

In the early months of the outbreak (2020–2022), COVID-19 was responsible for acute respiratory distress syndrome (ARDS) and an exceptional number of intensive care unit (ICU) admissions. Weaning difficulties from invasive mechanical ventilation (IMV) and many deaths related to COVID-19 were associated with persistent pulmonary hyperinflammation leading to pulmonary fibrosis and sometimes, in the first wave of the pandemic and before the use of dexamethasone was introduced, pulmonary cystic necrosis. A 72-year-old man hospitalized with severe COVID-19 required IMV and died on day 31 of refractory ARDS. Postmortem examination of the lungs found obliterative endotheliitis proximal to pulmonary cystic necrosis. The presence of SARS-CoV-2 envelope and complement/lectin (MASP-2) deposits near the endotheliitis lesions suggested that the virus acted directly on vascular involvement by a complement-mediated mechanism. Together with classic features of ARDS (epithelial lesions and diffuse alveolar damage), endothelial involvement with endotheliitis was the hallmark of severe COVID-19. Corticosteroids and complement blockade were sometimes beneficial for treating severe COVID-19, perhaps by preventing microvascular damage. [ABSTRACT FROM AUTHOR]

Here, we report the case of a patient with multiple parallel-line endotheliitis with myopic shift, which has not been previously reported. A 36-year-old man visited our clinic with blurred vision in his left eye. A slit lamp examination revealed an interesting pattern of multiple parallel lines of keratic precipitates, along with subtle corneal edema. The spherical equivalents measured in the right and left eyes were −9.25 and −11.875 diopter, respectively, with the left eye showing more myopic progression. On specular microscopy, endothelial cell loss was found in the left eye. After administration of a weak topical steroid, keratic precipitates and corneal edema resolved completely within 2 days. The myopic shift in his left eye recovered to −10.0 diopters. Multiple parallel-line endotheliitis can be easily treated with a weak topical steroid in a short period. A temporary myopic shift may occur, which in this case resolved upon disease recovery. However, corneal endothelial cell loss is inevitable; therefore, careful monitoring is needed. [ABSTRACT FROM AUTHOR]

To report bilateral Herpes Simplex virus (HSV) keratitis in a patient on latanoprost for primi]k=8ary open angle glaucoma (POAG). Case report. A 76-year-old healthy male on latanoprost monotherapy for POAG polresented with sudden bilateral decreased vision. Examination showed bilateral dense corneal edema with loose epithelium. Aqueous fluid was positive for HSV-1 DNA on polymerase chain reaction (PCR). Latanoprost was discontinued, topical prednisolone acetate 1% eye, acyclovir 400 mg 5 times a day and combination of dorzolamide hydrochloride 2% and timolol maleate 0.5% twice daily were prescribed. The vision rapidly improved to 20/25 along with complete resolution of corneal edema within four weeks, with no recurrences over the next one year. Bilateral simultaneous HSV endotheliitis is a rare condition and positive PCR test can help rule in the diagnosis. HSV keratitis is a known adverse event with Latanoprost use and can present atypically. [ABSTRACT FROM AUTHOR]

Po-Jui Chen,1 I-Huang Lin,1 Yi-Chun Chi,2 Chun-Chieh Lai,1 Jia-Horung Hung,1 Sung-Huei Tseng,1 Yi-Hsun Huang1 1Department of Ophthalmology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan; 2Department of Ophthalmology, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, TaiwanCorrespondence: Yi-Hsun Huang, Department of Ophthalmology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan, Email jackhyh@gmail.comAbstract: Purpose: This study aimed to evaluate the therapeutic efficacy and long-term outcomes of treatment with topical 2% ganciclovir solution in immunocompetent patients with aqueous humor polymerase chain reaction (PCR)-proven cytomegalovirus (CMV) anterior uveitis and corneal endotheliitis.Methods: We retrospectively reviewed the findings for immunocompetent patients diagnosed with CMV uveitis or endotheliitis based on clinical manifestations and polymerase chain reaction (PCR) examination results and treated with topical 2% ganciclovir solution at National Cheng Kung University Hospital. Clinical outcome measurements included evaluations of the response rate, relapses, resolution of anterior chamber inflammation, visual acuity, and intraocular pressure.Results: The study included 38 eyes of 32 patients. Long-term administration of topical 2% ganciclovir significantly decreased keratic precipitates (p = 0.001), anterior chamber cells (p = 0.001), and reduced intraocular pressure (p < 0.001). Only one eye was unresponsive to topical ganciclovir treatment, and the recurrence decreased to 0.13 relapses per year. The presence of keratic precipitates and higher intraocular pressure at the initial presentation were significantly associated with recurrence (p = 0.036 and p = 0.001, respectively).Conclusions:: Long-term use of topical 2% ganciclovir solution is effective, safe, and applicable when commercialized ganciclovir gel is not available.Keywords: cytomegalovirus, endotheliitis, ganciclovir, uveitis

Given the scarcity of data regarding ocular complications following COVID‐19 vaccination, the approach toward patients with suggestive symptoms and established clinical practice is lacking. Herein, we report the first case of herpetic endotheliithis and secondary stromal keratitis following inactivated COVID‐19 vaccination who experienced a relapse due to poor adherence. [ABSTRACT FROM AUTHOR]

We hypothesize that the presence of iris depigmentation is associated with the prediction of cytomegalovirus (CMV) as the etiology of chronic or recurrent anterior uveitis. A prospective cohort study on patients with recurrent or chronic anterior uveitis. Pre-operative data on iris depigmentation and corneal endothelial cell densities were compared between eyes with and without CMV. Forty-one eyes of 38 subjects with a mean age of 61.1 ± 11.2 years old were recruited. Seventeen eyes were positive for CMV. A greater proportion of eyes with CMV showed severe or diffuse iris depigmentation than eyes without CMV, and possessed larger corneal endothelial cells (p =.028). When severe iris depigmentation was present with a reduced endothelial cell density, the positive and negative predictive values were raised to 100.0% and 64.9% from 41.5% and 58.5%, respectively. Iris depigmentation is a potential clinical biomarker in predicting CMV in chronic or recurrent anterior uveitis. [ABSTRACT FROM AUTHOR]

We describe 3 patients in California, USA, with trichodysplasia spinulosa polyomavirus (TSPyV) infection of endothelium after steroid administration. We detected TSPyV RNA in tissue specimens by in situ hybridization, which revealed localization to endothelial cells. These cases suggest that diseases associated with endothelial inflammation could be associated with TSPyV infection.

Abstract Background The current case report presents acute hemorrhagic necrotizing encephalopathy (AHNE) as an example of a fatal complication, the etiology of which could be coronavirus disease 2019 (COVID-19) with multiple organ damage along with the existing respiratory tuberculosis. Case presentation A male in his 20s had severe symptoms of central nervous system lesion, which developed against the background of COVID-19 and respiratory tuberculosis, for which he was treated in the intensive care unit. Autopsy confirmed that he died from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) associated AHNE in adults with severe fatal endothelial dysfunction and respiratory tuberculosis. The main morphological signs of brain damage were desquamative endotheliitis, thrombosis, parenchymal hemorrhagic necrosis, encephalitis, severe necrobiotic neuronal damage. Conclusion The defeat of endothelial cells with the development of generalized endotheliitis in COVID-19, especially in conjunction with comorbid pathology, in particular tuberculosis, can lead to a fatal complication that affects the nervous system—AHNE. Therefore, it is worth paying close attention to the appearance of neurological symptoms in patients with a similar combination of diseases.

Abstract Given the scarcity of data regarding ocular complications following COVID‐19 vaccination, the approach toward patients with suggestive symptoms and established clinical practice is lacking. Herein, we report the first case of herpetic endotheliithis and secondary stromal keratitis following inactivated COVID‐19 vaccination who experienced a relapse due to poor adherence.

COVID-19 receives a lot of attention due to its threat to global public health. Research is ongoing to find universal methods to assess the baseline health status of a patient to determine prognosis and management strategies. This study aims to assess the predictive potential of the EASIX (Endothelial Activation and Stress Index) and two of its modifications (mEASIX and sEASIX) in terms of the need for admission to the ICU (intensive care unit), the use of IMV (invasive mechanical ventilation) and death due to COVID-19. The medical data of 370 severely ill patients hospitalised in the COVID-19 departments of the Regional Specialist Hospital in Wroclaw (Poland), including the ICU, were analysed retrospectively. The mortality rate in the group studied was 65.7% (243 cases). In the case of all three indices, EASIX, mEASIX and sEASIX, there was a statistically significant correlation between the need for admission to the ICU (p = 0.026, p = 0.019, p = 0.001, respectively) and the risk of death (p < 0.001). In terms of the risk of death, the high values of the assessed indices (EASIX ≥ 2.36, mEASIX ≥ 704.03, sEASIX ≥ 3.81) were characterised by low sensitivity (≤40%), high specificity (approximately 90%) and low NPV (negative predictive value) (approximately 40%) with high PPV (positive predictive value) (approximately 80%). Due to the ease of implementation and the low cost of performing basic laboratory tests, the above-mentioned indices can be used as an additional, but not universal tool for the initial assessment of the health condition of patients admitted to the hospital. [ABSTRACT FROM AUTHOR]

Cytomegalovirus (CMV) anterior uveitis is the most common form of ocular manifestation of CMV in immunocompetent individuals. The difficulty in diagnosing CMV anterior uveitis may delay adequate treatment and affect outcomes. We sought to review systemically the overall clinical characteristics and compare treatment outcomes in CMV anterior uveitis and endotheliitis. A literature search was performed, and studies describing clinical characteristics, treatment regimens, and outcomes that included more than 5 treated eyes were included. In these 23 studies, acute CMV anterior uveitis commonly presented with high intraocular pressure (95.31%, 95% CI 90.45–98.60) and mild anterior chamber inflammation (cells >2+ = 3.18%, 95% CI 0.21–0.54). About two-thirds of CMV endotheliitis cases presented with high intraocular pressure and coin-shaped corneal lesions. Acute CMV anterior uveitis showed good clinical response to topical 0.15% ganciclovir (GCV) gel or oral valganciclovir (VGCV) (90%, 95% CI 74–100% and 95%, 95% CI 88–100%, respectively). For chronic CMV anterior uveitis, both topical GCV and oral VGCV yielded comparable results. Topical 0.5–2% GCV or a combination of topical and oral VGCV for CMV endotheliitis both resulted in good clinical response. Recurrence of inflammation was common after cessation of maintenance therapy. Overall, topical GCV resulted in an optimal outcome for CMV anterior uveitis. Escalated concentration and frequency of usage are needed for chronic CMV anterior uveitis and endotheliitis. Adequate induction and maintenance phases of anti-CMV treatment seem necessary to prevent recurrences. [ABSTRACT FROM AUTHOR]

Virus induced endothelial dysregulation is a well-recognised feature of severe Covid-19 infection. Endothelin-1 (ET-1) is the most highly expressed peptide in endothelial cells and a potent vasoconstrictor, thus representing a potential therapeutic target. ET-1 plasma levels were measured in a cohort of 194 Covid-19 patients stratified according to the clinical severity of their illness. Hospitalised patients, including those who died and those developing acute myocardial or kidney injury, had significantly elevated ET-1 plasma levels during the acute phase of infection. The results support the hypothesis that endothelin receptor antagonists may provide clinical benefit for certain Covid-19 patients. [Display omitted] • Dysregulation of endothelial function is a feature of severe Covid-19 infection. • The endothelial peptide, ET-1 is a potential therapeutic target. • Higher circulating ET-1 levels are associated with more severe infection. • Endothelin receptor antagonists may be of clinical benefit in Covid-19. [ABSTRACT FROM AUTHOR]

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the ongoing global coronavirus (COVID-19) pandemic. Although initially viewed as an acute respiratory illness, COVID-19 is clearly a complex multisystemic disease with extensive cardiovascular involvement. Emerging evidence shows that the endothelium plays multiple roles in COVID-19 physiopathology, as both a target organ that can be directly infected by SARS-CoV-2 and a mediator in the subsequent inflammatory and thrombotic cascades. Arterial stiffness is an established marker of cardiovascular disease. The scope of this review is to summarize available data on the acute and long-term consequences of COVID-19 on vascular function. COVID-19 causes early vascular aging and arterial stiffness. Fast, noninvasive bedside assessment of arterial stiffness could optimize risk stratification in acute COVID-19, allowing for early escalation of treatment. Vascular physiology remains impaired at least 12 months after infection with SARS-CoV-2, even in otherwise healthy adults. This raises concerns regarding the extent of arterial remodeling in patients with preexisting vascular disease and the potential development of a persistent, chronic COVID-19 vasculopathy. Long-term follow up on larger cohorts is required to investigate the reversibility of COVID-19-induced vascular changes and their associated prognostic implications. [ABSTRACT FROM AUTHOR]

The SARS-CoV-2 virus ACE-2 receptor utilization for cellular entry and the defined ACE-2 receptor role in cardiovascular medicine hinted at dysregulated endothelial function or even direct viral endotheliitis as the key driver of severe COVID-19 vascular immunopathology including reports of vasculitis. In this article, we critically review COVID-19 immunopathology from the vasculitis perspective and highlight the non-infectious nature of vascular endothelial involvement in severe COVID-19. Whilst COVID-19 lung disease pathological changes included juxta-capillary and vascular macrophage and lymphocytic infiltration typical of vasculitis, we review the evidence reflecting that such "vasculitis" reflects an extension of pneumonic inflammatory pathology to encompass these thin-walled vessels. Definitive, extrapulmonary clinically discernible vasculitis including cutaneous and cardiac vasculitis also emerged- namely a dysregulated interferon expression or "COVID toes" and an ill-defined systemic Kawasaki-like disease. These two latter genuine vasculitis pathologies were not associated with severe COVID-19 pneumonia. This was distinct from cutaneous vasculitis in severe COVID-19 that demonstrated pauci-immune infiltrates and prominent immunothrombosis that appears to represent a novel immunothrombotic vasculitis mimic contributed to by RNAaemia or potentially diffuse pulmonary venous tree thrombosis with systemic embolization with small arteriolar territory occlusion, although the latter remains unproven. Herein, we also performed a systematic literature review of COVID-19 vasculitis and reports of post-SARS-CoV-2 vaccination related vasculitis with respect to the commonly classified pre-COVID vasculitis groupings. Across the vasculitis spectrum, we noted that Goodpasture's syndrome was rarely linked to natural SARS-CoV-2 infection but not vaccines. Both the genuine vasculitis in the COVID-19 era and the proposed vasculitis mimic should advance the understanding of both pulmonary and systemic vascular immunopathology. [ABSTRACT FROM AUTHOR]

Abstract Background Cytomegalovirus (CMV) can manifest as corneal endotheliitis in immunocompetent individuals. Early diagnosis is prudent to prevent endothelial cell loss, which could ultimately lead to corneal decompensation. CMV DNA was first detected in an eye with corneal endotheliitis in 2006; since then, clinical evidence from numerous case reports and case series have accumulated. Main text In this narrative review, we identified several drugs, including ganciclovir, valganciclovir, and their combination in oral, intravenous, intravitreal, and topical forms in different concentrations, together with the judicious use of topical steroids, have reported variable success. There has yet to be any prospective comparative study evaluating the efficacy and safety of these assorted forms of treatment; clinical evidence is based on case reports and case series. CMV endotheliitis presenting with corneal edema can masquerade as other corneal diseases and thus poses a great challenge especially in post-keratoplasty eyes. Heightened awareness is needed before and after keratoplasty to start prompt prophylaxis and treatment. Conclusion There is no consensus on the management of CMV endotheliitis. Further studies are much needed to elucidate the optimal treatment modality, regime, and duration in the treatment and prophylaxis of CMV endotheliitis.

Cardiovascular dysfunction and disease are common and frequently fatal complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Indeed, from early on during the SARS-CoV-2 virus pandemic it was recognized that cardiac complications may occur, even in patients with no underlying cardiac disorders, as part of the acute infection, and that these were associated with more severe disease and increased morbidity and mortality. The most common cardiac complication is acute cardiac injury, defined by significant elevation of cardiac troponins. The potential mechanisms of cardiovascular complications include direct viral myocardial injury, systemic inflammation induced by the virus, sepsis, arrhythmia, myocardial oxygen supply-demand mismatch, electrolyte abnormalities, and hypercoagulability. This review is focused on the prevalence, risk factors and clinical course of COVID-19-related myocardial injury, as well as on current data with regard to disease pathogenesis, specifically the interaction of platelets with the vascular endothelium. The latter section includes consideration of the role of SARS-CoV-2 proteins in triggering development of a generalized endotheliitis that, in turn, drives intense activation of platelets. Most prominently, SARS-CoV-2–induced endotheliitis involves interaction of the viral spike protein with endothelial angiotensin-converting enzyme 2 (ACE2) together with alternative mechanisms that involve the nucleocapsid and viroporin. In addition, the mechanisms by which activated platelets intensify endothelial activation and dysfunction, seemingly driven by release of the platelet-derived calcium-binding proteins, SA100A8 and SA100A9, are described. These events create a SARS-CoV-2–driven cycle of intravascular inflammation and coagulation, which contributes significantly to a poor clinical outcome in patients with severe disease. [ABSTRACT FROM AUTHOR]

Background: Although the lung is seen as the main target organ affected by SARS-CoV-2, other organs are also damaged. Aim: We aimed to determine the extrapulmonary findings of autopsies performed on cases with positive results with postmortem polymerase chain reaction test. Methods: Pathological changes in extrapulmonary organs were examined with light microscopy. Results: Heart, liver, spleen, kidney, pancreas, and central nervous system samples of these cases were evaluated. About 80% of the cases were men, and 20% were women. In the examination of heart, 28 of the cases had scar, 14 had acute myocardial infarction, 6 had acute and previous myocardial infarction findings, 2 had myocarditis, and 4 had interstitial mononuclear inflammatory cell infiltration. In the examination of the liver, portal inflammation was observed in 84 of the cases, steatosis in 54, centrilobular necrosis in 9, and capillary endotheliitis in the portal area in 7 of them. In the evaluation of the kidney, 37 cases had chronic pyelonephritis, 36 had tubular damage, 15 had tubulointerstitial necrosis, 16 had subcapsular microhemorrhage, 10 had capillary endothelitis, and 9 had a microvascular fibrin trombosis in their glomerular capillaries. In the central nervous system, 8 cases had infarction and liquefaction, 56 had perivascular petechial hemorrhage, 54 had acute hypoxic ischemic change, 3 had parenchymal microhemorrhage, and 52 had capillary endotheliitis. Conclusion: Autopsies play an important role in systematically examining the damage caused by the virus in all organs in order to elucidate the pathogenesis of SARS-CoV-2 infection and contribute to the clinical management of infected patients. [ABSTRACT FROM AUTHOR]

Cardiovascular dysfunction and disease are common and frequently fatal complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Indeed, from early on during the SARS-CoV-2 virus pandemic it was recognized that cardiac complications may occur, even in patients with no underlying cardiac disorders, as part of the acute infection, and that these were associated with more severe disease and increased morbidity and mortality. The most common cardiac complication is acute cardiac injury, defined by significant elevation of cardiac troponins. The potential mechanisms of cardiovascular complications include direct viral myocardial injury, systemic inflammation induced by the virus, sepsis, arrhythmia, myocardial oxygen supply-demand mismatch, electrolyte abnormalities, and hypercoagulability. This review is focused on the prevalence, risk factors and clinical course of COVID-19-related myocardial injury, as well as on current data with regard to disease pathogenesis, specifically the interaction of platelets with the vascular endothelium. The latter section includes consideration of the role of SARS-CoV-2 proteins in triggering development of a generalized endotheliitis that, in turn, drives intense activation of platelets. Most prominently, SARS-CoV-2–induced endotheliitis involves interaction of the viral spike protein with endothelial angiotensin-converting enzyme 2 (ACE2) together with alternative mechanisms that involve the nucleocapsid and viroporin. In addition, the mechanisms by which activated platelets intensify endothelial activation and dysfunction, seemingly driven by release of the platelet-derived calcium-binding proteins, SA100A8 and SA100A9, are described. These events create a SARS-CoV-2–driven cycle of intravascular inflammation and coagulation, which contributes significantly to a poor clinical outcome in patients with severe disease.

BackgroundThe diagnosis of antibody-mediated rejection (AMR) in the lung transplant is still an area under investigation. We performed a blinded multicenter study to determine if any statistically significant histologic findings in transbronchial biopsy specimens from lung transplant patients correlate with the presence of donor-specific antibodies (DSAs).MethodsWe asked 9 pathologists with experience in lung transplantation to evaluate 161 lung transplant biopsy specimens for various histologic parameters. The findings were correlated with antibody status positive for DSAs, positive for non-DSAs, and no antibodies (NABs) present. The significance of each histologic variable was reviewed.ResultsWe found no statistically significant association with acute cellular rejection, airway inflammation, or bronchiolitis obliterans and the presence or absence of antibodies. However, biopsy specimens with DSAs had a statistically significant difference vs NABs in the setting of acute lung injury, with or without diffuse alveolar damage (p = 0.0008), in the presence of capillary neutrophilic inflammation (p = 0.0014), and in samples with endotheliitis (p = 0.0155). In samples with complement 4d staining, there was a trend but no statistically significant difference between specimens associated with DSAs and specimens with NABs.ConclusionsCapillary inflammation, acute lung injury, and endotheliitis significantly correlated with DSAs. The infrequently observed diffuse staining for complement 4d limits the usefulness of this stain.

The SARS‐CoV‐2 is a new coronavirus responsible for the COVID‐19 disease and has caused the pandemic worldwide. A large number of cases have overwhelmed the healthcare system worldwide. The COVID‐19 infection has been associated with a heightened risk of thromboembolic complications. Various mechanisms are leading to the high thrombotic risk in COVID‐19 patients such as inflammation, endotheliitis, hyperviscosity, and hypercoagulability. We searched PubMed, EMBASE, and CINAHL from January 2020 to December 2020. We used the following search terms: COVID‐19, coagulopathy, and thrombosis. We reviewed the epidemiology, clinical features, mechanisms, and treatment of COVID‐19‐associated coagulopathy. [ABSTRACT FROM AUTHOR]

Background: The current case report presents acute hemorrhagic necrotizing encephalopathy (AHNE) as an example of a fatal complication, the etiology of which could be coronavirus disease 2019 (COVID-19) with multiple organ damage along with the existing respiratory tuberculosis. Case presentation: A male in his 20s had severe symptoms of central nervous system lesion, which developed against the background of COVID-19 and respiratory tuberculosis, for which he was treated in the intensive care unit. Autopsy confirmed that he died from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) associated AHNE in adults with severe fatal endothelial dysfunction and respiratory tuberculosis. The main morphological signs of brain damage were desquamative endotheliitis, thrombosis, parenchymal hemorrhagic necrosis, encephalitis, severe necrobiotic neuronal damage. Conclusion: The defeat of endothelial cells with the development of generalized endotheliitis in COVID-19, especially in conjunction with comorbid pathology, in particular tuberculosis, can lead to a fatal complication that affects the nervous system—AHNE. Therefore, it is worth paying close attention to the appearance of neurological symptoms in patients with a similar combination of diseases. [ABSTRACT FROM AUTHOR]

Arterial thromboembolic complications reported in patients with COVID-19 infection suggested that SARS-CoV-2 can trigger atherosclerotic plaque vulnerability. While endothelial cells in healthy subjects protect against thrombus formation, after injury they show prothrombotic activity. In addition, it has been hypothesized that "cytokine storm" might stimulate the production of neo-platelets triggering an abnormal "immunothrombosis" responsible for the hypercoagulable state induced in COVID-19 patients. The aim of this study is to report a case of severe COVID-19 infection characterized by the occurrence of microthrombosis in the vasa vasorum of the aorta. A 67-year-old male patient, in good health status and without comorbidities, who underwent a severe COVID-19 infection with fatal outcome, showed scattered aortic atherosclerotic plaques, characterized by multiple occlusive micro-thromboses in the vasa vasorum, spread out lymphocytic infiltrates and foci of endotheliitis and endothelial detachment. This case report confirms the previously described thrombotic involvement of vasa vasorum in COVID-19. The occurrence of the synchronous damage involving both the lumen surface (endothelial dysfunction, endotheliitis and endothelial detachment) and the adventitia (inflammation and occlusive thrombosis of vasa vasorum) could be the key points related to the fatal outcome of the SARS-CoV-2 patients. In our opinion, vasa vasorum thrombosis may thus initiate an atherogenic process that could be characterized by a much more rapid development. [ABSTRACT FROM AUTHOR]

Extrapulmonary manifestations of COVID-19 (Coronavirus disease 2019) are increasingly recognized. Secondary spinal infections are dangerous complications reported in a few cases in the literature. However, to our knowledge, there is no reported case of a severe spondylodiscitis (SD) complicated with a large psoas abscess in a COVID-19 patient. We would like to report a 43-year-old male patient living in central Anatolia and dealing with farming who presented to the hospital with a complaint of severe back pain. The patient who was given oral treatment with analgesic, anti-inflammatory, and myorelaxant agents was readmitted with increased complaints. His nasopharyngeal swab was positive for COVID-19 without pneumonia on chest computed tomography (CT). He spent the quarantine and treatment period at home but was admitted to our outpatient clinic with a wheelchair with increased complaints and right leg pain preventing daily activities. The control nasopharyngeal swab was negative for COVID-19 but further increase in C-reactive protein (CRP) (152,8 mg/L) and creatine kinase (CK) level (549 IU/L) were revealed. Lumbar magnetic resonance imaging (MRI) showed SD in the L3-L4 level along with right-sided prevertebral inflammatory soft tissue and a large right psoas muscle abscess. Pyogenic lumbar SD complicated with the right psoas abscess in the setting of COVID-19 was considered and antibacterial treatment was started following hospitalization. On the same day, percutaneous aspiration from the psoas abscess under CT guidance was performed and revealed no growth in the culture. After 3 weeks, follow-up MRI showed worsening of all the bone, soft tissue and disc findings. Myalgia is a common manifestation in viral infections, which was also demonstrated in COVID-19 patients, with possible increase in muscle enzymes. Secondary spinal infections and its soft-tissue complications should be considered in the management of COVID-19 patients with neuromuscular symptoms, and detailed neurological and neurosurgical evaluation should be performed in order to avoid progression and permanent damage.

We describe 3 patients in California, USA, with trichodysplasia spinulosa polyomavirus (TSPyV) infection of endothelium after steroid administration. We detected TSPyV RNA in tissue specimens by in situ hybridization, which revealed localization to endothelial cells. These cases suggest that diseases associated with endothelial inflammation could be associated with TSPyV infection. [ABSTRACT FROM AUTHOR]

Myocarditis has been reported as a possible clinical presentation or complication in patients with coronavirus disease (COVID)-19 due to SARS-CoV-2. Despite the alarm that this possibility generated among physicians, there is paucity of information about mechanisms, prevalence, prognosis, diagnosis and therapy of myocarditis in the context of COVID-19. This brief review has the goal to revise and summarize current knowledge on myocarditis in COVID-19 patients and underline problems especially related to diagnosis and treatment. [ABSTRACT FROM AUTHOR]

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Background: Early identification of patients at high risk of progression to severe COVID- 19 constituted an unsolved challenge. Although growing evidence demonstrates a direct association between endotheliitis and severe COVID- 19, the role of endothelial damage biomarkers has been scarcely studied. We investigated the relationship between circulating mid- regional proadrenomedullin (MR- proADM) levels, a biomarker of endothelial dysfunction, and prognosis of SARS- CoV- 2- infected patients. Methods: Prospective observational study enrolling adult patients with confirmed COVID- 19. On admission to emergency department, a blood sample was drawn for laboratory test analysis. Primary and secondary endpoints were 28- day all- cause mortality and severe COVID- 19 progression. Area under the curve (AUC) and multivariate regression analysis were employed to assess the association of the biomarker with the established endpoints. Results: A total of 99 patients were enrolled. During hospitalization, 25 (25.3%) cases progressed to severe disease and the 28- day mortality rate was of 14.1%. MR- proADM showed the highest AUC to predict 28- day mortality (0.905; [CI] 95%: 0.829- 0.955; P < .001) and progression to severe disease (0.829; [CI] 95%: 0.740- 0.897; P < .001), respectively. MR- proADM plasma levels above optimal cut- off (1.01 nmol/L) showed the strongest independent association with 28- day mortality risk (hazard ratio [HR]: 10.470, 95% CI: 2.066- 53.049; P < .005) and with progression to severe disease (HR: 6.803, 95% CI: 1.458- 31.750; P = .015). Conclusion: Mid- regional proadrenomedullin was the biomarker with highest performance for prognosis of death and progression to severe disease in COVID- 19 patients and represents a promising predictor for both outcomes, which might constitute a potential tool in the assessment of prognosis in early stages of this disease. [ABSTRACT FROM AUTHOR]

Coronavirus disease 19 (COVID‐19) is a rapidly evolving pandemic caused by the coronavirus Sars‐CoV‐2. Clinically manifest central nervous system symptoms have been described in COVID‐19 patients and could be the consequence of commonly associated vascular pathology, but the detailed neuropathological sequelae remain largely unknown. A total of six cases, all positive for Sars‐CoV‐2, showed evidence of cerebral petechial hemorrhages and microthrombi at autopsy. Two out of six patients showed an elevated risk for disseminated intravascular coagulopathy according to current criteria and were excluded from further analysis. In the remaining four patients, the hemorrhages were most prominent at the grey and white matter junction of the neocortex, but were also found in the brainstem, deep grey matter structures and cerebellum. Two patients showed vascular intramural inflammatory infiltrates, consistent with Sars‐CoV‐2‐associated endotheliitis, which was associated by elevated levels of the Sars‐CoV‐2 receptor ACE2 in the brain vasculature. Distribution and morphology of patchy brain microbleeds was clearly distinct from hypertension‐related hemorrhage, critical illness‐associated microbleeds and cerebral amyloid angiopathy, which was ruled out by immunohistochemistry. Cerebral microhemorrhages in COVID‐19 patients could be a consequence of Sars‐ CoV‐2‐induced endotheliitis and more general vasculopathic changes and may correlate with an increased risk of vascular encephalopathy. [ABSTRACT FROM AUTHOR]

The new coronavirus disease (COVID-19) is a systemic disease. Mounting evidence depict signs and symptoms involving multiple organs, most of which supported by pathological data. A plausible link to these manifestations is vascular and endothelial dysfunction/damage. However, much of the current knowledge relies on opinion and incipient evidence. We aim to objectively appraise current evidence on the association between COVID-19 and vascular disease, specifically endotheliitis and vasculitis. Two researchers independently entered the search terms COVID-19 OR SARS-CoV-2 AND vasculitis, endotheliitis OR endothelium in the following online platforms: MedRxiv and LitCovid (PubMed). The search period was set from November 1, 2019 to August 28, 2020. Manuscripts with unavailable full texts, not in English, mainly on pre-clinical data, presenting only study designs or not directly related to the topics of this review were excluded. Retrospective and prospective studies, especially longitudinal ones, were given priority to the purpose of this review. Since there was paucity of prospective controlled evidence, case reports/series were also considered. A total of 318 manuscripts were initially found. Sixty-seven (21%) were excluded: 59 (18.5%) met exclusion criteria and 8 (2.5%) were duplicates. One hundred and forty-two manuscripts (44,6%) did not provide original data and were also excluded: 35 (11%) were comments, 108 (33.9%) reviews; 1 (0.3%) position paper. One hundred and seven (33.6%) studies were considered for the present scoping review: 81 (25,5%) case reports/series; 18 (5.7%) prospective; 8 (2.5%) retrospective. Viral inclusions in endothelial cells, mononuclear cell infiltrates in the intima of small vessels and markers of endothelial cell apoptosis were demonstrated. Specificities of COVID-19 may lead to diverse vascular manifestations in different levels of the vascular bed. Evidence indicates that COVID-19 targets vasculature and endothelium. However, high quality data is still lacking and studies with prospective designs and appropriately matched controls are needed. [Display omitted] • The new coronavirus disease (Covid-19) is a systemic disease. • Vascular and endothelial dysfunction/damage at different levels is a plausible link through which the disease can occur. • Endothelial cell damage and apoptosis could lead to basal membrane exposure and a thrombotic macro- and/or microangiopathy. • Endothelial cell dysfunction due to unbalanced angiotensin II could drive vasoconstriction in virtually any affected organ. • Endothelial cells are recognized as part of the innate immune system and could play a role in an exacerbated inflammation. [ABSTRACT FROM AUTHOR]

To describe an immunocompetent patient with corneal endotheliitis caused by concomitant infection of cytomegalovirus and varicella zoster virus (VZV). A 37-year-old immunocompetent woman was referred to our hospital because of persistent corneal endotheliitis in the left eye. Slit-lamp examination revealed mild conjunctival injection, localized stromal corneal edema with underlying pigmented keratic precipitates, and inferior superficial corneal neovascularization. Anterior chamber examination revealed grade 2+ inflammatory cells. Real-time polymerase chain reaction analysis of aqueous humor supported a diagnosis of concomitant cytomegalovirus and VZV corneal endotheliitis. Treatment comprised oral valganciclovir and oral acyclovir for 6 weeks. During 12 months of follow-up, the cornea was clear, keratic precipitates were absent, and anterior chamber inflammation was resolved. No recurrences were noted. Untreated corneal endotheliitis can cause corneal decompensation and permanent endothelial cell loss. Dual infection must be considered in patients with corneal endotheliitis, particularly those with inadequate treatment responses. Timely detection of causative agents and administration of an appropriate treatment regimen can prevent corneal damage. [ABSTRACT FROM AUTHOR]

Abstract The corneal endothelium plays an integral role in regulating corneal hydration and clarity. Endotheliitis, defined as inflammation of the corneal endothelium, may disrupt endothelial function and cause subsequent visual changes. Corneal endotheliitis is characterized by corneal edema, the presence of keratic precipitates, anterior chamber inflammation, and occasionally limbal injection, neovascularization, and co-existing or superimposed uveitis. The disorder is classified into four subgroups: linear, sectoral, disciform, and diffuse. Its etiology is extensive and, although commonly viral, may be medication-related, procedural, fungal, zoological, environmental, or systemic. Not all cases of endothelial dysfunction leading to corneal edema are inflammatory in nature. Therefore, it is imperative that practitioners consider a broad differential for patients presenting with possible endotheliitis, as well as familiarize themselves with appropriate diagnostic and therapeutic modalities.

COVID-19 receives a lot of attention due to its threat to global public health. Research is ongoing to find universal methods to assess the baseline health status of a patient to determine prognosis and management strategies. This study aims to assess the predictive potential of the EASIX (Endothelial Activation and Stress Index) and two of its modifications (mEASIX and sEASIX) in terms of the need for admission to the ICU (intensive care unit), the use of IMV (invasive mechanical ventilation) and death due to COVID-19. The medical data of 370 severely ill patients hospitalised in the COVID-19 departments of the Regional Specialist Hospital in Wroclaw (Poland), including the ICU, were analysed retrospectively. The mortality rate in the group studied was 65.7% (243 cases). In the case of all three indices, EASIX, mEASIX and sEASIX, there was a statistically significant correlation between the need for admission to the ICU (p = 0.026, p = 0.019, p = 0.001, respectively) and the risk of death (p < 0.001). In terms of the risk of death, the high values of the assessed indices (EASIX ≥ 2.36, mEASIX ≥ 704.03, sEASIX ≥ 3.81) were characterised by low sensitivity (≤40%), high specificity (approximately 90%) and low NPV (negative predictive value) (approximately 40%) with high PPV (positive predictive value) (approximately 80%). Due to the ease of implementation and the low cost of performing basic laboratory tests, the above-mentioned indices can be used as an additional, but not universal tool for the initial assessment of the health condition of patients admitted to the hospital.