Reactivation of Acute Retinal Necrosis following SARS-CoV-2 Infection.

PURPOSE: To report on a case of reactivation of acute retinal necrosis following SARS-CoV-2 infection. METHODS: Observational case report. Observations. A 32-year-old female with a distant history of left retinal detachment secondary to necrotizing herpetic retinitis complained of right-eye vision loss, pain, redness, and photophobia. An ophthalmological examination revealed findings consistent with acute retinal necrosis of the right eye. A polymerase chain reaction (PCR) analysis of the right vitreous was positive for herpes simplex virus type 2 (HSV-2). A coronavirus disease 2019 (COVID-19) screening test using reverse transcriptase- (RT-) PCR was positive for SARS-CoV-2 RNA. CONCLUSIONS: Our case suggests that COVID-19 may cause a latent HSV infection to reactivate, causing contralateral involvement in patients with a prior history of HSV-associated acute retinal necrosis.

Pharmacotherapy as an adjunct to vitrectomy.

Vitreoretinal surgery has advanced extensively from the first days of vitrectomy. During the last decade, new developments in intravitreal pharmacotherapy have created new opportunities to enhance the surgical outcomes of our patients. In this article, we review and discuss some of the supporting evidence of different pharmacotherapies that may be used as an adjunct to vitrectomy for select common etiologies. Triamcinolone acetonide, dexamethasone, and angiogenesis inhibitors are among the most commonly used drugs given their safety profile and proven efficacy. Other pharmaceuticals have also shown promising results in small studies. The adoption of individualized medical treatments prior, during, and after vitrectomy will continue to increase as new evidence supporting the benefit of pharmacotherapy as an adjunct to vitrectomy becomes available.

Unilateral morning glory disc anomaly in a patient with prenatal Zika virus exposure.

BACKGROUND: To report a case of morning glory disc anomaly (MGDA) in a pediatric patient with prenatal Zika virus (ZIKV) exposure. CASE PRESENTATION: A 3-year-old male with prenatal exposure to ZIKV, confirmed by real-time polymerase chain reaction testing during the second trimester of pregnancy, was evaluated due to visual loss. Physical examination was remarkable for unilateral MGDA. Neuroimaging showed a base of skull encephalocele through the floor of the sella and callosal dysgenesis. CONCLUSIONS: This is the first report to suggest an association between prenatal ZIKV exposure and MGDA. Prenatal ZIKV exposure may be associated to a wider pathologic spectrum than previously reported.

Nonalcoholic fatty liver disease with cirrhosis increases familial risk for advanced fibrosis.

BACKGROUND: The risk of advanced fibrosis in first-degree relatives of patients with nonalcoholic fatty liver disease and cirrhosis (NAFLD-cirrhosis) is unknown and needs to be systematically quantified. We aimed to prospectively assess the risk of advanced fibrosis in first-degree relatives of probands with NAFLD-cirrhosis. METHODS: This is a cross-sectional analysis of a prospective cohort of 26 probands with NAFLD-cirrhosis and 39 first-degree relatives. The control population included 69 community-dwelling twin, sib-sib, or parent-offspring pairs (n = 138), comprising 69 individuals randomly ascertained to be without evidence of NAFLD and 69 of their first-degree relatives. The primary outcome was presence of advanced fibrosis (stage 3 or 4 fibrosis). NAFLD was assessed clinically and quantified by MRI proton density fat fraction (MRI-PDFF). Advanced fibrosis was diagnosed by liver stiffness greater than 3.63 kPa using magnetic resonance elastography (MRE). RESULTS: The prevalence of advanced fibrosis in first-degree relatives of probands with NAFLD-cirrhosis was significantly higher than that in the control population (17.9% vs. 1.4%, P = 0.0032). Compared with controls, the odds of advanced fibrosis among the first-degree relatives of probands with NAFLD-cirrhosis were odds ratio 14.9 (95% CI, 1.8-126.0, P = 0.0133). Even after multivariable adjustment by age, sex, Hispanic ethnicity, BMI, and diabetes status, the risk of advanced fibrosis remained both statistically and clinically significant (multivariable-adjusted odds ratio 12.5; 95% CI, 1.1-146.1, P = 0.0438). CONCLUSION: Using a well-phenotyped familial cohort, we demonstrated that first-degree relatives of probands with NAFLD-cirrhosis have a 12 times higher risk of advanced fibrosis. Advanced fibrosis screening may be considered in first-degree relatives of NAFLD-cirrhosis patients. UCSD IRB: 140084. FUNDING: National Institute of Diabetes and Digestive and Kidney Diseases and National Institute of Environmental Health Sciences, NIH.

Shared genetic effects between hepatic steatosis and fibrosis: A prospective twin study.

Nonalcoholic fatty liver disease is associated with metabolic risk factors including hypertension and dyslipidemia and may progress to liver fibrosis. Studies have shown that hepatic steatosis and fibrosis are heritable, but whether they have a significant shared gene effect is unknown. This study examined the shared gene effects between hepatic steatosis and fibrosis and their associations with metabolic risk factors. This was a cross-sectional analysis of a prospective cohort of well-characterized, community-dwelling twins (45 monozygotic, 20 dizygotic twin pairs, 130 total subjects) from southern California. Hepatic steatosis was assessed with magnetic resonance imaging-proton density fat fraction and hepatic fibrosis with magnetic resonance elastography. A standard bivariate twin additive genetics and unique environment effects model was used to estimate the proportion of phenotypic variance between two phenotypes accounted for by additive genetic effects and individual-specific environmental effects. Genetic correlations estimated from this model represent the degree to which the genetic determinants of two phenotypes overlap. Mean (± standard deviation) age and body mass index were 47.1 (±21.9) years and 26.2 (±5.8) kg/m2 , respectively. Among the cohort, 20% (26/130) had hepatic steatosis (magnetic resonance imaging-proton density fat fraction ≥5%), and 8.2% (10/122) had hepatic fibrosis (magnetic resonance elastography ≥3 kPa). Blood pressure (systolic and diastolic), triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high-density lipoprotein had significant shared gene effects with hepatic steatosis. Triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high-density lipoprotein had significant shared gene effects with hepatic fibrosis. Hepatic steatosis and fibrosis had a highly significant shared gene effect of 0.756 (95% confidence interval 0.716-1, P < 0.0001). CONCLUSIONS: Genes involved with steatosis pathogenesis may also be involved with fibrosis pathogenesis. (Hepatology 2016;64:1547-1558).