Postpartum Recovery From Meningioma-Related Oculomotor Palsy.

BACKGROUND: We summarize a case of transient oculomotor nerve palsy in a pregnant woman with a cavernous sinus meningioma. When pregnant women present with acute ophthalmic signs and symptoms, meningioma should be considered during diagnostic workup given the common proximity of growing meningiomas to visual pathways and ocular motor nerves within the parasellar region. CASE: A 32-year-old woman, gravida 2 para 1, at 37 weeks of gestation, presented with 2 weeks of diplopia, left-sided ptosis, and left periocular headache. There were no signs of preeclampsia. Examination revealed a left mydriatic pupil, complete left-sided ptosis, and motility deficits consistent with a left pupil-involving oculomotor nerve palsy. Magnetic resonance imaging of the brain revealed a cavernous sinus meningioma. Five days after cesarean birth, the ptosis significantly improved; 2 weeks later, the diplopia resolved. CONCLUSION: Pregnancy is associated with increased likelihood of intracranial meningioma growth, particularly in the parasellar region. We highlight a rare case of a transient cranial nerve III palsy in a pregnant patient due to cavernous sinus meningioma and review prior published reports.

Indications for Wear, Visual Outcomes, and Complications of Custom Imprint 3D Scanned Scleral Contact Lens Use.

PURPOSE: To report indications for wear, visual outcomes, and complications of EyePrintPRO (EPP) scleral contact lens (SCL) use. METHODS: A retrospective review identified all patients fitted with this device between December 2013 and March 2018. Baseline demographics, wear indication, and contact lens history were determined. Habitual-corrected visual acuity was measured at baseline and follow-up. Adverse wear symptoms and signs, reprinting, and device cessation were tracked. RESULTS: Ninety-five eyes from 69 patients were followed for a median of 12.1 months (interquartile range 4.4-19.6). Indications for wear included vision improvement and/or ocular surface stabilization in the setting of irregular corneal shape (n = 68 eyes, 72%), ocular surface disease (n = 17, 18%), exposure keratopathy (n = 7, 7%), neurotrophic keratitis (n = 5, 5%), and extracorneal topographical abnormalities preventing noncustom lens fitting such as glaucoma drainage devices (n = 8, 8%). Median habitual-corrected visual acuity improved from 0.67 to 0.08 (P = 0.0003). One-third of eyes (33.1%) developed adverse wear symptoms. Fifteen of 95 eyes (16%) developed adverse wear signs. Device cessation occurred in 10 eyes (10.5%) and reprinting occurred in 14 eyes (14.7%) unrelated to prior lens wear or indication (P = 0.67 and 0.15, respectively). In eyes that previously failed SCLs (n = 56), 12 eyes required reprinting and 49 eyes continued use. CONCLUSIONS: Indications for EPP wear include irregular corneal shape, ocular surface disease, and extracorneal topographic abnormalities. Visual acuity improves with the use of EPP. Clinicians and patients should be aware of potential adverse wear symptoms/signs and device cessation that may occur with EPP use. EPP is a viable salvage therapy in eyes that previously failed SCLs.

Neutrophil Subsets, Platelets, and Vascular Disease in Psoriasis.

Psoriasis is an inflammatory skin disease associated with increased cardiovascular risk and serves as a reliable model to study inflammatory atherogenesis. Because neutrophils are implicated in atherosclerosis development, this study reports that the interaction among low-density granulocytes, a subset of neutrophils, and platelets is associated with a noncalcified coronary plaque burden assessed by coronary computed tomography angiography. Because early atherosclerotic noncalcified burden can lead to fatal myocardial infarction, the low-density granulocyte-platelet interaction may play a crucial target for clinical intervention.

Chronic skin inflammation accelerates macrophage cholesterol crystal formation and atherosclerosis.

Inflammation is critical to atherogenesis. Psoriasis is a chronic inflammatory skin disease that accelerates atherosclerosis in humans and provides a compelling model to understand potential pathways linking these diseases. A murine model capturing the vascular and metabolic diseases in psoriasis would accelerate our understanding and provide a platform to test emerging therapies. We aimed to characterize a new murine model of skin inflammation (Rac1V12) from a cardiovascular standpoint to identify novel atherosclerotic signaling pathways modulated in chronic skin inflammation. The RacV12 psoriasis mouse resembled the human disease state, including presence of systemic inflammation, dyslipidemia, and cardiometabolic dysfunction. Psoriasis macrophages had a proatherosclerotic phenotype with increased lipid uptake and foam cell formation, and also showed a 6-fold increase in cholesterol crystal formation. We generated a triple-genetic K14-RacV12-/+/Srb1-/-/ApoER61H/H mouse and confirmed psoriasis accelerates atherogenesis (~7-fold increase). Finally, we noted a 60% reduction in superoxide dismutase 2 (SOD2) expression in human psoriasis macrophages. When SOD2 activity was restored in macrophages, their proatherogenic phenotype reversed. We demonstrate that the K14-RacV12 murine model captures the cardiometabolic dysfunction and accelerates vascular disease observed in chronic inflammation and that skin inflammation induces a proatherosclerotic macrophage phenotype with impaired SOD2 function, which associated with accelerated atherogenesis.

Association Between Skin and Aortic Vascular Inflammation in Patients With Psoriasis: A Case-Cohort Study Using Positron Emission Tomography/Computed Tomography.

Importance: Inflammation is critical in the development of atherosclerosis. Psoriasis is a chronic inflammatory skin disease that is associated with increased vascular inflammation by 18fluorodeoxyglucose positron emission tomography/computed tomography in vivo and future cardiovascular events. It provides a human model to understand the effect of treating inflammation in a target organ (eg, the skin) on vascular diseases. Objective: To investigate the association between change in skin disease severity and change in vascular inflammation at 1 year and to characterize the impact of 1 year of anti-tumor necrosis factor therapy on vascular inflammation. Design, Setting, and Participants: In this prospective cohort study, 220 participants from outpatient practices were recruited at the US National Institutes of Health. A total of 115 consecutively recruited patients with psoriasis were followed up at 1 year. The study was conducted from January 1, 2013, through October 31, 2016, with data analyzed in November 2016. Exposure: Skin inflammation measured as Psoriasis Area and Severity Index (PASI) score. Main Outcomes and Measures: Vascular inflammation assessed as target-to-background ratio by 18fluorodeoxyglucose positron emission tomography/computed tomography. Results: Among the 115 patients, the mean (SD) age at 1-year follow-up was 50.8 (12.8) years and 68 were men (59%). The cohort had a low cardiovascular risk by Framingham risk score and mild-to-moderate psoriasis, with a median PASI score of 5.2 (interquartile range, 3.0-8.9). At follow-up, the total cohort had a median improvement in PASI score of 33%, with use of topical therapy (60%), biological therapy (66%, mostly anti-tumor necrosis factor) and phototherapy (15%) (P < .001). Moreover, improvement in PASI score was associated with improvement in target-to-background ratio of 6%, mainly driven by those with higher responses in PASI score (P < .001). This association persisted beyond traditional risk factors (ß = 0.19; 95% CI, 0.012-0.375; P = .03) and was the strongest in those initiated with anti-tumor necrosis factor therapy (ß = 0.79; 95% CI, 0.269-1.311; P = .03). Conclusions and Relevance: Improvement in psoriasis skin disease severity was associated with improvement in aortic vascular inflammation by 18fluorodeoxyglucose positron emission tomography/computed tomography, with greater improvement in aortic vascular inflammation observed in those who had higher than 75% reduction in skin disease severity. These findings suggest that controlling remote target organ inflammation (eg, in the skin) may improve vascular diseases; however, randomized clinical trials are needed to confirm these findings.

Self-reported depression in psoriasis is associated with subclinical vascular diseases.

BACKGROUND AND AIMS: Psoriasis is a chronic inflammatory disorder associated with vascular inflammation, measured by 18-fluorodeoxyglucose positron emission tomography/computed tomography (18-FDG PET/CT), and an increased risk of myocardial infarction. Patients with psoriasis are also more likely to suffer from comorbid depression. Whether depression accelerates the development of subclinical atherosclerosis in psoriasis is unknown. METHODS: Patients were selected from within a larger psoriasis cohort. Those who reported a history of depression (N = 36) on survey were matched by age and gender to patients who reported no history of psychiatric illness (N = 36). Target-to-background ratio from FDG PET/CT was used to assess aortic vascular inflammation and coronary CT angiography scans were analyzed to determine coronary plaque burden. Multivariable linear regression was performed to understand the effect of self-reported depression on vascular inflammation and coronary plaque burden after adjustment for Framingham risk (standardized ß reported). RESULTS: In unadjusted analyses, vascular inflammation and coronary plaque burden were significantly increased in patients with self-reported depression as compared to patients with psoriasis alone. After adjustment for Framingham Risk Score, vascular inflammation (ß = 0.26, p = 0.02), total plaque burden (ß = 0.17, p = 0.03), and non-calcified burden (ß = 0.17, p = 0.03) were associated with self-reported depression. CONCLUSIONS: Self-reported depression in psoriasis is associated with increased vascular inflammation and coronary plaque burden. Depression may play an important role in promoting subclinical atherosclerosis beyond traditional cardiovascular risk factors.