Upper lid crease approach for margin rotation in trachomatous cicatricial entropion without external sutures

ABSTRACT Purpose: To describe the use of a lid crease incision for upper eyelid margin rotation in cicatricial entropion combining internal traction on the anterior lamella, tarsotomy, and tarsal overlap without external sutures. Methods: Surgical description: The main steps of the procedure consisted of exposure of the entire tarsal plate up to the eyelashes followed by tarsotomy through the conjunctiva. A double-armed 6.0 polyglactin suture was then passed through the distal tarsal fragment to the marginal section of the orbicularis oculi muscle. As the sutures were tied, the distal tarsus advanced over the marginal section, and traction was exerted on the marginal strip of the orbicularis muscle. There were no bolsters or external knots. The pretarsal skin-muscle flap was closed with a 6.0 plain gut suture. Results: We used this procedure at a tertiary hospital in Saudi Arabia from 2013 to 2014. Sixty upper lids of 40 patients (23 women and 17 men) were operated on, with an age range of 44-99 years [mean ± standard deviation (SD) = 70.9 ± 13.01 years]. Bilateral surgery was performed on 21 patients. Follow-up ranged from 1 to 12 months (mean 3.0 ± 2.71 months). Forty percent of the patients (24 lids) had more than 3 months' follow-up. The postoperative lid margin position was good in all cases. Trichiasis (two lashes) was observed in only one patient with unilateral entropion on the medial aspect of the operated lid. Conclusions: The upper lid margin can be effectively rotated through a lid crease incision with internal sutures. The technique combines the main mechanisms of the Wies and Trabut approaches and avoids the use of bolsters or external sutures, which require a second consultation to be removed. Some other lid problems, such as ptosis, retraction, or dermatochalasis, can be concomitantly addressed during the procedure

Epidemiology of traumatic spinal cord injury in Galicia, Spain: trends over a 20-year period

[Abstract] Study design: Observational study with prospective and retrospective monitoring. Objective: To describe the epidemiological and demographic characteristics of traumatic spinal cord injury (TSCI), and to analyze its epidemiological changes. Setting: Unidad de Lesionados Medulares, Complejo Hospitalario Universitario A Coruña, in Galicia (Spain). Methods: The study included patients with TSCI who had been hospitalized between January 1995 and December 2014. Relevant data were extracted from the admissions registry and electronic health record. Results: A total of 1195 patients with TSCI were admitted over the specified period of time; 76.4% male and 23.6% female. Mean patient age at injury was 50.20 years. Causes of injury were falls (54.2%), traffic accidents (37%), sports/leisure-related accidents (3.5%) and other traumatic causes (5.3%). Mean patient age increased significantly over time (from 46.40 to 56.54 years), and the number of cases of TSCI related to traffic accidents decreased (from 44.5% to 23.7%), whereas those linked to falls increased (from 46.9% to 65.6%). The most commonly affected neurological level was the cervical level (54.9%), increasing in the case of levels C1–C4 over time, and the most frequent ASIA (American Spinal Injury Association) grade was A (44.3%). The crude annual incidence rate was 2.17/100 000 inhabitants, decreasing significantly over time at an annual percentage rate change of −1.4%. Conclusions: The incidence rate of TSCI tends to decline progressively. Mean patient age has increased over time and cervical levels C1–C4 are currently the most commonly affected ones. These epidemiological changes will eventually result in adjustments in the standard model of care for TSCI

Anti-tumour necrosis factor discontinuation in inflammatory bowel disease patients in remission: study protocol of a prospective, multicentre, randomized clinical trial

Background: Patients with inflammatory bowel disease who achieve remission with anti-tumour necrosis factor (anti-TNF) drugs may have treatment withdrawn due to safety concerns and cost considerations, but there is a lack of prospective, controlled data investigating this strategy. The primary study aim is to compare the rates of clinical remission at 1?year in patients who discontinue anti-TNF treatment versus those who continue treatment. Methods: This is an ongoing, prospective, double-blind, multicentre, randomized, placebo-controlled study in patients with Crohn?s disease or ulcerative colitis who have achieved clinical remission for ?6?months with an anti-TNF treatment and an immunosuppressant. Patients are being randomized 1:1 to discontinue anti-TNF therapy or continue therapy. Randomization stratifies patients by the type of inflammatory bowel disease and drug (infliximab versus adalimumab) at study inclusion. The primary endpoint of the study is sustained clinical remission at 1?year. Other endpoints include endoscopic and radiological activity, patient-reported outcomes (quality of life, work productivity), safety and predictive factors for relapse. The required sample size is 194 patients. In addition to the main analysis (discontinuation versus continuation), subanalyses will include stratification by type of inflammatory bowel disease, phenotype and previous treatment. Biological samples will be obtained to identify factors predictive of relapse after treatment withdrawal. Results: Enrolment began in 2016, and the study is expected to end in 2020. Conclusions: This study will contribute prospective, controlled data on outcomes and predictors of relapse in patients with inflammatory bowel disease after withdrawal of anti-TNF agents following achievement of clinical remission. Clinical trial reference number: EudraCT 2015-001410-1

Higher COVID-19 pneumonia risk associated with anti-IFN-α than with anti-IFN-ω auto-Abs in children

We found that 19 (10.4%) of 183 unvaccinated children hospitalized for COVID-19 pneumonia had autoantibodies (auto-Abs) neutralizing type I IFNs (IFN-alpha 2 in 10 patients: IFN-alpha 2 only in three, IFN-alpha 2 plus IFN-omega in five, and IFN-alpha 2, IFN-omega plus IFN-beta in two; IFN-omega only in nine patients). Seven children (3.8%) had Abs neutralizing at least 10 ng/ml of one IFN, whereas the other 12 (6.6%) had Abs neutralizing only 100 pg/ml. The auto-Abs neutralized both unglycosylated and glycosylated IFNs. We also detected auto-Abs neutralizing 100 pg/ml IFN-alpha 2 in 4 of 2,267 uninfected children (0.2%) and auto-Abs neutralizing IFN-omega in 45 children (2%). The odds ratios (ORs) for life-threatening COVID-19 pneumonia were, therefore, higher for auto-Abs neutralizing IFN-alpha 2 only (OR [95% CI] = 67.6 [5.7-9,196.6]) than for auto-Abs neutralizing IFN-. only (OR [95% CI] = 2.6 [1.2-5.3]). ORs were also higher for auto-Abs neutralizing high concentrations (OR [95% CI] = 12.9 [4.6-35.9]) than for those neutralizing low concentrations (OR [95% CI] = 5.5 [3.1-9.6]) of IFN-omega and/or IFN-alpha 2

Tetrahydrocannabinolic acid A (THCA-A) reduces adiposity and prevents metabolic disease caused by diet-induced obesity

Medicinal cannabis has remarkable therapeutic potential, but its clinical use is limited by the psychotropic activity of \u3949-tetrahydrocannabinol (\u3949-THC). However, the biological profile of the carboxylated, non-narcotic native precursor of \u3949-THC, the \u3949-THC acid A (\u3949-THCA-A), remains largely unexplored. Here we present evidence that \u3949-THCA-A is a partial and selective PPAR\u3b3 modulator, endowed with lower adipogenic activity than the full PPAR\u3b3 agonist rosiglitazone (RGZ) and enhanced osteoblastogenic effects in hMSC. Docking and in vitro functional assays indicated that \u3949-THCA-A binds to and activates PPAR\u3b3 by acting at both the canonical and the alternative sites of the ligand-binding domain. Transcriptomic signatures in iWAT from mice treated with \u3949-THCA-A confirmed its mode of action through PPAR\u3b3. Administration of \u3949-THCA-A in a mouse model of HFD-induced obesity significantly reduced fat mass and body weight gain, markedly ameliorating glucose intolerance and insulin resistance, and largely preventing liver steatosis, adipogenesis and macrophage infiltration in fat tissues. Additionally, immunohistochemistry, transcriptomic, and plasma biomarker analyses showed that treatment with \u3949-THCA-A caused browning of iWAT and displayed potent anti-inflammatory actions in HFD mice. Our data validate the potential of \u3949-THCA-A as a low adipogenic PPAR\u3b3 agonist, capable of substantially improving the symptoms of obesity-associated metabolic syndrome and inflammation