To report and analyze cases of sterile intraocular inflammation (IOI) following intravitreal faricimab injections in patients treated for neovascular age-related macular degeneration (nAMD) and diabetic macular edema (DME). This double-center case series included nine eyes of six patients who developed uveitis after faricimab therapy. Comprehensive clinical evaluation was performed, including slit-lamp examination, intraocular pressure (IOP) measurement, fluorescein and indocyanine green angiography (ICGA), and laboratory tests. Inflammatory responses were treated with topical or systemic corticosteroids, and patients were monitored for visual acuity and inflammatory activity. The incidence of IOI was 0.8% per patient (Innsbruck) and 0.23% (Czechia), with inflammation typically occurring between the third and sixth injection (mean interval: 10d post-injection). Inflammatory presentations ranged from anterior uveitis to posterior segment involvement. One notable case demonstrated novel choroidal hypofluorescent lesions on angiography, suggesting deeper ocular involvement. The mean patient age was 76y; five of six affected patients were female. All cases responded to local and systemic corticosteroids, with full recovery of initial visual acuity. Sterile IOI after faricimab appears to be a rare but relevant adverse event. Although the incidence falls within expected ranges for anti-vascular endothelial growth factor (anti-VEGF) agents, the observed choroidal involvement represents a potentially new safety signal. Prompt diagnosis and corticosteroid therapy are effective in all cases. Our findings support the need for vigilant post-marketing surveillance and further studies to better understand the underlying mechanisms and risk factors of faricimab-associated inflammation.

BackgroundThe monocyte substate MS1, identified through single-cell RNA sequencing (scRNA-seq), is enriched in sepsis and shares a transcriptional profile with monocytic myeloid-derived suppressor cells (M-MDSCs), which inhibit T cell activation and cytotoxicity in cancer and chronic inflammation. M-MDSCs can be induced by a range of signals, including inflammatory cytokines such as IL-6 and IL-1β, as well as growth factors like GM-CSF and M-CSF involved in emergency myelopoiesis. While MS1 expansion has been observed in sepsis, the cytokine drivers of this response remain incompletely defined.Figure 1.IL-6 levels parallel the early expansion and subsequent decline of an immunosuppressive monocyte state in sepsis.(a) MS1 monocyte fractional abundance within PBMCs decreases progressively from presentation through recovery.(b) IL-6 plasma concentrations follow a similar temporal trajectory.Samples per timepoint: Day 0 – sepsis (n=67), sterile inflammation (n=26); Day 1 – sepsis (n=60), sterile inflammation (n=23); Day 3 – sepsis (n=53), sterile inflammation (n=15); Day 7 – sepsis (n=27), sterile inflammation (n=3); Convalescence (Day 28+) – sepsis (n=14), sterile inflammation (n=3). Points and lines represent individual subjects, colored by phenotype; boxes show median and interquartile range. IL-6 concentrations (pg/mL) were measured in matched plasma samples using multiplex proteomics. Significance was assessed using Wilcoxon rank-sum test with Benjamini-Hochberg correction. Statistical comparisons between sepsis and sterile inflammation (SI) are shown within the plotting area; comparisons versus healthy controls (HC) are shown outside the plotting area. *p < 0.05, **p < 0.01, ***p < 0.001.MethodsWe performed scRNA-seq with paired surface protein profiling on peripheral blood mononuclear cells (PBMCs) from patients with sepsis and sterile inflammation, sampled at presentation to the emergency department and longitudinally through recovery. In total, we analyzed samples from 130 individuals: 71 with sepsis, 27 with sterile inflammation, and 12 healthy controls recruited outside the ED. After quality control, 560,867 high-quality single cells were analyzed using multimodal integration. Matched plasma samples were profiled using a high-plex cytokine proteomics platform to assess candidate inducers of the MS1 state.ResultsMS1 monocytes were elevated at sepsis onset and declined progressively through day 7, remaining low into convalescence (Fig. 1a). Among candidate cytokines, only IL-6 exhibited a parallel temporal decline (Fig. 1b). Spearman correlations between IL-6 levels and MS1 abundance ranged from ρ=0.39 at day 0 to ρ=0.69 at convalescence. Other cytokines, including IL-1β, IL-8, TNF-α, and IL-10, showed less consistent trajectories and weaker correlations.ConclusionThese findings demonstrate an association between IL-6 and early expansion of an immunosuppressive monocyte state during sepsis, suggesting a putative IL-6–dependent emergency myelopoiesis program. The observed temporal relationship may reflect an early, IL-6–driven adaptation that transitions toward immune restoration during recovery. Defining cytokine–cell state relationships in acute infection may inform strategies to modulate myeloid cell dysregulation in patients with sepsis.DisclosuresAll Authors: No reported disclosures

Neuroimmune regulation of inflammation: RNA-Seq study of somatostatin-6 effects in gilthead seabream (Sparus aurata) skin and brain.

To report five cases of postoperative sterile endophthalmitis in patients who underwent pars plana vitrectomy with silicone oil injection for retinal detachment. Review of the medical records of five patients who underwent pars plana vitrectomy with silicone oil injection at Southend University Hospital and the Royal Eye Infirmary, Derriford Hospital, University Plymouth Hospitals NHS Trust, for rhegmatogenous or tractional retinal detachment. All five patients presented with signs of anterior chamber inflammation exhibiting flare, fibrin, and hypopyon in the early or late postoperative period following vitrectomy with silicone oil injection. Treatment with topical antibiotics and steroids was began, with rapid resolution of the anterior chamber inflammatory reaction and no further intervention required. The use of silicone oil as a tamponade agent for retinal detachment can rarely induce sterile anterior chamber inflammation with signs resembling infectious endophthalmitis. Onset of symptoms, absence of pain, and good response to topical steroids can help differentiate between the two entities.

Engineered mesenchymal stem cells for targeted delivery of H2S to suppress cGAS-STING inflammation and enhance cardioprotection in myocardial ischemia-reperfusion.

Microcystin-LR drives hepatic meta-inflammation and insulin resistance by hijacking the PP2A-JNK signaling axis.

ZFP36L1-mediated PRDM1 mRNA degradation inhibits inflammatory activation of Kupffer cells and ameliorates DCD liver ischemic-reperfusion injury.

ABSTRACT The article provides valuable insight on presentation and management of isolated anterior uveitis and with vitritis following intravitreal (IVT) faricimab. We highlight additional points. First sterile intraocular inflammation (IOI) onset ranges from 1–35 days; however, two patterns have been described: acute onset within 5 days and delayed onset at approximately 14 days following a mean of four IVT injections, although it may occur after the first. Sterile IOI may be recognised by delayed onset, suggestive of a type IV hypersensitivity reaction rather than infectious causes and by absence of hypopyon, although may present in severe cases. Second, faricimab’s dual inhibition may alter ocular immune surveillance, potentially facilitating herpes simplex virus reactivation. Increased vigilance for dendritic ulcers is therefore warranted, and antiviral therapy should be initiated prior to corticosteroids. Finally, management should be guided by severity, with anterior or vitreous tap considered to exclude exogenous endophthalmitis. Resolution typically occurs within 15 days.

BackgroundIn the context of liver resection and transplantation, hepatic ischemia-reperfusion injury (hepatic IRI) remains a significant clinical challenge, profoundly impacting both postoperative short- and long-term recovery. A novel cell death pathway, PANoptosis, is implicated in infections, malignancies and sterile inflammation. While the specific role of PANoptosis in the development of hepatic IRI remains unclear, this study aims to provide new insights and perspectives into the underlying mechanisms, thereby addressing this knowledge gap.MethodsWe constructed a panoptosis-related gene panel and analyzed seven gene expression datasets on hepatic IRI available in the GEO database. Differential expression analysis, enrichment analysis, and multi-omics consensus analysis were performed on panoptosis-hepatic IRI DEGs. Core genes associated with hepatic IRI were identified using ten machine learning algorithms. Single-cell analysis and two immune infiltration algorithms were employed to assess immune cell infiltration and their interplay with core genes. To validate our findings, core gene expression was validated via serum detection, H&E staining, and quantitative real-time PCR in a mouse hepatic IRI.ResultsWe identified 52 DE-PANRGs from a constructed panoptosis-related gene set of 485 genes. Functional enrichment analysis indicated their participation in necroptosis, apoptosis, cytokine-cytokine receptor interaction, NOD-like receptor signaling, and other related processes. Three distinct molecular subtypes of hepatic IRI were identified, with subtype C2 showing high expression of DE-PANRGs. Machine learning identified eight feature genes (IER3, CDKN1A, EMP1, IL1B, BTG3, JUN, HSPB1, and IL1A) with diagnostic potential. The function and correlation of core genes were confirmed through single-cell and immune infiltration analyses, and validated in a mouse hepatic IRI model.ConclusionUtilizing a panoptosis gene set, this study identified eight core genes involved in hepatic IRI, providing novel insights into panoptosis’ role in hepatic IRI.

We report a rare case of concurrent cutaneous and prostatic pyoderma gangrenosum (PG) in a man in his 70s. The patient initially presented with dysuria, pelvic discomfort and a boggy prostate, consistent with bacterial prostatitis. Despite prolonged antibiotic therapy, his symptoms progressed and imaging revealed a prostatic abscess. Following transurethral resection of the prostate, he developed painful necrotic ulcers across the trunk and extremities. Histopathological examination of both the prostate and skin demonstrated sterile neutrophilic inflammation, consistent with PG. Dermatology initiated systemic corticosteroids, mycophenolate mofetil and infliximab, resulting in partial disease control. This case highlights a unique presentation of simultaneous visceral and cutaneous PG in the absence of prior trauma or surgery and underscores the importance of considering non-infectious neutrophilic dermatoses in patients with refractory prostatitis and evolving systemic inflammation.

Reactive arthritis is defined as a sterile inflammation of the joint space, following a remote infection, which can be bacterial or viral in origin. Although leptospirosis is not a frequent cause, it has been reported as a potential trigger. We herein report an 11-year-old boy who presented with fever, jaundice, and acute onset of right hip pain with restricted movement. Laboratory investigations were done to evaluate for infectious causes. IgM antibodies for Leptospira were equivocal, suggesting the possibility of an acute infection. This case highlights that reactive arthritis can develop early in the course of leptospiral infection, as early as within 3 days of symptom onset, and may coincide with active systemic illness. Early recognition of this rare association is essential for the diagnosis and management.

Introduction Monogenic systemic autoinflammatory diseases (SAIDs) are driven by innate immune dysregulation, often due to aberrant inflammasome activation. Inflammasomopathies, those involving NLRP3, MEFV, MVK, and TNFRSF1A mutations, constitute a subgroup marked by sterile inflammation and overlapping symptoms like fever, serositis, rash, and arthritis. However, diagnostic complexity from phenotypic variability and incomplete penetrance makes genetic and immunological confirmation essential. This study aimed to characterize the clinical, biochemical, immunological, and genetic profiles of pediatric patients with confirmed or suspected inflammasomopathies at a tertiary care center. Methods Data were obtained from a monogenic SAID registry. Genetic analysis was performed using panel-based exome sequencing, and inflammatory biomarkers (C-reactive protein [CRP], erythrocyte sedimentation rate [ESR], MRP8/14) were evaluated. Results Over a 10-year period, 36 patients were assessed, of whom 13 (36%) had definitive diagnoses. Median age at symptom onset was 18 months, while diagnosis occurred at a mean age of 99 months, highlighting diagnostic delay. Predominant symptoms included fever (25%), ocular inflammation (12.5%), rash, arthritis, and aphthous ulcers (9% each). Despite identical NLRP3 mutations, phenotypic variation suggested roles for modifier genes or environmental factors. All patients showed laboratory signs of systemic inflammation—elevated ESR, CRP, MRP8/14, leukocytosis, and thrombocytosis—with absence of autoantibodies, consistent with autoinflammatory etiology. Overall variants were classified according to the ACMG (American College of Medical Genetics and Genomics) in inflammasome-related genes. Tailored to treatment strategies included IL-1 and TNF inhibitors. Conclusions This cohort reinforces the pivotal role of the inflammasome in monogenic autoinflammatory diseases. Clinical heterogeneity, even among patients with identical mutations, underscores the need for individualized evaluation. Early integration of clinical, immunological, and genetic data guiding targeted cytokine therapies that can mitigate innate immune dysregulation improving outcomes in children.

Autoinflammatory diseases (AIDs) represent a heterogeneous group of conditions pathogenetically associated with dysregulation of innate immunity and clinically characterized by recurrent episodes of sterile inflammation in affected organs in the absence of infection, allergy, and high titers of circulating autoantibodies or autoreactive T cells. The overwhelming majority of monogenic AIDs (mAIDs) are accompanied by skin rashes, the type of which is determined by the specific disease and, to some extent, by differing pathogenetic mechanisms. The first part of the article presents the cutaneous characteristics of the most common mAIDs: Familial Mediterranean fever (FMF), cryopyrinassociated periodic syndromes (CAPS), tumor necrosis factor receptor-associated periodic syndrome (TRAPS), periodic syndrome with hyperimmunoglobulinemia D / mevalonate kinase deficiency (HIDS/MKD). Skin involvement in these diseases reflects systemic inflammation associated with hyperproduction of the key pro-inflammatory cytokine interleukin (IL)-1β. In other AIDs, symptoms mainly depend on increased levels of cytokines such as IL-18, IL-36, etc. (NLRC4-associated autoinflammatory disease; deficiency of the IL-36 receptor antagonist – DITRA), as well as activation of interferon signaling pathways (interferonopathies). Different pathogenetic mechanisms determine the diversity of clinical phenotypes, including cutaneous manifestations. Knowledge of these features helps establishing a correct diagnosis, obtaining genetic confirmation (without which accurate identification of these rare conditions is impossible today) and selecting appropriate therapy. Pathological examination plays a special auxiliary role and should be used in diagnostically challenging situations.

ObjectiveNontraumatic osteonecrosis of the femoral head (NONFH) is a devastating condition characterised by immune dysregulation and sterile inflammation, which are increasingly acknowledged as central pathogenic mechanisms. This study aims to identify the core herbal combination for NONFH and systematically explore its immunomodulatory effects and underlying pharmacological mechanisms, with a focus on immune system interactions.MethodsThe core combination ‘Rehmanniae radix praeparata (SDH)‐achyranthes root (NX)‐Chinese angelica root (DG)’ (SND) was identified via data mining of clinical literature using the Traditional Chinese Medicine Inheritance Support System (TCMISS) V2.5 platform. Its chemical constituents were characterised by ultrahigh performance liquid chromatography‐quadrupole time‐of‐flight mass spectrometry (UHPLC‐Q‐TOF‐MSE) technology, yielding 127 identified compounds, 47 of which were selected as bioactive components based on drug‐likeness screening. The potential molecular targets of SND and NONFH were predicted and intersected, with a focus on immune‐related targets. Subsequent comprehensive enrichment analysis was performed, emphasising immune pathway involvement, along with immune infiltration profiling. A support vector machine (SVM) model was constructed to identify key immune‐related targets, and interactions were validated via molecular docking and molecular dynamics (MD) simulations.ResultsSND shared 46 candidate targets with NONFH. Enrichment analysis revealed these targets were significantly enriched in immune‐inflammatory pathways, especially those related to immune cell activation and regulation. Notably, pathways involved in neutrophil extracellular trap (NET) formation and other innate immune responses were prominent. Machine learning identified five key targets: ACP1, NDUFAF3, haematopoietic cell kinase (HCK), CXCR2 and platelet‐activating factor receptor (PTAFR)—all of which play critical roles in the modulation, signalling and activation of immune cells, particularly neutrophils and macrophages. Subsequent immune infiltration analysis demonstrated a strong correlation between these key targets (e.g. HCK, CXCR2 and PTAFR) and neutrophil abundance in NONFH. Molecular docking (MD) and molecular dynamics simulations (MDS). MD confirmed stable binding between the active components and these targets, with the HCK‐chrysophanic acid complex exhibiting the strongest affinity (binding energy: −8.7 kcal/mol).ConclusionOur integrated analysis suggests that SND alleviates NONFH primarily through multi‐target immunomodulation, explicitly involving suppression of NET formation and regulation of immune cell activity, especially neutrophils and osteoclasts. This study presents a novel, immunologically explicit hypothesis for the mechanism of SND against NONFH, providing a solid theoretical foundation for future experimental validation and clinical application.

Damage-associated molecular patterns (DAMPs) are endogenous molecules released during cellular stress or injury that trigger sterile inflammation. In perioperative settings, common triggers include surgical trauma, ischemia–reperfusion injury, cardiopulmonary bypass, blood transfusion, and mechanical ventilation. When released extracellularly, DAMPs activate innate immune receptors such as Toll-like receptors (TLRs) and the receptor for advanced glycation end products (RAGE), initiating signaling cascades that amplify inflammation, disrupt endothelial integrity, and promote coagulation and metabolic imbalance. This sterile inflammatory response may extend local tissue injury into systemic organ dysfunction, manifesting clinically as acute lung injury, acute kidney injury, myocardial dysfunction, disseminated intravascular coagulation, and perioperative neurocognitive disorders. Recognizing the central role of DAMPs reframes these complications as predictable consequences of endogenous danger signaling rather than solely as results of infection or hemodynamic instability. This understanding supports the use of established strategies such as protective ventilation and restrictive transfusion to minimize DAMP release. Emerging evidence also suggests that anesthetic agents may influence DAMP-mediated inflammation: propofol and dexmedetomidine appear to exert anti-inflammatory effects, whereas volatile anesthetics show variable results. Although clinical data remain limited, anesthetic choice and perioperative management may significantly affect systemic inflammatory burden and recovery. Future research validating DAMPs as biomarkers and therapeutic targets may inform precision anesthetic strategies aimed at modulating sterile inflammation, ultimately enhancing perioperative outcome.

Accurate diagnosis of post-neurosurgical bacterial infection of central nervous system is challenging due to the nonspecific nature of clinical signs and cerebrospinal fluid (CSF) parameters, which often overlap with sterile postoperative inflammation. This study aimed to develop and validate a stepwise diagnostic strategy integrating readily available clinical and basic laboratory indicators to improve the early identification of post-neurosurgical bacterial infection of the central nervous system. A retrospective cohort study was conducted at Tianjin Huanhu Hospital, a tertiary neurosurgical center, from October 2018 to June 2025. We enrolled 176 patients suspected of post-neurosurgical bacterial infection of the central nervous system who underwent CSF metagenomic next-generation sequencing (mNGS). Six diagnostic prediction models, combining clinical features (fever, altered mental status) and CSF parameters (white blood cell count, glucose levels), were constructed. Their diagnostic performance was evaluated against a composite reference standard (mNGS, culture, and clinical treatment response) using receiver operating characteristic analysis. The area under the curve (AUC), sensitivity, and specificity were calculated. Among the 6 models, two demonstrated superior performance. Model 5 (T > 38.0°C + [CSF white blood cell ≥ 2000 × 106/L OR CSF glucose < 2.2 mmol/L OR CSF/Blood glucose ratio < 0.4]) achieved an AUC of 0.768. Notably, Model 6 (T > 39.0°C + Altered Mental Status + Intermittent Fever), relying solely on clinical indicators, achieved a comparable AUC of 0.769. For individual parameters, a high fever threshold (T > 39.8°C) and profoundly low CSF glucose (<1.01 mmol/L) showed high specificities of 99%and 97%, respectively, for ruling in infection. A diagnostic strategy combining severe clinical manifestations (high fever and altered mental status) with high-threshold CSF parameters enables effective risk stratification for post-neurosurgical bacterial infection of the central nervous system. The high performance of a purely clinical model (Model 6) offers a valuable tool for rapid bedside assessment, especially in resource-limited settings. Future prospective, multicenter studies are recommended to validate these algorithms and further refine variable definitions for broader clinical application.

BackgroundLong Interspersed Nucleotide Element-1 (LINE-1, or L1) sequences occupy approximately 17% of the human genome. L1 RNA expression, required for embryogenesis, is low in middle childhood, but increases in adults, eroding heterochromatin and leading to ectopic gene misexpressions, sterile chronic inflammation, and physiological deterioration. To our knowledge, no studies have yet tested whether adults with high L1 RNA levels for their age are shorter-lived, and whether the women with higher L1 RNA levels have shorter reproductive lifespans, as would be expected if higher L1 RNA expressions accelerate both systemic and reproductive aging.MethodsThe RNA levels of 127 subfamilies of L1 elements in lymphoblastoid cell lines (LCLs) from 43 grandmothers and 43 grandfathers of the three-generation Utah CEPH (Centre d’Étude du Polymorphisme Humain) families were obtained from the Genetic European Variation in Disease (GEUVADIS) project. Survival and reproductive lifespan data for these subjects were obtained from the University of Utah. The sum of the RNA levels across all 127 L1 element subfamilies (a.k.a. total L1 RNA level), and the variance of RNA levels across the 127 subfamilies, were calculated for each research subject and tested for associations with longevity in both sexes and with age at last birth (ALB) for the women.ResultsWomen in the top half of summed L1 RNA expressions, or in the top half of variance in RNA expression across the L1 subfamilies, had significantly higher mortality rates than women in the bottom half for those measures (for top half vs. bottom half total L1 RNA levels, Hazard Ratio (HR) 4.00, 95% CI 1.50–10.67, P = 0.0057; for top half vs. bottom half variance across the L1 subfamilies, HR 3.84, 95% CI 1.49–10.72, P = 0.0068). No significant associations of L1 RNA levels, or their variance, with mortality were observed in the full set of 43 men; however, restricting the analysis to the men who were 68 years or older at blood draw and survived at least four years after the blood draw (n = 31) revealed significantly higher mortality rates, within this subset of men, for those in the top half of total L1 RNA levels vs. men in the bottom half (HR 2.79, 95% CI 1.11–7.05, P = 0.03). Among the 37 women whose ALB was ≥ 30 years, the approximate age when fertility begins to decline, higher total L1 RNA levels were associated, though not significantly, with a younger ALB. However, selecting for relatively healthy individuals by restricting the analyses to women who were younger than 75.5 years at blood draw and survived at least five years after the blood draw (n = 27) revealed a strong association of higher intra-individual variance in L1 RNA expression across the 127 L1 subfamilies with a younger ALB (Pearson r = −0.44, p = 0.02).ConclusionsThese results from a small cohort of research subjects lend support to the hypothesis that the regulation of L1 RNA expressions in adults significantly influences the rates of both systemic and reproductive aging. Expanded studies of similar design are needed to further test this hypothesis.

Exposure to respirable particles such as multiwalled carbon nanotubes (MWCNTs) can provoke acute lung inflammation and tissue injury, potentially progressing to chronic disease. Lipid mediators (LMs), including proinflammatory and pro-resolving species, play a critical role in regulating this process. This study investigated LM biosynthesis in acute lung inflammation induced by fibrogenic MWCNTs. Adult C57BL/6J mice were exposed to MWCNTs (Mitsui-7; 1860.4 μg/kg) via oropharyngeal aspiration. Lung tissues collected 24 h postexposure exhibited neutrophil infiltration, elevated inflammatory cytokines, and tissue damage. Enzymes involved in prostanoid synthesis─phospholipase A2, cyclooxygenase-2, and prostaglandin E synthase─were significantly upregulated. Lipidomic profiling was performed by using C18 spin column enrichment and UPLC-MS/MS. MWCNT exposure significantly increased the levels of prostanoids (PGE2, PGD2, PGF2α, thromboxane B2) and hydroxyeicosatetraenoic acids (5-, 12-, 15-HETE). Elevated levels of protectin DX, 14(S)-, and 17-HDHA derived from docosahexaenoic acid, and 12-, 15-, and 18-HEPE derived from eicosapentaenoic acid were also observed. In vitro, MWCNTs induced intracellular lipid accumulation in macrophages. These findings reveal rapid activation of LM biosynthetic pathways, particularly those producing proinflammatory prostanoids, in mouse lungs following nanoparticle exposure. The study underscored the utility of lipidomic profiling for mechanistic insights into nanoparticle-induced sterile inflammation and toxicity in limited tissue samples.

Background: Cataract surgery is a highly successful ophthalmic procedure; however, the immediate postoperative period remains critical for wound healing and infection prevention. The use of postoperative patching is intended to protect the surgical site, but the optimal duration—whether one day or two days—remains debated. Aim: To assess the safety and outcomes of two-day postoperative patching without topical medication following cataract surgery, with specific focus on the incidence of endophthalmitis, early anterior segment stability, and visual recovery. Methods: This retrospective descriptive study included 120 eyes of 120 patients who underwent cataract extraction with posterior chamber intraocular lens implantation between January 2014 and August 2022 at three centers in Baghdad: Al-Kindy Teaching Hospital and Imam Ali Hospital. All patients received subconjunctival gentamicin (20 mg/mL) and dexamethasone (4 mg/mL) at the end of surgery. The operated eye was patched continuously for 48 hours without any topical eye drops. Postoperative assessments at day 3, day 7, and two weeks evaluated wound integrity, corneal clarity, anterior chamber depth, inflammation, and best-corrected visual acuity (BCVA). Results: The study population included 72 males (60.00%) and 48 females (40.00%), mostly aged over 40 years (91.66%). Phacoemulsification was the predominant surgical technique (79.17%), followed by MSICS (15.00%) and ECCE (05.83%). The intraoperative course was uneventful in 89.17% of cases; posterior capsule rupture ± vitreous loss occurred in 06.67%. Early postoperative evaluation (within 48 hours) revealed normal healing in 93.33%, mild corneal edema in 04.17%, and shallow anterior chamber in 01.67%. Importantly, no confirmed cases of endophthalmitis (00.00%) were identified, and only one case (00.83%) presented with mild sterile inflammation. At two weeks, BCVA ranged between 6/6 and 6/12 in 80.83% of patients, indicating excellent visual recovery. Conclusion: Two-day postoperative patching after cataract surgery is safe, effective, and protective. It does not increase the risk of endophthalmitis and may enhance wound stability during the most critical healing phase. This low-cost, easily applicable protocol may be particularly valuable in resource-limited or high-volume surgical settings, providing added protection without delaying visual rehabilitation

Sterile inflammation in laminopathies.