Proliferative Retinopathy Research Articles

High prevalence of comorbidities in older adult patients with type 2 diabetes: a cross-sectional survey

BackgroundDiabetes is a global health problem, and its incidence and complications increase with the duration of the disease and over time. This increase in complications in older patients can lead to disability and a lower quality of life. This study aimed to investigate the rate of diabetes control and complications in older adults.MethodThis was a cross-section of an ongoing cohort of patients with type 2 diabetes mellitus (T2DM) aged 65 years and older. The clinical and laboratory characteristics of older adult patients with T2DM in good and intermediate health conditions were collected between 2010 and 2022.ResultsA total of 2,770 older adult patients with T2DM were enrolled, including 1,530(55.3%) female and 1,240 (44.7%) male participants. Metabolic syndrome, hypertension, and coronary artery disease were the most common comorbidities, affecting 1,889 (71.4%), 1,495 (54.4%), and 786 (29.2%) patients, respectively. Albuminuria was present in 626 (22.6%) patients, while retinopathy was detected in 408 (14.7%) patients, including 6% with proliferative retinopathy. Most patients were treated with oral antidiabetic agents (88.9%), with metformin being the most prescribed medication (85.6%). Statins were prescribed to 71.8% of the patients. The most prescribed antihypertensive medications were angiotensin receptor blockers and angiotensin-converting enzyme inhibitors, prescribed to 54% and 15% of patients, respectively. The hemoglobin A1c (HbA1c) goal (HbA1c < 7.5%) was achieved in 1,350 (56.4%) patients, and the low-density lipoprotein cholesterol (LDL-C) goal (LDL < 100) was achieved in 1,165 (45.6%) patients. Blood pressure control (BP < 140/90) was achieved in 1,755 (65.4%) patients. All three goals were achieved in 278 (10.3%) patients. There were no significant differences in clinical laboratory results and the patients’ characteristics based on gender.ConclusionThe rate of progression of complications in older adult patients is higher than the effectiveness of the treatment, indicating the need for increased social support for this age group.

Vascular endothelial growth factor/connective tissue growth factor and proteomic analysis of aqueous humor after intravitreal conbercept for proliferative diabetes retinopathy.

To investigate the role of connective tissue growth factor (CTGF) and vascular endothelial growth factor (VEGF) in the protein profile of the aqueous humor in patients with proliferative diabetic retinopathy (PDR) following intravitreal injection of conbercept. This study included 72 PDR patients and 8 cataract patients as controls. PDR patients were divided into 3 groups according to the intervals of 3, 5, and 7d between intravitreal conbercept (IVC, 0.5 mg/0.05 mL) injection and pars plana vitrectomy (PPV) performed. Aqueous humor samples were collected before and after IVC and PPV for VEGF and CTGF levels detected with enzyme-linked immunosorbent assay (ELISA). The differential proteomics of 10 patients who underwent PPV surgery 5d after IVC and 8 normal controls was studied, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed on the data, and the protein interaction network of 23 differential proteins was studied. Post-IVC, VEGF levels decreased and CTGF levels increased significantly in aqueous humor, with the CTGF/VEGF ratio rising significantly at all intervals. Liquid chromatography tandem mass spectrometry (LC-MS/MS) identified differentially expressed proteins between pre- and post-IVC samples. GO and KEGG analyses revealed involvement in immune response, stress response, complement and coagulation cascades, ferroptosis, and PPAR signaling pathways. PPI analysis highlighted key proteins like APOA1, C3, and transferrin (TF). ELISA assay confirmed the differential expression of proteins such as HBA1, SERPINA1, COL1A1, and ACTB, with significant changes in the IVC groups. The study demonstrates that IVC effectively reduces VEGF levels while increasing CTGF levels, thereby modifying the CTGF/VEGF ratio, and IVC significantly alters the protein profile in the aqueous humor of patients with PDR. Proteomic analysis reveals that these changes are associated with critical biological pathways and protein interactions involved in immune response, stress response, and cellular metabolism.

Baseline characteristics of Ghanaian children and adults enrolled in PIVOT, a randomised clinical trial of hydroxyurea in HbSC disease in sub-Saharan Africa.

HbSC disease is a common form of sickle cell disease with significant morbidity and early mortality. Whether hydroxyurea is beneficial for HbSC disease is unknown. Prospective Identification of Variables as Outcomes for Treatment (PIVOT, Trial ID PACTR202108893981080) is a double-blind, randomised, placebo-controlled phase II trial of hydroxyurea for people with HbSC, age 5-50 years, in Ghana. After screening, participants were randomised to placebo (standard of care) or hydroxyurea. The primary outcome is the cumulative incidence of haematological toxicities during 12 months of blinded treatment; secondary outcomes include multiple laboratory and clinical assessments. Between April 2022 and June 2023, 112 children and 102 adults were randomised, including 44% females and average age 21.6 ± 14.5 years. Participants had substantial morbidity including previous hospitalisations (93%), vaso-occlusive events (86%), malaria (79%), often received transfusions (20%), with baseline haemoglobin 11.0 ± 1.2 g/dL and foetal haemoglobin 1.8% ± 1.5%. The spleen was palpable in six children and one adult, and ultrasonographic volumes were collected. Proliferative sickle retinopathy was common (30% children, 75% adults), but proteinuria was less common (3% children, 8% adults). Whole blood viscosity, ektacytometry, point-of-sickling, transcranial Doppler, near-infrared spectrometry (NIRS), 6-minute walk, and quality of life were also measured. Now fully enrolled, PIVOT will document the safety and potential benefits of hydroxyurea on clinical and laboratory outcomes in HbSC disease.

Vitreoretinal Surgery in Retinopathy of Prematurity

In this article, vitreoretinal surgical procedures applied for retinopathy of prematurity (ROP) are discussed in comparison with indications such as traction retinal detachments (tRDs), secondary to other ischemic neovascular proliferative retinopathies such as proliferative diabetic retinopathy (PDR). Thus, by comparing the clinical features of ROP, the rationale of vitreoretinal surgical procedures applied, and the currently accepted pathogenetic hypotheses with the clinical features and vitreoretinal surgery procedures of other ischemic neovascular proliferative retinopathies as PDR, a determination of why the accepted pathogenetic hypotheses of ROP are wrong and what is the correct pathogenesis has been made.

Optical coherence tomography (OCT) and OCT Angiography in Stages 3 and 4 proliferative sickle cell retinopathy

PurposeTo investigate macular findings in Goldberg stages 3 and 4 proliferative sickle cell retinopathy (PSCR) using optical coherence tomography (OCT) and OCT Angiography MethodsA case-control study using retrospective OCT and OCTA data from PSCR eyes (cases) and prospective data from age and sex-matched normal (controls). OCTA data included vessel density (VD) in the superficial capillary vascular plexus (SCP) and deep capillary vascular plexus (DCP), foveal avascular zone (FAZ) characterization, including the shape (in the SCP & DCP), size (area covered), and perimeter. OCT data were whole, superior, and inferior hemi-retina thickness for the superficial and deep retina. ResultsThere were 38 OCT / OCTA scans of PSCR eyes of 21 SCD patients; ten eyes were excluded for not meeting inclusion criteria. We analyzed nineteen (19) patients (ten unilateral and 9 bilateral), 28 eyes, nine SS eyes (32%), and nineteen SC eyes (68%). The controls consisted of 29 eyes of 16 normal subjects (three unilateral and 13 bilateral). The commonest FAZ shape in PSCR was “irregular” in 14 eyes (50%), followed by “round” in 11 eyes (39.3%) versus controls, the commonest shape “round” in 18 eyes (62%), followed by “irregular” 9 eyes (31%) (p = 0.165). FAZ area and perimeter were larger in PSCR (p > 0.05). The deep and superficial VD was reduced in PSCR. The mean whole deep VD for cases was 48.9 ± 6.1 versus 52.9 ± 6.4 for controls (p = 0.019). Mean whole superficial VD for cases was 47.4 ± 5.5 versus 49.8 ± 3.4 for controls (p = 0.058).Retina thickness in the whole, superior and inferior hemi-retina, for superficial and deep retina, was higher in PSCR compared to controls (p < 0.05). Superficial whole thickness for cases and controls were 287.0 µm [IQR 35.3 µm] versus 273.0 µm [IQR 18 µm] respectively (p = 0.008). Deep whole thickness for cases and controls was 287.0 µm [IQR 35.25 µm] versus 273.0 µm [IQR 18 µm] (p = 0.008).VD was reduced in SS compared to SC eyes (deep whole VD: 50.28 ± 6.01 vs 46.78 ± 5.80) (p = 0.139). Retina thickness in SS was reduced relative to SC. Peripheral retinal laser photocoagulation did not affect VD, though it was associated with a thinner macula. ConclusionOCT/OCTA of stage 3 and 4 PSCR revealed reduced VD in the DCP and SCP. Despite the thin temporal retina in SCD, there is a thicker whole, superior, and inferior hemiretina in both the superficial and deep retina. An irregularly shaped FAZ is common, a reflection of abnormal microcapillary loss in the perifoveal area.

Modulation of diabetes-related retinal pathophysiology by PTX3

Diabetic retinopathy (DR) is a common complication of diabetes characterized by vascular pathology and neuroinflammation. Pentraxin 3 (PTX3) is a soluble pattern recognition molecule that functions at the crossroads between innate immunity, inflammation, and tissue remodeling. DR is known to involve inflammatory pathways, although the potential relevance of PTX3 has not been explored. We found that PTX3 protein levels increased in the retina of diabetic mice. Similarly, evaluation of a publicly available transcriptomic human dataset revealed increased PTX3 expression in DR with diabetic macular edema and proliferative retinopathy, when compared to nondiabetic retinas or diabetic retinas without complications. To further understand the role of PTX3 within DR, we employed the streptozotocin-induced diabetes model in PTX3 knockout mice (PTX3KO), which were followed up for 9 mo to evaluate hallmarks of disease progression. In diabetic PTX3KO mice, we observed decreased reactive gliosis, diminished microglia activation, and reduced vasodegeneration, when compared to diabetic PTX3 wild-type littermates. The decrease in DR-associated pathological features in PTX3KO retinas translated into preserved visual function, as evidenced by improved optokinetic response, restored b-wave amplitude in electroretinograms, and attenuated neurodegeneration. We showed that PTX3 induced an inflammatory phenotype in human retinal macroglia, characterized by GFAP upregulation and increased secretion of IL6 and PAI-1. We confirmed that PTX3 was required for TNF-α-induced reactive gliosis, as PTX3KO retinal explants did not up-regulate GFAP in response to TNF-α. This study reveals a unique role for PTX3 as an enhancer of sterile inflammation in DR, which drives pathogenesis and ultimately visual impairment.

Characterization and Automatic Discrimination between Predominant Hypoperfusion and Hyperperfusion Stages of NPDR.

Diabetic retinopathy (DR) is a common diabetes complication that can lead to blindness through vision-threatening complications like clinically significant macular edema and proliferative retinopathy. Identifying eyes at risk of progression using non-invasive methods could help develop targeted therapies to halt diabetic retinal disease progression. A set of 82 imaging and systemic features was used to characterize the progression of nonproliferative diabetic retinopathy (NPDR). These features include baseline measurements (static features) and those capturing the temporal dynamic behavior of these static features within one year (dynamic features). Interpretable models were trained to distinguish between eyes with Early Treatment Diabetic Retinopathy Study (ETDRS) level 35 and eyes with ETDRS levels 43-47. The data used in this research were collected from 109 diabetic type 2 patients (67.26 ± 2.70 years; diabetes duration 19.6 ± 7.26 years) and acquired over 2 years. The characterization of the data indicates that NPDR progresses from an initial stage of hypoperfusion to a hyperperfusion response. The performance of the classification model using static features achieved an area under the curve (AUC) of the receiver operating characteristics equal to 0.84 ± 0.07, while the model using both static and dynamic features achieved an AUC of 0.91 ± 0.05. NPDR progresses through an initial hypoperfusion stage followed by a hyperperfusion response. Characterizing and automatically identifying this disease progression stage is valuable and necessary. The results indicate that achieving this goal is feasible, paving the way for the improved evaluation of progression risk and the development of better-targeted therapies to prevent vision-threatening complications.

Spotlight on Expanded Field Imaging Findings in Proliferative Sickle Cell Retinopathy

Spotlight on Expanded Field Imaging Findings in Proliferative Sickle Cell Retinopathy

Association of Anemia and Diabetic Retinopathy Among Patients With Type 2 Diabetes Mellitus: Retrospective Cross-Sectional Study.

Introduction Type 2 diabetes mellitus (T2DM) is a common metabolic disorder characterized by the combination of defective insulin secretion and the inability of insulin-sensitive tissues to respond appropriately to insulin. Diabetic retinopathy (DR) is a common microvascular complication that can result in a preventable cause of blindness. Research to determine the prevalence of anemia among diabetic patients is necessary to assess whether treatment practices should be changed. Anemia is a common complication in patients with T2DM and has been associated with the progression of DR. In this study, our aim is to determine the prevalence of DR and its association with hemoglobin levels in patients diagnosed with T2DM in Dubai, UAE. Methods In this retrospective cross-sectional study, we extracted the data using electronic medical records. The study was performed over a span of three years in Dubai from 2019 to 2022. A total of 368 T2DM patients were included based on retinal exam findings classified into mild, moderate, severe non-proliferative retinopathy, and proliferative retinopathy. Descriptive statistics were used for categorical (frequency, percentage) and continuous variables (mean, SD), with chi-square/Fisher exact tests for categorical associations, ANOVA for continuous variables, and multiple logistic regression to identify DR risk factors, using OR, 95% CI, and p < 0.05 for significance. Results The prevalence of anemia (defined as hemoglobin levels ≤13 mg/dL for men and ≤12 mg/dL for women) was observed in 39.4% of individuals with DR aged between 40 and 88 years; 60.6% of the patients had normal hemoglobin, while 91 individuals (24.7%) exhibited mild anemia, 53 individuals (14.4%) showed moderate anemia, and only one individual (0.3%) had severe anemia. DR grading was as follows: mild non-proliferative DR (16.8%), moderate non-proliferative DR (30.2%), severe non-proliferative DR (13.3%), and proliferative DR (39.7%). Macular edema was present in 59.2% of patients, showing a statistically significant association with more severe DR stages (p < 0.0001). No significant association was found between hemoglobin levels and DR severity (p = 0.568). However, among males, a significant difference in mean hemoglobin levels across DR grades was observed (p = 0.009), with higher hemoglobin levels associated with lower odds of severe DR (OR = 0.775, p = 0.036). Macular edema strongly predicted DR severity, with significant odds ratios across all stages (p < 0.0001). Conclusions There is a significant prevalence of anemia among the examined population. DR severity was notably associated with lower hemoglobin levels in males, and macular edema was significantly linked to more severe stages of DR. Vigilant monitoring and integrated care for both anemia and DR are crucial to optimize patient outcomes and mitigate complications. Regular retinopathy screening is essential for early detection and timely intervention, particularly considering the challenges posed by anemia, such as delayed wound healing and increased infection risk post-screening.

Agonism of β3-Adrenoceptors Inhibits Pathological Retinal Angiogenesis in the Model of Oxygen-Induced Retinopathy.

In response to hypoxia, sympathetic fibers to the retina activate β-adrenoceptors (β-ARs) that play an important role in the regulation of vascular and neuronal functions. We investigated the role of β3-AR using the mouse model of oxygen-induced retinopathy (OIR). Mouse pups were exposed to 75% oxygen at postnatal day 7 (PD7) followed by a return to room air at PD12. The β3-AR preferential agonist BRL37344 was subcutaneously administered once daily at different times after the return to room air. At PD17, the OIR mice underwent flash and pattern electroretinogram. After sacrifice, retinal wholemounts were used for vessel staining or immunohistochemistry for astrocytes, Müller cells, or retinal ganglion cells (RGCs). In retinal homogenates, the levels of markers associated with neovascularization (NV), the blood-retinal barrier (BRB), or astrocytes were determined by western blot, and quantitative reverse-transcription polymerase chain reaction was used to assess β3-AR messenger. Administration of the β3-AR antagonist SR59230A was performed to verify BRL37344 selectivity. β3-AR expression is upregulated in response to hypoxia, but its increase is prevented by BRL37344, which counteracts NV by inhibiting the pro-angiogenic pathway, activating the anti-angiogenic pathway, recovering BRB-associated markers, triggering nitric oxide production, and favoring revascularization of the central retina through recovered density of astrocytes that ultimately counteracts NV in the midperiphery. Vasculature rescue prevents dysfunctional retinal activity and counteracts OIR-associated retinal ganglion cell loss. β3-AR has emerged as a crucial intermediary in hypoxia-dependent NV, suggesting a role of β3-AR agonists in the treatment of proliferative retinopathies.

A study of diabetic retinopathy in diabetic foot syndrome in Western Regional Institute of India

Background: Diabetes is a rapidly growing health challenge and potential epidemic across low-and-middle-income countries like India. Diabetic retinopathy (DR) is a consequence of diabetic microangiopathy, which may cause visual deterioration due to macular edema in any stage and vitreous hemorrhage or tractional retinal detachment in the advanced proliferative retinopathy stages. Aims and Objectives: The aim was to study the retinopathy status in diabetic patients with a risk of diabetic foot syndrome (DFS) visiting a western regional hospital in India. Materials and Methods: In this cross-sectional study, all patients with diabetes mellitus (DM) with a risk of DFS, visiting a tertiary care hospital during the study period, underwent an ophthalmological evaluation for documentation of their retinopathy status. Results: One hundred and fourteen patients diagnosed to have a risk profile for DFS were included in the study. Their mean age was 61.22 years and 81.6% were males. The mean duration of DM was 12.24 years, respectively. Of the 114 patients, 72 had DR. An increased presence of retinopathy in patients with an increased risk grade of diabetic foot (DF) was found significant by the Chi‐square test. (P&lt;0.001). Conclusion: Our study found an increased presence of DR in Western Indian cohort with DFS. The severity of retinopathy was greater in patients with higher grades of risk for DF, therefore establishment of an association between DR and DFS will help in developing an integrated management strategy for these two grave consequences of diabetes.

A neutrophil elastase-generated mature form of IL-33 is a potent regulator of endothelial cell activation and proliferative retinopathy

Human interleukin-33 (IL-33) is a 270 amino acid protein that belongs to the IL-1 cytokine family and plays an important role in various inflammatory disorders. Neutrophil proteases (Cathepsin G and Elastase) and mast cell proteases (tryptase and chymase) regulate the activity of IL-33 by processing full-length IL-33 into its mature form. There is little evidence on the role of these mature forms of IL-33 in retinal endothelial cell signaling and pathological retinal angiogenesis. Here, we cloned, expressed, and purified the various mature forms of human IL-33 and then evaluated the effects of IL-3395-270, IL-3399-270, IL-33109-270, and IL-33112-270 on angiogenesis in human retinal microvascular endothelial cells (HRMVECs). We observed that IL-3395-270, IL-3399-270, IL-33109-270, and IL-33112-270 significantly induced HRMVEC migration, tube formation and sprouting angiogenesis. However, only IL-3399-270 could induce HRMVEC proliferation. We used a murine model of oxygen-induced retinopathy (OIR) to assess the role of these mature forms of IL-33 in pathological retinal neovascularization. Our 3′-mRNA sequencing and signaling studies indicated that IL-3399-270 and IL-33109-270 were more potent at inducing endothelial cell activation and angiogenesis than the other mature forms. We found that genetic deletion of IL-33 significantly reduced OIR-induced retinal neovascularization in the mouse retina and that intraperitoneal administration of mature forms of IL-33, mainly IL-3399–270 and IL-33109–270, significantly restored ischemia-induced angiogenic sprouting and tuft formation in the hypoxic retinas of IL-33–/– mice. Thus, our study results suggest that blockade or inhibition of IL-33 cleavage by neutrophil proteases could help mitigate pathological angiogenesis in proliferative retinopathies.

The molecular mechanism responsible for HbSC retinopathy may depend on the action of the angiogenesis-related genes ROBO1 and SLC38A5.

HbSC disease, a less severe form of sickle cell disease, affects the retina more frequently and patients have higher rates of proliferative retinopathy that can progress to vision loss. This study aimed to identify differences in the expression of endothelial cell-derived molecules associated with the pathophysiology of proliferative sickle cell retinopathy (PSCR). RNAseq was used to compare the gene expression profile of circulating endothelial colony-forming cells from patients with SC hemoglobinopathy and proliferative retinopathy (n = 5), versus SC patients without retinopathy (n = 3). Real-time polymerase chain reaction (qRT-PCR) was used to validate the RNAseq results. A total of 134 differentially expressed genes (DEGs) were found. DEGs were mainly associated with vasodilatation, type I interferon signaling, innate immunity and angiogenesis. Among the DEGs identified, we highlight the most up-regulated genes ROBO1 (log2FoldChange = 4.32, FDR = 1.35E-11) and SLC38A5 (log2FoldChange = 3.36 FDR = 1.59E-07). ROBO1, an axon-guided receptor, promotes endothelial cell migration and contributes to the development of retinal angiogenesis and pathological ocular neovascularization. Endothelial SLC38A5, an amino acid (AA) transporter, regulates developmental and pathological retinal angiogenesis by controlling the uptake of AA nutrient, which may serve as metabolic fuel for the proliferation of endothelial cells (ECs) and consequent promotion of angiogenesis. Our data provide an important step towards elucidating the molecular pathophysiology of PSCR that may explain the differences in ocular manifestations between individuals with hemoglobinopathies and afford insights for new alternative strategies to inhibit pathological angiogenesis.

Heterotypic macrophages/microglia differentially contribute to retinal ischaemia and neovascularisation.

Diabetic retinopathy is characterised by neuroinflammation that drives neuronal and vascular degenerative pathology, which in many individuals can lead to retinal ischaemia and neovascularisation. Infiltrating macrophages and activated retina-resident microglia have been implicated in the progression of diabetic retinopathy, although the distinct roles of these immune cells remain ill-defined. Our aim was to clarify the distinct roles of macrophages/microglia in the pathogenesis of proliferative ischaemic retinopathies. Murine oxygen-induced retinopathy is commonly used as a model of ischaemia-induced proliferative diabetic retinopathy (PDR). We evaluated the phenotype macrophages/microglia by immunostaining, quantitative real-time RT-PCR (qRT-PCR), flow cytometry and scRNA-seq analysis. In clinical imaging studies of diabetic retinopathy, we used optical coherence tomography (OCT) and OCT angiography. Immunostaining, qRT-PCR and flow cytometry showed expression levels of M1-like macrophages/microglia markers (CD80, CD68 and nitric oxide synthase 2) and M2-like macrophages/microglia markers (CD206, CD163 and macrophage scavenger receptor 1) were upregulated in areas of retinal ischaemia and around neo-vessels, respectively. scRNA-seq analysis of the ischaemic retina revealed distinct ischaemia-related clusters of macrophages/microglia that express M1 markers as well as C-C chemokine receptor 2. Inhibition of Rho-kinase (ROCK) suppressed CCL2 expression and reduced CCR2-positive M1-like macrophages/microglia in areas of ischaemia. Furthermore, the area of retinal ischaemia was reduced by suppressing blood macrophage infiltration not only by ROCK inhibitor and monocyte chemoattractant protein-1 antibody but also by GdCl3. Clinical imaging studies of diabetic retinopathy using OCT indicated potential involvement of macrophages/microglia represented by hyperreflective foci in areas of reduced perfusion. These results collectively indicated that heterotypic macrophages/microglia differentially contribute to retinal ischaemia and neovascularisation in retinal vascular diseases including diabetic retinopathy. This adds important new information that could provide a basis for a more targeted, cell-specific therapeutic approach to prevent progression to sight-threatening PDR.

Evaluation of peripheral blood inflammatory biomarkers in sickle cell disease with and without retinopathy.

The aim of this study was to evaluate the clinical significance of blood-cell associated inflammation markers in patients with sickle cell disease (SCD) and sickle cell retinopathy (SCR). Neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), monocyte to lymphocyte ratio (MLR), systemic immune inflammation index (SIII), systemic inflammation response index (SIRI), systemic inflammation modulation index (SIMI) and aggregate systemic inflammation index (AISI) were calculated. This study included 45 healthy controls (Group 1) and 100 SCD (Group 2). Patients in Group 2 were then divided into two groups: without SCR (Group 3) and with SCR (Group 4), and patients with SCR (Group 4) were further divided into two groups: non-proliferative sickle cell retinopathy (NPSCR) (Group 5) and proliferative sickle cell retinopathy (PSCR) (Group 6). The mean values for NLR, PLR, SIII, SIRI, AISI, and SIMI were significantly higher in Group 2 compared to Group 1 (p = 0.011 for NLR, p = 0.004 for SIII, and p < 0.001 for others). Furthermore, AISI and SIMI parameters demonstrated statistically significant discriminatory power to distinguish Group 5 from Group 6 (p = 0.0016 and p = 0.0006, respectively). Given the critical role of inflammatory mechanisms in the pathogenesis of SCD and its related complications, the assessment of blood-cell-associated inflammatory markers may present a pragmatic and advantageous approach to the clinical oversight and therapeutic intervention of SCD.

Clinical serum lipidomic profiling revealed potential lipid biomarkers for early diabetic retinopathy

Diabetic retinopathy (DR) is a serious complication of diabetes featuring abnormal lipid metabolism. However, the specific lipid molecules associated with onset and progression remain unclear. We used a broad-targeted lipidomics approach to assess the lipid changes that occur before the proliferative retinopathy stage and to identify novel lipid biomarkers to distinguish between patients without DR (NDR) and with non-proliferative DR (NPDR). Targeted lipomics analysis was carried out on serum samples from patients with type I diabetes, including 20 NDRs and 20 NPDRs. The results showed that compared with the NDR group, 102 lipids in the NPDR group showed specific expressions. Four lipid metabolites including TAG58:2-FA18:1 were obtained using the Least Absolute Shrink And Selection Operator (LASSO) and Support Vector Machine Recursive Feature Elimination (SVM-RFE) methods. The four-lipid combination diagnostic models showed good predictive ability in both the discovery and validation sets, and were able to distinguish between NDR patients and NPDR patients. The identified lipid markers significantly improved diagnostic accuracy within the NPDR group. Our findings help to better understand the complexity and individual differences of DR lipid metabolism.

Linking Diabetic Retinopathy Severity to Coronary Artery Disease Risk Factors in Type 2 Diabetic Patients.

Diabetes mellitus (DM) is a common metabolic disorder characterized by hyperglycemia, leading to chronic complications, notably cardiovascular diseases such as coronary artery disease (CAD). Diabetic retinopathy (DR), a leading cause of blindness, may serve as a non-invasive marker for CAD. This study investigates the correlation between DR and CAD to explore its diagnostic potential in diabetic populations. A cross-sectional study was conducted over one year in a general hospital, involving 100 type 2 DM patients with retinopathy. DR was classified as mild non-proliferative diabetic retinopathy (NPDR), moderate NPDR, severe NPDR, or proliferative retinopathy, based on fundus examinations. Data on age, duration of diabetes, cholesterol levels, glycated hemoglobin (HbA1C), and ECG (electrocardiography) findings were collected. Statistical analysis included frequency analysis, chi-square tests for association between categorical variables, and significance testing with p-values. Data were analyzed using IBM SPSS Statistics for Windows, Version 20.0 (Released 2011; IBM Corp., Armonk, New York, United States). Descriptive statistics were characterized by categorical and continuous variables. The chi-square test determined associations between qualitative variables, with significance set at p<0.05. The mean age of patients was 57.13 ± 8.51 years. Age and duration of diabetes were significant predictors of retinopathy severity (p<0.001). Proliferative retinopathy was found exclusively in patients over 70 years. Lower cholesterol levels (<200 mg/dL) were significantly associated with less severe retinopathy (p=0.033), whereas higher cholesterol levels (>200 mg/dL) did not show a statistically significant association with retinopathy severity (p=0.772). Patients with HbA1C levels between 6.5% and 8.5% predominantly had milder forms of retinopathy, as indicated by the significant p-value (<0.001). In contrast, patients with HbA1C levels above 8.5% are more likely to have severe NPDR or proliferative diabetic retinopathy (PDR), but this association was not statistically significant (p=0.582). ECG abnormalities increased with retinopathy severity (p=0.002). Hypertension was significantly linked to cardiac changes in retinopathy patients (p<0.001), while smoking and family history of CAD were not significant factors.This study's cross-sectional design limits causality inference. The single-center sample of 100 patients may not be broadly generalizable. Reliance on self-reported data introduces potential recall bias, and confounding factors such as diet, physical activity, and additional comorbidities were not accounted for. The lack of a control group further limits comparative analysis. Future longitudinal studies with larger, diverse samples are needed. Retinopathy in DM patients is significantly associated with cardiac changes and other risk factors such as hypertension, dyslipidemia, and poor glycemic control. Aggressive management of these factors is essential. Retinopathy can serve as a predictor of CAD in diabetic patients.

Evaluation of the Role of Prolactin in the Prevention of Diabetic Retinopathy

Aim: Investigating the potential role of prolactin in the prevention of diabetic retinopathy Methods: The study was conducted on 90 diabetic patients who were divided into a group that included 37 patients without retinopathy and a group that included 27 patients with non-proliferative retinopathy and 26 patients with proliferative retinopathy who attended the Endocrinology clinic and Division at Tishreen University Hospital in Lattakia during the period from 2023 to 2024. Results: Independent samples T-test analysis showed Significant decreased in prolactin level in diabetic patients with DR in comparison to diabetic patients without DR (p=0.0001). Person correlation showed a statistically significant inverse relationship between prolactin levels and Glycosylated hemoglobin levels between patient groups. Conclusions: From this study it can be concluded that diabetic patients with retinopathy had lower level of prolactin and serum prolactin does seem to have protective role in diabetic retinopathy.

Двухэтапное хирургическое лечение регматогенной отслойки сетчатки, осложненной выраженной пролиферативной витреоретинопатией, с применением первичной круговой ретинотомии и отсроченной эндолазеркоагуляцией сетчатки в уменьшенном объеме

Abstrakt Primary retinotomy in the surgical treatment of complicated rhegmatogenous retinal detachment with severe proliferative vitreoretinopathy D.O. Shkvorchenko, B.E. Malyugin, A.Yu. Kornienko, E.S. Khrisanfova, O.B. Klepinina S. Fyodorov Eye Microsurgery Federal State Institution, Moscow, Russian Federation Purpose. To develop a method of surgical treatment of rhegmatogenous retinal detachment with severe proliferative retinopathy (stage C) using primary circumferential retinotomy, short-term perfluorocarbon liquid (PFCL) endotamponade and deferred laser endophotocoagulation in a reduced volume. To evaluate the effectiveness of the developed method in the treatment of complicated rhegmatogenous retinal detachment with severe proliferative vitreoretinopathy. Material and methods. 12 patients (12 eyes) with the diagnosis of rhegmatogenous retinal detachment with severe proliferative retinopathy were operated using developed method of two-stage surgical treatment with a reduced volume of laser endophotocoagulation. All 12 patients had a concomitant diagnosis of complicated cataract. Results. A new method of two-stage surgical treatment with reduced volume of laser endophotocoagulation was developed in the S. Fyodorov Eye Microsurgery Federal State Institution. After the follow-up period of 12 months retina was attached in all 12 cases, best corrected visual acuity (BCVA) was 0.38±0.08; 5 eyes had silicone oil endotamponade, in 7 cases silicone oil was removed. Conclusion. Primary 360-degree retinotomy is an effective method of surgical treatment of rhegmatogenous retinal detachment with severe proliferative retinopathy. The most preferable in these cases is to carry out surgical treatment in several stages with short-term PFCL tamponade, which allows to achieve maximum adaptation of the retina. Laser retinopexy in the PFCL environment during the second stage of surgery allows it to be carried out fully and at the same time in a minimal volume. Key words: retinal detachment, proliferative vitreoretinopathy, primary retinotomy, circumferential retinotomy, perfluorocarbon liquid, laser endophotocoagulation

Successful treatment of retinopathy of prematurity in oculocutaneous albinism with OCA2 variants: a case report and review of literature

BackgroundOculocutaneous albinism (OCA) is a group of autosomal recessive hereditary disorders that affect melanin biosynthesis, resulting in abnormalities in hair, skin, and eyes. Retinopathy of prematurity (ROP) is a proliferative retinopathy mainly observed in premature infants with low birth weight and early gestational age, but it can also affect full-term infants or children with normal weight, particularly in developing countries. The coexistence of ROP and OCA is rare. There is limited documentation regarding treatment approaches, with few studies reporting positive outcomes with laser treatment due to the absence of melanin pigment. This study discusses the treatment challenges in a female infant diagnosed with ROP and OCA, and underscores the importance of genetic analysis in guiding therapeutic decisions for this rare comorbid condition.Case presentationThe study presents a case of ROP occurring concurrently with OCA. Genetic testing revealed two variants, c.727C > T (p.R243C) and c.1832 T > C (p.L611P), in the OCA2 gene, inherited from the patient's mother and father, respectively. The identified mutations were consistent with a diagnosis of OCA2, classified as a subtype of OCA. The patient initially received intravitreal anti-vascular endothelial growth factor (anti-VEGF) injection, followed by laser photocoagulation therapy for a recurrent event. A favorable outcome was observed during the 2-month follow-up period.ConclusionsThe co-occurrence of ROP and OCA is a rare phenomenon, and this is the first recorded case in the Chinese population. The current case supports the use of laser as the primary treatment modality for ROP in OCA2 patients with partial pigmentation impairment. Furthermore, genetic analysis can aid in predicting the effectiveness of laser photocoagulation in this patient population.