Inexpensive HIV Med Improves Vision in Diabetic Eye Disease
Oral lamivudine, an inflammasome inhibitor originally approved for suppressing HIV, was a relatively safe and effective treatment for improving visual acuity in adults with center-involving diabetic macular edema, a serious complication of diabetic retinopathy.
METHODOLOGY:
Researchers conducted a clinical trial to assess the effectiveness of oral lamivudine vs placebo in improving visual acuity in 24 adults (mean age, 62.7 years; 55% women) with type 2 diabetes and center-involving diabetic macular edema from a tertiary center in São Paulo, Brazil.
Best-corrected visual acuity was less than 69 letters in this cohort.
The participants were randomly assigned to receive either oral lamivudine (150 mg twice daily; 10 participants; 16 eyes) or placebo (14 participants; 21 eyes) for 8 weeks, with intravitreous bevacizumab (1.25 mg) administered at week 4.
Primary outcomes were the mean changes in best-corrected visual acuity from baseline to weeks 4 and 8, and secondary outcomes included changes in retinal thickness and adverse events.
Outcomes in the lamivudine group were compared with those in a historical cohort of individuals who received aflibercept, bevacizumab, or ranibizumab.
TAKEAWAY:
Participants who received lamivudine experienced a significant improvement in visual acuity as early as week 4, with a mean gain of 9.8 letters on the eye chart, whereas those on placebo had a mean loss of 1.8 letters ( P < .001) ; 94% of eyes in the lamivudine group showed an improvement in best-corrected visual acuity compared with just 24% in the placebo group.
< .001) ; 94% of eyes in the lamivudine group showed an improvement in best-corrected visual acuity compared with just 24% in the placebo group. Following injection of bevacizumab at week 4, patients in the lamivudine group showed greater improvement in visual acuity than those who received placebo (16.9 vs 5.3 letters; P < .001) at week 8.
< .001) at week 8. When compared with drugs in the historical cohort, lamivudine was at least as effective as aflibercept and more effective than bevacizumab or ranibizumab.
No significant differences were observed in retinal thickness or adverse events between the lamivudine and placebo groups; no serious systemic adverse events such as lactic acidosis or hepatic or renal toxicity were reported during the study period.
IN PRACTICE:
Continual intravitreous administration of anti–vascular endothelial growth factor drugs, 'which requires frequent visits to doctors' offices, imposes a substantial burden on patients and healthcare systems,' the researchers reported. 'Repurposing existing drugs such as lamivudine enables potentially immediate translation to practice and could obviate the aforementioned challenges by reducing medication costs and eliminating intravitreous injection costs. Such an oral medication would also avoid the potentially blinding complications of intravitreous injections.'
'These findings open the door to a more accessible and less invasive treatment approach for DME [diabetic macular edema], with the potential to benefit millions of patients globally,' they added.
SOURCE:
This study was led by Felipe Pereira of the Universidade Federal de São Paulo, São Paulo, Brazil. It was published online on May 27, 2025, in Med .
LIMITATIONS:
The relatively small number of participants was a major limitation. The 8-week duration of the study — imposed because of safety concerns over lamivudine's potential toxicity — precluded assessment of its long-term efficacy and safety. This study took place at a single center in Brazil and involved participants whose characteristics differed from those from the historical cohort who were based in the United States.
DISCLOSURES:
This study received support from the Universidade Federal de São Paulo, Latinofarma, the National Institutes of Health, and other sources. Some authors declared receiving consultancy fees, were named as inventors on matter-related patent applications, served as scientific consultants, and had other ties with many sources, including the funding agencies.
Hashtags
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Medscape
18 minutes ago
- Medscape
New Hyperkalemia Risk Model for CKD and Diabetes
A new risk model may help identify which patients with chronic kidney disease (CKD) and diabetes are more likely to develop hyperkalemia, granting physicians more confidence in prescribing medications like finerenone. However, researchers caution that further validation is needed. The model is based on pooled data from two phase 3 trials of finerenone: FIDELIO-DKD (Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease) and FIGARO-DKD (Finerenone in Reducing Cardiovascular Mortality and Morbidity in Diabetic Kidney Disease). The combined dataset, known as FIDELITY, includes 6355 patients in the placebo groups. Researchers used this dataset to develop the risk score, identifying seven factors independently associated with the primary outcome of new onset of hyperkalemia (incident serum potassium level > 5.5 mmol/L): Serum potassium > 4.5 mmol/L Prior history of hyperkalemia No use of sodium-glucose co-transporter 2 inhibitor Urine albumin-to-creatinine ratio > 1000 mg/g Hemoglobin < 12 g/dL No use of thiazide-type diuretics Estimated glomerular filtration rate < 45 mL/min/1.73 m2 The model was subsequently validated using data from the finerenone groups in FIDELITY. In their paper, published online in the European Heart Journal , João Pedro Ferreira, MD, PhD, of the Cardiovascular Research and Development Center at the University of Porto, Porto, Portugal, and coauthors noted that the model could be used to reduce the risk for hyperkalemia among high-risk patients receiving finerenone. 'This could include tailoring of individualized treatment and follow-up strategies (eg, frequency of visits and serum potassium assessments, and use of potassium binders), thus optimizing patient management and potentially improving outcomes,' they noted. Welcome Results, Validation Required CKD, which affects more than 800 million people worldwide, is a common complication of diabetes. An estimated 15%-40% of people with CKD in the setting of diabetes may have hyperkalemia, noted Bernard G. Jaar, MD, MPH, clinical director for Nephrology at Johns Hopkins School of Medicine, Baltimore, who was not involved in the study. In an email exchange with Medscape Medical News , Jaar described the study as 'welcome and much needed.' He noted that hyperkalemia poses a challenge for clinicians, as many medications required for optimal care in CKD — including renin-angiotensin-aldosterone system (RAAS) blockade agents and finerenone — can raise serum potassium. 'This is a true barrier to care,' Jaar wrote. 'Clinicians are worried about the potential complications associated with hyperkalemia, such as arrhythmias and even death.' Jaar noted that the FIDELITY analysis has several strengths, including its large sample size of patients with varying stages of CKD and degrees of proteinuria, and a risk score model that incorporated readily available clinical variables. He added that it reports a stepwise increase in hyperkalemia risk across risk score tertiles in both placebo and finerenone groups, even though all patients were already on a maximally tolerated RAAS blockade agent. However, he questioned the study's generalizability, given that it excluded patients if their serum potassium was > 4.8 mmol/L. 'This risk model in predicting hyperkalemia needs to be validated in other populations where diet may be different,' Jaar wrote. 'Also, this needs to be validated in at-risk populations during real-life experience and not only in patients enrolled in clinical trials, who are typically highly motivated and selected.' Future Applications Rajiv Agarwal, MD, MS, professor emeritus of medicine at Indiana University and a lead researcher in the finerenone clinical studies, echoed the need for further validation of this tool. Although not involved with the development of the risk model, Agarwal was an author on key publications from the FIGARO-DKD, FIDELIO-DKD, and FIDELITY studies. Agarwal suggested that this model's approach could be applied to other therapies, including aldosterone synthase inhibitors in a similar population with CKD. He also noted the importance of incorporating validated risk models for hyperkalemia into electronic medical records or apps, particularly in countries with limited access to care, like China and India. This would allow more nuanced approaches for following up patients taking drugs with established hyperkalemia risk. 'If the patient cannot come after a month, can I make a clinical judgment and say, 'Okay, if you came back after 3 months, your risk of hyperkalemia is low enough that I'm willing to take that risk,'' he said. 'Or if the risk of hyperkalemia is high, you can tell the patient who can't come back in 30 days, 'I don't think I want to prescribe this drug for you'.' The work on the risk model was supported by Bayer, which also funded the FIDELIO-DKD and FIGARO-DKD studies and pooled analysis. The study's authors included Bayer employees. Other financial relationships of the authors included research support, consulting and other fees from companies including: Abbott Vascular, Amgen, Astellas, AstraZeneca, Bayer, BioVentrix, Boehringer Ingelheim, Brahms, Brainstorm Medical, Cardiac Dimensions, Cardior, Cereno Scientific, CSL Vifor, CVRx, Edwards, Eli Lilly, G3 Pharmaceuticals, Gilead, GSK, Impulse Dynamics, Janssen, KBP Biosciences, Mundipharma, Novartis, Novo Nordisk, Occlutech, PhaseBio, Proton Intel, Respicardia, Sanofi, Sarfez, scPharmaceuticals, Servier, SQ Innovation, Tricida, Vectorious, Vifor International, and V-Wave. Agarwal had received support from Bayer. He also had received consulting fees and other support from Boehringer Ingelheim, Novartis, Akebia, Intercept Pharma, Alnylam, and Vertex. Jaar reported no relevant financial disclosures.
New York Times
an hour ago
- New York Times
Should We Test Babies for Incurable Diseases?
In every postpartum hospital unit across the country, 1-day-old babies undergo the same ritual: A nurse pricks the newborn's heel and stamps tiny drops of blood onto a paper filter, which is then sent off for a standard screening panel. Today, that panel checks for unusual bio-markers that may indicate a rare but treatable disease like sickle cell anemia or cystic fibrosis. But what if that same dried blood spot could tell you about the baby's risk of developing certain conditions later in life — some with no method of prevention or cure? What if that heel prick could tell you that the baby was almost certainly going to be diagnosed with autism by the time they turned 5? Or that the child would be more likely to develop breast cancer as an adult? Would you want to know? Would she? These questions are no longer hypothetical. Tens of thousands of parents have sought such insights by enrolling their newborns in research projects that examine the baby's genome — the full blueprint for her growing body. As the cost of sequencing plummets, the practice of analyzing hundreds of genes in healthy babies is quietly on the rise, ushering in new questions about where to draw the boundaries of knowledge — and who should get to decide. Scientifically speaking, the possibilities are almost endless. Since virtually every disease has some basis in our genes, the full genome — with three billion base pairs, coding some 20,000 genes — contains a wealth of data to be mined for lifesaving intel and gut-wrenching secrets. But the experts are divided. Some say that revealing a risk of an incurable illness will only put parents in distress, bombarding them with despairing predictions for their young child's life. Others believe any data about diseases that arise in adulthood, like breast or colon cancer, must be excluded, since they violate that future adult's privacy and autonomy — in other words, the right not to know. Want all of The Times? Subscribe.
Medscape
2 hours ago
- Medscape
Continuing Metformin Reduces PCOS Pregnancy Risks
Continuing metformin throughout the first trimester in women with polycystic ovary syndrome (PCOS) showed the potential to reduce miscarriage risk (odds ratio [OR], 0.64) and increase clinical pregnancy rates (OR, 1.57) compared with placebo. A meta-analysis of 12 randomized controlled trials involving 1708 women suggested that stopping metformin at pregnancy confirmation might be less beneficial than continuation through the first trimester. METHODOLOGY: Researchers conducted a systematic review and meta-analysis of randomized controlled trials evaluating metformin started preconception and continued at least until positive pregnancy test compared with placebo or no treatment in women with PCOS. The analysis included 12 trustworthy studies with 1708 participants, with trials conducted across 14 countries spanning five continents, all graded as low to moderate quality evidence. The primary outcome measure focused on miscarriage rate, defined as pregnancy loss prior to 20 completed weeks of gestation, while secondary outcomes included clinical pregnancy and live birth rates. Investigators performed indirect comparisons between treatment groups using the Bucher technique to evaluate clinical pregnancy, miscarriage, and live birth rates for metformin treatment continued throughout first trimester vs stopped at a positive pregnancy test. TAKEAWAY: Women receiving preconception metformin continued throughout the first trimester had higher clinical pregnancy rates (OR, 1.57; 95% CI, 1.11-2.23), potential reduction in miscarriage (OR, 0.64; 95% CI, 0.32-1.25), and possible increase in live birth (OR, 1.24; 95% CI, 0.59-2.61) compared with placebo or no treatment. Participants who stopped metformin once pregnant showed an increased clinical pregnancy rate (OR, 1.35; 95% CI, 1.01-1.80) but suggested higher miscarriage risk (OR, 1.46; 95% CI, 0.73-2.90) compared with placebo or no treatment. Indirect comparisons consistently favored continuing metformin through first trimester vs stopping at pregnancy confirmation for clinical pregnancy (OR, 1.16; 95% CI, 0.74-1.83), miscarriage (OR, 0.44; 95% CI, 0.17-1.16), and live birth (OR, 1.14; 95% CI, 0.41-3.13). IN PRACTICE: 'Women with PCOS have been shown to have a fivefold increased risk per year of developing insulin resistance and subsequent type 2 diabetes. Insulin resistance has been shown to be independently associated with a higher risk of miscarriage. Metformin acts by decreasing gluconeogenesis, lipogenesis and enhancing glucose uptake, all of which in turn reduce insulin resistance,' wrote the authors of the study. SOURCE: The study was led by James Cheshire, PhD, Birmingham Women's and Children's NHS Foundation Trust in Birmingham, England. It was published online in American Journal of Obstetrics and Gynecology . LIMITATIONS: According to the authors, the main limitation was the inherent heterogeneous nature of the study population and the overall low quality of evidence. Women with PCOS have different phenotypes and varying degrees of hyperandrogenism and insulin resistance, which could not be accounted for in the analyses. Additionally, many studies did not subdivide pregnancy outcome data by body mass index (BMI), preventing meaningful analyses in BMI subgroups. The limited outcome data in spontaneously conceiving populations (only 30 women from two studies) make it difficult to extrapolate findings to this group. DISCLOSURES: The authors reported having no conflicts of interest. The study received no external funding.
