Shiga-producing E. coli Growing More Resistant to Antibiotics

Photo by CDC on Unsplash

Resistance to antimicrobial agents is rising among human infections with Escherichia coli bacteria that produce the Shiga toxin, according to a study analysing data from nearly 2000 infections in the United States between 2010 and 2021.

The increase in resistance points to a need for antibiotic stewardship in the food production chain as well as in human health, says study leader Csaba Varga, a professor of pathobiology at the University of Illinois Urbana-Champaign.

“Shiga toxin–producing E. coli is a type of foodborne bacteria that can cause anything from mild diarrhoea to very serious illness. About 100 000 people in the U.S. get sick from this strain each year, and some end up in the hospital,” Varga said. “The biggest concern is for children under five years of age, who are more likely to develop serious complications, such as kidney failure.”

Varga and graduate student Tarjani Bhatt used data reported by the U.S. Centers for Disease Control and Prevention, which collects the information through a national surveillance system. They focused on the E. coli strain O157, which produces the Shiga toxin responsible for the majority of severe illnesses. They looked at 1995 samples collected between 2010 and 2021 to see whether there was any change in antimicrobial resistance rates over time, and whether there were any patterns in age or geography.

“Most of the previous studies have looked at snapshots in time, not how resistance changes year by year. We didn’t have a clear picture of long-term trends, whether resistance was increasing, decreasing or staying the same,” Varga said. “Resistance doesn’t stay in one place; it moves through people, animals and the environment. Our study helps fill those gaps by looking at when, where and in whom resistance is emerging over time.”

The group found that, while overall resistance remains low, it has steadily increased over time – especially for the common antibiotics tetracycline and sulfisoxazole. They also found that resistance varied by geographical region and by age group, with younger adults in their 20s and 30s most likely to have infections resistant to some antibiotics.

The most mystifying aspect of the findings is that antibiotics are not typically recommended for Shiga-producing E. coli infections, Varga said. Though the treatment kills the bacteria, that action triggers the release of more Shiga toxin, making the illness more dangerous and increasing the risk for serious complications. Antibiotics are avoided unless the patient has another severe infection at the same time.  

“Even though we don’t usually treat this infection with antibiotics, we’re still seeing resistance emerging and spreading, which tells us these bacteria are being exposed to antibiotics somewhere along the way,” Varga said.

The researchers propose a “One Health” approach to the issue, taking into account not only human health and antibiotic use, but animals and environment as well, particularly because the illness is foodborne.

“Better antibiotic stewardship in agriculture, along with food safety and environmental controls, will be key to slowing this trend. What happens on farms, in food production and in the environment can directly impact human health. Prevention has to happen from farm to fork,” Varga said.

Source: University of Illinois at Urbana-Champaign

New Evidence Offers Hope for Ketogenic Therapy in Treatment of Anorexia Nervosa

Pilot trial reports reduced eating disorder and depressive symptoms in difficult-to-treat psychiatric condition

Photo from Freepik.

A pilot study published today in Communications Medicine demonstrates the potential of a new approach to treating anorexia nervosa, a disorder for which effective treatments have been significantly limited. The research from UC San Diego School of Medicine reports that a ketogenic nutritional intervention – a high-fat, low-carbohydrate, moderate-protein diet – was feasible and safe for patients with weight-normalised and mildly underweight anorexia nervosa. The ketogenic intervention was well-tolerated by participants, with high adherence rates and no significant weight loss observed throughout the program.

Furthermore, significant improvements were observed in eating disorder symptoms, with nearly 3 in 4 of study completers in the recovered range at study end, no longer meeting criteria for an anorexia nervosa diagnosis, and all completers experiencing an improvement in depression scores.

Anorexia nervosa is a devastating psychiatric disorder with among the highest mortality rate of any mental illnessin the United States, a death occurs every 52 minutes as a result of this disorder or its complications. Even after successful weight restoration, patients often struggle with persistent psychological symptoms — including body dissatisfaction, an intense fear of eating, and a preoccupation with shape — that drive an alarmingly high risk of relapse.

Study lead Guido Frank, MD, Professor of Psychiatry at UC San Diego School of Medicine, who has been studying and treating anorexia patients for over 25 years, launched this study to broaden treatment options for this high-risk population. “We urgently need new approaches to anorexia nervosa. Our work with ketogenic therapy looks beyond standard therapies and potentially at the underlying physiology of the disorder,” states Dr. Frank. “Growing evidence links anorexia nervosa to neurometabolic dysfunction, and we are hopeful that direct metabolic intervention can regulate neural function and address the psychological symptoms patients experience.”

The outpatient, nationwide, single-arm clinical study delivered a supervised 14-week ketogenic intervention, with 18 of the 22 enrolled participants (82%) completing the study. No significant change in weight was observed throughout the program (as measured by BMI). By the end of the study, 72% of study completers reached the recovered range of eating disorder symptoms as measured by eating disorder scales (Eating Disorder Examination Questionnaire, EDE-Q, and Eating Disorder Inventory-3, EDI-3) and all showed improvements in depression scores (as measured by the Beck Depression Inventory, BDI), with 72% within normal range.

For co-author Barbara Scolnick, MD, an internal medicine physician in Waban, Massachusetts, this study is the culmination of a decade-long personal journey. “The scientific inquiry that led to this research began in search of answers for my niece, Caroline Beckwith,” Dr. Scolnick shared. “Ketogenic therapy, a standard in epilepsy care, was the major catalyst, when combined with other interventions, that allowed Caroline to achieve remission after a 15-year struggle with anorexia nervosa. I am encouraged by these preliminary findings, which indicate that this treatment may provide a path forward for others like Caroline.”

While the authors acknowledge the clinical sensitivities of dietary interventions in this patient population, this study builds on prior preliminary evidence to provide proof of concept. The findings indicate that, when delivered with specialized medical supervision and trained support, ketogenic therapy holds potential for those who have failed to respond to traditional treatments.

“This study highlights the promise of dietary interventions that target normalizing underlying neurometabolic function for even the most intractable psychiatric conditions like anorexia nervosa,” said Jan Ellison Baszucki, co-founder and president of Baszucki Group, who funded the study. “We hope this work drives awareness and support for researching and delivering ketogenic therapy for eating disorders, providing new hope for patients and their families.”

A current extension of this study, for patients with both anorexia nervosa and bulimia nervosa diagnoses, is underway and recruiting participants nationally. Those interested in learning more or joining the study can find more information at the study site.

Source: Bazsucki Group

Most Cases of HIV Persistence in Blood After Treatment Explained by Defective Copies

Study strongly suggests that most persistent cases of viral detection, despite ideal HIV drug therapy, are not due to virus transmission or a rebound of active disease

Colourised transmission electron micrograph of an HIV-1 virus particle (yellow/gold) budding from the plasma membrane of an infected H9 T cell (purple/green).

Antiretroviral drugs for HIV infection have enabled most people living with the virus to live long and healthy lives. However, a small portion of people experience detectable – and worrisome – traces of the virus that causes AIDS despite strict adherence to long-term treatment regimens and the absence of symptoms. New findings published in Nature Communications suggest that most cases of this phenomenon, which is called non-suppressible viraemia, are explained by defective and noninfectious copies of the virus. The research was partially supported by grants from the National Institutes of Health (NIH).

The study, which involved more than 50 people, found that while traces of HIV-1 RNA can persist in blood after optimal therapy, cases of non-suppressible viraemia are driven by HIV-1 RNA with defects in a piece of the RNA known as 5’-leader.

“From a clinical perspective, this is important because people with HIV are taught that the absolute goal of their medication is to achieve undetectable viral load and they worry,” says Francesco R. Simonetti, MBChBD, PhD, the senior study author and an assistant professor of medicine in the Division of Infectious Diseases at Johns Hopkins University School of Medicine. The new findings, says Simonetti and his team, should provide relief to many people living with HIV who fear a viral rebound or who are concerned about transmitting the virus to partners despite taking effective treatment.

For the study, the investigators examined blood samples from 52 people living with HIV who had detectable loads of the virus despite taking long-term antiretroviral drug therapy.

These samples, which were assessed from 32 people and compared to an additional 20 samples, were collected between 2021 and 2025. The majority of participants were white men, between ages 58 and 68, and received care in the U.S., Canada and Denmark. The researchers found that most detectable forms of the virus, around 95%, were due to defective copies, and most defects were due to mutations or deletions in the 5’-leader region of HIV-1 RNA. This region is known to orchestrate the production of copies of the virus, but in this case the defects prevented the generation of infectious virus.

Modern antiretroviral therapies, which date back to 1996, prevent HIV from infecting new populations of immune system cells, but aren’t able to retroactively prevent previously infected cells from releasing HIV viral particles. Since those cells usually represent a small portion of infected cells after a person is on stable therapy, most people who take antiretroviral therapies are able to bring their viral loads to clinically undetectable levels in their blood. 

However, in some cases, which are estimated to occur less than 1% of the time, people may experience clinically detectable levels after taking long-term antiretroviral drug therapy. This could happen years later, or, in less frequent cases, they may have never achieved undetectable levels.

This new study offers evidence that clinicians can now study the virus in blood plasma and confirm if clinically detectable levels are due to defective copies released from one or a few T-cell clones, says Simonetti. If so, he adds, this could eliminate the need for extra medications and could prevent related complications. It could also help people living with HIV have access to surgeries or other procedures, such as hip or knee replacements or organ transplants, and participate in clinical studies if they know they have HIV under control.

The assay taht the researchers created and used to confirm the defective copies of the virus for this study is cost-effective and can be broadly used in HIV clinics and research settings. Similar to using a liquid biopsy to detect cancer mutations in DNA, the assay, which is called CLAWS (Capturing 5′ Leader Anomalies Without Sequencing), uses advanced technology to identify detectable viral loads that are due to defective copies.

“We know that these defective proviruses cannot infect new cells, but they are still clinically relevant,” says Simonetti. “Think of how many extra visits, extra drugs, extra costs and tests they’ve been causing.”

“It’s also clear from the new study that, over time on treatment, intact proviruses that make virus are pruned away, while defective ones escape the immune system,” he says. “Now we want to understand these differences in immune recognition to uncover HIV’s vulnerabilities.”

Source: John Hopkins Medicine

56% of New SA Stem Cell Donors Are Under 25 and Saving Lives

Photo by Elizeu Dias on Unsplash

More than half of all new stem cell donors registered in South Africa in 2025 were between the ages of 17 and 25. And, according to a growing body of medical research, they are also the most valuable donors on the planet.

Research analysing more than 10 000 stem cell transplants has found that for every ten-year increase in donor age, patient survival rates two years after transplant decline by approximately 6 to 7%. Donors aged 17 to 25 consistently provide patients with the best chance of survival. A separate long-term study found that transplants from younger donors successfully engrafted up to 30 000 stem cells that continued contributing to blood production for decades, compared to a tenfold decrease in transplants from older donors. It has also been confirmed that donor age has a greater influence on transplant success than previously assumed, with younger donors associated with improved overall survival and reduced relapse risk.

The evidence is bearing out in South Africa’s own numbers. DKMS Africa’s donor base has grown from 18 801 in 2021 to more than 173 000 by the end of 2025, a ninefold increase in four years. New sign-ups in 2025 alone reached more than 60 000, nearly double the 2023 figure. The 17 to 25 age group has led that charge, growing from 19% of new donors in 2021 to 56% in 2025. Forty percent of last year’s new donors were between 17 and 21.

Context matters: every hour, someone in South Africa is diagnosed with blood cancer. For many patients, a stem cell transplant from a matched, unrelated donor is the only viable path to survival. The match they need may already be on the registry. Or it may not exist yet.

“In South Africa, finding a compatible donor depends on human leukocyte antigen (HLA) characteristics that are inherited and vary significantly across ethnic groups. Patients have the highest probability of finding a match within a registry that reflects their own background. Currently, patients from black, coloured and Indian communities face considerably lower odds than those from communities better represented in local and international registries. A registry that grows without also diversifying fails the patients who need it most. That is why more young people of diverse backgrounds need to step forward and close this gap,” says Palesa Mokomele, Head of Community Engagement and Communications at DKMS Africa.

She adds, “This Youth Month, we need every young person who has not yet registered to know that their moment is now, and every adult who has not yet registered to ask themselves honestly: what is my excuse?”

The registration process takes minutes: a free swab kit arrives by post, is completed at home, and returned. No blood is drawn. No appointment is made. A registered donor is only contacted if they prove to be a genetic match for a patient in need, and even then, the decision to proceed remains entirely theirs. Registering is the first step. Following through, if called upon, is the one that saves a life.

To register, visit www.dkms-africa.org.

Certain Combinations of Antihypertensives Are More Tolerable, Study Finds

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Getting patients to adhere to antihypertensive drugs is a major obstacle in controlling hypertension and cardiovascular risk. To find out which drugs or combinations of drugs have the best adherence rates, researchers conducted a comprehensive network meta-analysis of the five primary classes of blood pressure-lowering medications. The research, published in JAMA Network, examined short-term tolerability and side-effect profiles in data from over 700 clinical trials, and identifies significant variations in treatment discontinuation rates across different drug categories and combinations.

The most well-tolerated options were angiotensin II receptor blockers (ARBs), both alone and paired with calcium channel blockers – often showing fewer withdrawals than placebos. While most therapies successfully reduced headaches, they simultaneously increased instances of dizziness and hypotension-related symptoms. These findings suggest that specific combination therapies may offer better patient outcomes and superior symptomatic improvement compared to traditional single-drug treatments. Ultimately, the study provides a robust framework for clinicians to better manage patient-reported adverse events during the initial months of hypertension care.

New Research Finds Peppermint Oil Can Reduce Blood Pressure

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Daily doses of peppermint oil have been proved to lower blood pressures for patients with mildly high readings, new research has found.

A team of University of Lancashire academics discovered a daily intake of 100 microlitres of peppermint oil, taken twice a day over 20 days, lowered the systolic blood pressure by an average of 8.5mmHg.

The findings have been published in PLOS One Journal and prove there could be a simple, inexpensive, and well‑tolerated way to help treat people with slightly raised blood pressure.

Lead author Dr Jonnie Sinclair, Reader in Sport and Health Sciences, said: “High blood pressure is one of the biggest causes of heart disease and death worldwide, and it costs a huge amount of money to treat. Although medicines are commonly used to treat it, it’s not always clear how well they work in the long-term, and they can cause unwanted side effects.”

Peppermint oil is low in calories and price so it’s proved to be a very simple and cost-effective solution to potentially treat millions of people around the world.

– Lead author Dr Jonnie Sinclair, Reader in Sport and Health Sciences

Peppermint contains substances like menthol and flavonoids and in the study, 40 18 to 65-years-olds were randomly split into two groups. One group in the pre‑hypertension and stage 1 hypertension phases took a small daily dose of oil and saw the improvement while the other took a peppermint‑flavoured placebo that did not contain the active oil and saw no real change.

Researchers measured the change in systolic blood pressure, but they also looked at body measurements, blood results, diastolic blood pressure (the bottom number in a blood pressure reading), heart rate, mental wellbeing and sleep quality.

Dr Sinclair added: “Our findings were very positive and they have significant clinical implications, especially given arterial hypertension is the most common preventable risk factor for cardiometabolic disease and the greatest single risk factor for global mortality.

“Peppermint oil is low in calories and price so it’s proved to be a very simple and cost-effective solution to potentially treat millions of people around the world.”

A copy of the research paper, Effects of peppermint (Mentha x piperita L.) oil on cardiometabolic outcomes in patients with pre- and stage 1 hypertension: A placebo randomized controlled trial, is available on the PLOS One Journal website.

Source: University of Lancashire

TB is Curable. South Africans Can’t Wait Around for Someone Else’s Rescue.

Tuberculosis (TB) is not a medical mystery, writes AI Diagnostics CEO, Braden van Breda. It’s a detection failure. And with technology like AI at our disposal, he believes the MedTech industry has the power to step up and fix it.

Tuberculosis bacteria. Credit: CDC

TB remains the deadliest infectious disease in the world, but it’s not killing people indiscriminately, it’s killing people in poor, developing countries.

Data from the World Health Organization makes this very clear. In 2024, most TB cases were concentrated in developing regions, especially South-East Asia, the Western Pacific, and Africa. In South Africa, an estimated 54 000 people died of TB in 2024. That’s a soccer stadium full of people wiped out by TB in a single year. Meanwhile, the Americas accounted for just 3.3% of global cases and Europe 1.9%.

The danger is that we get complacent about these numbers because we’re so used to hearing them. It’s not normal that people’s loved ones are dying from TB by the tens of thousands in some parts of the world, while in others, the incidence is low enough to be almost negligible.

Detection is the crisis

We already know what causes TB. We know how it spreads, how to diagnose it, and how to treat it. South Africa is losing this fight because the tools we currently have don’t catch cases early enough.

Since TB is easiest to treat (and least likely to spread) when it’s found early, the result compounds. Too many people are only diagnosed once they become seriously ill. By then, they’ve already infected others, and the cost and effort of accessing care often becomes a barrier in itself.

The science is there; the failure now lies in access to quality screening. The question we need to ask ourselves is whether we’re serious about bringing healthcare to people instead of forcing people to chase healthcare.

Start designing TB screening around the communities that need it most

Too much of our TB diagnostic infrastructure remains concentrated in too few facilities, and that depends on expensive equipment, medical specialists, and referral pathways.

For many people, especially in rural areas and poorer communities, getting to a hospital means losing a day’s wages, while having to pay for transport they can’t afford. The result is that people wait or don’t go at all. In 2024, only about 184 000 of the estimated 249 000 South Africans who fell ill with TB were diagnosed and started on treatment. That leaves around 65 000 people who were missed altogether.

This is why community-level screening matters so much. We can’t build specialist diagnostic centres next to every rural clinic. Even if we could, we don’t have enough specialists to run them. The answer is to put simpler, portable, and locally workable screening tools into the hands of frontline healthcare workers, especially nurses in primary care settings.

South Africa can’t wait around to be rescued

If the bottleneck is access, then innovation has to begin where access fails. That means building around the healthcare system we have, not the one we wish we had. How do we equip the nurse at the overcrowded community clinic? If we’re serious about combating TB, that’s the question we have to answer.

It’s also why South Africa can’t keep assuming that imported solutions from European or American healthcare systems will automatically fit our realities. We need tools designed for our burden of disease, clinic environments, and constraints. The countries carrying the heaviest burden should also be shaping the next generation of practical, scalable solutions.

The local MedTech sector needs to decide whether it’s serious about that responsibility. It’s one thing to produce impressive technology for conferences and investor decks, but can it be used in a crowded community clinic by a healthcare worker at the end of an 18-hour shift? If the answer is no, it’s not solving the real problem.

When a curable disease is killing tens of thousands of people, we can’t afford to sit around and wait to solve the problem. Thanks to advances in technology, the tools to close the screening gap are no longer beyond our reach. Failing to use them is inexcusable.

How an Anti-inflammatory Helps the Heart After a Heart Attack

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Every day, thousands of people worldwide suffer a heart attack, often leading to lasting damage to the heart muscle. New research from the University of Oslo suggests that targeting inflammation in the body helps protect the heart and improve recovery after a heart attack.

“In a small country like Norway alone, we see around 11 000 heart attacks every year,” says postdoctoral fellow Camilla Huse at the Research Institute for Internal Medicine, at University of Oslo and Oslo University Hospital. “Forty heart attacks every day is a lot.”

Fortunately, modern treatments are so effective that most patients survive a heart attack.

Inflammation damages the heart

However, a heart attack triggers a strong inflammatory reaction in the body. While this inflammation is part of the body’s natural response, it also causes damage to the heart muscle during a heart attack.

Such injury can lead to poorer health, a reduced quality of life and fewer working years for those affected. It also increases the risk of developing new heart diseases later in life.

So, how can we protect the heart during a heart attack?

Can anti-inflammatory medication improve heart attack treatment?

For some time, the researchers at the University of Oslo and Oslo University Hospital have been studying a medicine that blocks the effect of a substance that stimulates inflammation, a substance called IL-6. Previously, they have shown that administering this medicine in addition to established treatment for heart attacks has promising results: the patients suffered less damage to their hearts.

“This could be a new way of treating patients,” senior researcher Tuva Børresdatter Dahl says, and continues:

“To move forward with treatment, we need to understand what happens in the body when we block inflammation. Which processes inside the cells are affected by the medicine being tested? Which are not? And how does this relate to damage to the heart and to the improved recovery of the patient?”

How to investigate the effect of the treatment

The researchers conducted a study in which they examined the immune cells of 200 patients with STEMI. STEMI is a type of heart attack where the risk of serious complications is high.

The patients were randomly divided into two groups. Half of them received the anti-inflammatory medication, blocking the IL-6 signal, while the other half received a placebo, i.e. a treatment without any active ingredient.

The researchers then monitored how the treatment affected the immune cells in the blood. They also measured how much of the heart muscle was damaged.

Monocytes at the front line of our immune system

The researchers found that the treatment affects a type of immune cell called monocytes, which play an important role in all forms of inflammation.

“The monocytes are right at the front line of our immune system. They are among the first immune cells to arrive to the heart when a heart attack occurs,” Huse says.

Shortly after a heart attack, a strong inflammatory mobilisation occurs in the body, and monocytes flow to the heart muscle.

“The monocytes help to repair and clean up after a heart attack. But they can often get a little too eager. Thus, they also contribute to worsening the damage to the heart muscle after the heart attack,” she explains.

Reduced inflammation linked to better heart attack recovery

The study showed that the patients who received the anti-inflammatory medication had fewer monocytes in their blood shortly after the heart attack.

Normally, having high levels of these immune cells soon after a heart attack are linked to more heart damage and worse outcomes for the patients. Lower levels, on the other hand, are associated with less damage to the heart and better healing.

The researchers also found that the medicine made the cells in the heart muscle more resistant to damage, so that more heart cells survived the heart attack.

The study showed that patients who received the anti-inflammatory drug (dark blue) had fewer monocytes in their blood shortly after the heart attack. Illustration from the researchers.

Changing immune cell behaviour to protective

As a result of the treatment, the way the monocytes behave was also changed.

“The function of the monocytes changed, from being more harmful to becoming more protective. The “good” functions of the immune cells were strengthened,” Huse says.

“We believe that those functions are the reason why patients suffer less damage after the heart attack. The heart is helped towards recovery,” she adds.

The study also showed another important effect: mechanisms that normally draw inflammatory cells into the damaged area were prevented in the patients who received the medicine.

What could this mean for heart attack patients in the future?

The research provides new insight into how inflammation affects the heart during a heart attack, and how this treatment can protect the heart from damage following STEMI.

This creates an opportunity for anti-inflammatory drugs to become part of a standard treatment for heart attacks and give patients a better life afterwards.

“The study shows that monocytes play an important role in the development of heart attacks. We believe that affecting these cells, which the blocking of IL-6 does, is beneficial. It could be a new and important additional treatment for these patients,” Dahl points out.

Why mechanism-focused research matters

The researcher believes that more such in-depth studies are needed when new medicines are tested.

“They provide a better understanding of the mechanisms behind illness and how the medicine affects the body. It doesn’t just tell us whether a treatment has worked, but also why or why not.

“Such knowledge can make new treatment options possible. This type of research should therefore be prioritised in future clinical studies,” Dahl says.

Reference

Huse C, Murphy SL, Yang K, Balzer NR, Stokke MK, Anstensrud AK, et al. The effects of interleukin-6-receptor inhibition on monocytes in STEMI: a substudy of the ASSAIL-MI trial. EBioMedicine. 2025. doi:10.1016/j.ebiom. 2025.105960 

By Julie Nybakk Kvaal, Institute of Clinical Medicine

Source: University of Oslo

Common Class of Antihypertensives Linked to Worse Diabetic Kidney Outcomes

Dihydropyridine calcium-channel blockers linked to poorer kidney outcomes in people with type 2 diabetes

Photo by Towfiqu Barbhuiya on Unsplash

Commonly prescribed blood pressure medications known as dihydropyridine calcium-channel blockers (DCCBs) may be associated with poorer kidney outcomes in people with Type 2 diabetes (T2D) and diabetic kidney disease (DKD), according to new research presented at the 63rd European Renal Association (ERA) Congress in Glasgow, Scotland.1

Kidney Outcomes Worse with DCCBs in T2D

The findings suggest that patients receiving DCCBs alongside current standard-of-care kidney-protective therapies face a significantly higher risk of major adverse kidney events compared with those treated with alternative antihypertensive medications.

DKD remains one of the leading causes of kidney failure worldwide and is driven by chronic damage to the kidney’s filtering system caused by prolonged hyperglycaemia.2 Effective blood pressure control is a cornerstone of management, particularly alongside renin-angiotensin system (RAS) inhibitors and sodium-glucose cotransporter-2 (SGLT2) inhibitors, which have transformed outcomes for patients by slowing kidney disease progression and reducing the risk of kidney failure.

Researchers analysed data from 31 031 adults with T2D treated between 2016 and 2021. All participants were receiving both RAS and SGLT2 inhibitors. Of these, 12 172 patients were also prescribed DCCBs, while 18 859 received alternative blood pressure therapies. Participants were followed for a median of approximately 3.5 years.

After adjusting for baseline demographic and clinical differences, DCCB use was associated with a 33% increased risk of major adverse kidney events compared with other antihypertensive treatments. The composite outcome included a decline of at least 40% in estimated glomerular filtration rate (eGFR) or progression to end-stage kidney disease requiring dialysis or kidney transplantation.

Lead author Dr Timna Agur noted that DCCBs are widely used as second-line blood pressure therapies in DKD, making the findings particularly relevant to current clinical practice. The researchers propose that the observed association may stem from the drugs’ effects on kidney haemodynamics. By preferentially dilating blood vessels entering the kidney’s filtering units, DCCBs may increase pressure within these structures, potentially contributing to ongoing damage despite concurrent kidney-protective therapies.

Blood Pressure Treatment Choice May Matter

Although the study was observational and cannot establish causality, the investigators emphasised that the results warrant further investigation. Prospective studies and randomised controlled trials will be needed to determine whether alternative blood pressure treatment strategies could offer greater kidney protection for patients with DKD.

References

Li J et al. Epidemiological status, development trends, and risk factors of disability-adjusted life years due to diabetic kidney disease: a systematic analysis of Global Burden of Disease Study 2021. Chin Med J. 2025;138(5):568-578.

Agur T et al. DCCB therapy and risk of CKD progression in type 2 diabetes on RASi and SGLT2i. Abstract 597. ERA Congress, 3-6 June 2026.

Source: EMJ Reviews

Africa CDC and WHO Launch Joint Continental Ebola Response Plan

The plan complements national response plans launched by the Governments of the Democratic Republic of the Congo and Uganda

The Africa Centres for Disease Control and Prevention (Africa CDC) (www.AfricaCDC.org) and the World Health Organization (WHO) today launched a joint continental preparedness and response plan on the ongoing Ebola outbreak caused by the Bundibugyo virus. The plan aims to raise US$ 518 million to support African countries together with partners to prepare for, rapidly detect and respond to the outbreak.

The six-month plan, covering June to November 2026, brings together governments, partners and communities under a unified ‘One Response’ approach to strengthen outbreak response measures, including emergency coordination, disease surveillance, laboratory testing, infection prevention and control, clinical care, community engagement, research, logistics and support for essential health services.

The plan complements national response plans launched by the Governments of the Democratic Republic of the Congo and Uganda.

“Ebola moves fast. Africa must move faster. This joint plan gives the continent a clear path to act with speed and unity: to save lives, support the affected countries and protect neighbouring communities, said Africa CDC Director-General Dr Jean Kaseya. “With Member States, WHO and partners, Africa CDC is turning commitment into action and resources into response for the communities at risk.”

WHO Director-General Dr Tedros Adhanom Ghebreyesus said: “The only way to beat this outbreak is through close partnership, working together under the leadership of the affected countries in one coordinated effort, guided by a simple principle: one plan, one budget, one team.”

He added: “Containing Ebola depends on political commitment, sustained financing, and the trust and engagement of communities. This plan places communities at the centre, because without their participation, contact tracing falters, safe care is delayed, and transmission continues.”

The plan also focuses on protecting vulnerable populations, strengthening cross-border collaboration, and supporting countries to respond quickly to new cases. At a time when there are no licensed vaccines or therapeutics specifically approved for the Bundibugyo species of Ebola, the plan aims to strengthen health systems to ensure resilience even as countries respond to acute health emergencies.

Implementation of preparedness and response activities is already underway across affected and at-risk countries. Furthermore, in 10 priority countries critical measures are being strengthened to enhance public health emergency preparedness and ensure early detection and swift response

.The plan emphasizes the need to maintain support for other ongoing health emergencies, including mpox, cholera and measles, to prevent disruptions to critical response efforts and safeguard progress towards stronger, more resilient health systems.

This coordinated effort comes as response operations accelerate in the Democratic Republic of the Congo, where authorities, with support from Africa CDC, WHO and partners, are ramping up efforts to curb the spread of the virus and end the outbreak.

Africa CDC and WHO urge Member States to strengthen screening and public health measures at points of entry and enhance cross-border coordination and solidarity to support a timely, effective and evidence-based response to the outbreak.

Through the joint preparedness and response plan, the continent is mobilising its collective expertise and resources to reinforce response measures, acting as one to control the outbreak and protect communities across the region. Its successful implementation will require strong political commitment, sustained investment and close collaboration among governments, health workers, communities and partners.

Drawing on lessons learned from previous Ebola outbreaks and recent public health emergencies, the plan also provides a pathway to broadly strengthen Africa’s capacity to prevent, detect and respond to future health threats while protecting lives and livelihoods.

DOWNLOAD | JOINT CONTINENTAL EBOLA RESPONSE PLAN: https://apo-opa.co/49KMxG2