Category: 8. Health

Led by the World Health Organization (WHO) and the UN’s Special Programme in Human Reproduction (HRP), the day underscores the importance of sexual health across all stages of life. Sexual health goes beyond physical safety; it embraces dignity, consent, pleasure, and freedom from coercion and discrimination.

This year’s theme, “Sexual Justice – What Can We Do?”, calls on us to recognize sexual health as a cornerstone of well-being. It emphasizes the need for equitable, rights-based solutions that ensure justice and access for everyone, everywhere.

Sexual justice means that all people have the power and resources to make free, informed, and healthy decisions about their bodies, sexuality, and reproduction. It ensures equal access to education, healthcare, and services, while promoting a world free from discrimination, violence, and exclusion, where everyone can experience sexual health, rights, and pleasure.

For seafarers, the maritime profession presents unique challenges in maintaining sexual health, due to prolonged time away from family and limited shore leave. Recognizing the importance of sexual well-being at sea is essential for fostering healthy mental, emotional, and physical states among crews.

The growing conversation around sexual health

Over the past decade, there has been an expanded cultural conversation around sexuality, improvements in sexual education, and growing awareness of the sexual-health challenges which has led to a surge in demand for sexual-health products.

According to McKinsey, research shows that 87% of U.S. consumers reported spending the same or more on sexual-health products in the past year, reflecting the recognition of sexual health as a vital aspect of personal well-being. Affirmative sexual health encourages positive, safe, and consensual sexual experiences, contributing to emotional and social well-being.

Research insights

In March 2025, HRP researchers conducted a systematic review of HIV public communication campaigns using a pleasure-based approach. The study, analyzing 29 campaigns across multiple regions, found that integrating pleasure – through enjoyment, empowerment, and emotional connection – reduces stigma, improves knowledge, and encourages safer behaviors like condom use and HIV testing.

Similarly, in December 2024, WHO published a special issue in the Bulletin of the World Health Organization on advancing sexual health and rights. It covered topics ranging from sexual empowerment and harmful gender norms to menstrual hygiene, endometriosis, and HIV prevention. The publication highlighted the need for inclusive, people-centered interventions to achieve global health equity.

WHO also released global research priorities for sexually transmitted infections (STIs), identifying 40 key research areas to improve prevention, diagnosis, management, and epidemiology.

HRP and WHO are advancing sexual health measurement using tools like the Sexual Health Assessment of Practices and Experiences (SHAPE) questionnaire, enabling countries to generate comparable data for better monitoring and intervention.

Key considerations about sexual health

Maintaining sexual health at sea, or anywhere, requires attention to the following:

#1 Secured consent

Consent is essential for any sexual activity. Both partners must explicitly agree to the activity, with the ability to withdraw at any time. Key considerations include:

• Consent is required for every sexual act; past consent does not guarantee future consent.
• Consent applies to long-term partners and casual encounters alike.
• Silence does not imply agreement.
• Alcohol or drug use can compromise a person’s ability to consent. 

2. Preventing Sexually Transmitted Infections

STIs, including HIV, chlamydia, gonorrhea, syphilis, and hepatitis B, are transmitted primarily through unprotected sexual contact. Effective treatment is currently available for several STIs. If left untreated, they can cause infertility, cancer, or even death. Symptoms may be absent, so regular testing is critical.

Sexual health challenges in maritime work

Seafaring is a profession marked by long separations, isolation, and restricted access to shore facilities. Prolonged sexual abstinence, when involuntary, can impact on psychological health, job satisfaction, and overall well-being.

Research indicates that lack of sexual activity in isolated settings can lead to:

• Emotional distress, depression, and irritability
• Increased risk-taking behaviors during port visits
• Heightened sexual frustration and potential aggression 

Mental health support onboard often focuses on fatigue and stress, while the emotional impact of sexual frustration remains largely unaddressed. Tackling these challenges requires open dialogue, access to counselling, and the normalization of conversations about sexual well-being among seafarers.

In this context, OneCare Group announced in June its commitment to reducing stigma and promoting sexual health awareness by providing tailored training for its seafarers. The programmes, delivered both online and in person, cover key areas such as STIs, safe sex practices, and common misconceptions about sexual health.

Sexual harassment onboard

Women working at sea face additional risks, including sexual harassment and assault. Studies by the Seafarers International Research Centre (SIRC) and Seafarers’ Charity found that female seafarers experience higher isolation and fear of reporting incidents.

Similarly, surveys by the Norwegian Seafarers’ Union (NSU) indicate that 31% of members reported experiencing sexual harassment, with women, younger crew, and new recruits disproportionately affected. It is also important to note that male seafarers can be victims as well.

Therefore, zero-tolerance approach to harassment, combined with awareness campaigns and clear reporting protocols, is essential for a safe and equitable maritime workplace.

Promoting sexual health awareness at sea

Several organizations, including OneCare Group and Marine Medical Solutions (MMS), are actively addressing sexual health in the maritime sector. Their initiatives include:

• Online and in-person sexual health training for crew members
• Education on STIs, safe sex practices, and contraception
• Support for gender- and sexuality-specific needs, including LGBTQ+ seafarers
• Encouraging peer-to-peer dialogue to reduce stigma and foster emotional support

Experts stress that open communication, access to medical care, and psychological support are key to mitigating the mental and physical impacts of prolonged sexual abstinence and sexual frustration among seafarers.

Sexual health is an essential part of overall well-being. As WHO reminds us, health is more than the absence of disease – it is a state of complete physical, mental, and social well-being.  

Sudan’s Darfur region is grappling with a deadly cholera outbreak amid a complex humanitarian crisis marked by heavy rains, mass displacement, fragile water, sanitation and hygiene (WASH) infrastructure, along with limited access to healthcare.

New figures from the Africa Centres for Disease Control and Prevention (Africa CDC) show that all five Darfur states have reported high cases, with North Darfur accounting for 57% of all cases. Yet South Darfur bears the heaviest death burden – 66 out of 136 deaths recorded in the region so far in 2025.

In all, cholera has been reported across all 18 states in Sudan, with children over the age of 10 accounting for 15% of infections. Khartoum State alone has recorded 24,252 cases and 427 deaths in 2025.

Darfur is particularly vulnerable due to restricted access, ongoing conflict and the possibility of significant under-reporting. Displacement has increased the risk of cross-border transmission, with Chad already reporting cases in refugee settlements near the border with Sudan.

 The crisis in Sudan is part of a broader regional emergency, with cholera surging across the continent and exposing deep weaknesses in public health systems. The country is one of 23 African nations currently facing cholera outbreaks, and among the worst affected alongside South Sudan, the Democratic Republic of Congo, and Angola.

In response, African leaders have launched the Continental Cholera Preparedness and Response Plan 1.0, spearheaded by Africa CDC and the World Health Organization (WHO), and championed by Zambian President H.E. Hakainde Hichilema. The six-month plan requires over $231 million in funding, with additional resources needed for long-term vaccine production and health system strengthening.

Yet the plan goes beyond coordination and resource mobilisation, showing how strong political leadership can bring multiple sectors together to address urgent public health challenges. It builds on the successful mpox response model, leveraging the Incident Management Support Team (IMST) to coordinate efforts across countries.

“The elimination of cholera is not only a health goal — it is a moral imperative, a catalyst for economic growth, and a decisive step toward achieving Agenda 2063: The Africa We Want,” said President Hichilema.

The IMST’s “4-One” principle — one team, one plan, one budget, one monitoring framework — ensures strategic coherence and operational efficiency. Cholera specialists will guide technical implementation, while a Continental Task Force will oversee progress toward the 2030 goal of eliminating cholera in over 20 countries, reducing deaths by 90%, and keeping fatality rates below 1%.

Without urgent action, Africa could see over 200,000 cholera cases and 6,000 deaths between September 2025 and February 2026. However, rapid interventions —including the deployment of 10 million vaccine doses, the establishment of treatment centres, and robust community engagement — could dramatically reduce the toll.

“Cholera is not just a health emergency — it is a reflection of deeper systemic inequalities,” said Africa CDC Director General Dr Jean Kaseya. “Our response must be swift, coordinated and rooted in solidarity. We cannot afford to let vulnerable communities bear the brunt of preventable disease.”

Back in Sudan, inadequate WASH infrastructure is a significant contributor to the outbreak. Ninety per cent of Khartoum’s water treatment plants are currently out of service. This has severely limited access to clean water and increased the risk of disease transmission. Compounding the situation, Sudan is also battling concurrent outbreaks of dengue fever, diphtheria, measles, and pertussis.

Flooding on 17 August displaced nearly 900 people in North Darfur, compounding the already dire conditions. Ongoing conflict has made parts of the region inaccessible, with shortages of medical supplies, clean water, and isolation centres complicating containment efforts.

Access to vaccines remains uneven across Sudan, with some regions facing severe challenges. In Darfur, oral cholera vaccine coverage is virtually non-existent, compared to a national average of just 5.4%. This gap is mainly due to ongoing civil conflict, which has made large parts of the region inaccessible to vaccination teams. As a result, displaced populations — many living in overcrowded camps — are especially vulnerable to cholera outbreaks.

Thus, the true extent of the outbreak may be obscured by the ongoing humanitarian crisis. Under-reporting, limited healthcare access, and delays in data collection continue to hinder a full understanding of the situation.

While the decline in new cases in the affected African countries offers a glimmer of hope, the overall situation underscores the extreme vulnerability of communities in conflict-affected regions like Darfur. The cholera outbreak is a stark reminder of the broader challenges African countries face in managing preventable diseases under strained conditions.

Health authorities stress the urgent need for increased support to improve water and sanitation facilities, expand access to treatment, and implement vaccination campaigns in affected areas.

The Continental Cholera Preparedness and Response Plan offers a practical and coordinated framework to support national efforts. But its success will depend on timely implementation, sustained funding and the ability to adapt to complex, on-the-ground realities.

Sudan’s ongoing crisis highlights the urgency of these efforts.

“This cholera crisis is not just a public health emergency but is also a powerful reminder and a call to our leaders that there is no health without peace,” said Dr Jean Kaseya, Director General of Africa CDC.

Northwestern University chemists have developed a new nanostructure that improves the efficiency of CRISPR gene editing by up to three times while reducing toxicity. Due to be published on 05 September in the Proceedings of the National Academy of Sciences, the study details how these lipid nanoparticle spherical nucleic acids (LNP-SNAs) deliver CRISPR machinery into cells more effectively than current methods and increase the success rate of precise DNA repair.

The LNP-SNAs are tiny DNA-coated spheres that protect the CRISPR components and guide them to specific tissues. Each particle carries Cas9 enzymes, guide RNA and a DNA repair template, all protected within a dense DNA shell. That shell not only shields the contents but also determines which organs and tissues the particles reach while aiding their entry into cells.

In tests across multiple human and animal cell types, the system outperformed existing delivery methods by a wide margin. LNP-SNAs entered cells up to three times more effectively than the lipid particles used in COVID-19 vaccines, produced significantly less toxicity and boosted editing efficiency threefold. The particles also increased the success rate of precise DNA repair by more than 60 percent.

Chad A. Mirkin, who led the study at Northwestern, said the team focused on overcoming the main barrier to CRISPR’s use in medicine: delivering the editing components into the right cells and tissues.

“CRISPR is an incredibly powerful tool that could correct defects in genes to decrease susceptibility to disease and even eliminate disease itself,” he said. “But it’s difficult to get CRISPR into the cells and tissues that matter. Reaching and entering the right cells – and the right places within those cells – requires a minor miracle. By using SNAs to deliver the machinery required for gene editing, we aimed to maximise CRISPR’s efficiency and expand the number of cell and tissue types that we can deliver it to.”

The delivery dilemma

CRISPR is a gene-editing system that can cut, disable or repair genes once it is inside a cell’s nucleus. The main challenge is delivery, as the CRISPR components cannot cross cell membranes on their own and require a vehicle.

Researchers have typically turned to viral vectors, which are naturally skilled at infiltrating cells but come with the risk of triggering strong immune responses. Lipid nanoparticles (LNPs), the type used in mRNA vaccines, are considered safer than viral vectors but less effective because they often become trapped inside endosomes within cells, preventing release of their contents.

As Mirkin explained: “Only a fraction of the CRISPR machinery actually makes it into the cell and even a smaller fraction makes it all the way into the nucleus. Another strategy is to remove cells from the body, inject the CRISPR components and then put the cells back in. As you can imagine, that’s extremely inefficient and impractical.”

Enter the spherical nucleic acid

Mirkin’s group took inspiration from spherical nucleic acids (SNAs), a nanostructure he originally invented at Northwestern. Unlike linear DNA and RNA, SNAs form globular shells around a nanoparticle core, typically around 50 nanometres in diameter. These shells interact easily with cell-surface receptors, making them highly effective at penetrating cells. Seven SNA-based therapies are already in clinical trials, including a Phase II trial for Merkel cell carcinoma.

In this study, the team engineered hybrid structures with an LNP core carrying the CRISPR components, surrounded by a dense DNA shell. The DNA strands improved uptake and could be customised to target specific tissues.

“Simple changes to the particle’s structure can dramatically change how well a cell takes it up,” said Mirkin. “The SNA architecture is recognised by almost all cell types, so cells actively take up the SNAs and rapidly internalise them.”

Results across the board

When tested on cultures of skin cells, white blood cells, human bone marrow stem cells and kidney cells, the LNP-SNAs consistently excelled. They entered cells more effectively, caused less toxicity and achieved higher rates of successful gene edits than existing methods. Crucially, the system showed it could support complex DNA repairs – a major hurdle in moving CRISPR-based therapies beyond proof of concept.

The next stage is to test the approach in living disease models, with plans to expand into clinical applications. Flashpoint Therapeutics, a Northwestern spin-out, is already commercialising the platform.

The study shows that the structure of a nanomaterial can be as important as its composition, a concept that forms the basis of structural nanomedicine, a field in which Mirkin has played a leading role.

“CRISPR could change the whole field of medicine,” said Mirkin. “But how we design the delivery vehicle is just as important as the genetic tools themselves. By marrying two powerful biotechnologies – CRISPR and SNAs – we have created a strategy that could unlock CRISPR’s full therapeutic potential.”

Antimicrobial resistance (AMR) is one of the gravest public health threats of our time—yet it remains largely invisible. In 2019, drug-resistant infections were linked to 4.95 million deaths globally, with 1.27 million of these directly caused by resistant pathogens, making AMR a leading global killer (The Lancet, 2022). This “silent pandemic” is not only a medical emergency; it is rapidly becoming an economic crisis.

Pakistan stands at the epicentre of this growing catastrophe. According to new national estimates, AMR was directly responsible for 59,200 deaths in the country in 2019 and contributed to an additional 221,300 fatalities—making it the third leading cause of death in Pakistan. By 2022, the number of drug-resistant infections rose to 1.15 million, with 64,690 deaths directly caused by AMR and over 306,000 deaths associated with it. These figures reveal a rapidly escalating burden that extends far beyond hospitals and clinics.

The Fleming Fund Country Grant Pakistan (FFCGP) emerged as a key player in the fight against AMR, investing in laboratory capacity, expanding surveillance systems across human and animal health sectors, and enabling critical research. Among its most consequential contributions is the first-ever national economic burden analysis of AMR in Pakistan—a groundbreaking study that has provided evidence to shape both policy and resource allocation. The findings are alarming: In 2022 alone, AMR cost Pakistan an estimated US$3.5 billion, or nearly 1% of the national GDP. These costs accrue from longer hospital stays, the need for expensive second- and third-line treatments, repeat diagnostic testing, and vast productivity losses due to premature deaths and disability. The economic burden is projected to rise to US$4.32 billion in 2023 and US$5.04 billion by 2025, amounting to 1.35% of GDP—a great loss Pakistan can hardly afford.

The World Health Organization has set bold targets: a 10% reduction in AMR-related deaths, 80% access to essential antimicrobials, and a ban on the use of last-resort antibiotics in agriculture

Behind these numbers are real human consequences. Drug-resistant infections disproportionately impact the poor, pushing families deeper into poverty. Treating a severe resistant infection can cost up to PKR 700,000 (US$3,100) per patient—an unaffordable sum for most households in a country where 38.3% of the population (93 million people) lives in multidimensional poverty. With limited financial protection and high out-of-pocket health spending, AMR doesn’t just threaten lives, it destroys livelihoods. Deepening this crisis is the unchecked misuse of antibiotics: over-the-counter sales of antimicrobials without prescription, poor diagnostic practices, limited awareness, and weak regulatory enforcement. Alarmingly, up to 70% of common infections in Pakistan no longer respond to first-line antibiotics, leading doctors to rely on more toxic and expensive last-resort medications. This fuels a dangerous cycle of resistance, illness, and financial strain.

Despite the clear and growing threat, Pakistan’s policy response remains vastly under-resourced. The proposed allocation for implementing the National Action Plan on AMR in 2025 is just PKR 923 million (US$3.29 million)—a figure that is less than one-thousandth of the anticipated annual economic loss due to AMR. This gap reflects a serious underestimation of the crisis and a lack of political urgency.

Globally, the World Health Organization has set bold targets: a 10% reduction in AMR-related deaths, 80% access to essential antimicrobials, and a ban on the use of last-resort antibiotics in agriculture. Pakistan must align with these global goals and commit to substantial investment, stronger governance, and robust public awareness.

AMR is dismantling health systems, undermining decades of medical progress, and draining national economies. For Pakistan, this is no longer a future threat—it is a present and growing emergency. Without swift, coordinated action and bold leadership, AMR may prove to be the defining health and development challenge of our generation. Further, shrinking donor support is leading to the closure of donor-supported programmes like the Fleming Fund Country Grant Pakistan, which calls for urgent action at national and international levels.

‘Instead of one pill, I prescribed ‘6 pills’

He said, “A 35-year-old consulted me today, as he wanted me to prescribe an aspirin pill to prevent a stroke. His father, aged 60, had recently suffered from stroke (paralysis), and he was concerned about his higher risk of getting a stroke in future. Instead of one pill (aspirin), I prescribed ‘6 pills’ (mentioned in the recommendations section of my prescription).”

So what did Dr Kumar actually prescribe to the man, who at the time, ‘weighed 80 kg, had a BMI (body mass index) of 26.2 with mildly elevated total and LDL cholesterol, normal homocysteine and cardiac evaluation’?

7-8 hours of sleep to 9-10K steps a day

As per the prescription he shared on X, Dr Kumar advised the man to follow these habits and come back for a ‘review after three months’:

1. Regular sleep: 7-8 hours a night.

2. Brisk walking or running: 30-40 minutes a day. Aim for 9-10K steps per day.

3. Healthy diet: Avoid soft drinks, sugar, and ultra-processed packaged foods. Reduce carb intake and increase fruits (within limits), vegetables, and nuts (a handful/day), poultry, fish, and eggs.

4. Reduce working hours: from current 13-14 hours to 8-9 hours.

5. Reduce stress.

6. Complete abstinence from alcohol.

Can aspirin prevent a stroke?

Aspirin is in a group of medications called salicylates. It works by stopping the production of certain natural substances that cause fever, pain, swelling, and blood clots. Sharing details of daily aspirin therapy, Mayo Clinic said that taking an aspirin a day can be a lifesaving option and may lower the risk of heart attack and stroke, but it’s not for everyone.

Per Mayo Clinic, daily aspirin therapy may be used in two ways:

⦿ Primary prevention

This means that you’ve never had a heart attack or stroke. You’ve never had coronary bypass surgery or coronary angioplasty with stent placement. You’ve never had blocked arteries in your neck, legs or other parts of the body. But you take a daily aspirin to prevent such heart events. The benefit of aspirin for this use has been debated.

⦿ Secondary prevention

This means that you had a heart attack or stroke, or you have known heart or blood vessel disease. You’re taking a daily aspirin to prevent a heart attack or stroke. The benefit of daily aspirin therapy in this situation is well established.

Note to readers: This report is based on user-generated content from social media. HT.com has not independently verified the claims and does not endorse them.

This article is for informational purposes only and not a substitute for professional medical advice.

Introduction

Diffuse large B-cell lymphoma (DLBCL) is an aggressive B-cell lymphoma, the most common pathological type of NHL, accounting for approximately 30% to 40% of all NHL cases across different geographical regions.^1,2 The median age at initial diagnosis of DLBCL is over 60 years, and 30% of patients are over 75 years old. The incidence of DLBCL increases with age.^3,4 Epidemiological studies indicate that DLBCL has a complex and multifactorial etiology, including genetic characteristics, clinical features, and immune disorders, in addition to risk factors related to viruses, environment, high weight in youth, and occupational exposure.^5,6 Although the prognostic significance of the International Prognostic Index (IPI) has been validated in many subtypes of NHL since 1993, its prognostic value in DLBCL remains controversial.

ABO blood group antigens, which play an important role in the physiology and pathology of cells, are defined by carbohydrate moieties on the extracellular surface of red blood cell membrane.^7,8 Our previous research has elaborated on the relationship between ABO blood group and lymphoma, and summarized the current knowledge of the underlying pathogenic mechanisms of the association.⁹ It has been observed that ABO blood group is not only associated with the risk and prognosis of lymphoma, but may also be associated with the pathological classification of lymphoma patients.⁹ However, we did not specifically compare DLBCL with other lymphoma subtypes in our previous research. Given this background, we conducted a retrospective study specifically focusing on a representative pathological type, namely DLBCL, with the aim of investigating whether ABO blood group correlates with the risk of onset and prognosis of this disease. This study provides preliminary and exploratory evidence supporting ABO blood group as a potential biomarker for DLBCL. Its cost-effective and readily accessible nature warrants further validation in larger-scale studies, which may offer novel perspectives for future understanding of DLBCL-specific disease risk stratification and prognostic assessment.

Materials and Methods

We retrospectively analyzed 220 patients with newly diagnosed DLBCL at two medical institutions between January 2012 and December 2022. The research was conducted in full compliance with the guidelines set forth in the Declaration of Helsinki and obtained official authorization from the Institutional Review Board of the First Affiliated Hospital of Henan University of Science (No. 2024–1592 Fast). All patients with DLBCL participating in this study met the following inclusion criteria: (1) A diagnosis of DLBCL was confirmed by specialized pathologists according to the World Health Organization (WHO) classification. (2) No prior anti-cancer treatment had been administered. (3) Data on ABO blood group was accessible. (4) Sufficient clinical, laboratory, and follow-up records were available. Exclusion criteria include: (1) Transformed from other types of lymphoma to DLBCL. (2) Suffering from other tumors or having a history of tumor. (3) Suffering from other severe systemic diseases.

The baseline clinical data of patients were collected, including gender, age, Eastern Cooperative Oncology Group performance status (ECOG PS), primary tumor location, extranodal invasion details (sites and count), B symptoms, treatment modalities and response, ABO blood group, Ann Arbor stage, serum lactate dehydrogenase (LDH) levels, baseline serum CRP levels, serum β₂-Microglobulin (β₂-MG) levels, cellular origin, and IPI score. Overall survival (OS) is defined as the duration extending from the date of first diagnosis until either the occurrence of death from any cause or the last recorded date, when patient data is censored.

Additionally, we randomly selected age- and sex-matched hospitalized patients as controls (case-control ratio = 1) from the same institutions. Controls were diagnosed with non-malignant, non-hematological, and non-immunological disorders based on surgery or other routine clinical management (eg, hernia, cholelithiasis, osteoarthritis, cataract). Computerized randomization ensured equal numbers of controls per institution relative to DLBCL cases. ABO blood group data for controls were retrieved from hospital information systems (HIS) or laboratory databases using identical procedures as cases.

Within the DLBCL patient cohort, associations between ABO blood types and baseline clinical/laboratory variables were evaluated using Chi-square test or Fisher’s exact test for categorical data. When performing multiple pairwise comparisons among different blood groups for a specific variable, the Bonferroni correction was applied, adjusting the significance level to α’ = α / [k(k-1)/2], where k represented the number of blood groups, to account for all possible pairwise comparisons. The Log rank test and Kaplan-Meier method was applied for a univariate survival analysis. Variables demonstrating a univariate association with OS at P < 0.2 were included in multivariate Cox proportional hazards regression models. Hazard ratios (HRs) with 95% CIs were reported for significant predictors. A two-tailed P < 0.05 was deemed indicative of statistical significance. The statistical software package SPSS 26.0 (SPSS Inc., Chicago, IL, USA) was used for statistical calculations.

Result

Patient Characteristics

A total of 220 patients diagnosed with DLBCL, including 101 males and 119 females, with a median age of 60 years, were enrolled in the study. The clinical characteristics of the patients are listed in Table 1. Of the enrolled patients, 166 (75.5%) exhibited an optimal performance status (ECOG PS 0–1). B symptoms were present in 76 patients (34.5%). Involvement of at least two extranodal sites was displayed by 81 patients (36.8%). Elevated LDH levels were observed in 111 (50.5%) patients. The serum CRP levels were available for 108 patients, and the serum β₂-MG data were available for 158 patients. Localized disease (stage I/II) was observed in 73 patients (33.2%). High-risk disease (IPI ≥ 3) was present in 79 patients (35.9%). Ki-67 antigen levels were available for 195 patients. Among the 220 patients with DLBCL, 115 (73.2%) originated from the non-germinal center B cell-like (GCB) subtype. The ABO blood group exhibited no significant association with patient age, gender, ECOG PS, B symptoms, the number of extranodal sites, LDH levels, CRP levels, serum β₂-MG levels, Ann Arbor stage, IPI score, Ki-67 levels, or cellular origin (all P > 0.05, Table 1).

Table 1 Basic Characteristics of DLBCL Patients in Distinct ABO Blood Type Groups

The Effect of ABO Blood Group on Risk of DLBCL

In the DLBCL cohort, the distribution of ABO blood types was as follows: blood type A in 66 patients (30.0%), blood type B in 56 patients (25.5%), blood type AB in 24 patients (10.9%), and blood type O in 74 patients (33.6%). A control group comprising 220 individuals with nonmalignant conditions was randomly selected for comparison. The distribution of ABO blood types within the control group was as follows: blood group A accounted for 65 patients (29.5%), blood group B accounted for 72 patients (32.8%), blood group AB accounted for 17 patients (7.7%), and blood group O accounted for 66 patients (30.0%). No statistically significant disparity was observed in the distribution of ABO blood groups between DLBCL patients and the control cohort (P = 0.301, Supplementary Table 1).

Upon conducting a gender-stratified comparative analysis, we identified a statistically significant disparity among female patients with DLBCL compared to the control group (P = 0.012, Figure 1). Conversely, an analysis of the ABO blood group distribution among male DLBCL patients relative to the control group revealed no statistically significant differences (P = 0.757, Figure 1).

Figure 1 Distribution of ABO blood types among DLBCL patients and controls by gender. Significant difference observed in females (P = 0.012, chi-square test); no significant difference observed in males (P = 0.757, chi-square test). Abbreviation: DLBCL, diffuse large B cell lymphoma.

In the study comparing female patients with DLBCL to a female control group without the disease, the prevalence rate of DLBCL were observed to be 54.5%, 34.3%, 70.0%, and 54.1% respectively in individuals with blood type A, B, AB, and O. To account for multiple pairwise comparisons across blood groups, Bonferroni correction was applied, yielding an adjusted significance threshold of α = 0.05/[4(4−1)/2] = 0.0083. Subsequent pairwise analysis demonstrated a significantly lower DLBCL risk in individuals with blood type B compared to blood type AB (P = 0.005, Table 2). No statistically significant differences in DLBCL risk were observed between other blood group pairs (P > 0.0083, Table 2).

Table 2 DLBCL and the Distribution of ABO Blood Groups in Females

The Effect of ABO Blood Group on Survival of Patients with DLBCL

By the conclusion of the final follow-up period, a cumulative total of 77 (35.0%) patients had unfortunately passed away. The deaths were due to tumor progression (n = 69), severe pulmonary infections (n = 5), cardiovascular disease (n = 1), and other causes (n = 2). The 3-year OS rates for blood type A, B, AB, and O groups were 51.0%, 58.8%, 74.9%, and 74.0%, respectively (P = 0.458, Figure 2). Upon stratifying by age groups, we observed that among patients with DLBCL aged over 60 years, the 3-year OS rates for blood type A, B, AB, and O groups were 32.0%, 23.7%, 87.5%, and 69.0%, respectively, yielding a statistically significant difference (P = 0.043, Figure 3a). Considering that DLBCL patients with blood type B had the shortest 3-year OS rate, we categorized those aged over 60 into two distinct groups: blood type B and non-B (A, AB, and O). Patients with blood type B demonstrated a significantly reduced 3-year OS rate compared to those with non-B blood types (23.7% vs 53.6%, P = 0.030, Figure 3b). In contrast, among DLBCL patients aged 60 years or younger, no significant difference in survival rates was observed between individuals with blood type B and those with non-B blood types, with 3-year OS rates of 83.3% and 73.7%, respectively (P = 0.196, Figure 3c). Given that the 3-year OS rates of patients aged over 60 years with A and B blood types were shorter than those with AB and O blood types, we conducted a further comparison between blood type AB/O and blood type A/B to investigate the impact of ABO blood type on survival outcomes. The analysis revealed that the OS for patients with A/B blood types was significantly shorter compared to those with AB/O blood types (P = 0.014, Figure 3d). Notably, the 106 DLBCL patients aged over 60 years shared a similar clinical background (all P > 0.05, Supplementary Table 2).

Figure 2 The Kaplan-Meier curves for OS in patients with DLBCL according to ABO blood type (P = 0.458 by Log rank test). Abbreviation: OS, overall survival; DLBCL, diffuse large B-cell lymphoma; A, blood type A; B, blood type B; AB, blood type AB; O, blood type O.

Figure 3 The Kaplan-Meier curves for OS in patients with DLBCL according to ABO blood type. (a): OS in patients aged >60 years stratified by blood types A, B, AB, and O c. (b): OS in patients aged >60 years comparing blood type B vs non-B (A, O, and AB) (P = 0.030 by Log rank test). (c): OS in patients aged ≤60 years comparing blood type B vs non-B (A, O, and AB) (P = 0.196 by Log rank test). (d): OS in patients aged >60 years comparing blood types A/B vs AB/O (P = 0.014 by Log rank test). Abbreviation: OS, overall survival; DLBCL, diffuse large B-cell lymphoma; A, blood type A; B, blood type B; AB, blood type AB; O, blood type O; A/B, blood type A and blood type B; AB/O, blood type AB and blood type O.

Univariate and Multivariate Cox Regression Analysis

Table 3 presented the findings from both univariate and multivariate regression analyses regarding potential predictors of OS in patients with DLBCL aged over 60 years. The univariate analysis indicated that Ann Arbor stage, LDH levels, IPI score, and ABO blood type were significant prognostic factors influencing OS in patients with DLBCL (P < 0.05). Blood type B was linked to a significantly shorter OS when compared to non-B blood types (HR 2.013, 95% CI 1.056–3.839, P = 0.034). In the multivariate analysis, IPI score ≥ 3 (HR 2.247, 95% CI 1.226–4.120, P = 0.009), elevated LDH levels (HR 1.890, 95% CI 1.015–3.520, P = 0.045), and blood type B (HR 2.050, 95% CI 1.069–3.933, P = 0.031) emerged as adverse factors for OS.

Table 3 Univariate and Multivariate Analysis of Prognostic Factors for OS in DLBCL Patients Aged Over 60 years

Discussion

In the present study, we found that females with blood type B might exhibit a reduced risk of DLBCL compared to those with blood type AB. The prognostic implications of ABO blood group distinctions were not apparent across the entire cohort of DLBCL patients. However, our analysis found notable prognostic significance associated with ABO blood group specifically among DLBCL patients aged over 60 years. Among these patients, those with blood type B experienced a significantly shorter OS compared to patients with non-B blood groups.

The ABO gene is located on chromosome 9q34 and encodes two alleles (ie, A and B) for specific glycosyltransferases that catalyze the covalent linkage of N-acetyl-D-galactosamine or D-galactose to a common precursor side chain (ie, the H antigen), eventually forming A and B antigens respectively.^10,11 Unlike the A and B alleles, the O variant encodes a non-functional glycosyltransferase, so the H antigen remains unmodified.¹² In recent years, researchers have found a possible association between ABO blood group and the development of cancers. Studies have indicated that individuals with blood type A may be at an increased risk of tumorigenesis, whereas those with blood type B appear to have a reduced risk.^13–17 Previous investigations did not observe statistically significant results regarding the correlation between ABO blood group and the risk of DLBCL.^18,19 This study provided evidence that among female patients, individuals with blood type B may have exhibited a decreased risk of developing DLBCL in comparison to those with AB blood types.

Epidemiological studies have shown that the incidence of DLBCL is significantly higher among males compared to females.²⁰ This disparity may be linked to the presence of estrogen in the female population. Studies propose that estrogen potentially exhibits antitumor properties, capable of inhibiting the proliferation and dissemination of tumor cells through a variety of mechanisms.²¹ It has been reported that the use of high-dose oral contraceptives for pregnancy prevention or exposure to estrogen via postmenopausal hormone replacement therapy may reduce the risk of aggressive lymphoma.²² Furthermore, B-cell lymphomas treated with estrogen receptor β were shown to have effectively inhibit tumor growth in vivo.²³ These findings provided additional evidence that estrogen played a significant role in the development and progression of lymphoma. The study suggested that, compared to females with blood type AB, those with blood type B might exhibit a reduced risk of developing DLBCL. The study suggested that, compared to females with blood type AB, those with blood type B might exhibit a reduced risk of developing DLBCL. We hypothesize that this may be partially mediated by the higher estrogen levels typically found in individuals with blood type B, though this remains speculative in the absence of direct hormonal measurements. Further research is warranted to substantiate this hypothesis.

There were few studies exploring the prognostic relationship between ABO blood groups and DLBCL, and the results were inconsistent. A study in Turkey revealed that there was no significant correlation between ABO blood groups and the prognosis of patients with DLBCL.¹⁹ This finding was consistent with the result of this study conducted among the entire cohort of DLBCL patients. Nevertheless, what distinguished it was that our subgroup analysis identified blood type B as a negative prognostic factor specifically for patients older than 60 years. Osada et al reported that DLBCL patients with blood type B had a shorter OS than those with non-B blood types, and this trend was more significant among male DLBCL patients.¹⁸ A large-scale, population-based study on DLBCL series showed that male patients had worse prognosis outcomes than female patients.²⁴ Although our study observed similar results in DLBCL patients aged over 60 years, we did not find any relationship between gender and the survival of DLBCL patients.

The underlying mechanisms of how the ABO blood group may interact with the development and progression of cancers, including lymphoma, are still poorly understood. Several plausible hypotheses have been formulated to elucidate the link between ABO blood group and cancer risk. It is hypothesized that the absence of blood group antigen expression – particularly A and B antigens – may enhance tumor malignancy by increasing cellular motility and migration, thereby correlating with adverse clinical outcomes and poorer overall prognosis.^25–27 Studies have indicated that the reduction or absence of ABO blood group antigen expression might be related to the deletion of ABO allele or relative down-regulation of the glycosyltransferase necessary for blood group antigen synthesis caused by hypermethylation of the ABO promoter region.^28–32 The absence of ABO blood group antigens has been observed in hematological malignancies, including Hodgkin’s lymphoma (HL).^33,34 We hypothesize that analogous mechanisms may be present in patients aged over 60 years with DLBCL, which could lead to the reduction or absence of B-type antigens, ultimately resulting in unfavorable prognostic outcomes. The glycosylation of ABO blood group antigens can lead to conformational changes in proteins that not only affect intercellular signaling, cell adhesion, and immune surveillance, but also stimulate tumor growth and metastasis.^35–40 Some studies have reported that the ABO gene locus is associated with circulating levels of tumor necrosis factor-alpha, soluble intercellular adhesion molecule (ICAM)-1, E-selectin, and P-selectin.^41–43 These adhesion molecules play a crucial role in the recruitment processes associated with chronic inflammation. Chronic inflammation is linked to tumor growth, invasion, and migration.^44–46 Chronic inflammation is also associated with lymphatic malignancies.⁴⁷ For example, the lymphomas that appear in mice deficient in GM-CSF and IFNγ are caused by infections and subside after antibiotic treatment.⁴⁸ Although this study did not find a significant association between ABO blood group antigens and CRP, there may be other inflammatory cytokines that serve as intermediaries linking ABO blood group antigens to DLBCL. It is possible that ABO blood group antigens influence tumor progression and metastasis by altering the inflammatory state of the host. ABO glycosyltransferase can regulate plasma von Willebrand factor (vWF) levels, affecting the risk of venous thromboembolism.^49,50 vWF plays an important role in inhibiting angiogenesis, promoting wound healing, and inducing tumor cell apoptosis; particularly, angiogenesis and apoptosis are also involved in tumorigenesis.^51–54 Therefore, ABO blood group may contribute to the development of tumors by regulating plasma vWF levels.⁹ In this study, we observed a case of patients with DLBCL and blood type B who died from a pulmonary embolism. We observed one blood type B patient dying from pulmonary embolism, suggesting thromboembolic events as another potential mechanism.

This study has several limitations. First, Retrospective design inherently restricts causal inference and may introduce unmeasured confounders. Second, Absence of data on estrogen levels precludes validation of the proposed biological hypotheses. Third, the relatively small sample size with regionally constrained recruitment limits population-level generalizability and increases susceptibility to selection bias. Last, reduced statistical power after Bonferroni correction for multiple comparisons may have obscured subtle associations between other blood group.

Conclusion

In summary, our research found that females with blood type B may have a lower risk of developing DLBCL compared to females with blood type AB. Furthermore, blood type B may serve as a poor prognostic factor for patients over the age of 60 who have DLBCL. To better understand the role of ABO blood groups in DLBCL, future studies are recommended in a large number of different populations (Asian, Caucasian, African) as well as in various regions.

Data Sharing Statement

The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the corresponding authors.

Ethics Approval and Consent to Participate

The studies involving humans were approved by the ethics committee of The First Affiliated Hospital of Henan University of Science and Technology. The studies were conducted in accordance with the local legislation and institutional requirements. All participants confirmed their informed consent by responding to yes/no inquiries. All information collected from this study was treated with utmost confidentiality.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Funding

This work was supported by the Doctoral Research Funds of Henan University of Science and Technology.

Disclosure

The authors report no conflicts of interest in this work.

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Introduction

Klebsiella pneumoniae (KP) is a highly adaptable opportunistic pathogen and a major contributor to global mortality associated with antimicrobial resistance.¹ Taxonomically, it is a member of the family Enterobacteriaceae and genus Klebsiella. It is a Gram-negative, facultatively anaerobic bacillus characterized by the presence of a prominent capsule, frequent occurrence of pili, and the absence of both spores and flagella.² Based on virulence and pathogenic features, KP strains are broadly classified into two distinct types: classical KP (cKP) and hypervirulent KP (HvKP). Compared to cKP, HvKP exhibit potent virulence and are capable of causing community-acquired infections in otherwise healthy individuals. These infections involve multiple organ systems and can manifest as pneumonia, liver abscesses, endophthalmitis, and meningitis.³ According to systematic reviews, KP is a leading etiological agent of Gram-negative meningitis and bacteremia in low-and middle-income countries.⁴ Infections caused by HvKP are typically acute in onset, characterized by rapid progression to disseminated systemic infections, and associated with significant morbidity and poor prognostic outcomes. According to the 2017 Infectious Diseases Society of America (IDSA) recommendations, intraventricular drainage and intrathecal antibiotic administration may be implemented for meningitis patients with severe central nervous system (CNS) infections.⁵ In this case, the primary genetic markers of the hvKP strain were associated with rmpA and siderophore systems.

Case Presentation

The patient was a 63-year-old female with a four-year history of diabetes mellitus. She had been receiving drug treatment and was able to maintain a relatively normal lifestyle, although glycemic control remained poor. Before acute deterioration, for 72 hours, the patient developed prodromal symptoms including fatigue and anorexia. She presented to the emergency department with a 24-hour history of progressive delirium, altered mental status, and tympanic fever, and was subsequently hospitalized for urgent evaluation and treatment. Initial laboratory tests showed leukocytosis, with a white blood cell (WBC) count of 20.81×10⁹ /L (normal range: 4.0–9.5×10⁹ /L) and neutrophil predominance at 90.6% (normal range: 40.0–75.0%). Blood glucose was significantly elevated at 24.13 mmol/L (normal range: 4.1–5.9 mmol/L), and C-reactive protein (CRP) level was significantly elevated at 328.25 mg/L (normal range: ≤10 mg/L). Blood gas analysis indicated a pH of 7.49 (normal range: 7.35–7.45), PaO₂ of 83 mmHg (normal range: 80–100 mmHg), PCO₂ of 19 mmHg (normal range: 35–45 mmHg), HCO₃⁻ of 13.2 mmol/L (normal range: 21–27 mmol/L), and substantially elevated levels of lactic acid at 2.9 mmol/L (normal range: 0.9–1.7 mmol/L). Procalcitonin (PCT) was significantly elevated at 23.15 ng/mL (normal range: 0–0.05 ng/mL). Brain MRI scans revealed multiple intracranial infectious lesions accompanied by pneumocephalus (Figure 1A). Chest CT scans revealed bilateral lung inflammation, multiple pulmonary abscesses, and small bilateral pleural effusions (Figure 1B and C). Abdominal CT revealed cavitary changes in the right hepatic lobe (Figure 1D).

Figure 1 Imaging findings suggest multiple infectious lesions. (A) Brain MRI scan: multiple intracranial infectious lesions accompanied by pneumocephalus. Arrow points to the high signal areas in the temporal lobes. (B) Chest CT: multiple areas of consolidation in the right lung, with an arrow indicating one such consolidation. (C) Chest CT: mediastinal window shows consolidation with cavity in the right lung. Arrow indicates the cavity. (D) Abdominal CT: liver Abscess and arrow points to the liver lesion.

The patient was diagnosed with sepsis and admitted to the intensive care unit (ICU) for further treatment. Empiric antibiotic therapy was initiated with intravenous meropenem (2.0 g every 8 hours, administered for over 3 hours) in combination with linezolid (600 mg every 12 hours). Shortly thereafter, the patient exhibited progressive neurological deterioration, characterized by deepening coma, bilateral anisocoria, and respiratory distress. Mechanical ventilation was employed to manage dyspnea. Subsequently, a lumbar puncture was performed to access the cerebrospinal fluid (CSF), which appeared purulent and turbid (Figure 2D1), with an opening pressure of 375 mmH₂O (equivalent to approximately 3.68 kPa). Biochemical analysis of the CSF revealed the following abnormalities: elevated glucose 1.11 mmol/L, increased levels of chlorine at 119.3 mmol/L, elevated levels of protein at 10.36 mg/L, and significantly elevated nucleated cell count of 85000 × 10⁶/L (Table 1).

Table 1 Susceptibility Test Result of the Bronchoalveolar Lavage Fluid and Cerebrospinal Fluid Culture Was Obtained on October 14, 2022 (Day 2)

Figure 2 Cerebrospinal fluid (CSF) samples demonstrating varying degrees of appearance. (D1) Appearance of CSF on day 1. (D2–D5) The appearance of CSF following CSF exchange therapy and intrathecal injection was gradually cleared from day 2 to day 5.

On the second day of hospitalization, the patient demonstrated a deteriorated condition. The glasgow coma scale (GCS) score decreased from 7 to 4. Due to the high viscosity of the CSF, drainage was ineffective, prompting the placement of a lumbar cisternal drainage catheter via subarachnoid puncture to facilitate CSF replacement therapy. Daily CSF exchange therapy was initiated, involving the removal of 10 mL of CSF followed by the infusion of an equal volume of normal saline, for a total of approximately 30 mL per day. To further reduce inflammatory response and enhance antibiotic concentration, intrathecal injection of 3 mg dexamethasone combined with 50 mg amikacin was conducted following each CSF exchange. Concurrent intravenous anti-infective therapy was continued with meropenem (2.0 g every 8 hours) and linezolid (600 mg every 12 hours). This combined regimen of CSF exchange and intrathecal injections was continued for five consecutive days, CSF, during which the CSF was gradually cleared (Figure 2D1–D5).

On the fourth day after admission, KP was isolated from blood, bronchoalveolar lavage fluid (BALF), and CSF cultures (Table 2), with a positive string test indicative of a hypervirulent phenotype (Figure 3A and B). Whole-genome sequencing (WGS) further confirmed the hypervirulent phenotype of the KP strain, multilocus sequence typing (MLST) analysis confirmed that the isolate belongs to sequence type 65 (ST65-K1), identifying key virulence determinants including the rmpA transcriptional activator, aerobactin synthesis gene cluster (iucABCD), salmochelin siderophore system (iroBCDE), enterobactin biosynthesis genes (entABCDEFS), iron uptake-related genes (fepABCDG), type 3 fimbrial genes (mrkABCDFHIJ), type 1 fimbrial genes (fimABCDEFGHIK), and K1 capsular serotype-associated loci. Collectively, the clinical presentation and laboratory findings were consistent with the diagnosis of a disseminated infection due to HvKP (Table S1).

Table 2 Laboratory Data in Cerebrospinal Fluid Laboratory During Treatment

Figure 3 Klebsiella pneumoniae (KP) identification. (A) Shows a petri dish containing a bacterial culture on a blood agar plate. An arrow points to a specific colony morphology. (B) Blood agar plate showing positive string test for the KP isolated from the patient.

By the eighth day of hospitalization, the patient exhibited improvement in neurological functions, presenting with lethargy but able to open her eyes spontaneously. The motor function of the upper extremities was partially preserved, with the ability to perform simple command-based movements. However, due to persistent severe pulmonary infection, a tracheostomy was performed (Figure 4A and B). Ongoing treatment included intravenous antimicrobial therapy, which was de-escalated to ceftriaxone (2 g IV once daily) combined with moxifloxacin (0.4 g IV once daily), based on antimicrobial susceptibility testing. Supportive care comprised albumin infusion, parenteral nutrition, and symptomatic management.

Figure 4 Repeat chest CT on day 8 reveals bilateral cavitary infectious lung lesions. (A) Demonstrating right lower lobe consolidation (arrow). (B) Showing cavitation within the consolidated area and progression of the infection (arrow).

Following comprehensive treatment, the patient exhibited marked improvement in consciousness level, including regained spontaneous eye-opening and command-following movements of the upper extremities. Successful weaning from invasive mechanical ventilation was achieved on day 11 of hospitalization. Repeat brain MRI on day 11 demonstrated complete resolution of the previously identified purulent meningoencephalitis lesions (Figure 5A and B), while concurrent thoracic and abdominal CT scans revealed significant therapeutic response with >80% reduction in pulmonary and hepatic abscesses volumes (Figure 5C and D). A multidisciplinary team implemented a stepwise decannulation protocol on day 20, resulting in the successful removal of the tracheostomy tube and the initiation of structured neurorehabilitation. The patient was discharged on hospital day 33 after successful clinical cure. At discharge, final neurological examination revealed a GCS score of 15, preserved language function, and full muscle strength (grade V) in all four limbs, without residual neurological deficits. At the six-month follow-up, the patient could independently perform all activities of daily living.

Figure 5 Repeat imaging involving brain MRI, chest and abdominal CT scans on day 11. (A and B) Brain MRI shows that intracranial infection lesions have been cleared. (C) Chest CT shows that the right lung abscess has significantly reduced in size (arrow indicates lesion). (D) Abdominal CT shows that the liver abscess has significantly reduced in size (arrow indicates lesion).

Discussion

Etiologically, HvKP is primarily associated with community-acquired infections. It is significantly prevalent among Asian, Pacific Islanders, and Hispanic populations. While HvKP typically affects individuals with diabetes or a compromised immune system, it has also been shown to affect healthy individuals. Typically, the disease is invasive, with liver abscesses representing the most prevalent initial presentation, followed by metastatic infections such as endophthalmitis, pulmonary abscesses, meningitis, splenic abscesses, and necrotizing fasciitis. These infections progress rapidly, resulting in exacerbated neurological functioning and suboptimal prognostic outcomes.⁶ Additionally, studies have reported cases of post-traumatic systemic invasive infections due to HvKP.⁷ Studies indicate that diabetes is an independent risk factor for systemic HvKP infections, a phenomenon potentially attributable to the reduced immunity under hyperglycemic conditions.⁸

For instance, the patient in this case report had pre-existing diabetes, resulting in rapidly progressing disseminated infections involving the brain, lungs, and liver following HvKP infection. Key virulence factors for KP include capsular serotypes (K1 and K2), hypermucoviscous phenotype, virulence plasmids, lipopolysaccharides, iron acquisition systems, and fimbriae.^9,10 Hypermucoviscous KP strains expressing K1 and K2 capsular serotypes are strongly associated with treatment-resistant liver abscesses and recurrent invasive infections. HvKP exhibits enhanced iron acquisition capabilities, capsule production, and biofilm formation compared to cKP. These pathological mechanisms contribute to its enhanced invasiveness.¹¹ The ST65-K1 hypervirulent Klebsiella pneumoniae (hvKP) strain described in this study carries key virulence determinants, including the capsular hypermucoviscosity regulator rmpA and siderophore gene clusters. The rmpA gene drives excessive capsular polysaccharide expression, conferring a hypermucoid phenotype that promotes invasive dissemination. Concurrently, the siderophore clusters enable high-affinity ferric iron (Fe³⁺) scavenging, breaching host nutritional immunity in iron-restricted organs such as the liver, thereby confirming the diagnosis of the HvKP infection. Research has shown that HvKP-related mortality increases significantly with invasion of multiple organs (such as liver, brain, lungs), with reported mortality rates of 45% for KP meningitis.^12,13 Empirical antibiotic regimens for KP infections recommend cephalosporins combined with aminoglycosides. For intracranial infections, third-generation cephalosporins—such as ceftriaxone or cefotaxime—with high CSF penetration capability are recommended as first-line treatment options. Additionally, carbapenem agents—such as imipenem and meropenem—are recommended in cases where extended-spectrum β-lactamase (ESBL) production is suspected.¹⁴ Meropenem is recommended as the first-line therapy for severe infections involving multiple sites,¹⁵ particularly in critically ill diabetic patients undergoing intensive care.¹⁶ For HvKP, antibiotics with strong tissue penetration are highly recommended, coupled with abscess drainage in cases where the procedure is clinically feasible. In this case, percutaneous drainage was not conducted given the small size (3 cm) of the liver abscess size.¹⁷ HvKP-related intracranial infections progress rapidly, characterized by significantly high mortality rates, and an undefined optimal treatment duration. Studies indicate that survival and favorable neurological outcomes are associated with initial GCS scores ≤7 at the time of antibiotic initiation.¹⁸ Aztreonam, aminoglycosides, and carbapenems are the primary therapeutic options for KP meningitis, although they exhibit varying efficacy. According to the 2023 statistics from the CHINET China Bacterial Resistance Surveillance Network (www.chinets.com), KP ranks as the second most common pathogen among clinical isolates, accounting for 14.22% of cases. Notably, carbapenem resistance rates have exceeded 20%. Key resistance mechanisms identified include ESBLs, carbapenemases such as KPC, and metallo-β-lactamases, including the NDM.¹⁹ HvKP-induced community-acquired meningitis with septic shock is associated with a high hospitalization rate, with a 28-day mortality.²⁰ In this case, intrathecal amikacin and dexamethasone were administered based on the results from the susceptibility test. Intrathecal administration of amikacin enables direct attainment of therapeutic concentrations in the CSF, thereby enhancing antimicrobial efficacy.²¹ Additionally, findings from meta-analyses indicate that intrathecal dexamethasone exhibits significant efficacy in reducing capillary permeability, inflammation, cerebral edema, and intracranial pressure, while enhancing antibiotic activity.²²

The patient in this case presented with an acute-onset, a history of diabetes mellitus, and disseminated invasive infection. The disease progressed rapidly, resulting in impaired consciousness and respiratory failure. Based on clinical manifestations and genomic sequencing, the diagnosis was confirmed to be HvKP invasive syndrome complicated by severe intracranial infection. Due to the high viscosity of the CSF, preventing drainage through conventional methods, an integrated approach involving CSF exchange and intrathecal injections with amikacin and dexamethasone was used to treat the patient. This approach was therapeutically efficacious, resulting in improved clinical outcomes and subsequent discharge of the patient in stable condition.

Conclusion

Efficacious treatment of HvKP-related intracranial infections necessitates early recognition, potent antibiotic therapy with high tissue penetration ability, and quick CSF drainage. In this case, CSF exchange, combined with intrathecal injection with amikacin and dexamethasone, significantly improved clinical outcomes. This case represents the first reported application of this integrated regimen for HvKP meningitis, highlighting its significant therapeutic potential for broader clinical utility. However, this case provides an example but does not establish a generalizable standard of care, and that further studies or reports are needed to validate safety and outcomes.

Abbreviations

KP, Klebsiella pneumoniae; cKP, classical KP; HvKP, Hypervirulent KP; IDSA, Infectious Diseases Society of America; CNS, central nervous system; WBC, white blood cell; CRP, C-reactive protein; PCT, Procalcitonin; ICU, intensive care unit; CSF, cerebrospinal fluid; GCS, glasgow coma scale; BALF, bronchoalveolar lavage fluid; WGS, whole-genome sequencing; MLST, multilocus sequence typing; ESBL, extended-spectrum β-lactamase.

Data Sharing Statement

Data on the case clinical information, informed consent form, and images are available for review from the corresponding author upon request.

Ethical Approval

The publication of de-identified case details was expressly authorized under the original study approval by theAffiliated Lu’an Hospital of Anhui Medical University Institutional Review Board (Approval No. 2025LLKS-KY-042).

Consent for Publication

Written informed consent was obtained from patient and her families for the publication of case details and images. The complete signed consent form is archived at the Institutional Review Board (IRB) of Affiliated Lu’an Hospital of Anhui Medical University under approval number (Approval No. 2025LLKS-KY-042).

Acknowledgments

The authors thank the patient’s family for their consent to participatein this study as well as the medical, nursing, radiologist, and laboratory staff who were involved in the patient’s care.

Funding

The authors declare that financial support was received for the research in publication of this article. This research is supported by the Lu’an City Science and Technology Bureau Research Project (No.2024lakj013).

Disclosure

The authors report no conflicts of interest in this work.

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Published in the journal Brain Communications the study by academics from the University of Bath and the University of Bristol, reports that Fastball EEG, a three-minute passive test that records electrical activity in the brain while participants view a stream of images, can reliably identify memory problems in people with Mild Cognitive Impairment (MCI) — a condition that can lead to Alzheimer’s. This follows the group’s previous study in 2021 that demonstrated Fastball was sensitive to memory impairment in Alzheimer’s disease.

Crucially, the research team has demonstrated for the first time that the test can be administered in people’s homes, outside of a clinical environment. Researchers say this opens the door to wider screening and monitoring using accessible, low-cost technology.

With the development of the breakthrough Alzheimer’s drugs, donanemab and lecanemab, an early diagnosis is more important than ever before. The drugs are clinically proven to be the most effective in the early stages of Alzheimer’s. Despite this, in England, it is estimated that as many as 1 in 3 people do not currently have a dementia diagnosis, delaying treatments, support and research opportunities to tackle the condition.

The study was led by Dr George Stothart, a cognitive neuroscientist in the Department of Psychology at the University of Bath. He said:

“We’re missing the first 10 to 20 years of Alzheimer’s with current diagnostic tools. Fastball offers a way to change that — detecting memory decline far earlier and more objectively, using a quick and passive test.”

How the test works

Fastball is a passive EEG test that monitors the brain’s automatic responses to images — without requiring participants to follow instructions or recall information. This makes it more objective and accessible than traditional memory tests.

Key findings:

• Detected early memory issues in people with MCI likely to develop Alzheimer’s.
• Delivered reliable results in real-world home settings.
• Showed reduced memory responses even in patients who later progressed to dementia.

Researchers say Fastball could be scaled for use in GP surgeries, memory clinics, or at home — helping deliver earlier, more accurate diagnoses.

Dr Stothart added: “There’s an urgent need for accurate, practical tools to diagnose Alzheimer’s at scale. Fastball is cheap, portable, and works in real-world settings.”

The study was funded by the Academy of Medical Sciences and supported by dementia research charity BRACE.

Chris Wiliams, CEO of BRACE Dementia Research, said: “Fastball is an incredible tool that could offer anyone who, for whatever reason, cannot access a dementia diagnosis in a clinical setting.

BRACE has been supporting the development of Fastball for several years, and we are excited to see what Dr Stothart’s team will achieve over the next few years with ongoing support from the charity.”

What is perimenopause?

Perimenopause is defined as the transitional phase that can last anywhere from 8 to 10 years before menopause, which is marked by 12 consecutive months without a menstrual period. During this time, fluctuations in estrogen and progesterone levels create hormonal chaos that triggers various symptoms. Unfortunately, many women misattribute these symptoms to stress, overwork, or mental health issues, as per the National Institute of Mental Health.

How do you know if it is PMS or perimenopause?

The key difference between PMS and PMM lies in duration and unpredictability. PMS usually arises predictably, following ovulation and is alleviated by menstruation. PMM, however, often feels like an ongoing battle with no apparent cause or solution, radically altering women’s lives, as per Harvard Health.

How does mood change during perimenopause?

The hormonal shifts of perimenopause impact neurotransmitters like serotonin and dopamine, which influence mood, focus, and motivation, as per the Journal of Midlife Health. As a result, many women experience heightened emotions such as irritability, anxiety, and sadness.

These emotional fluctuations can be invisible to others, leading women to feel misunderstood and unappreciated. They may be dismissed as “overreacting” or “too sensitive.” “The impact on relationships and work productivity can be profound, while medical professionals sometimes fail to connect the symptoms to hormonal changes, prescribing antidepressants or sleep aids instead. This dismissive attitude can foster feelings of shame, frustration, and isolation,” menopause coach Tammana Singh tells Health Shots.

What are the symptoms of hormonal changes in women?

Recognising the signs of perimenopause can help you take control of your health and overall well-being. Menopause coach Tammana Singh shares seven key indicators:

1. Heightened anxiety or depressive spells: Unexplained emotional lows and anxiety attacks may become more frequent.
2. New or worsening PMS symptoms: If your PMS seems to be intensifying or changing, it might be a sign of perimenopause.
3. Night sweats and insomnia: Experiencing sudden sweating during the night or difficulty sleeping can significantly disrupt rest.
4. Brain fog or forgetfulness: Mental clarity may decrease, resulting in forgetfulness or difficulty concentrating.
5. Sudden weight gain: Weight gain, particularly around the abdomen, can signal hormonal changes.
6. Migraines or joint pain: Increased headaches or joint discomfort may indicate shifts in hormone levels.
7. Irregular or heavier periods: Changes in menstrual cycle regularity or flow can be a telling sign.

How to manage hormonal changes during perimenopause?

Awareness is crucial when navigating this transitional phase. Understanding that hormonal changes drive these symptoms allows women to seek appropriate help rather than blaming themselves.

Here are some methods to consider:

1. Track your hormonal patterns: Using apps, journals, or simple calendar notes can help you connect mood changes with variations in your menstrual cycle, as per the Journal of Medical Internet Research. Look for patterns that emerge over time.
2. Rethink self-care: The approach to self-care during this phase requires more than just surface-level solutions, as per the American Psychological Association. Focus on restorative practices such as:

• Deep breathing exercises
• Journaling
• Professional therapy
• Gentle movements like yoga or tai chi can help regulate cortisol and estrogen levels.

3. Build a menopause-ready lifestyle: Healthy lifestyle choices can alleviate some perimenopausal symptoms. Consider:

• Introducing foods rich in phytoestrogens (flaxseeds, sesame seeds, tofu).
• Maintaining good sleep hygiene—consistent sleep schedules, a comfortable sleep environment, and practices that promote relaxation.
• Starting a strength-training regimen to support muscle and bone health.

4. Get informed support: Seek out professionals well-versed in hormonal health, such as:

• Functional medicine practitioners
• Integrative gynaecologists
• Specialists knowledgeable about Ayurveda
• Therapists who can guide you through lifestyle shifts based on current research

Hormonal changes may challenge us, but they also open the door to deeper body awareness and self-acceptance.