Category: 8. Health

  • Researchers use AI to identify “hidden fat” on routine bone scans-Xinhua

    SYDNEY, Sept. 4 (Xinhua) — Researchers in Australia are developing an artificial intelligence (AI) algorithm that estimates dangerous hidden fat, or visceral fat, from bone density scans used to detect spine fractures.

    Visceral fat, the harmful deep belly fat that surrounds organs, is a “troublemaker” strongly linked to serious health problems like heart disease, diabetes and cancer, according to a statement released Thursday by Australia’s Edith Cowan University (ECU).

    The ECU team is training its machine learning algorithm to analyze lateral spine Dual-energy X-ray Absorptiometry (DXA) scans, used to assess bone density, to accurately predict visceral fat levels from these images, offering valuable new health insights without requiring additional tests.

    Current methods to estimate visceral fat, like body mass index, waist circumference, and waist-to-hip ratio, have limitations as they cannot distinguish between different types of body fat, leading to inconsistent obesity assessments, researchers said.

    Imaging techniques such as MRI and CT provide accurate visceral fat measurement but are costly and, in the case of CT, expose patients to higher radiation, they said.

    “The machine-learning model has been trained on thousands of images; the next step is to incorporate further datasets from around the world, so it learns from the largest, most diverse cohort possible and becomes as effective as possible,” said Syed Zulqarnain Gilani, a senior lecturer and lead AI scientist at ECU.

    Continue Reading

  • Cardiologist shares real reasons even fit and sporty people suffer heart attacks, sudden cardiac arrest during workout | Health

    Cardiologist shares real reasons even fit and sporty people suffer heart attacks, sudden cardiac arrest during workout | Health

    In an interview with HT Lifestyle, Dr Lakshmi Navya, consultant cardiologist at Manipal Hospitals Vijayawada, shared that sudden cardiac death occurs when the heart suddenly stops functioning, often within an hour, and can happen to anyone, even during physical activity like exercise or sports. She explained that addressing modifiable risk factors can reduce the likelihood of experiencing a heart attack. Also read | 52-year-old man dies of heart attack while working out at gym: Doctors explain how to prevent such tragedies

    Fit and sporty individuals can suffer heart attacks or sudden cardiac arrests due to various reasons. Here is what to know. (Freepik)

    Dr Navya said, “Sudden cardiac death is the cessation of all life activities immediately within one hour. So nowadays we see many people who succumb to sudden cardiac arrest while working out at the gym, while walking on the road, or while playing sports, and all. So why does this happen so often?”

    According to her, when the body exerts itself, the heart works harder, which can lead to stress and potentially fatal consequences, especially if there are underlying heart issues. Dr Navya said, “When the body is at rest, the energy requirement is also lower. When the body exerts, the heart needs to work more in accordance with the amount of work we do. When the amount of work increases, the heart is under stress. There is a surge of catecholamine activity in the body, which can lead to multiple factors.”

    What causes sudden cardiac death?

    Dr Navya shared that sudden cardiac death can occur due to pre-existing blocks – rupture of existing blockages in the heart, leading to massive heart attacks – or ventricular arrhythmias – abnormal heart rhythms, such as ventricular tachycardia or fibrillation, often genetically transmitted.

    She said, “One being, if there are already pre-existing blocks in the heart, it can cause rupture of any pre-existing plugs, that is, any blocks that happen in the heart, leading to a massive heart attack. This is one of the major causes of sudden cardiac death. So by the time the patient reaches the hospital, there will be cardiac arrest because of the very high prevalence of massive heart attacks.”

    She added, “And the second cause is ventricular arrhythmias. So there will be some inherent genetically transmitted diseases which can cause an increase in heart rate called ventricular tachycardia or ventricular fibrillation, which do not need have any pre-existing phenomenon. So this is the second most important cause, and the majority of the time, this is transmitted genetically.”

    Lifestyle habits like smoking, alcohol consumption, stress, poor diet, lack of sleep, and inadequate physical activity are linked to your heart health.(Shutterstock)
    Lifestyle habits like smoking, alcohol consumption, stress, poor diet, lack of sleep, and inadequate physical activity are linked to your heart health.(Shutterstock)

    Increasing incidence of heart attacks can be attributed to?

    So why are heart attacks among the young increasing? According to Dr Navya, the increasing incidence of young heart attacks can be attributed to genetic predispositions, familial hypercholesterolemia, and innate genetic disorders, as well as lifestyle habits like smoking, alcohol consumption, stress, poor diet, lack of sleep, and inadequate physical activity.

    She explained, “The non-modifiable risk factors include those that are genetically transmitted, such as familial hypercholesterolemia, some lipid disorders, and some innate genetic disorders leading to early atherosclerosis. Hence, those are non-modifiable and not available to change in our hands.”

    What are the modifiable risk factors? Dr Navya said, “The modifiable ones are the lifestyle habits that include smoking, alcohol, high amounts of stress, lack of sleep, junk food, and inadequate diet intake. So these and all cause the modifiable risk factors, which we do not follow. And also keeping in check hypertension, diabetes, the other metabolic syndrome parameters, that is, waist to hip ratio, abdominal circumference, keeping the weight in check, lipids in check, these are not commonly done very common. So these factors affect the formation of blocks in the heart, thereby causing massive heart attacks.”

    Note to readers: This article is for informational purposes only and not a substitute for professional medical advice. Always seek the advice of your doctor with any questions about a medical condition.

    Continue Reading

  • Spatial Orientation Deficits Signal Alzheimer’s Risk

    Spatial Orientation Deficits Signal Alzheimer’s Risk


    Register for free to listen to this article

    Thank you. Listen to this article using the player above.

    Individuals with an increased risk for dementia due to Alzheimer’s disease can have impaired spatial orientation skills. DZNE researchers come to this conclusion based on a study involving around 100 older adults who were tasked with determining their position within a virtual environment. In this, participants with “subjective cognitive decline” (SCD) – a risk factor for Alzheimer’s disease – performed worse than members of the control group. In contrast, there were no significant differences in conventional tests of cognitive performance. In view of this, the current research results, published in the journal Science Advances, could pave the way for more sensitive testing methods. Potential areas of application include early diagnosis of Alzheimer’s and drug studies.

    The term “subjective cognitive decline” (SCD) refers to the condition in which someone believes that their memory is deteriorating, despite standard tests showing no decline in mental performance. “This condition has been the focus of research in recent years, because people with SCD are known to be at an increased risk of developing Alzheimer’s dementia later in life,” explains Prof. Thomas Wolbers, a research group leader at DZNE’s Magdeburg site and a member of the Collaborative Research Centre “Neural Resources of Cognition”. “It is therefore reasonable to assume that SCD may indicate a preclinical stage of Alzheimer’s.”

    Novel approach

    In the current study, the team led by the Magdeburg-based neuroscientist explored an approach for detecting cognitive impairments that goes beyond conventional test methods. Experts from the US and the Czech Republic collaborated on this research. Together, they assessed what is known as path integration: This refers to the ability to determine position and navigate spatially based on body awareness and the perception of one’s movement. “For this task, we humans use special neuronal circuits. They are located in an area of the brain called the entorhinal cortex. Hence, in a sense, we carry a compass inside our heads,” says Wolbers. Alzheimer’s disease typically affects this area in its earliest stages, even before symptoms of dementia manifest. “This brings us full circle to our current study. To my knowledge, our findings are the first to show that SCD can be associated with subtle orientation problems. We hope this will lay the foundation for novel testing methods that can detect very early effects of Alzheimer’s disease,” says Wolbers.

    A world without reference points

    The study included 102 older women and men, aged between 55 and 89. Thirty of the participants had SCD. However, all study subjects scored within the normal range on conventional cognitive tests. For the actual experiment, they wore a virtual reality headset. Equipped with these, they walked through real space while simultaneously moving through a computer-generated environment: They saw an endlessly vast plain with no landmarks under a blue sky. However, the irregular texture of the ground enabled them to perceive their movements across the digital landscape. “Since there were no visual landmarks in this virtual world, the only way to orient oneself was with the help of the brain’s navigation system. This is precisely the ability we wanted to test,” says Dr. Vladislava Segen, first author of the current publication and a member of Wolbers’ research group.

    Putting the brain’s compass to the test

    The task began with the study participants following a ball that floated near the ground while moving along a curved trajectory until it finally came to a stop. Once the participants had caught up with the ball, they were asked to turn toward their original starting point and mark its presumed position. To do this, they used a virtual pointer that could be operated via a hand controller. The participants were also asked to align themselves with the direction they had been facing at the initial start of their path. “This allowed us to test how well the study subjects could remember their initial orientation,” says Segen. The ball then hovered on to the next stop, where the responses had to be repeated. With two stops per run, the total distance covered in real space was approximately six meters, and each participant completed about 70 trials. This allowed to collect extensive data on the movements of the study subjects and how accurately they performed their orientation tasks.

    Less accurate with SCD

    “Some found these tasks easier than others. They were certainly challenging. In general, there was a clear age-related effect with the oldest individuals showing larger errors. This applied regardless of whether SCD was existent or not,” says Segen. “However, when comparing the groups, it became obvious that participants with SCD performed worse overall. They were less accurate in path integration. Our data suggest that these orientation difficulties did not arise from movement dynamics, such as walking faster or looking at the ground more often while walking. The causes of the imprecise orientation were not related to motion, but cognitive in nature.”

    Deeper insights with mathematical modelling

    To identify the causes of this impairment in more detail, the research team applied complex mathematical modelling to the collected data. “The brain has to process various data to determine position. This includes correctly perceiving the speed at which you are moving and the direction in which you are going. With the help of our model, we were able to identify which sources of error had the greatest impact on position determination and which had only minor influence,” says Segen. One factor stood out, with its influence on position accuracy differing significantly between the two study groups. “To determine your position in space while moving, you have to constantly update your position in your mind. This requires you to remember previous positions. To do this, you unconsciously draw on a mental history. In people with SCD, this type of memory was particularly faulty. We therefore refer to this as memory leak. We suspect that functional disturbances in the entorhinal cortex are responsible for this”, explains Segen.

    Clinical Implications and Future Directions

    The entorhinal cortex contains a special type of neurons called “grid cells”. Based on incoming sensory information, those cells generate a kind of coordinate system for the environment in which a person currently finds themselves. Studies by other research groups suggest that these neural circuits store a history of previous, successive locations in memory – similar to the sequence of images in a flipbook. “The evidence is converging that path integration is very sensitive to grid cell dysfunction and thus to preclinical stages of Alzheimer’s disease,” says Thomas Wolbers. Thus, the researchers want to further develop their experimental setup so that it can be used in clinical trials. “I am thinking, for example, about testing new drugs. When evaluating the effects of novel active substances, path integration could supplement existing assessments to provide a more detailed overall picture,” says Wolbers. “In the long term, I also see potential for use in clinical routine, specifically in the early diagnosis of Alzheimer’s disease. However, this technique first needs to be further tested and simplified. Also, we intend to relate our findings to biomarkers for Alzheimer’s disease derived from blood or cerebrospinal fluid. This should provide further insights into the capability of our approach for detecting neurodegeneration.”

    Reference: Segen V, Kabir MR, Streck A, et al. Path integration impairments reveal early cognitive changes in subjective cognitive decline. Sci Adv. 2025;11(36):eadw6404. doi: 10.1126/sciadv.adw6404

    This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source. Our press release publishing policy can be accessed here.

    Continue Reading

  • Varying psychological stress among Rwandan patients with chronic disea

    Varying psychological stress among Rwandan patients with chronic disea

    Abdullateef Isiaka Alagbonsi,1 Clothilde Manishimwe,2,* Muhirwa Serge,2,* Divine Aimee Agahozo,2,* Shema Tito2,*

    1Department of Physiology, School of Medicine and Pharmacy, College of Medicine and Health Sciences, University of Rwanda, Huye, Southern Province, Republic of Rwanda; 2Department of Primary Health, School of Medicine and Pharmacy, College of Medicine and Health Sciences, University of Rwanda, Kigali, Republic of Rwanda

    Background: While psychological stress cannot be dissociated from chronic diseases, the extent to which it impacts the management of chronic diseases is poorly understood. This cross-sectional study investigated the prevalence and impact of psychological stress among Rwandan patients with chronic diseases, particularly hypertension, heart failure, malignancies, diabetes, and kidney failure.
    Methods: This cross-sectional study was conducted among internal medicine patients receiving treatment for chronic diseases at the University Teaching Hospital of Kigali (n = 81) and the University Teaching Hospital of Butare (CHUB) (n = 78) between May 1 and June 30, 2024.
    Results: There was a very high prevalence of psychological stress (91.8%) among Rwandan patients with various forms of chronic diseases. Despite the regular monitoring of their disease progression by their healthcare providers (92.4%) and compliance with their medication (89.9%) and dietary (89.3%) regimens, many of them still experienced frequent complications (96.8%) and worsening outcomes (95.5%), though there was an improvement in symptoms (94.3%). Furthermore, there was a weak relationship (r = 0.210, ρ = 0.000) between the severity of psychological stress experienced by patients with chronic diseases and their treatment outcomes. Finally, patients with heart failure (p< 0.001), hypertension (p< 0.001), diabetes (p< 0.001), and malignancies (p< 0.001) experienced higher levels of psychological stress.
    Conclusion: Hypertension, heart failure, malignancies, and diabetes, but not kidney failure, predict psychological stress among Rwandan patients.

    Keywords: diabetes, heart failure, hypertension, kidney failure, malignancy, psychological stress

    Introduction

    Psychological stress, manifested through perceived stress, anxiety, depression, post-traumatic stress disorder (PTSD), and obsessive-compulsive disorder, has emerged as a pivotal factor influencing the management and prognosis of chronic illnesses.1 People with chronic illnesses have a higher chance of developing psychological stress than the general population.2,3 Moreover, the global burden of chronic diseases is exacerbated by the pervasive presence of psychological stressors. In Sub-Saharan Africa, where healthcare resources are often scarce, the confluence of chronic diseases and psychological stress presents formidable challenges. Limited healthcare infrastructure, inadequate access to essential medications, and socio-economic disparities compound the impact of chronic diseases in Sub-Saharan Africa.4 Chronic stress not only compromises individuals’ mental well-being but also causes physiological dysregulation, like inflammation and oxidative stress. These biological mechanisms have been implicated in the pathogenesis and progression of various chronic diseases, such as cancer, diabetes, and cardiovascular ailments.5

    Most of the currently used procedures for diagnosing various medical conditions in the healthcare system are based on the biomedical model, which relies on bodily concepts such as the pathophysiology of diseases and derangements of organ-system functions.6 This model has been criticized for regarding patients as disease-based objects, ignoring the importance of subjective patients’ experiences in clinical care. However, the biopsychosocial model that assumes that the disease outcomes are attributed to the intricate blend of biological, psychological, and social factors is now believed to be an ideal representation of science and humanism in medical practice, even though it is hard to implement in clinical practice.7 It accommodates social contexts in the understanding of the aetiology of diseases. The biopsychosocial model faces criticism because its application needs a thorough evaluation of the behavioural, psychological, sociocultural, and spiritual dimensions of patients’ problems, which requires huge efforts of the healthcare providers who are already overburdened with clinical, administrative, and possibly research tasks. It is believed that diseases demonstrating structural changes in tissues and organs will benefit more from the biomedical approach, while those without known pathological changes may be suitable for the biopsychosocial approach.8 The relevance of the biopsychosocial model is well appreciated when considering the comorbidity of chronic diseases and psychological stress from the context of the diathesis–stress model, which explains the emergence of psychological disorders from an interaction between an individual’s inherent vulnerability (diathesis) and the individual’s experience of stressful events. Based on this model, the greater an individual’s vulnerability to a disorder, the smaller the amount of stress needed to trigger the development of the disorder.9

    Data from the World Health Organisation (WHO) revealed that in 2019, NCDs accounted for 51% of all deaths in Rwanda, including cardiovascular diseases (17%), cancers (9%), chronic respiratory diseases (3%), diabetes (3%), and other NCDs (18%). During that period, the probability of premature mortality from NCDs was 20%, the percentage of NCD deaths occurring under 70 years was 63%, and the NCD age-standardized death rate was 615 per 100,000 population.10 A recent countrywide study among 19,110 Rwandan population showed the prevalence of mental disorders to be 23.2% in women and 16.6% in men, and the prevalent mental disorders were major depressive episode (12.0%), panic disorder (8.1%), and PTSD (3.6%). Specifically, among the 1271 survivors of the 1994 genocide in Rwanda, the prevalence of any mental disorder was 53.3% for women and 48.8% for men, and the most prevalent disorders were major depressive episode (35.0%), PTSD (27.9%), and panic disorder (26.8%).11 While psychological stress cannot be dissociated from chronic diseases, the extent to which such stress impacts the management of chronic diseases is not well understood. Through an examination of the prevalence of psychological stress among individuals with chronic diseases, this research sought to establish the impact of psychological stress on the treatment outcomes among patients with chronic diseases in Rwanda, which could reveal insights about the appropriate interventions and support for the patients. In this Rwandan study, we reported the prevalence of psychological stress among patients with chronic diseases, the treatment outcome of chronic diseases among patients exhibiting psychological stress, and the type of chronic diseases with a high risk of psychological stress.

    Methodology

    Research Design

    The cross-sectional study employed three research design methods. The descriptive evaluative research design was used to evaluate the effectiveness of treatment modalities in managing chronic diseases among patients with psychological stress. A descriptive correlational research design was employed to investigate the relationship between the severity of psychological stress and treatment outcomes for chronic diseases. The descriptive comparative research design was used to compare the prevalence of psychological stress among various forms of chronic diseases.

    Study Setting

    This study was conducted in 2024 at two tertiary hospitals in Rwanda. They were selected due to their significance in providing healthcare services to a diverse patient population in Rwanda, covering different catchment areas.

    Study Population and Sampling Techniques

    All internal medicine patients receiving treatment for chronic diseases at the University Teaching Hospital of Kigali (CHUK) and the University Teaching Hospital of Butare (CHUB) between 1st May and 30th June 2024, particularly those with hypertension, heart failure, malignancies, diabetes, and kidney failure, were invited to participate in the study. To ensure that the sample represents the population and responds to the geographical diversity, a stratified random sampling technique was employed. Two strata-specific “fishbowls” were created, one for each hospital. In each fishbowl, 81 patients from CHUK and 78 patients from CHUB were randomly selected, ensuring consistency and fairness across the strata. This approach yielded a total sample size of 159 patients, chosen based on Slovin’s formula.12 Adult patients who were recently diagnosed with hypertension, heart failure, malignancies, diabetes, and kidney failure were included in the study. Patients who were less than 18 years old, had advanced cases of chronic diseases, had underlying psychiatric illnesses, and/or refused to consent were excluded from the study.

    Instrumentation and Data Collection

    Before administering the questionnaire, a content validation process was conducted to ensure clarity, adequacy of items for data collection, alignment with study objectives, lack of bias, and relevance. Seven experts and two laymen participated in the content validation process. The expert panel included a statistician, a methodologist, four medical doctors, and one public health specialist, while two laymen provided additional perspectives. Suggestions and corrections from these experts were carefully considered when formulating the final questionnaire. Furthermore, a pilot test of the questionnaire was conducted among 20 patients from an unselected pool. The data collection primarily involved a face-to-face survey (with an online option for a few patients who could not attend the in-person session) to capture quantitative data on the prevalence of psychological stress and qualitative insights into the experiences and perceptions of patients regarding their psychological well-being and chronic disease management. The survey questionnaire comprised four self-constructed sections, with 12 questions in section 1 and 14 questions each in sections 2–4.

    The first section extracted valuable insights from the patients about their perceptions and experiences of their treatment outcomes, focusing on disease progression, management adherence, and quality of life (QoL). A true or false test was administered to gauge the patient’s understanding of disease progression, adherence to treatment regimens, and the impact of their condition on their overall QoL. Each correct response (true) was assigned a score of 1 point, while an incorrect response (false) received a score of 0 points. The composite score was calculated by tallying the frequency of correct answers and computing the percentage. The descriptive interpretation of scores was categorized as follows: Very Low (0–64, 0–25%); Low (65–95, 26–50%); High (96 −127, 51–75%); and Very High (128–159, 76–100%).

    The second section delved into the medical history, diagnosis, and current management strategies for chronic diseases. The third section explored the patients’ perception of the common contributing factors to psychological stress among patients with chronic diseases, where patients were asked to identify and rate various factors that they believed contributed to their psychological stress. The last section assessed the level of psychological stress among patients with chronic diseases, where the patients were asked to self-report their levels of psychological stress and indicate the specific stressors or challenges they faced. In sections 2–4, each was scored on a 4-point Likert scale: 1 – Very Low (Strongly Disagree with a mean interval score of 0.5–1.5); 2 – Low (Disagree with a mean interval score of 1.51–2.5); 3 – High (Agree with a mean interval score of 2.51–3.5), and 4 – Very High (Strongly Agree with a mean interval score of 3.51–4.0). Assessment of psychological stress was done by a subjective method, which measures the individuals’ perception of how stressful they regard their general life.13

    Informed Consent and Ethical Approval

    The participating patients provided informed consent and knew that their responses would be published as an undergraduate dissertation and an article in a peer-reviewed journal. The study protocol got ethical approval from the ethics committee of the University of Rwanda College of Medicine and Health Sciences, CHUK, and CHUB. Furthermore, the study complies with the Declaration of Helsinki.

    Data Analysis

    The data were analysed using the Statistical Package for Social Sciences (SPSS) version 21.0. Frequency and percentage distributions were calculated to determine the prevalence rate of psychological stress among patients with chronic diseases. Pearson’s product-moment correlation coefficient was used to examine the relationship between variables, particularly exploring the correlation between the severity of psychological stress and treatment outcomes among patients with chronic diseases. One-way ANOVA and t-test were used to compare means between groups and determine whether there were significant differences in treatment outcomes among patients with chronic diseases who experienced psychological stress compared to those who did not. Regression analyses were limited to disease type as a predictor of psychological stress, since detailed sociodemographic (eg, age, sex, and income) and clinical variables (eg, disease severity and treatment duration) were not collected.

    Results

    Patients with Chronic Diseases Have a Very High Prevalence of Psychological Stress and Poor Treatment Outcomes

    There was a very high prevalence of psychological stress (91.8%) among Rwandan patients with various forms of chronic diseases. This psychological stress was mostly in the form of being overwhelmed by the demands of managing the chronic illness (98.7%). Moreover, many patients associated the financial burden of their chronic illness with their high psychological stress (88.1%) and further expressed frustration about how their chronic illness negatively affected their mental well-being (96.8%) and daily life (94.3%), raising serious concerns about their future health (95.5%). They also had challenges in managing their emotional burdens (92.4%) and communicating their concerns to healthcare providers (93.1%), leading to discouragement and defeat (91.1%), hopelessness and difficulty in maintaining a positive outlook (89.3%), and disconnect and social isolation (81.7%). These findings highlight the multifaceted nature of psychological stress experienced by patients with chronic diseases in Rwanda, encompassing emotional, financial, and social dimensions (Table 1).

    Table 1 Psychological Stress Among Patients with Chronic Diseases in Rwanda (n=159)

    Furthermore, most patients also reported a very high understanding of the stages and progression of their chronic diseases (98.7%). Despite the regular monitoring of their disease progression by their healthcare providers (92.4%) and compliance with their medication (89.9%) and dietary (89.3%) regimens, many of them still experienced frequent complications (96.8%) and worsening outcomes (95.5%), though there were improvement in symptoms (94.3%) (Table 2).

    Table 2 Treatment Outcomes Among Patients with Chronic Diseases (N=159)

    The Severity of Psychological Stress is Weakly Associated with Treatment Outcomes of Chronic Diseases

    Pearson correlation was used to test the relationship between the severity of psychological stress experienced by patients with chronic diseases and their treatment outcomes. We noted a weak but significantly positive relationship between the severity of psychological stress and outcome of chronic disease treatments (r = 0.210, ρ =0.000). This suggests that additional factors other than the severity of psychological stress could be impacting the treatment outcomes of chronic diseases in the Rwandan population.

    Prediction of Psychological Stress Among Chronic Disease Patients

    Regression analysis demonstrated that heart failure, malignancies, diabetes, and hypertension were significant predictors of psychological stress (p<0.001). Analyses were restricted to disease type due to the available data (Table 3).

    Table 3 Regression Analysis for Predictors of Psychological Stress Among Patients

    Discussion

    The extent to which psychological stress impacts the management of chronic diseases among Rwandan patients is not well understood. In this study, we reported the prevalence of psychological stress among patients with chronic diseases, the treatment outcome of chronic diseases among patients exhibiting psychological stress, and the type of chronic diseases with a high risk of psychological stress. This study provides three key information. Firstly, there is a very high prevalence of psychological stress among chronic disease patients in Rwanda, leading to poor treatment outcomes. Secondly, the severity of psychological stress is weakly associated with treatment outcomes of chronic diseases in Rwanda. Finally, hypertension, heart failure, malignancies, and diabetes, but not kidney failure, predict psychological stress among Rwandan patients. However, we were unable to adjust for potential confounders such as age, sex, income, and disease severity, since these were not collected in the present study. Consequently, our regression model may not fully capture the independent contribution of disease type to psychological stress.

    A study in Ethiopia reported that the prevalence of psychological stress among patients (62%) with chronic diseases surpasses that seen in the general population.14 Another study in Ghana noted an elevated level of psychological stress among chronic kidney disease patients undergoing haemodialysis.15 In South Africa, 89% of patients with chronic diseases experienced psychological stress.16 Similarly, in Rwanda, varying levels of psychological stress have been reported among patients with chronic diseases,17 which was further exacerbated by the COVID-19 pandemic.14,18 The same observation has been made in the non-African population in India,19 Greece,20 and China.21,22 Factors like marital status, family history of chronic illness, low social support, rural residence, co-infection with HIV, stigma, presence of other chronic diseases, and smoking have been associated with psychological stress among patients with chronic diseases in some African countries.14,23 Furthermore, age,14 gender,24 and socio-economic status14 have been shown to affect psychological stress among patients with chronic diseases. Consistent with these findings, we also observed that 91.8% of patients with chronic diseases, including hypertension, heart failure, diabetes, malignancies, and kidney failure, have psychological stress in Rwanda. Our data show that the psychological stress among Rwandans with chronic diseases was multifaceted, such as being overwhelmed by the demands of managing the chronic illness and the financial burden of their chronic illness, among others.

    It is known that chronic diseases can cause various forms of psychological stress and vice versa.25,26 We investigated whether the severity of psychological stress determines the treatment outcomes of chronic diseases among the Rwandan population. We noted that the comorbidity of psychological stress and chronic diseases among the patients leads to frequent complications and worsening treatment outcomes, albeit with improved symptoms. Despite the regular monitoring of their disease progression by their healthcare providers and patient compliance with their medication and dietary regimen, many of them still experienced frequent complications and worsening outcomes. Our finding agrees with Zhang et al27 who demonstrated the detrimental effect of psychological stress on the treatment outcomes of chronic diseases among the Chinese population. It is also consistent with previous reports that psychological stress harms the disease progression,28 management adherence,29 the QoL,30 and treatment outcomes14 of patients with chronic diseases. Interestingly, a review study showed that the comorbidity of depression with other chronic diseases consistently worsens health compared with depression alone, with any of the chronic diseases alone, and with any combination of chronic diseases without depression.31 However, there was a weak, albeit significantly positive, relationship between the severity of psychological stress and treatment outcomes of chronic diseases among the patients. Simply put, this means that as psychological stress increases, the treatment outcomes become adversely affected. Notwithstanding, this weak relationship suggests that additional factors other than the severity of psychological stress could impact the treatment outcomes of chronic diseases in the Rwandan population.

    Findings on the relationship between psychological stress and chronic diseases have been inconsistent. Some reported that chronic stress positively correlates with chronic diseases,30–35 including ischaemic heart disease,36 diabetes,37 obesity,38,39 and other metabolic syndromes.40 Suffering from a chronic disease is a stressful factor in itself that influences individual psychological well-being.41,42 Where this interconnection exists, psychotherapeutic interventions as an essential part of chronic disease treatment have been suggested since they are effective in reducing symptoms of psychological distress that may affect the progression of and mortality from chronic diseases.43–45 On the contrary, other researchers reported that there is no correlation between various forms of psychological stress and the development or progression of some chronic diseases.46–48 In this study, we noted that psychological stress is significantly associated with heart failure, hypertension, diabetes, and malignancies, as patients with these diseases reported a higher incidence of psychological stress. Interestingly, kidney failure did not emerge as a significant predictor of stress in our regression model. However, we could not stratify patients by treatment duration or dialysis status, variables that may influence psychological stress in this population. The lack of these data may partly explain the absence of association in our findings.

    Physiologically, disturbing stimuli are sensed and responded to by the cortical centres by activating pathways that stimulate peripheral networks through the limbic system, including the sympathetic-adrenal-medullary axis and the renin-angiotensin system, followed later by the hypothalamic-pituitary-adrenal (HPA) axis.49 Most body tissues and organs express glucocorticoid receptors and respond to the glucocorticoids induced by stress, which regulate stress-associated processes like modulation of cardiovascular and immune functions and dampening of the stress response by inhibition of the HPA axis when adaptation is attained.50 Chronic stress arises when the stressor is overwhelmed and cannot be resolved, and glucocorticoid-dependent negative feedback that controls the stress response does not work due to glucocorticoid receptor resistance, leading to elevated levels of molecular stress mediators, a compromised immune system, and long-term damage to multiple tissues and organs.51 Psychological stress increases the levels of circulating cytokines and various biomarkers of inflammation,49 as it is perceived by the brain as “danger” and elicits neuroimmune circuits to prevent or repair the damage and restore homeostasis.52 Thus, psychological stress promotes inflammation, oxidative and nitrosative stress, and decreases immunosurveillance, in addition to its potential to cause dysfunctional activation of the autonomic nervous system and the HPA axis.53,54 Furthermore, stress induces adrenaline release, which downregulates chemokine CXCL12 in the mesenchymal stem cells, thereby causing cell division and leukocyte mobilisation into the bloodstream.55 These have adverse effects on the progression and recovery from chronic diseases like hypertension, atherosclerosis, diabetes, heart failure, malignancies, and kidney failure, among others.50

    Conclusions

    In conclusion, this study shows a high prevalence of psychological stress among patients with chronic diseases in Rwanda. It also shows that psychological stress is apparent among patients with hypertension, heart failure, malignancies, and diabetes, but not kidney failure. This study has some limitations. First, we did not collect detailed sociodemographic and clinical variables such as income, disease severity, or treatment duration, which limited our ability to perform multivariate regression analyses controlling for these factors. Future research should include such variables to provide a more robust assessment of predictors of psychological stress among patients with chronic diseases. Second, we did not collect treatment-specific data (eg, dialysis status, duration of illness), which limited our ability to perform subgroup analyses in the kidney failure population. Third, the patients were only those referred to CHUK and CHUB hospitals, which may not fully represent the broader population of individuals with chronic diseases in Rwanda. Fourth, the duration of the study is short, thereby necessitating a longitudinal study in the future. Despite these limitations, the study has a strength in enriching our understanding of the relationship between psychological stress and chronic diseases in Rwanda. Thus, a country-wide longitudinal study assessing the prevalence and impact of psychological stress among Rwandan patients with chronic diseases within Rwanda’s broader healthcare system, including private hospitals, is worth conducting in the future. Moreover, there is a need to develop a validated and Rwanda-compliant stress assessment tool to assess the progression of psychological stress among chronic disease patients by controlling for the prevalent genocide-induced psychological disorders. Based on the study’s findings, policymakers and healthcare providers are advised to adopt a multifaceted approach to healthcare delivery that addresses physical, psychological, socioeconomic, and educational aspects to reduce the high levels of psychological stress among patients with chronic diseases in Rwanda. Some of these should include integrating mental health services into routine chronic disease management protocols, developing tailored patient education programs that focus on stress management techniques, providing training programs for healthcare providers to improve communication skills, and empowering patients to actively participate in their treatment plan, among others. If adopted, an interventional trial that will subsequently assess the impact of the multifaceted healthcare delivery approach on the psychological stress among chronic disease patients will be useful in the future.

    Data Sharing Statement

    The corresponding author would provide information about the raw data for this study upon a reasonable request.

    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, or interpretation. They also participated in the drafting, revising, or critically reviewing the article; gave final approval of the version to be published; agreed on the journal to which the article had been submitted; and agreed to be accountable for all aspects of the work.

    Funding

    The authors declare that no financial support was received for the Research, Authorship, or Publication of this Article.

    Disclosure

    The authors report no conflicts of interest in this work.

    References

    1. Monroe SM, Slavich GM. Psychological stressors: overview. Stress. 2016;1:109–115.

    2. Moussavi S, Chatterji S, Verdes E, et al. Depression, chronic diseases, and decrements in health: results from the world health surveys. Lancet. 2007;370(9590):851–858. doi:10.1016/S0140-6736(07)61415-9

    3. Walker ER, McGee RE, Druss BG. Mortality in mental disorders and global disease burden implications: a systematic review and meta-analysis. JAMA Psychiatry. 2015;72(4):334–341. doi:10.1001/jamapsychiatry.2014.2502

    4. Rayner BL, Jones ESW, Davidson B, et al. Advances in chronic kidney disease in Africa. Appl Sci. 2023;13(8):1–17. doi:10.3390/app13084924

    5. Denis F, Mahalli R, Delpierre A, et al. Psychobiological factors in global health and public health. Int J Environ Res Public Health. 2022;19(11):6728. doi:10.3390/ijerph19116728

    6. Fava GA, Sonino N. The biopsychosocial model thirty years later. Psychother Psychosom. 2008;77(1):1–2. doi:10.1159/000110052

    7. Borrell-Carrió F, Suchman AL, Epstein RM. The biopsychosocial model 25 years later: principles, practice, and scientific inquiry. Ann Fam Med. 2004;2(6):576–582. doi:10.1370/afm.245

    8. Williams N, Wilkinson C, Stott N, Menkes DB. Functional illness in primary care: dysfunction versus disease. BMC Fam Pract. 2008;9(1):30. doi:10.1186/1471-2296-9-30

    9. Broerman R. Diathesis-Stress Model. In: Zeigler-Hill V, Shackelford TK, editors. Encyclopedia of Personality and Individual Differences. Cham: Springer; 2020. doi:10.1007/978-3-319-24612-3_891.

    10. World Health Organisation (WHO). Non-Communicable Diseases – rwanda. Available from: https://ncdportal.org/CountryProfile/GHE110/RWA. Accessed 17, July, 2025.

    11. Kayiteshonga Y, Sezibera V, Mugabo L, et al. Prevalence of mental disorders, associated co-morbidities, health care knowledge and service utilization in Rwanda – towards a blueprint for promoting mental health care services in low- and middle-income countries? BMC Public Health. 2022;22(1):1858. doi:10.1186/s12889-022-14165-x

    12. Stephanie E. Slovin’s formula sampling techniques. Silencing. 2020;2020:1–3.

    13. Russ TC, Stamatakis E, Hamer M, et al. Association between psychological distress and mortality: individual participant pooled analysis of 10 prospective cohort studies. BMJ. 2012;345(jul31 4):e4933. doi:10.1136/bmj.e4933

    14. Tareke M, Bayeh AB, Birhanu M, et al. Psychological distress among people living with chronic medical illness and the general population, Northwest Ethiopia: a comparative cross-sectional study. PLoS One. 2022;17(12):1–13. doi:10.1371/journal.pone.0278235

    15. Ganu VJ, Boima V, Adjei DN, et al. Depression and quality of life in patients on long term hemodialysis at a national hospital in Ghana: a cross-sectional study. Ghana Med J. 2018;52(1):22–28. doi:10.4314/gmj.v52i1.5

    16. de-Graft Aikins A, Sanuade O, Baatiema L, et al. How chronic conditions are understood, experienced and managed within African communities in Europe, North America and Australia: a synthesis of qualitative studies. PLoS One. 2023;18(2):1–32. doi:10.1371/journal.pone.0277325

    17. Nshimyiryo A, Barnhart DA, Cubaka VK, et al. Barriers and coping mechanisms to accessing healthcare during the COVID-19 lockdown: a cross-sectional survey among patients with chronic diseases in rural Rwanda. BMC Public Health. 2021;21(1):1–12. doi:10.1186/s12889-021-10783-z

    18. Melaku T, Assefa D, Bayisa B, et al. Research and intervention priorities for mental health of people living with chronic disease(s) in the midst of the COVID-19 pandemic in low-resource settings: a commentary. Ann Med Surg. 2020;57:268–269. doi:10.1016/j.amsu.2020.07.051

    19. Swathi M, Manjusha S, Isatrin JV, et al. Prevalence and correlates of stress, anxiety, and depression in patients with chronic diseases: a cross-sectional study. Middle East Curr Psychiat. 2023;30(1):66. doi:10.1186/s43045-023-00340-2

    20. Gerontoukou EI, Michaelidoy S, Rekleiti M, et al. Investigation of anxiety and depression in patients with chronic diseases. Health Psychol Res. 2015;3(2):2123. doi:10.4081/hpr.2015.2123

    21. Wong WS, Chen PP, Yap J, et al. Chronic pain and psychiatric morbidity: a comparison between patients attending specialist orthopaedics clinic and multidisciplinary pain clinic. Pain Med. 2011;12(2):246–259. doi:10.1111/j.1526-4637.2010.01044.x

    22. Liu X, Cao H, Zhu H, et al. Association of chronic diseases with depression, anxiety and stress in Chinese general population: the CHCN-BTH cohort study. J Affect Disord. 2021;1(282):1278–1287. doi:10.1016/j.jad.2021.01.040

    23. Ayana TM, Roba KT, Mabalhin MO. Prevalence of psychological distress and associated factors among adult tuberculosis patients attending public health institutions in Dire Dawa and Harar cities, Eastern Ethiopia. BMC Public Health. 2019;19(1):1–9. doi:10.1186/s12889-019-7684-2

    24. Heim L, Schaal S. Rates and predictors of mental stress in Rwanda: investigating the impact of gender, persecution, readiness to reconcile and religiosity via a structural equation model. Int J Ment Health Syst. 2014;8(1):1–9. doi:10.1186/1752-4458-8-37

    25. Scott KM, Bruffaerts R, Tsang A, et al. Depression–anxiety relationships with chronic physical conditions: results from the world mental health surveys. J Affect Disord. 2007;103(1–3):113–120. doi:10.1016/j.jad.2007.01.015

    26. Kohlmann S, Gierk B, Hilbert A, et al. The overlap of somatic, anxious and depressive syndromes: a population-based analysis. J Psychosom Res. 2016;1(90):51–56. doi:10.1016/j.jpsychores.2016.09.004

    27. Zhang C, Xiao S, Lin H, et al. The association between sleep quality and psychological distress among older Chinese adults: a moderated mediation model. BMC Geriatr. 2022;22(1):1–10. doi:10.1186/s12877-021-02658-0

    28. Ballesio A, Zagaria A, Musetti A, et al. Longitudinal associations between stress and sleep disturbances during COVID-19. Stress Heal. 2022;38(5):919–926. doi:10.1002/smi.3144

    29. Shafique F, Qasim MF, Kamal A, et al. The quantitative study on psychological distress of patients regarding hospital management. Pakistan J Med Heal Sci. 2023;17(3):37–39. doi:10.53350/pjmhs202317337

    30. Stathopoulou A, Fragkiadakis GF. Assessment of psychological distress and quality of life of family caregivers caring for patients with chronic diseases at home. AIMS Public Heal. 2023;10(2):456–468. doi:10.3934/publichealth.2023032

    31. Clarke DM, Currie KC. Depression, anxiety and their relationship with chronic diseases: a review of the epidemiology, risk and treatment evidence. Med J. 2009;190:S54–S60.

    32. McFarlane AC. The long-term costs of traumatic stress: intertwined physical and psychological consequences. World Psychiatry. 2010;9(1):3–10. doi:10.1002/j.2051-5545.2010.tb00254.x

    33. Renzaho AMN, Houng B, Oldroyd J, et al. Stressful life events and the onset of chronic diseases among Australian adults: findings from a longitudinal survey. Eur J Public Health. 2013;24(1):57–62. doi:10.1093/eurpub/ckt007

    34. Afari N, Ahumada S, Wright LJ, et al. Psychological trauma and functional somatic syndromes: a systematic review and meta-analysis. Psychosom Med. 2014;76(1):2–11. doi:10.1097/PSY.0000000000000010

    35. Marazziti D, Tomaiuolo F, Dell’Osso L, et al. Neuropsychological testing in interventional cardiology staff after long-term exposure to ionizing radiation. J Int Neuropsychol Soc. 2015;21(9):670. doi:10.1017/S135561771500082X

    36. Engstrom G, Khan FA, Zia E, et al. Marital dissolution is followed by an increased incidence of stroke. Cerebrovasc Dis. 2004;18(4):318–324. doi:10.1159/000080770

    37. Cosgrove M. Do stressful life events cause type 1 diabetes? Occup Med. 2004;54(4):250–254. doi:10.1093/occmed/kqh047

    38. Barry D, Petry N. Gender differences in associations between stressful life events and body mass index. Prev Med. 2008;47(5):498–503. doi:10.1016/j.ypmed.2008.08.006

    39. Pyykkonen AJ, Ra¨ikko¨Nen K, Tuomi T, et al. Stressful life events and the metabolic syndrome: the prevalence, prediction and prevention of diabetes (PPP)-Botnia study. Diabetes Care. 2010;33(2):378–384. doi:10.2337/dc09-1027

    40. Raikkonen K, Matthews KA, Kuller LH. Depressive symptoms and stressful life events predict metabolic syndrome among middle-aged women: a comparison of world health organization, adult treatment panel III, and international diabetes foundation definitions [corrected] [published erratum appears in]. Diabetes Care. 2007;30(4):872–877. doi:10.2337/dc06-1857

    41. Alonzo AA. The experience of chronic illness and post-traumatic stress disorder: the consequences of cumulative adversity. Soc Sci Med. 2000;50(10):1475–1484. doi:10.1016/S0277-9536(99)00399-8

    42. Chaturvedi S, Clancy M, Schaefer N, et al. Depression and post-traumatic stress disorder in individuals with hereditary hemorrhagic telangiectasia: a cross-sectional survey. Thrombosis Res. 2017;153:14–18. doi:10.1016/j.thromres.2017.03.003

    43. Tanzilli A, Lingiardi V, Hilsenroth M. Patient SWAP-200 personality dimensions and FFM traits: do they predict therapist responses? Pers Dis. 2018;9:250–262.

    44. Perry JC, Banon E, Bond M. Change in defense mechanisms and depression in a pilot study of antidepressive medications plus 20 sessions of psychotherapy for recurrent major depression. J Nerv Ment Dis. 2020;208(4):261–268. doi:10.1097/NMD.0000000000001112

    45. Yonatan-Leus R, Strauss AY, Cooper-Kazaz R. Psychodynamic psychotherapy is associated with sustained reduction in health care utilization and cost. Clin Psychol Psychother. 2021;28(3):642–655. doi:10.1002/cpp.2527

    46. Strickland OL, Giger JN, Nelson MA, et al. The relationships among stress, coping, social support, and weight class in premenopausal African American women at risk for coronary heart disease. J Cardiovasc Nurs. 2007;22(4):272–278. doi:10.1097/01.JCN.0000278964.05748.d8

    47. Kriegbaum M, Christensen U, Lund R, et al. Job loss and broken partnerships: do the number of stressful life events influence the risk of ischemic heart disease in men? Ann Epidemiol. 2008;18(10):743–745. doi:10.1016/j.annepidem.2008.04.010

    48. Fallon P. The role of intrusive and other recent life events on symptomatology in relapses of schizophrenia: a community nursing investigation. J Psychiatr Ment Health Nurs. 2009;16(8):685–693. doi:10.1111/j.1365-2850.2009.01451.x

    49. Black PH. Stress and the inflammatory response: a review of neurogenic inflammation. Brain Behav Immun. 2002;16(6):622–653. doi:10.1016/S0889-1591(02)00021-1

    50. Mariotti A. The effects of chronic stress on health: new insights into the molecular mechanisms of brain–body communication. Future Sci OA. 2015;1(3):FSO23. doi:10.4155/fso.15.21

    51. Silverman MN, Sternberg EM. Glucocorticoid regulation of inflammation and its functional correlates: from HPA axis to glucocorticoid receptor dysfunction. Ann NY Acad Sci. 2012;1261(1):55–63. doi:10.1111/j.1749-6632.2012.06633.x

    52. Maier SF, Watkins LR. Cytokines for psychologists: implications of bidirectional immune-to-brain communication for understanding behavior, mood, and cognition. Psychol Rev. 1998;105(1):83–107. doi:10.1037/0033-295X.105.1.83

    53. Piccinni A, Origlia N, Veltri A, et al. Plasma b-amyloid peptides levels: a pilot study in bipolar depressed patients. J Affect Disord. 2012;138(1–2):160–164. doi:10.1016/j.jad.2011.12.042

    54. Bartolato B, Hyphantis TN, Valpione S, et al. Depression in cancer: the many biobehavioural pathways driving tumour progression. Cancer Treat Rev. 2017;52:58–70. doi:10.1016/j.ctrv.2016.11.004

    55. Heidt T, Sager HB, Courties G, et al. Chronic variable stress activates hematopoietic stem cells. Nat Med. 2014;20(7):754–758. doi:10.1038/nm.3589

    Continue Reading

  • Safe, healthy, and informed: Raising awareness on World Sexual Health Day

    Safe, healthy, and informed: Raising awareness on World Sexual Health Day

    Every year on September 4th, the world observes World Sexual Health Day – a moment to highlight sexual health as a vital part of overall health and well-being.

    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.  

    Continue Reading

  • Darfur Crisis Shows Why Peace and Multisectoral Action Are Essential – Africa CDC

    Darfur Crisis Shows Why Peace and Multisectoral Action Are Essential – Africa CDC

    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.

    Continue Reading

  • New nanostructure makes CRISPR edits safer and three times faster

    New nanostructure makes CRISPR edits safer and three times faster

    Northwestern University researchers have created DNA-coated nanoparticles that deliver CRISPR into cells three times more effectively while reducing toxicity. The advance could overcome one of the biggest barriers to gene-editing therapies.

    3D illustration of a DNA double helix with a missing segment being held by tweezers, symbolising genetic engineering and CRISPR gene editing.


    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.

    “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.”

    Illustration of a DNA double helix with glowing blue and pink strands, combined with mechanical gears symbolising genetic engineering and CRISPR gene-editing technology, on a dark blue background.Illustration of a DNA double helix with glowing blue and pink strands, combined with mechanical gears symbolising genetic engineering and CRISPR gene-editing technology, on a dark blue background.

    CRISPR is a powerful tool for editing DNA, allowing researchers to switch genes on or off, fix harmful mutations and explore how genes affect health and disease. It is seen as one of the most promising technologies in modern medicine. Image credit: Shutterstock/Butusova Elena

    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.

    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.

    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.”

    Related topics
    Analysis, Cell Cultures, CRISPR, cytotoxicity, DNA, Drug Delivery, Enzymes, Gene Therapy, Genetic Analysis, Genome Editing, Genomics, Nanomedicine, Nanoparticles

    Continue Reading

  • Antimicrobial Resistance: Pakistan’s Hidden Health Crisis

    Antimicrobial Resistance: Pakistan’s Hidden Health Crisis

    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.


    Continue Reading

  • Neurologist’s responds to 35-year-old man wanting him to ‘prescribe aspirin to prevent stroke’ after father’s paralysis | Health

    Neurologist’s responds to 35-year-old man wanting him to ‘prescribe aspirin to prevent stroke’ after father’s paralysis | Health

    Dr Sudhir Kumar, a neurologist, took to X on Jun 10, 2023, to share his prescription for a patient ‘who wanted advice regarding starting an aspirin pill,as his father had suffered from a stroke (recently) at age 60’. In the accompanying tweet, Dr Kumar shared details of the man’s case and what he actually prescribed him instead of aspirin. Also read | Neurosurgeon explains how to recognise a brain stroke: Most common warning signs, symptoms and what to do immediately

    Aspirin works by inhibiting the production of certain natural substances that cause fever, swelling, and blood clots, which can make it useful for stroke prevention. (Pixabay)

    ‘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.

    Continue Reading

  • ABO blood group and the risk and prognosis of diffuse large B-cell lym

    ABO blood group and the risk and prognosis of diffuse large B-cell lym

    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.

    References

    1. Swerdlow SH, Campo E, Pileri SA, et al. The 2016 revision of the world health organization classification of lymphoid neoplasms. Blood. 2016;127(20):2375–2390. doi:10.1182/blood-2016-01-643569

    2. Armitage JO, Gascoyne RD, Lunning MA, Cavalli F. Non-Hodgkin lymphoma. Lancet. 2017;390(10091):298–310. doi:10.1016/S0140-6736(16)32407-2

    3. Sehn LH, Salles G. Diffuse large b-cell lymphoma. N Engl J Med. 2021;384(9):842–858. doi:10.1056/NEJMra2027612

    4. Liu Y, Barta SK. Diffuse large B-cell lymphoma: 2019 update on diagnosis, risk stratification, and treatment. Am J Hematol. 2019;94(5):604–616. doi:10.1002/ajh.25460

    5. Cerhan JR, Kricker A, Paltiel O, et al. Medical history, lifestyle, family history, and occupational risk factors for diffuse large B-cell lymphoma: the interlymph non-hodgkin lymphoma subtypes project. J Natl Cancer Inst Monogr. 2014;2014(48):15–25. doi:10.1093/jncimonographs/lgu010

    6. De Roos AJ, Schinasi LH, Miligi L, et al. Occupational insecticide exposure and risk of non-hodgkin lymphoma: a pooled case-control study from the interlymph consortium. Int J Cancer. 2021;149(10):1768–1786. doi:10.1002/ijc.33740

    7. Mohandas N, Narla A. Blood group antigens in health and disease. Curr Opin Hematol. 2005;12(2):135–140. doi:10.1097/01.moh.0000153000.09585.79

    8. Storry JR, Olsson ML. The ABO blood group system revisited: a review and update. Immunohematology. 2009;25(2):48–59. doi:10.21307/immunohematology-2019-231

    9. Qin L, Gao D, Wang Q, et al. ABO blood group and the risk and prognosis of lymphoma. J Inflamm Res. 2023;16:769–778. doi:10.2147/JIR.S401818

    10. Yamamoto F. Molecular genetics of ABO. Vox Sang. 2000;78(2):91–103. doi:10.1111/j.1423-0410.2000.tb00045.x

    11. Yamamoto F, Cid E, Yamamoto M, Blancher A. ABO research in the modern era of genomics. Transfus Med Rev. 2012;26(2):103–118. doi:10.1016/j.tmrv.2011.08.002

    12. Lowe JB. The blood group-specific human glycosyltransferases. Baillieres Clin Haematol. 1993;6(2):465–492. doi:10.1016/s0950-3536(05)80155-6

    13. Poole EM, Gates MA, High BA, et al. ABO blood group and risk of epithelial ovarian cancer within the Ovarian Cancer Association Consortium. Cancer Causes Control. 2012;23(11):1805–1810. doi:10.1007/s10552-012-0059-y

    14. Sheng L, Sun X, Zhang L, Su D. ABO blood group and nasopharyngeal carcinoma risk in a population of Southeast China. Int J Cancer. 2013;133(4):893–897. doi:10.1002/ijc.28087

    15. Li X, Xu H, Ding Z, Jin Q, Gao P. Association between ABO blood group and HCV-related hepatocellular carcinoma risk in China. Medicine (Baltimore). 2016;95(49):e5587. doi:10.1097/MD.0000000000005587

    16. Li X, Xu H, Gao P. ABO blood group and diabetes mellitus influence the risk for pancreatic cancer in a population from China. Med Sci Monit. 2018;24:9392–9398. doi:10.12659/MSM.913769

    17. Huang JY, Wang R, Gao YT, Yuan JM. ABO blood type and the risk of cancer – Findings from the Shanghai Cohort Study. PLoS One. 2017;12(9):e0184295. doi:10.1371/journal.pone.0184295

    18. Osada Y, Ito C, Nishiyama-Fujita Y, et al. Prognostic impact of ABO blood group on survival in patients with malignant lymphoma. Clin Lymphoma Myeloma Leuk. 2020;20(2):122–129. doi:10.1016/j.clml.2019.09.607

    19. Ulu BU, Başcı S, Bakırtaş M, et al. Could blood groups have prognostic significance on survival in patients with diffuse large B cell lymphoma. Leuk Res. 2022;115:106810. doi:10.1016/j.leukres.2022.106810

    20. Morton LM, Wang SS, Devesa SS, Hartge P, Weisenburger DD, Linet MS. Lymphoma incidence patterns by WHO subtype in the United States, 1992-2001. Blood. 2006;107(1):265–276. doi:10.1182/blood-2005-06-2508

    21. Pierdominici M, Maselli A, Locatelli SL, et al. Estrogen receptor β ligation inhibits Hodgkin lymphoma growth by inducing autophagy. Oncotarget. 2017;8(5):8522–8535. doi:10.18632/oncotarget.14338

    22. Lee JS, Bracci PM, Holly EA. Non-Hodgkin lymphoma in women: reproductive factors and exogenous hormone use. Am J Epidemiol. 2008;168(3):278–288. doi:10.1093/aje/kwn119

    23. Yakimchuk K, Hasni MS, Guan J, Chao MP, Sander B, Okret S. Inhibition of lymphoma vascularization and dissemination by estrogen receptor β agonists. Blood. 2014;123(13):2054–2061. doi:10.1182/blood-2013-07-517292

    24. Székely E, Hagberg O, Arnljots K, Jerkeman M. Improvement in survival of diffuse large B-cell lymphoma in relation to age, gender, international prognostic index and extranodal presentation: a population based swedish lymphoma registry study. Leuk Lymphoma. 2014;55(8):1838–1843. doi:10.3109/10428194.2013.853297

    25. Hakomori S. Antigen structure and genetic basis of histo-blood groups A, B and O: their changes associated with human cancer. Biochim Biophys Acta. 1999;1473(1):247–266. doi:10.1016/s0304-4165(99)00183-x

    26. Le Pendu J, Marionneau S, Cailleau-Thomas A, Rocher J, Le Moullac-Vaidye B, Clément M. ABH and Lewis histo-blood group antigens in cancer. APMIS. 2001;109(1):9–31. doi:10.1111/j.1600-0463.2001.tb00011.x

    27. Dabelsteen E, Gao S. ABO blood-group antigens in oral cancer. J Dent Res. 2005;84(1):21–28. doi:10.1177/154405910508400103

    28. Stellner K, Hakomori S, Warner GS. Enzymic conversion of “H1-glycolipid” to A or B-glycolipid and deficiency of these enzyme activities in adenocarcinoma. Biochem Biophys Res Commun. 1973;55(2):439–445. doi:10.1016/0006-291x(73)91106-6

    29. Orlow I, Lacombe L, Pellicer I, et al. Genotypic and phenotypic characterization of the histoblood group ABO(H) in primary bladder tumors. Int J Cancer. 1998;75(6):819–824. doi:10.1002/(sici)1097-0215(19980316)75:6<819::aid-ijc1>3.0.co;2-y

    30. Iwamoto S, Withers DA, Handa K, Hakomori S. Deletion of A-antigen in a human cancer cell line is associated with reduced promoter activity of CBF/NF-Y binding region, and possibly with enhanced DNA methylation of A transferase promoter. Glycoconj J. 1999;16(10):659–666. doi:10.1023/a:1007085202379

    31. Kominato Y, Hata Y, Takizawa H, Tsuchiya T, Tsukada J, Yamamoto F. Expression of human histo-blood group ABO genes is dependent upon DNA methylation of the promoter region. J Biol Chem. 1999;274(52):37240–37250. doi:10.1074/jbc.274.52.37240

    32. Gao S, Bennett EP, Reibel J, et al. Histo-blood group ABO antigen in oral potentially malignant lesions and squamous cell carcinoma–genotypic and phenotypic characterization. APMIS. 2004;112(1):11–20. doi:10.1111/j.1600-0463.2004.apm1120103.x

    33. Scott GL, Rasbridge MR. Loss of blood group antigenicity in a patient with Hodgkin’s disease. Vox Sang. 1972;23(5):458–460. doi:10.1111/j.1423-0410.1972.tb03836.x

    34. Bianco T, Farmer BJ, Sage RE, Dobrovic A. Loss of red cell A, B, and H antigens is frequent in myeloid malignancies. Blood. 2001;97(11):3633–3639. doi:10.1182/blood.v97.11.3633

    35. Greenwell P. Blood group antigens: molecules seeking a function. Glycoconj J. 1997;14(2):159–173. doi:10.1023/a:1018581503164

    36. Pinho SS, Reis CA. Glycosylation in cancer: mechanisms and clinical implications. Nat Rev Cancer. 2015;15(9):540–555. doi:10.1038/nrc3982

    37. Stowell SR, Ju T, Cummings RD. Protein glycosylation in cancer. Annu Rev Pathol. 2015;10:473–510. doi:10.1146/annurev-pathol-012414-040438

    38. Xu Y, Chang R, Xu F, et al. N-glycosylation at asn 402 stabilizes n-cadherin and promotes cell-cell adhesion of glioma cells. J Cell Biochem. 2017;118(6):1423–1431. doi:10.1002/jcb.25801

    39. Läubli H, Borsig L. Altered cell adhesion and glycosylation promote cancer immune suppression and metastasis. Front Immunol. 2019;10:2120. doi:10.3389/fimmu.2019.02120

    40. Reily C, Stewart TJ, Renfrow MB, Novak J. Glycosylation in health and disease. Nat Rev Nephrol. 2019;15(6):346–366. doi:10.1038/s41581-019-0129-4

    41. Melzer D, Perry JR, Hernandez D, et al. A genome-wide association study identifies protein quantitative trait loci (pQTLs). PLoS Genet. 2008;4(5):e1000072. doi:10.1371/journal.pgen.1000072

    42. Kiechl S, Paré G, Barbalic M, et al. Association of variation at the ABO locus with circulating levels of soluble intercellular adhesion molecule-1, soluble P-selectin, and soluble E-selectin: a meta-analysis. Circ Cardiovasc Genet. 2011;4(6):681–686. doi:10.1161/CIRCGENETICS.111.960682

    43. Barbalic M, Dupuis J, Dehghan A, et al. Large-scale genomic studies reveal central role of ABO in sP-selectin and sICAM-1 levels. Hum Mol Genet. 2010;19(9):1863–1872. doi:10.1093/hmg/ddq061

    44. Fernandes JV, Cobucci RN, Jatobá CA, et al. The role of the mediators of inflammation in cancer development. Pathol Oncol Res. 2015;21(3):527–534. doi:10.1007/s12253-015-9913-z

    45. Singh R, Mishra MK, Aggarwal H. Inflammation, Immunity, and Cancer. Mediators Inflamm. 2017;2017:6027305. doi:10.1155/2017/6027305

    46. Greten FR, Grivennikov SI. Inflammation and cancer: triggers, mechanisms, and consequences. Immunity. 2019;51(1):27–41. doi:10.1016/j.immuni.2019.06.025

    47. Grivennikov SI, Greten FR, Karin M. Immunity, inflammation, and cancer. Cell. 2010;140(6):883–899. doi:10.1016/j.cell.2010.01.025

    48. Enzler T, Gillessen S, Manis JP, et al. Deficiencies of GM-CSF and interferon gamma link inflammation and cancer. J Exp Med. 2003;197(9):1213–1219. doi:10.1084/jem.20021258

    49. Ibrahim-Kosta M, Bailly P, Silvy M, et al. ABO blood group, glycosyltransferase activity and risk of venous thromboembolism. Thromb Res. 2020;193:31–35. doi:10.1016/j.thromres.2020.05.051

    50. Ward SE, O’Sullivan JM, O’Donnell JS. The relationship between ABO blood group, von Willebrand factor, and primary hemostasis. Blood. 2020;136(25):2864–2874. doi:10.1182/blood.2020005843

    51. Starke RD, Ferraro F, Paschalaki KE, et al. Endothelial von Willebrand factor regulates angiogenesis. Blood. 2011;117(3):1071–1080. doi:10.1182/blood-2010-01-264507

    52. Franchini M, Frattini F, Crestani S, Bonfanti C, Lippi G. von Willebrand factor and cancer: a renewed interest. Thromb Res. 2013;131(4):290–292. doi:10.1016/j.thromres.2013.01.015

    53. O’Sullivan JM, Preston R, Robson T, O’Donnell JS. Emerging roles for von willebrand factor in cancer cell biology. Semin Thromb Hemost. 2018;44(2):159–166. doi:10.1055/s-0037-1607352

    54. Ishihara J, Ishihara A, Starke RD, et al. The heparin binding domain of von Willebrand factosr binds to growth factors and promotes angiogenesis in wound healing. Blood. 2019;133(24):2559–2569. doi:10.1182/blood.2019000510

    Continue Reading