As a significant breakthrough in rare disease therapy, the U.S. Food and Drug Administration (FDA) has just approved Andembry (garadacimab‑gxii), the first-ever prophylactic treatment that aims for factor XIIa to prevent attacks of hereditary angioedema (HAE). This once-monthly injectable has provided patients 12 years and older with a new, convenient way to manage symptoms effectively—but its significance extends far beyond convenience, as it is a sea change in the way we treat this incapacitating illness.
Hereditary angioedema is an inherited, rare illness that results in sudden, aching swelling of the body's different regions, such as the face, limbs, or inner tissues like the airway or intestines. Blockages caused by it can result in life-threatening respiratory problems or severe abdominal pain. These occur because leakage from small blood vessels lets fluid seep into nearby tissues. HAE typically presents in childhood or adolescence, worsens after puberty, and strikes almost everyone diagnosed through age 20.
While the swelling may be painful and disfiguring, the most significant danger is airway involvement, which can be fatal. Conventional treatments are primarily concerned with treating these sudden attacks or maintaining regular infusions to prevent them. But until now, real long-term prevention was out of reach.
Andembry is a monoclonal antibody that directly blocks factor XIIa, a central protein in the cascade of processes that leads to HAE attacks. By blocking factor XIIa's action, Andembry stops the process before swelling occurs—making the first line of defense against unpredictable flare-ups.
Administered through a straightforward autoinjector that delivers the dose in 15 seconds or less, Andembry is designed to become an integral part of patients' lives. Users simply have to self-administer the injection on a monthly basis, making it a convenient option for teenagers as well as adults who are treating this condition.
The FDA's approval is based on powerful Phase III clinical trial data. During six months, 62% of Andembry patients were wholly attack-free—a remarkable benchmark for a disease characterized by constant flare-ups.
Like any drug, Andembry has potential side effects, although most were mild. The most frequent problems encountered involved nasal and upper throat inflammation and abdominal pain, each of which were observed in approximately 7% of patients. Most importantly, no severe adverse events or drop-outs from treatment were seen—testifying to the drug's overall safety and tolerability.
Such a positive profile represents an important victory for a long-term treatment—particularly one that will be repeatedly self-administered by families and patients.
Dr. Bill Mezzanotte, R&D Head at CSL (who created Andembry), refers to the drug as a "game-changer". He mentions it's the first monoclonal antibody to be created wholly by CSL and the only injectable treatment for factor XIIa. The fact that it's designed to give treatment in seconds speaks to a patient-centric focus—particularly necessary for a disease that is notoriously unpredictable and can hit at any time.
Apart from clinical efficacy, Andembry vows to greatly improve the daily lives of HAE patients. The benefits in everyday life are:
Preventing attacks before they occur can cut down school or workplace absences, decrease hospital visits, and reduce emergency care expenses—all substantial quality-of-life differences.
Andembry's approval represents a tipping point in the direction of personalized, preventive treatment for HAE. It changes the emphasis from responding to swelling attacks to actively preventing them, a shift with broad implications for patients and the health care system as a whole.
Providers now have a powerful, easy-to-use option to present to patients and families. Investigators are looking at whether Andembry can supplant or minimize the use of current prophylactics, like C1 inhibitor treatments or bradykinin receptor antagonists.
Economically, although monoclonal antibody therapies are generally very expensive, Andembry's ability to decrease emergency room visits and hospital stays could potentially yield dramatic cost savings for both patients and payers over time.
With Andembry's approval, individuals with hereditary angioedema can now receive a once-per-month injection that provides near-total attack prevention, outstanding safety, and improved quality of life. For the increasingly large population of diagnosed and undiagnosed patients, Andembry provides a new level of confidence and control in managing a condition long known to be capricious and highly restrictive.
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John Toshack, the Wales and Liverpool legend, has been diagnosed with dementia, his son Cameron has confirmed to the media.
After a glittering playing career with Liverpool, the now 77-year-old Toshack went on to manage several leading clubs across Europe, including Real Madrid, Real Sociedad, and Besiktas.
His son and ex-Leeds United assistant Cameron, now coaching in Thailand, told the Daily Mail that his father has "good days and bad days".
"It's a terrible disease," he added.
Cameron noted that while his father's memory of his glory days remains intact, his short-term memory is more affected. And his father often tends to forget matters they spoke about in short periods.
"It’s the short-term memory where we’re seeing it – I speak to him most days, and if we chat in the afternoon, he might not remember that we also spoke in the morning," the report said.
"But if I ask him about the Liverpool days, or Sociedad or Madrid, the detail is amazing; his memory was so clear".
Meanwhile, Football Association of Wales in a post on social media platform X shared: "Our thoughts are with former
@Cymru player and manager John Toshack and his family following his recent diagnosis".
Dementia is an umbrella term used to describe a significant decline in mental function that is serious enough to affect everyday life. It commonly impacts memory, thinking, and reasoning skills.
Dementia itself is not a single disease but a collection of symptoms caused by underlying conditions such as Alzheimer’s disease or vascular dementia.
Common signs include memory problems, confusion, difficulty finding words, changes in mood or behaviour, and trouble completing familiar tasks.
These symptoms usually worsen over time and are not considered a normal part of ageing. Although there is no cure, treatment options can help manage symptoms, and early diagnosis plays an important role in care planning.
Alzheimer's disease is one of the most common forms of dementia and mostly affects adults over the age of 65.
About 8.8 million Indians aged 60 and above are estimated to be living with Alzheimer's disease. Over seven million people in the US, 65 and older, live with the condition, and over 100,00 die from it annually.
Alzheimer's disease is believed to be caused by the development of toxic amyloid and beta proteins in the brain, which can accumulate in the brain and damage cells responsible for memory.
Amyloid protein molecules stick together in brain cells, forming clumps called plaques. At the same time, tau proteins twist together in fiber-like strands called tangles. The plaques and tangles block the brain's neurons from sending electrical and chemical signals back and forth.
Over time, this disruption causes permanent damage in the brain that leads to Alzheimer's disease and dementia, causing patients to lose their ability to speak, care for themselves, or even respond to the world around them.
While there is no clear cause of Alzheimer's disease, experts believe it can develop due to genetic mutations and lifestyle choices, such as physical inactivity, unhealthy diet, and social isolation.
Early symptoms of Alzheimer's disease include forgetting recent events or conversations. Over time, Alzheimer's disease leads to serious memory loss and affects a person's ability to do everyday tasks.
There is no cure for this progressive brain disorder, and in advanced stages, loss of brain function can cause dehydration, poor nutrition, or infection. These complications can result in death.
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Children under 5 in India remain at high risk of typhoid infections, hospitalization, and death due to growing antimicrobial resistance (AMR), according to an alarming study, which highlighted the urgent need to control drug resistance in the country.
Typhoid fever is a systemic illness caused by Salmonella enterica serovar Typhi (S. Typhi), and presents a significant health challenge in India.
The modelling study, published in The Lancet Regional Health – Southeast Asia, showed that typhoid fever caused an estimated 4.9 million cases and nearly 8,000 deaths in India in 2023.
However, more concerning was that a large proportion of infections were found resistant to fluoroquinolones — one of the main classes of antibiotics used to treat typhoid. They found that:
"Drug-resistant typhoid fever remains a serious public-health threat in India, with implications beyond national borders," said Dr Vijayalaxmi Mogasale, Joint PhD Candidate at the London School of Hygiene & Tropical Medicine and Nagasaki University.
"Tackling this problem does not lie solely in moving to newer antibiotics, but calls for timely preventive action, including responsible antibiotic use and the introduction of the typhoid vaccine into the national immunization program, prioritizing high-burden age groups and regions," she added.
Also read: Study Links Widespread Use of Antibiotics During COVID To Surge In AMR Cases
In Global Burden of Diseases (GBD) 2021, India contributed to 58 percent of global typhoid fever cases and 48 percent of global deaths.
The new study, including researchers from Christian Medical College in Vellore, estimated that more than two-thirds of typhoid cases in India are resistant to fluoroquinolones. This not only limits treatment options but also increases the risk of complications.
The major drivers of typhoid fever deaths were identified among those with no treatment and hospitalized cases with AMR-related complications. The highest burden of typhoid cases were reported from Delhi, Maharashtra, and Karnataka.
Further, the study found that drug-resistant typhoid infections accounted for at least 87 per cent of India's disease-related economic burden in 2023, the PTI reported.
The total economic burden due to typhoid fever was estimated at Rs 123 billion.
Children under the age of 10 incurred the highest economic burden, contributing to over half of the costs, researchers found.
In addition, they estimated that households bore 91 per cent of expenses, and 70,000 families faced "catastrophic" health expenditure.
A 2024 ICMR report also flagged that more Indians are developing antibiotic resistance against typhoid, pneumonia, and urinary infections. Over 95 percent of Salmonella typhi strains are now resistant to fluoroquinolones, making it difficult to treat infections caused by this bacterium.
Also read: Antimicrobial Resistance Explained: Why Is WHO Calling It A Serious Health Threat?
Typhoid fever is a water- and food-borne infectious disease. Major symptoms include
The World Health Organization (WHO) recommends TCV for children from six months of age and for adults up to 45–65 years, depending on the vaccine.
To achieve greater impact, the Lancet researchers suggested implementing:
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The US Centers for Disease Control and Prevention (CDC) has raised concerns about a highly mutated variant of COVID-19 -- BA.3.2 -- which has been reported in at least 23 countries, including 25 states in America.
The BA.3.2 variant was first identified in a respiratory sample in South Africa in November 2024.
The World Health Organization (WHO) has designated BA.3.2 as a Variant Under Monitoring (VUM). It does not boost immunity from previous infection or vaccination.
What makes the BA.3.2 variant special is the “70 to 75 substitutions and deletions in the gene sequence of its spike protein”, according to the CDC’s latest Morbidity and Mortality Weekly Report.
“BA.3.2 represents a new lineage of SARS-CoV-2, genetically distinct from the JN.1 lineages (including LP.8.1 and XFG) that have circulated in the US since January 2024,” said the CDC researchers.
“BA.3.2 mutations in the spike protein have the potential to reduce protection from a previous infection or vaccination,” they added.
BA.3.2 is a descendant of the Omicron BA.3 lineage. It is genetically distinct from the previously circulating JN.1 lineages (including LP.8.1 and XFG).
BA.3.2 comprises two major branches, BA.3.2.1 and BA.3.2.2. BA.3.2.2 also has substitutions like: K356T, A575S, R681H, and R1162P, the CDC report said.
The first BA.3.2 lineage sequence was detected in a respiratory sample collected on November 22, 2024, in South Africa from a boy aged 5 years.
It was then identified in 2025, in Mozambique (March), the Netherlands (April), and Germany (April). It began to increase in September 2025, with the highest number of detections reported during the week beginning December 7, 2025.
As of February 11, 2026, BA.3.2 had been detected in at least 23 countries.
Between November 2025 and January 2026, the weekly BA.3.2 detections increased and reached approximately 30 percent of sequences reported in three European countries (Denmark, Germany, and the Netherlands).
The strain was detected in the US on June 27, 2025, through the CDC’s Traveler-Based Genomic Surveillance program in a participant traveling to the US from the Netherlands.
The first US detection of BA.3.2 in a clinical specimen collected from a patient was reported on January 5, 2026. Since then, the CDC has detected the BA.3.2 variant from
The CDC stressed the need for “continued genomic surveillance to track SARS-CoV-2 evolution and determine its potential effect on public health”.
According to the WHO, BA.3.2 demonstrates antigenic drift and reduced neutralization in vitro from previously infected or vaccinated individuals.
However, the global health body noted that currently approved COVID-19 vaccines are expected to continue providing protection against severe disease.
Despite immune evasion, phenotypic data suggest BA.3.2 has reduced infectivity.
It shows resistance to some monoclonal antibodies (cilgavimab, bebtelovimab, sotrovimab) but increased sensitivity to tixagevimab-be, the WHO said.
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