Latest news with #asymptomatic
Yahoo
05-07-2025
- Health
- Yahoo
Could You Have 'Silent Celiac' And Not Know It?
You're likely somewhat familiar with celiac disease, a serious autoimmune disorder that causes certain people to experience small intestine damage when they consume gluten. Those afflicted often experience gastrointestinal symptoms like stomach pain, bloating, constipation, gas and diarrhea. But not everyone does. In fact, you can have 'silent celiac' and have no idea. Below, GI specialists explain what silent celiac is, how it's diagnosed and treated and what to look out for. ''Silent' celiac disease is when someone has celiac disease, a reaction to the gluten protein, but they do not manifest symptoms from the disease,' said Dr. Rabia De Latour, a gastroenterologist and assistant professor of medicine at NYU Grossman School of Medicine. 'They can have the physical manifestations of the disease like small bowel inflammation but without the GI symptoms like diarrhea and abdominal pain.' As such, the form of celiac often called 'silent' celiac can also be referred to as 'asymptomatic' celiac. 'This is a rare form of celiac, as usually patients develop GI symptoms from the malabsorption, which is secondary to the intestinal damage caused by the celiac disease,' said Dr. Kevin Cronley, a gastroenterologist with Gastro Health in Cincinnati. Although the idea of silent celiac presumes you have no symptoms of the disease, some people might simply not realize they're experiencing mild symptoms. 'For probably a portion of those patients who think they have no symptoms, they discover that they did have symptoms and feel much better once they go on a gluten-free diet,' said Dr. David Kastenberg, chief of the division of gastroenterology and hepatology at Jefferson Health in the Greater Philadelphia area. 'They weren't aware that they had symptoms because they thought things like headaches, joint aches, chronic sinus problems or muscle aches were just part of their normal everyday life rather than celiac.' Because this manifestation of celiac disease does not involve clear symptoms, many people go undiagnosed. 'Silent celiac disease is underdiagnosed, and physicians should have a low threshold to test for it if there are any laboratory abnormalities suggestive of celiac, family history of celiac disease, or other conditions which celiac can be associated with,' Cronley said. As he noted, further inspection of lab abnormalities are typically the way people with the disease wind up with a diagnosis. 'Someone might have silent GI symptoms but may have abnormal lab findings or nonspecific generalized symptoms like fatigue and headaches,' De Latour noted. 'Going to your doctor for regular checkups with appropriate blood work can pick up the lab work signs of celiac before your symptoms might. Someone might have blood work findings suggesting they are not absorbing certain nutrients well from their food due to the gut inflammation.' If a patient's bloodwork shows iron deficiency or elevated liver function, for instance, doctors may then check for celiac by doing a blood test for certain antibodies, like tissue transglutaminase antibody. They can also do an upper endoscopy to look at the GI tract and take a sample of tissue from the small intestine. 'Silent celiac might be 'unsilenced' if someone is getting an upper endoscopy for something separate like acid reflux and the findings suggest celiac, leading them to go on and do blood tests,' Kastenberg said. 'People also need to take notice when someone is at a higher risk for having celiac, like having a first-degree relative with celiac or concomitant medical problem like autoimmune thyroid disease.' He noted that conditions like type 1 diabetes, Down syndrome and certain skin rashes are also associated with increased risk of celiac disease. The good news is there's a clear and effective treatment for celiac disease, silent or otherwise. The bad news is it calls for a big lifestyle change. 'The treatment for celiac disease is a gluten-free diet,' Cronley said. 'Gluten is a protein that is found in wheat that the body will confuse with the lining of the patient's intestines, causing damage to the intestines. This intestinal injury can result in symptoms of malabsorption, vitamin deficiencies, and can increase the risk of cancer of the small intestine.' To remove this harmful protein from the equation and reduce the inflammation, patients must completely cut gluten out of their diets. 'For sicker patients, there are more intense therapies, but this is less common,' De Latour noted. Fortunately, there's now more awareness and understanding around gluten-free eating than in the past. 'Gluten-free diets are popular right now because in general, people feel better on a gluten-free diet by eating less processed foods,' Cronley said. 'If you think you may have celiac, seek an evaluation by a physician who can properly evaluate you for the disease.' Once you get the celiac diagnosis, it's important to make those dietary changes, even if you don't feel symptoms after eating gluten. 'Silent celiac is really celiac disease, so it's serious,' Kastenberg said. 'It's hard for people to accept that when they feel perfectly fine. If you feel terrible when you have gluten, you get that feedback that you shouldn't eat that thing. But if you aren't so sensitive and can eat gluten all the time without feeling it, you aren't getting that feedback that it's a problem for you.' But you need to recognize that silent celiac should be taken just as seriously. Ignoring it can lead to long-term issues. 'Even if you feel well, your small intestine is not well,' Kastenberg emphasized. 'It's not functioning properly, and there are lots of potential consequences like an increased risk for osteoporosis, nutritional deficiencies, malignancies and even reproductive and pregnancy-related issues like low birth weight or spontaneous abortion. If you have celiac, it's important to tell your family members to get screened as well. Catching it early makes a big difference.' If You're A Healthy Eater, Is It Possible You Get TOO Much Fiber? The Worst Foods To Eat Before Flying Why Are People Eating Oranges In The Shower On TikTok?
Medscape
09-06-2025
- Health
- Medscape
Study Reveals Malaria Parasite's Secrets
Malaria parasites can hide in people's bodies for years or even decades without causing symptoms by shutting down the genes that make them visible to the immune system, a new report found. This discovery explains how people can remain infected years after developing malaria and spread the disease through mosquitos that bite them, said Kirk W. Deitsch, PhD, professor with the Department of Microbiology and Immunology, Weill Medical College of Cornell University, New York City, and co-author of a study published in Nature Microbiology . 'What's probably happening in a place like Africa, where there's a lot of malaria transmission, is that people we thought didn't have malaria actually had these invisible parasites at really low levels in their system,' Deitsch told Medscape Medical News . The implications for elimination campaigns are significant. Currently, 'when we try to do a malaria elimination campaign, [we] treat the kids, the ones who are sick,' he said. The study suggests 'that we need to treat all asymptomatic people, the adults, because they're carrying these cryptic parasites that nobody knew about before.' Sticky Proteins and Spleen Avoidance The researchers sought to better understand how malaria persists in the body. 'There were these weird cases where a person who grew up in, let's say, Africa, had malaria several times, were no longer infected, and moved to the States. They lived in the States for a decade, maybe 12 or 13 years, and then they give blood for a transfusion, and the recipient of the transfusion gets really bad malaria,' Deitsch said. 'So clearly, those parasites have been hiding in this person for more than a decade, and nobody knew why. How are they hiding? Where are they?' Study authors focused on the var gene, which expresses an adhesive surface protein on the infected red blood cells in malaria. The protein is 'sticky,' allowing infected cells to attach to blood vessel walls and avoid being filtered out by the spleen, Deitsch said. But the parasite pays a price because the immune system can detect the sticky protein. Previous methods of analyzing the genetics of malaria looked at millions of parasites together. 'If you want to know which gene is being turned on in that population, you take all those parasites, you extract all the RNA from the population, and you look at which gene is turned on,' Deitsch explained. For the new study, researchers analyzed the malaria parasite at the single-cell level. 'We isolated single parasites and then looked at which gene is being expressed by just that individual parasite,' he said. 'We found there was always a group of parasites that had turned off the entire [ var ] gene family and were expressing no genes at all.' As a result, the red blood cells didn't produce the surface proteins, allowing them to be 'invisible' and evade the immune system. Like a Criminal The parasites don't turn invisible right away, Deitsch said. Instead, they constantly switch to different sticky proteins, like a criminal changing disguises, as the immune system swings into action. 'As soon as your antibody titer begins to rise, they just switch to a different adhesive protein.' 'The parasite only has so many copies of this adhesive protein that they can put out to the surface over their lifetime. So they run out of genes after about a year and a half or so.' Scientists used to think this meant the infection would be cleared. 'Everybody always assumed that once the parasite runs out of these genes, that the infection is over. You clear the infection, and then you're okay.' Deitsch used the metaphor of a criminal who has a closet full of 50-60 disguises. 'When you get to the last one, then you've run out, and the cops have figured out all your previous disguises. At the back of the closet, there's an invisibility cloak. They can put that on, and then the cops can't see you at all.' These invisible parasites exist at very low levels. 'Those parasites don't go to very high levels because your spleen is continuously filtering them,' Deitsch explained. 'But what they're able to do is maintain this low level of infection for a long time.' The only sign of continued infection may be a slightly enlarged spleen 'because the spleen is continuously clearing a lot of these invisible parasites by filtration,' Deitsch noted. Changes in Malaria Prevention Strategy? The findings suggest that anti-malaria efforts should treat entire populations with anti-malaria drugs, even healthy people, Deitsch said. And drugs could be developed to make the hidden parasites become visible to the immune system. However, neither strategy is simple, he said. What's next? 'We're going to continue working on the molecular mechanisms that mediate this process [and explore] how the parasites control their chromosomes and their genes to go into this silent, invisible state and then switch back out into a different state,' Deitsch said. Researchers are also studying basic questions about how parasites coordinate their disguise changes. 'There are literally trillions of parasites in the circulation of a sick individual, and they seem to coordinate switching their disguise,' Deitsch said. 'They all know to go to the same next disguise.' Outside Experts Weigh In Karine Le Roch, PhD, MS, director of the Center for Infectious Disease and Vector Research, University of California, Riverside, who was not involved with the paper, told Medscape Medical News that it's 'a rigorous, innovative, and impactful study that advances a long-standing question in malaria biology.' The report 'addresses a major paradox in malaria biology and offers a compelling explanation for asymptomatic chronic infections, which have long been poorly understood,' she said. Anna Bachmann, PhD, a research group leader at the Bernhard Nocht Institute for Tropical Medicine in Hamburg, Germany, also praised the study. Bachmann, who didn't work on the paper, said it suggests 'that P falciparum may possess even more sophisticated strategies to maintain long-term infections than previously understood.' She added that the findings have implications regarding whether migrants need more extensive screening and treatment for acute and chronic infections. 'Many parasitic infections in refugees from sub-Saharan Africa have been found to be clinically almost silent, leading to the recommendation that screening practices need to be improved, particularly with respect to parasitic infections,' she said. 'This is primarily to improve the health of migrants, but it could also become relevant in the context of a potential reintroduction of malaria in nonendemic regions as currently being observed in parts of the United States and southern Europe.' The National Institutes of Health supported Deitsch and another author via grants. Deitsch is a Stavros S. Niarchos Scholar and recipient of a William Randolph Hearst Endowed Faculty Fellowship Grant, and the William Randolph Hearst Foundation supported his institution. Another author received support from the Swiss National Science Foundation. The other authors had no disclosures.
Medscape
12-05-2025
- Health
- Medscape
Rituximab Shows Long-Term Benefits in Follicular Lymphoma
Early rituximab monotherapy led to a substantial delay in the need for new treatment in patients with advanced stage, asymptomatic, low tumour burden follicular lymphoma. After a median follow-up duration of 14.7 years, researchers found no detrimental effect on the time to initiation of second new treatment or overall survival. METHODOLOGY: Researchers conducted an open-label, randomised, phase 3 trial in which 455 patients with asymptomatic, stage II-IV, grade 1-3a low tumour burden follicular lymphoma were randomly assigned in a 1:1:1 ratio to the watchful waiting (n = 183), rituximab induction (n = 82), or rituximab maintenance (n = 190) group. Rituximab induction comprised 375 mg/m 2 intravenous doses weekly for 4 weeks, and the rituximab maintenance group received additional 12 doses every 8 weeks at the same dose. intravenous doses weekly for 4 weeks, and the rituximab maintenance group received additional 12 doses every 8 weeks at the same dose. The primary endpoint was the time to initiation of new treatment (TTNT), defined as the time from randomisation until the first day of systemic chemotherapy or radiotherapy initiation. This study reported long-term results of the trial over a median follow-up duration of 14.7 years. TAKEAWAY: At 15 years, 65% (95% CI, 56-72) of patients in the rituximab maintenance group, 48% (95% CI, 36-60) of patients in the rituximab induction group, and 34% (95% CI, 27-42) of patients in the watchful waiting group had not started new treatment. The median TTNT was 5.6 years (95% CI, 3.8-8.4) in the watchful waiting group, 14.8 years (95% CI, 7.5 to not reached) in the rituximab induction group, and not reached (95% CI, 15.6 to not estimable) in the rituximab maintenance group. The TTNT was significantly longer for patients in both rituximab groups than for those in the watchful waiting group (rituximab induction vs watchful waiting: hazard ratio [HR], 0.55; 95% CI, 0.38-0.80; P = .0019; rituximab maintenance vs watchful waiting: HR, 0.36; 95% CI, 0.26-0.50; P < .0001). = .0019; rituximab maintenance vs watchful waiting: HR, 0.36; 95% CI, 0.26-0.50; < .0001). No significant differences in overall survival were observed between the groups at 15 years (rituximab maintenance, 73%; rituximab induction, 66%; and watchful waiting, 68%). Similarly, no significant differences in the risk for high-grade transformation and the time to initiation of second new treatment were observed between the groups. IN PRACTICE: "Early rituximab monotherapy could therefore be considered a standard treatment option for patients with advanced stage, asymptomatic low tumour burden follicular lymphoma and the optimal approach should be considered on an individual patient basis," the authors concluded. SOURCE: This study was led by Michael Northend, University College London Hospitals NHS Foundation Trust, London, England. It was published online in The Lancet Haematology . LIMITATIONS: This study was limited by the lack of long-term toxicity data, especially for patients receiving rituximab maintenance, and the early closure of the rituximab induction group, which limited the power of any comparisons with the four-dose rituximab induction regimen. DISCLOSURES: This study received funding from Cancer Research UK, the Lymphoma Research Trust, Lymphoma Action, and Roche. Roche provided rituximab free of charge. Additional disclosures are noted in the original article. Several authors reported receiving honoraria and consultancy fees and having other ties with various sources.
