Showing posts sorted by relevance for query pylori. Sort by date Show all posts
Showing posts sorted by relevance for query pylori. Sort by date Show all posts

Wednesday, February 26, 2020

FDA Approves Talicia (omeprazole magnesium, amoxicillin and rifabutin) for the Treatment of H. pylori Infection in Adults

In continuation of my update on omeprazole and amoxicillin   

RedHill Biopharma Ltd. (Nasdaq: RDHL) (Tel-Aviv Stock Exchange: RDHL) (“RedHill” or the “Company”), a specialty biopharmaceutical company primarily focused on the development and commercialization of proprietary drugs for the treatment of gastrointestinal diseases,  announced that the U.S. Food and Drug Administration (FDA) has approved Talicia (omeprazole magnesium, amoxicillin and rifabutin) delayed-release capsules 10 mg1/250 mg/12.5 mg for the treatment of Helicobacter pylori (H. pylori) infection in adults. RedHill expects to launch Talicia1 in the U.S. in the first quarter of 2020 with its dedicated sales force.
Talicia is the only rifabutin-based therapy approved for the treatment of H. pylori infection and is designed to address the high resistance of H. pylori bacteria to current clarithromycin-based standard-of-care therapies. It is estimated that H. pylori resistance to clarithromycin more than doubled between 2009-2013.
Professor David Y. Graham, MD, MACG, Professor of Medicine, Molecular Virology and Microbiology at Baylor College of Medicine, Houston and Lead Investigator of the Talicia Phase 3 studies, said: “Talicia offers patients a much-needed new treatment option for H. pylori with an excellent safety and efficacy profile that is not compromised by clarithromycin or metronidazole resistance. The clinical studies for Talicia demonstrated high efficacy in eradication of H. pylori. Studies with Talicia found zero resistance to rifabutin and showed 17% resistance to clarithromycin, a current standard-of-care macrolide antibiotic, consistent with current data showing that clarithromycin-containing therapies fail in approximately 25-40% of cases.”
Colin W. Howden, MD, AGAF, FACG, Hyman Professor of Medicine & Chief of the Division of Gastroenterology, University of Tennessee Health Science Center, added: “H. pylori is a major cause of peptic ulcer and gastritis. It is also carcinogenic and is the leading cause of gastric cancer. Treatment of H. pylori infection has become increasingly difficult due to growing bacterial resistance and the lack of advances in treatment options over the past decade. Talicia offers a new effective treatment option to overcome bacterial resistance and provide optimal efficacy and I believe it could become a recommended first-line standard-of-care treatment for H. pylori infection.”
“The FDA’s approval of Talicia demonstrates our unwavering dedication to patients suffering from gastrointestinal diseases. We thank the patients, researchers and clinical staff who participated in the studies of Talicia and the RedHill team and vendors for this important milestone achieved by their commitment and hard work,” said Dror Ben-Asher, Chief Executive Officer of RedHill Biopharma. “We are working to expand our sales force to approximately 140 representatives who will promote Talicia, Aemcolo and other gastrointestinal-focused products in our basket.”

Saturday, June 6, 2009

Glutamine for stomach ulcer ?

We know that Glutamine is the most abundant naturally occurring, non essential amino acid in the human body and one of the few amino acids which directly crosses the blood brain barrier. In the body it is found circulating in the blood as well as stored in the skeletal muscles. It becomes conditionally essential (requiring intake from food or supplements) in states of illness or injury.

Dietary sources of L-glutamine include beef, chicken, fish, eggs, milk, dairy products, wheat, cabbage, beets, beans, spinach, and parsley. Small amounts of free L-glutamine are also found in vegetable juices and fermented foods, such as miso.

In one of my earlier blog, I did mention that broccoli, has been found useful against the H. pylori infection, now its the turn of Glutamine-that has been found useful against the infection. Dr. Susan Hagen, Associate Director of Research in the Department of Surgery at BIDMC and Associate Professor of Surgery at Harvard Medical School and group has found that extra glutamine in the diet could protect against gastric damage caused by H. pylori.

Gastric damage develops when the bacteria weakens the stomach's protective mucous coating, damages cells and elicits a robust immune response that is ineffective at ridding the infection. Eventually, she notes, years of infection result in a combination of persistent gastritis, cell damage and an environment conducive to cancer development. Dr. Hagen and her co-authors had previously shown that glutamine protects against cell death from H. pylori-produced ammonia. And further studies revealed that, the damaging effects of ammonia on gastric cells could be reversed completely by the administration of L-glutamine," explains Hagen. "The amino acid stimulated ammonia detoxification in the stomach - as it does in the liver - so that the effective concentration of ammonia was reduced, thereby blocking cell damage', which encouraged the group to hypothesize that a similar mechanism might be at work in the intact stomach infected with H. pylori.

The results are encouraging and are of great importance, because of the fact that the animals exhibited increased expression of three cytokines - interleukin 4, interleukin 10 and transforming growth factor-alpha mRNA. According to the authors these all play an important role in the stomach's ability to protect against damaging effects resulting from other responses to H. pylori infection. And more interestingly-glutamine supplementation may be an alternative therapy for reducing the severity of infection. Thus ptoviding a relief to the patients suffering from H.Pylori. H. pylori bacteria infect more than half of the world's population and were recently identified as a Group 1 carcinogen by the WHO. Hope this inexpensive, easy-to-use treatment could be used to modify the damaging effects of H. pylori infection inthe near future.
Congrats Dr. Susuan and group. ....

Ref : http://www.bidmc.org/News/InResearch/2009/May/StomachUlcers.aspx


Sunday, July 23, 2017

Study on common bacterium presents new pathway to combat gastric cancers

A common bacterium that more than half of people have in their gut can use hydrogen gas present in the gastrointestinal tract to inject a cancer-causing toxin into otherwise healthy cells, according to a recently published study led by University of Georgia researchers.

The bacterium's reliance on hydrogen presents a pathway to potential new treatment and preventive measures in fighting gastric cancers, which kill more than 700,000 people per year, said corresponding author Robert Maier, Georgia Research Alliance Ramsey Eminent Scholar of Microbial Physiology in the Franklin College of Arts and Sciences.

Previous studies solidified the relationship between stomach ulcers and cancer and certain strains of Helicobacter pylori, a stomach-dwelling bacterium that causes 90 percent of all gastric cancers. Earlier research also found a link between a toxin known as CagA, or cytotoxin-associated gene A, and cancer formation, but the new study exposes how the bacterium uses hydrogen as an energy source to inject CagA into cells, resulting in gastric cancer, Maier said.

"There are many known microbes in the human gut that produce hydrogen and others that use hydrogen. The implications of the study are that if we can alter a person's microflora, the bacterial makeup of their gut, we can put bacteria in there that don't produce hydrogen or put in an extra dose of harmless bacteria that use hydrogen," Maier said. "If we can do that, there will be less hydrogen for H. pylori to use, which will essentially starve this bacteria out and result in less cancer."

Changing the microbial makeup of a person's gut sounds complicated, but scientists are already exploring ways to do so through the use of probiotics, antibiotics, nutritional regimes and even fecal transplants.

Although many people carry the H. pylori bacterium, it can take decades for the infection to develop into cancer, providing an opening for aggressive preventive measures in people who have a high risk of developing tumors, said lead author Ge Wang, a senior research scientist in the Department of Microbiology. The presence of H. pylori strains with both CagA and high hydrogen-utilizing activity within patients can potentially serve as biomarkers for predicting future cancer development.

An earlier study led by Maier, "Molecular Hydrogen as an Energy Source for Helicobacter pylori," published by the American Association for the Advancement of Science in 2002, showed that the presence of hydrogen in the gastric chamber was important for bacterial growth, but it wasn't until the current study that researchers learned of the strong cancer connection: The bacterium harnesses the energy from hydrogen gas, via an enzyme known as hydrogenase, to severely disrupt host cell function, leading to cancer.

"If hydrogen is in the gastric mucosa, of course a bacterium will use it," Maier said. "It's an excellent energy source for many bacteria out in nature. But we didn't realize that pathogens like H. pylori could have access to it inside an animal in a way that enables the bacterium to inject this toxin into a host cell and damage it."

Not all strains of the bacteria cause cancer, but those with CagA are known carcinogens. Using human-derived gastric cells, Wang analyzed the hydrogenase activity in the cells that were infected with different strains — both cancer causing and non-carcinogenic — of H. pylori. He found more activity in the cancer-causing strains. After using genetic engineering to knock out the DNA fragment containing the hydrogenase-inducing genes, which prevented those strains from deriving energy from hydrogen, he found that the strain he created could no longer move the cancer-causing toxin into the gastric cells. Collaborators at Vanderbilt University took Wang's in vitro model and adapted it to test the theory in gerbils, which confirmed the UGA researchers' findings.

Sunday, October 18, 2009

Relationship between H pylori and gastric cancer

In my earlier blogs, I have covered lots of news about the Helicobacter pylori, (H. pylori a gram negative bacterium which infects about 50% of the world population). H. pylori colonization causes a strong systemic immune response. Various tools have been employed to identify the relationship between H pylori and gastric cancer, including c-DNA microarrays. However, most of these methods did not consider the systematic interaction of biological components. While reading science daily, I found this interesting info.

A research team from South Korea studied the complex reaction of gastric inflammation induced by H. pylori in a systematic manner using a protein interaction network.

The researchers drew a conclusion that immune-related proteins activated by H. pylori infection interact with proto-oncogene proteins. The hub and bottleneck proteins are potential drug targets for gastric inflammation and cancer.

Their study showed how a systematic approach such as the network construction produces meaningful information. It also offered a relatively easy and simple framework to understand the complexity of cellular interactions having functional importance. Therefore, the application of this tool may be an alternative to find important genes and drug targets in other diseases and in complex biological systems....

Ref : http://www.wjgnet.com/1007-9327/15/4518.asp

Monday, January 18, 2016

Seaweed extract shows promise in treating H. pylori-related diseases, gastric cancer


http://www.news-medical.net/

Effective treatments for H. pylori are limited with a rising percentage of treatment failures, primarily due to antibiotic resistance. Alternative and additional treatment options are widely recognised as a significant global healthcare issue. Results from this latest study show that fucoidan, a sulphated polysaccharide found in brown seaweed, may offer a solution.

The study took place at the University of Western Australia in the laboratories of Nobel Prize Laureate Professor Barry Marshall, who is recognised for his discovery of H. pylori and its role in gastritis and peptic ulcer disease. The research involved testing fucoidan extracts derived from the Fucus vesiculosus and Undaria pinnatifida species of brown seaweed. These certified organic, high-purity extracts were developed and produced by Australian biotechnology company, Marinova Pty Ltd.

The in vitro studies showed fucoidan extracts are extremely effective at dislodging H. pylori from infected human stomach cancer cells. This significant result positions fucoidan as a potential alternative to the increasingly inadequate antibiotic treatments.

Dr Alfred Chin-Yen Tay, Research Associate at The Marshall Centre for Infectious Diseases who supervised the study, said:

These research findings are an encouraging step forward in the control of H. pylori-related diseases. Fucoidan is a natural extract and oral delivery to the stomach is simple. It would be a welcome option for suffering patients, especially before having to undergo invasive diagnosis and treatment options.

Tuesday, September 13, 2011

Biologists identify mechanism of H. pylori that damages DNA of gastric mucosal cells

In continuation of my update on H.Pylorihttp://www.med-chemist.com/search?q=pylori..
We know that,  stomach bacterium Helicobacter pylori is one of the biggest risk factors for the development of gastric cancer, the third most common cause of cancer-related deaths in the world. Molecular biologists from the University of Zurich have now identified a mechanism of Helicobacter pylori that damages the DNA of cells in the gastric mucosa and sets them up for malignant transformation.

 More at :

Biologists identify mechanism of H. pylori that damages DNA of gastric mucosal cells

Sunday, July 1, 2012

Pernix Therapeutics introduces Omeclamox-Pak® for the treatment of H. pylori infection and duodenal ulcer disease

Pernix Therapeutics introduces Omeclamox-Pak® for the treatment of H. pylori infection and duodenal ulcer disease: Pernix Therapeutics Holdings, Inc., a specialty pharmaceutical company,  announced the introduction of Omeclamox-Pak®, a ten-day therapy of omeprazole (below 1st) delayed-release capsules (20 mg), clarithromycin (below 2nd) tablets (500 mg) and amoxicillin (below 3rd) capsules (500 mg) for the treatment of Helicobacter pylori (H. pylori) infection and duodenal ulcer disease (active or one-year history) to eradicate H. pylori in adult patients...


Saturday, March 17, 2012

H. pylori bacteria associated with elevated levels of HbA1c

In continuation of my update on H.Pylori

H. pylori bacteria associated with elevated levels of HbA1c: A new study by researchers at NYU Langone Medical Center reveals that the presence of Helicobacter pylori (H. pylori) bacteria is associated with elevated levels of glycosylated hemoglobin (HbA1c), an important biomarker for blood glucose levels and diabetes.

Tuesday, October 13, 2009

A special protien in the stomach against Helicobacter pylori ....

In my earlier blogs, I did mention with the help of Broccoli and Glutamine how one can avoid the stomach ulcer caused by H. pylori infection (which in turn lead to gastric adenocarcinoma and MALT lymphoma). But this is something interesting a special protein in the lining of the stomach has been shown to be an important part of the body’s defence against the stomach ulcer bacterium Helicobacter pylori in a new study from the Sahlgrenska Academy at the University of Gothenburg. The discovery may explain why the bacterium makes some people more ill than others.

The research team has shown that a protein called MUC1 found in the lining of the stomach is important for the body’s defence against the bacterium. Greatly magnified, MUC1 looks like a tree growing out of low bushes on the surface of the stomach. As MUC1 is taller than the other structures on the cell surface, Helicobacter pylori readily becomes attached to the protein and then rarely gets to infect the cell. As per the claim by the researchers MUC1 acts as a decoy which prevents the bacterium from coming into close contact with the cell surface. Genetic variations between people mean that MUC1 molecules vary in length, and this may be part of the reason why Helicobacter pylori makes some people more ill than others. Congrats for this improtant achievement..

Ref : http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000617

Wednesday, January 27, 2010

LOAD - a better combination therapy against Helicobater pylori....

In continuation of my update on Helicobater pylori infection and its treatment, I found this info interesting to share with. Dr. Patrick Basu and his colleagues at Columbia University College of Physicians and Surgeons found that,  a shorter course of the four-drug combination (LOAD), seven days vs. a ten-day treatment, is equally effective. As per the claim by the researchers  Helicobater pylori, a bacteria implicated in peptic ulcers and gastritis, was eradicated in 95 percent patients who took a 7-day course of combination therapy with  levofloxacin (L), omeprazole (O), nitazoxanide (Alinia®) (A) and doxycycline  (D) (LOAD) compared to eradication in only 80.9 percent of patients on lansoprazole, amoxicillin and clarithromycin (LAC) for seven days.

The study included 135 patients with treatment naïve Helicobacter pylori infection, who were randomized to LOAD (7 or 10 days) vs. LAC (10 days). There was a total wash out period of six weeks from any prior antibiotic and PPI use prior to the initiation of therapy.


Ref : http://www.acg.gi.org/media/releases/09ACGReleaseLOADTherapyforHPylori.pdf

Monday, April 13, 2009

Broccoli sprouts may help prevent stomach cancer !










Pict., of Broccoli (Structures of DIM & Sulforaphane respectively)

We knew that Broccoli has anticancer activity due to the presence Diindolylmethane, DIM (Str-1). DIM is a natural compound formed during the autolytic breakdown of glucobrassicin present in food plants of the Brassica genus, including broccoli, cabbage, Brussels sprouts, cauliflower and kale. The autolytic breakdown of glucobrassicin requires the catalytic reaction of the enzyme myrosinase which is endogenous to these plants and released upon rupture of the cell wall

(the same compound, has been tested for viral nfections,bacterial infections and immune deficiency diseases also). And boiling the Broccoli, will lead to the loss of this
compound has been also established
Now more interestingly, Dr. Jed Fahey has come out with something different and this time they have mentioned about a phytochemical from broccoli, i.e., sulforaphane. Though the cancer protective effects of sulforaphane is known two decades ago, but this is the first study to show an effect of broccoli in humans on the bacterial infection that leads to stomach cancer. In this study, researchers enrolled 48 Helicobacter-infected Japanese men and women and randomly assigned them to eat 70 grams of fresh broccoli sprouts daily for eight weeks or an equivalent amount of alfalfa sprouts.

Researchers assessed the severity of H. pylori infection at enrollment, and again at four and eight weeks using standard breath, serum and stool tests. H. pylori levels were significantly lower at eight weeks on all three measures among those patients who had eaten broccoli sprouts, while they remained the same for patients who had eaten alfalfa sprouts.
A reduction in H. pylori is expected to lead to a reduction in stomach cancer due to their well-established cause-and-effect link. Stomach cancer has a grim prognosis and is the second most common and the second deadliest cancer worldwide. Congrats Dr. Jed Fahey and group...

Saturday, December 22, 2012

Stroke drug kills bacteria that cause ulcers and tuberculosis


sc-223958

Now researchers  found that, a compound called ebselen (see structure) effectively inhibits the thioredoxin reductase system in a wide variety of bacteria, including Helicobacter pylori which causes gastric ulcers and Mycobacterium tuberculosis which causes tuberculosis. Thioredoxin and thioredoxin reductase proteins are essential for bacteria to make new DNA, and protect them against oxidative stress caused by the immune system. Targeting this system with ebselen, and others compounds like it, represents a new approach toward eradicating these bacteria.

Building on previous observations where ebselen has shown antibacterial properties against some bacteria, Holmgren and colleagues hypothesized that the bacteria sensitive to ebselen relied solely on thioredoxin and thioredoxin reductase for essential cellular processes. They investigated this by testing it on strains of E. coli with deletions in the genes for thioredoxin, thioredoxin reductase and the glutaredoxin system. They found that strains with deletions in the genes coding for glutaredoxin system were much more sensitive than normal bacteria. Researchers further tested ebselen againstHelicobacter pylori andMycobacterium tuberculosis, which both naturally lack the glutaredoxin system and are frequently resistant to many commonly used antibiotics, and found both to be sensitive to ebselen.

"As rapidly as these organisms evolve, we need new drugs sooner rather than later," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "The fact that these scientists have found a new target for killing some of the most resistant bacteria is great news, but the fact that we already have at least one drug which we could possibly use now makes the news even better."


Ref : http://www.fasebj.org/content/early/2012/12/17/fj.12-223305

Friday, August 9, 2013

Acid reflux drug may cause heart disease, study suggests

In human tissue and mouse models, the researchers found PPIs (proton pump inhibitors) caused the constriction of blood vessels. If taken regularly, PPIs could lead to a variety of cardiovascular problems over time, including hypertension and a weakened heart. In the paper, the scientists call for a broad, large-scale study to determine whether PPIs are dangerous.
"The surprising effect that PPIs may impair vascular health needs further investigation," said John Cooke, M.D., Ph.D., the study's principal investigator. "Our work is consistent with previous reports that PPIs may increase the risk of a second heart attack in people that have been hospitalized with an acute coronary syndrome. Patients taking PPIs may wish to speak to their doctors about switching to another drug to protect their stomachs, if they are at risk for a heart attack."
Commonly used proton pump inhibitors in the United States are lansoprazole (below left) and omeprazole (below right), 

and these drugs are purchasable over the counter as brands or generics. The FDA estimates about 1 in 14 Americans has used them. In 2009, PPIs were the third-most taken type of drug in the U.S., accounting for $13 billion in sales. PPIs are used to treat a wide range of disorders, including gastroesophageal reflux disease, or GERD, infection by the ulcer-causing Helicobacter pylori, Zollinger-Ellison syndrome, and Barrett's esophagus.
Recent studies of proton pump inhibitors use by people who've already experienced severe cardiovascular events have raised concern about the anti-reflux drugs, at least for this subgroup of patients, said Cooke, chair of the Department of Cardiovascular Sciences and director of the Center for Cardiovascular Regeneration at Houston Methodist DeBakey Heart & Vascular Center.
PPIs are initially inert. After oral consumption, they are activated by specialized cells in the stomach. Once active, the molecules suppress the movement of protons into the intestine, which reduces the amount of acid present there and in the stomach.
In mouse models and cultures of human endothelial cells, Cooke and lead author Yohannes Ghebramariam, Ph.D., found that PPIs suppressed the enzyme DDAH, dimethylarginine dimethylaminohydrolase. That caused an increase in the blood levels of ADMA (asymmetric dimethylarginine), an important chemical messenger. They found ADMA in turn suppressed the production of another chemical messenger, nitric oxide, or NO, proven by 1998 Nobel Prize winners Furchgott, Ignarro, and Murad to impact cardiovascular function. Quantitative studies in mouse models showed animals fed PPIs were more likely than controls to have tense vascular tissue.
"We found that PPIs interfere with the ability of blood vessels to relax," said Ghebremariam, a Houston Methodist molecular biologist. "PPIs have this adverse effect by reducing the ability of human blood vessels to generate nitric oxide. Nitric oxide generated by the lining of the vessel is known to relax, and to protect, arteries and veins."
The researchers found PPIs led to an approximately 25 percent increase in ADMA in mouse and tissue cultures, and reduced the ability of mouse blood vessels to relax by over 30 percent on average.