Over-the-counter drugs, dietary supplements and their effect on lab test results

Over-the-counter (OTC) drugs and dietary supplements are widely used and popular, with US households spending an average of almost USD 350 annually on OTC products. In 2006 an average of EUR 67.50 was spent per person on OTC products in Germany.

The use of various OTC drugs and dietary supplements is highly prevalent in Europe and patients are often not willing to disclose this information to laboratory staff and the ordering physician as a survey published in Clinical Chemistry and Laboratory Medicine, published by De Gruyter in association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM), shows.

The study reports on the results of a survey of patients in 18 European countries which shows that those taking OTC products and dietary supplements are not aware of the potential effects on laboratory test results they may have. In addition, patients do not believe that they need to disclose this use to medical and/or laboratory staff.

The study shows that dietary supplements and OTC drugs are more frequently used by middle-aged patients – especially women – with the most common being multivitamins, multiminerals, cranberry and aspirin. All of these compounds, if consumed shortly before blood sampling, may cause changes in lab test results, thus leading to interpretation difficulties and possibly incorrect diagnoses.

Although more data is needed about the frequency of the consumption of various dietary products, vitamins or OTC drugs, the authors believe that a multifaceted approach is necessary to draw attention to the issue using educational interventions which target both healthcare professionals and patients.

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There’s A New Antidepressant In Town, And It’s Poisoning People

Tianeptine, an unapproved drug meant to treat depression, is causing opioid-like highs — and poisonings.

While overdoses and serotonin syndrome can cause serious problems in those who take antidepressants, an unapproved antidepressant is causing an alarmingly high number of calls to poison control centers in the United States. The drug, a medication called tianeptine, is sold as an antidepressant in Latin America, Asia, and Europe. It has not been approved for use in the United States, and there’s a reason why.

The drug causes opioid-like highs, which has led many people to buy it instead of actual opioid drugs like fentanyl, codeine, hydrocodone, and heroin. However, it is not harmless in the slightest. According to Fox News, the drug has already been linked to two deaths in the United States. The deaths were caused by “tianeptine toxicity,” and occurred after the deceased bought the drug online.

Developed in France to treat depression and anxiety, the drug’s method of action was a mystery for decades. However, it was discovered that tianeptine interacts with the brain’s opioid receptors. This euphoric effect can cause relief from depression and anxiety symptoms, but it can also cause highs, addiction, and withdrawal.

In fact, those withdrawing from tianeptine experience many of the same symptoms as those withdrawing from opioid drugs. Considering the similarities between the two drugs, it’s no surprise that people are using it as a stand-in for actual opioids.

Troubling side effects were reported, including confusion, tachycardia, and nausea/vomiting. When taken in unison with other drugs, tianeptine becomes even more dangerous.

Most commonly taken with this antidepressant is phenibut. Phenibut, developed in Russia as an anti-anxiety medication, has gained a following online for being a “happy drug.” According to Vice News, there are entire online forums dedicated to discussing drugs like tianeptine and phenibut, and both drugs are described as having “euphoregenic effects.”

Many agree that the U.S. crackdown on illegal opioids is causing others to seek out replacements.

“We are also seeing a shift away from the use of prescription opioids toward plant materials containing unrecognized opioids or to OTC products with potentially lethal opioid effects,” an FDA official wrote in a paper recently published by the New England Journal of Medicine.

Tianeptine is the perfect substitute. Easily purchased online as a research chemical and diet supplement, it’s not hard to get your hands on. However, several studies and hundreds of poison control calls show that it’s just as dangerous as its illegal counterparts.

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Diabetes: Switching to common drugs raises risk of complications

Researchers set out to investigate how safe it is for patients with type 2 diabetes to switch from taking metformin, which is a standard “first-line” antidiabetic drug, to taking sulfonylureas, often prescribed to control blood sugar levels when metformin alone fails.

They were led by Prof. Samy Suissa, from McGill University in Quebec, Canada.

As Prof. Suissa and colleagues explain in their paper, numerous studies have confirmed the safety of sulfonylureas.

Fewer, however, have focused on their safety when patients have switched to the drugs or when they have added them to their previous treatment.

So, to fill this research gap, the scientists examined whether adding sulfonylureas or switching to them from metformin raises the risk of cardiovascular problems such as heart attack or stroke, or the risk of death from cardiovascular problems or from any other causes.

Also, the team examined whether or not switching to, or adding, sulfonylureas raised the risk of severe hypoglycemia, or low blood sugar. All these risks were compared with taking metformin alone.

Continuing metformin safer than switching

In order to study these links, the researchers examined over 77,138 people with type 2 diabetes who started taking metformin between 1998 and 2013.

Of these, 25,699 either added sulfonylureas to their treatment or switched to them altogether during the study period.

The team compared these people with age-matched controls who continued to take only metformin over a follow-up period of 1.1 years, on average.

Overall, when compared with staying on metformin, the study found that adding, or switching to, sulfonylureas was linked with a higher risk of a heart attack, death from any causes, and severe hypoglycemia.

More specifically, people adding, or switching to, the second-line treatment were 26 percent more likely to have a heart attack, 28 percent more likely to die from any causes, and over seven times more likely to have severe hypoglycemia, on average.

The researchers also discovered a trend toward a higher likelihood of stroke and death from heart problems in those switching to, or adding, sulfonylureas.

Finally, when comparing just adding sulfonylureas to metformin with switching to sulfonylureas completely, the latter raised the risk of a heart attack by 51 percent and mortality from all causes by 23 percent.

However, no differences were found in the risk of stroke, cardiovascular death, or hypoglycemia between just adding the drugs and switching to them.

Prof. Suissa and colleagues conclude, “Sulfonylureas as second-line drugs are associated with an increased risk of myocardial infarction, all-cause mortality, and severe hypoglycemia, compared with remaining on metformin monotherapy.”

Thus, in line with current recommendations on the treatment of type 2 diabetes, continuing metformin when introducing sulfonylureas is safer than switching.”

As with any observational study, causality cannot be inferred from the results. But researchers Lucy D’Agostino McGowan and Christianne Roumie deem the study “well designed and the relations […] strong and consistent” in an accompanying editorial, which is also published in the BMJ.

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Focussed ultrasound used to improve effects of cancer drugs

Researchers have made a breakthrough in more precisely targeting drugs to cancers. Using ultrasound and lipid drug carriers (liposomes), a multi-disciplinary team of biomedical engineers, oncologists, radiologists and anaesthetists at the University of Oxford have developed a new way to improve the targeting of cancer drugs to tumours.

The new technology has been used in humans for the very first time, with ultrasound remotely triggering and enhancing the delivery of a cancer drug to the tumour.

“Reaching therapeutic levels of cancer drugs within a tumour, while avoiding side effects for the rest of the body is a challenge for all cancer drugs, including small molecules, antibodies and viruses,” said Professor Constantin Coussios, Director of the Oxford Centre for Drug Delivery Devices (OxCD3) and of the Institute of Biomedical Engineering at the University of Oxford. “Our study is the first to trial this new technique in humans, and finds that it is possible to safely trigger and target the delivery of chemotherapy deep within the body from outside the body using focussed ultrasound. Once inside the tumour, the drug is released from the carrier, supplying a higher dose of chemotherapy directly to the tumour, which may help to treat tumours more effectively for the same or a lower systemic dose of the drug.”

Published in The Lancet Oncology journal, the 10-patient phase 1 clinical trial used focussed ultrasound from outside the body to selectively heat liver tumours and trigger drug release from heat-sensitive carriers, known as thermosensitive liposomes. Building on over a decade of preclinical studies, the study demonstrated the ultrasound technique to be feasible, safe, and capable of increasing drug delivery to the tumour between two-fold and ten-fold in the majority of patients. Ongoing research worldwide is investigating the applicability of this technique to other tumour types, and future research could explore the combination of ultrasound with other drugs.

All 10 patients treated had inoperable primary or secondary tumours in the liver and had previously received chemotherapy. The procedure was carried out under general anaesthesia and patients received a single intravenous dose of 50 mg/m2 of doxorubicin encapsulated within low-temperature-sensitive liposomes (ThermoDox, Celsion Corporation, USA). The target tumour was selectively heated to over 39.5o C using an approved ultrasound-guided focussed ultrasound device (JC200, Chongqing HAIFU, China) at the Early Phase Clinical Trials Unit at the Churchill Hospital in Oxford. In six out of 10 patients, the temperature at the target tumour was monitored using a temporarily implanted probe, whilst in the remaining four patients ultrasonic heating was carried out non-invasively.

Before ultrasound exposure, the amount of drug reaching the tumour passively was low and estimated to be below therapeutic levels. In seven out of 10 patients, chemotherapy concentrations within the liver tumour following focussed ultrasound were between two and ten times higher, with an average increase of 3.7 times across all patients.

“Only low levels of chemotherapy entered the tumour passively. The combined thermal and mechanical effects of ultrasound not only significantly enhanced the amount of doxorubicin that enters the tumour, but also greatly improved its distribution, enabling increased intercalation of the drug with the DNA of cancer cells,” said Dr. Paul Lyon, lead author of the study.

“This trial offers strong evidence of the rapidly evolving role of radiology in not only diagnosing disease but also in planning, guiding and monitoring therapy. The treatment was delivered under ultrasound guidance and patients were subsequently followed up by CT, MRI and PET-CT, evidencing local changes in tumours exposed to focussed ultrasound,” commented Professor Fergus Gleeson, radiology lead co-investigator for the trial.

“A key finding of the trial is that the tumour response to the same drug was different in regions treated with ultrasound compared to those treated without, including in tumours that do not conventionally respond to doxorubicin,” added Professor Mark Middleton, principal investigator of the study. “The ability of ultrasound to increase the dose and distribution of drug within those regions raises the possibility of eliciting a response in several difficult-to-treat solid tumours. This opens the way not only to making more of current drugs but also targeting new agents where they need to be most effective. We can now begin to realize the promise of precision cancer medicine.”

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‘Microbubbles’ could destroy more than half of hard-to-treat tumours

Chemotherapy breakthrough: ‘Microbubbles’ loaded with drugs could destroy more than half of hard-to-treat tumours without any side effects

  • Destroy 60% of hard-to-treat cancers, such as breast and lung, in mice
  • Therapy only targets immune cells that work to fight off tumours
  • Therefore avoids the side effects of treating all cells, like inflammation
  • Means drugs could be administered at around 100 times higher doses
  • Lung and breast cancers are typically difficult to treat due to them being solid 

Scientists have unveiled a potential chemotherapy breakthrough.

‘Microbubbles’ loaded with immune-stimulating drugs destroy 60 percent of hard-to-treat cancers, such as lung and breast, in mice, a US study found today.

The therapy only targets immune cells that work to fight off tumours and therefore avoids the side effects of treating all cells, such as inflammation, the research adds.

A lack of adverse events could allow drugs to be administered at around 100 times higher doses than they are currently given, the study found.

Lung and breast cancers are typically difficult to treat due to them being solid, which prevents them from reacting to immune-stimulating drugs as well as blood tumours such as lymphoma or leukemia. 

Scientists have unveiled a potential chemotherapy breakthrough (stock)


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WHAT CANCER DRUGS ARE IN DEVELOPMENT? 

Research released in January 2018 suggested a cancer drug is in development that could stop the disease in its tracks.

The unnamed medication targets a specific enzyme that fuels the spread of tumours.

It does this by binding to the membrane of rapidly multiplying cells, a study found.

This hijacks cancer’s ‘survival mechanism’ and prevents tumours from attaching to the protein they need to thrive.

It is unclear when the drug could be available.

The anti-cancer drug binds to cancerous cells’ membrane protein, known as dehydroorotate dehydrogenase (DHODH).

The researchers analysed how fats, which are the building blocks of cell membranes, and drugs bind to DHODH.

Study author Dr Erik Marklund, from Uppsala University, said: ‘Our simulations show the enzyme uses a few lipids as anchors in the membrane.

‘When binding to these lipids, a small part of the enzyme folds into an adapter that allows the enzyme to lift its natural substrate [the substance an enzyme acts on] out of the membrane.

‘It seems the drug, since it binds in the same place, takes advantage of the same mechanism.’

Co-author Sir David Lane, from the Karolinska Institute, Sweden, added: ‘The study helps to explain why some drugs bind differently to isolated proteins and proteins that are inside cells.

‘By studying the native structures and mechanisms for cancer targets, it may become possible to exploit their most distinct features to design new, more selective therapeutics.’

How does the treatment work?

To ensure the treatment only targets tumour-specific immune cells, the researchers attached small spheres to these cells.

Coming into contact with these spheres causes the microbubbles to release the drug they are carrying. 

This leads to a chemical change to occur on the surface of the immune cells, which triggers the microbubbles to break down.

Cured 60% of tumours in mice  

The microbubbles were given to mice who were genetically engineered to express immune cells that target skin-cancer tumours.

In around 60 per cent of the mice, the tumours disappeared.

The researchers, from the Massachusetts Institute of Technology, were able to give the rodents around eight times as much immune-stimulating drug, known as IL-15, without side effects compared to injecting a drug that targets all of the animals’ immune cells.

A second experiment involved the scientists attaching the microbubbles to human immune cells that were engineered to target an aggressive cancer in the brain, known as glioblastoma.

This caused the destruction of glioblastoma much more efficiently than conventional treatment, according to the scientists. 

The researchers plan to assess this treatment’s effectiveness in many different tumour types, including solid and blood versions of the disease. 

They also wish to discover whether other drugs could stimulate the immune system as effectively.

The findings were published in the journal Nature Biotechnology. 

Cancer vaccine may be available in just one year 

This comes after research released last March suggested a cancer vaccine that cured 97 per cent of blood tumours in mice will be tested on humans with low-grade lymphoma later this year.

Patients receiving the vaccine, which contains two drugs proven for their safety, will not require any chemotherapy, with the jab’s side effects expected to be just fever and injection-site soreness.

If approved, researchers, from the University of California, San Fransisco, do not expect the treatment will be be available for another year or two.

Rather than creating lasting immunity, the jab works by activating the immune system to attack tumours.

This is expected to be effective in low-grade lymphoma, which affects certain white blood cells and generally responds to treatment, due to it often being detected by the immune system, unlike other forms of the disease, such as bowel cancer. 

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Drugs that block structural changes to collagen could prevent lung fibrosis

Scientists have found that it is the structure of collagen, rather than the amount, that leads to the devastating condition of lung fibrosis, according to a report in the journal eLife.

The study provides the first evidence in humans that altered collagen structure affects tissue stiffness during progression of lung fibrosis and identifies a potential new target for drugs to prevent the condition.

It is widely thought that fibrosis occurs when components that hold together a tissue’s architecture (called the extracellular matrix (ECM)) build up in the tissue and lead to tissue stiffness. But recently evidence has suggested that this increased stiffness causes the build-up of yet more ECM components, resulting in a cycle that causes more scar tissue.

“We knew that stiffness is an important factor in the build-up of scar tissue in the lung,” explains lead author Mark Jones, NIHR Clinical Lecturer in Respiratory Medicine at the NIHR Southampton Biomedical Research Centre and University of Southampton, UK. “But we didn’t understand what specifically causes increased stiffness in diseased human tissue. Given that excessive build-up of collagen is considered a hallmark of fibrosis, we wanted to see whether this molecule has a role in tissue stiffness.”

They started by looking at the biological and mechanical features of lung tissue from people with lung fibrosis and compared this to healthy lung tissue. They found that the lung fibrosis samples were much stiffer than those from healthy people but, surprisingly, had similar levels of collagen.

However, when they looked at enzymes that give collagen its unique ‘cross-linked’ structure within the ECM, they found that a family of these enzymes (the LOXL family) was more abundant in the fibrosis samples. This led them to further investigate the types of collagen structures found in the fibrosis samples—which are broadly grouped into immature and mature collagen cross-links. They found that increased lung tissue stiffness only occurred where there were higher amounts of the mature cross-linked collagen and that, in these samples, the structure of each collagen building block—or fibril—was altered. This suggested that it is collagen structure, controlled by the LOXL family, that determines tissue stiffness.

Having made this discovery, the team tested whether they could alter the structure of collagen by blocking the LOXL enzymes, with a view to preventing lung fibrosis. They tested a compound called PXS-S2A that blocks LOXL-2 and LOXL-3 in lung tissue cells isolated from people with fibrosis. They found that the number of cross-linked collagen molecules declined with an increasing dose of PXS-S2A.The compound also reduced tissue stiffness, even at low concentrations, suggesting that blocking LOXL-2/LOXL-3 could be an effective way to reduce tissue stiffness.

Finally, they tested the LOXL-2/3 inhibitor in rats with lung fibrosis and found that although there was no effect on total collagen content in the lungs, the treated rats had reduced fibrosis and improved lung function, with no adverse effects.

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