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Hope rises for drug-resistant malaria treatment

By Chukwuma Muanya, Assistant Editor
18 April 2016   |   4:39 am
There is fresh hope for the treatment of drug-resistant malaria even as more reasons are emerging why more Nigerians are coming down with kidney damage.

Malaria

• Heartburn, stomach acid drug linked to increased kidney failure

There is fresh hope for the treatment of drug-resistant malaria even as more reasons are emerging why more Nigerians are coming down with kidney damage.

Scientists in a study published yesterday in the journal, Science, found that resistance to a key anti-malarial drug cannot be passed on by mosquitoes in a breakthrough they believe could drastically improve the way the disease is battled.

They say the discovery could potentially shut down the avenue for mass drug-resistance to spread, making malaria treatment significantly more effective for the 3.2 billion people at risk.

The international research project was led by the University of Melbourne, Australia, and focused on the drug atovaquone.

Atovaquone introduced in 2000 is safe for pregnant women and children is one of the few anti-malarials that can be used in mass administration approaches. It was largely phased out of use because resistance was initially observed.

According to the new study, although some malaria parasites have developed a genetic mutation that protect them against the drug in early life, the mutation eventually kill the parasites by stopping the production of an essential type of energy as they grow.

Meanwhile, a new study published yesterday in the Journal of the American Society of Nephrology found that a long-term use of popular drugs commonly used to treated heartburn, acid reflux and ulcers could lead to kidney damage and severe kidney disease.

The drugs are known as proton pump inhibitors (PPIs) Proton pump inhibitors which reduce the stomach acid made by glands in the lining of the stomach. This is not the same as antacids, which reduce excess acid after it enters the stomach.

Common types of PPI include omeprazole (brand name Prilosec, also available over the counter), esomeprazole (Nexium), lansoprazole (Prevacid), rabeprazole (AcipHex), pantoprazole (Protonix), dexlansoprazole (Dexilant) and Zegerid (omeprazole with sodium bicarbonate).

The researchers came to the conclusion that PPIs could lead to kidney damage and severe kidney disease after analysing large collections of patient data held in the Department of Veterans Affairs (VA) national databases.

They are commonly used to relieve symptoms of acid reflux or gastroesophageal reflux disease (GERD) – a condition where food or liquid from the stomach moves up into the esophagus or food pipe.

PPIs are also used to treat peptic or stomach ulcers and damage to the lower esophagus caused by acid reflux. There are many names and brands of PPIs. Most work equally as well, although side effects may vary. Some are also available over the counter – that is, without a prescription.

The researchers suggest the actual number of PPI users in the U.S. is likely to be higher, because some types are available without a prescription.

For their study, the team examined five years of VA records for 173,000 new users of PPIs and 20,000 new users of H2 receptor blockers – another type of drug that also suppresses stomach acid – and looked for incidence of kidney problems.

Their analysis finds that patients taking PPIs were more likely to experience declining kidney function than patients taking H2 receptor blockers.

Senior author and a nephrologist with the VA Saint Louis Health Care System in Missouri, United States (US), Dr. Ziyad Al-Aly, said their findings emphasised the importance of only using PPIs when medically necessary, and also limiting the duration of use to the shortest possible. He noted: “A lot of patients start taking PPIs for a medical condition, and they continue much longer than necessary.”

The study adds to a body of research that is raising questions about long-term use of PPIs.

The lead authors of the malaria study, Prof. Geoff McFadden and Dr. Dean Goodman, are calling it a ‘genetic trap’ that could prove to be a significant step forward in the anti-malaria fight.

The pair, along with long-term collaborator Vanessa Mollard, led a team investigating the evolution and life cycle of the malaria parasite for the past six years.

They said: “These results are very exciting because the spread of drug resistance is currently destroying our ability to control malaria,” said McFadden from the School of Biosciences at the University of Melbourne.

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