HealthWatch Africa January 2009

Blood typeBlood typeBlood typeBlood type could becould becould becould be the new the new the new the new weapon weapon weapon weapon in thein thein thein the battle battle battle battle againstagainstagainstagainst HIV/AIDSHIV/AIDSHIV/AIDSHIV/AIDS

Can we

give Malaria

The card test?

New avenue for TB therapyNew avenue for TB therapyNew avenue for TB therapyNew avenue for TB therapy

HIV/AIDS

Blood type – the new weapon in battle against HIV infection Researchers have discovered a potentially important new resistance factor in the battle against HIV: blood types.

n international team of researchers from Canadian Blood Services, The Hospital for Sick Children (SickKids) and Lund University in Sweden have discovered that certain blood types are more predisposed to contracting HIV, while others are

more effective at fending it off. A carbohydrate-containing antigen, termed Pk blood group which is distinct from the well-known ABO and Rh blood grouping systems, is present at variable levels on the surface of white and red blood cells in the general population. A study published recently in Blood, which is currently available online, shows that cells from rare individuals (<1 in a million) who produce excess of this blood group antigen have dramatically reduced sensitivity to HIV infection. Conversely, another slightly more common subgroup of people who do not produce any Pk (<5 in a million) was found to be much more susceptible to the virus. "This study is not suggesting that your blood type alone determines if you will get HIV," says lead author Dr. Don Branch of Canadian Blood Services. "However, it does suggest that individuals who are exposed to the virus, may be helped or hindered by their blood

status in fighting the infection." Increasing the level of the Pk antigen in cells in the laboratory also resulted in heightened resistance to HIV, while lowering it increased susceptibility. The Pk molecule has been previously studied extensively by The Research Institute at the Hospital for Sick Children Senior Scientist Dr. Cliff Lingwood; Lund University's Dr. Martin Olsson has identified underlying genetic reasons for Pk blood group variation. "This discovery implicates the Pk level as a new risk factor for HIV infection and demonstrates the

importance of blood-group-related science," says Dr. Olsson.

A This study is not suggesting that your blood type

alone determines if you will get HIV

"The conclusions of this study pave the way for novel therapeutic approaches to induce HIV resistance and promote further understanding of the pandemic as a whole," says Dr. Lingwood. http://www.blood.ca

Potential new target in the war on HIV/AIDS Researchers at the Indiana University School of Medicine have identified a potential new target in the war on HIV/AIDS.

he information was published in the January 16 issue of the journal Molecular Cell. The study revealed that a variant of a protein involved in HIV pathogenesis can suppress production of an HIV protein, known as Nef. Nef is required for the

human immunodeficiency virus to develop into AIDS through a series of complex events involving viral elements and cellular proteins. Nef has never been a target for drug treatment in HIV patients. Johnny J. He, Ph.D., principal author of the research and the

director of the Indiana University Center for AIDS Research, said a drug affecting Nef could complement existing therapies to provide protection against the virus. The current treatment for HIV/AIDS is highly active anti-retroviral therapy (HAART). It is a combination of drugs that target two HIV enzymes - reverse transcriptase (RT) and protease (PR) or RT or PR inhibitors. Dr. He said another encouraging outcome of the research was the discovery that Nef could be

suppressed on the molecular level to prevent it from translating into protein. "These scientific advances have therapeutic potential to interrupt the progression of the virus into AIDS," said Dr. He, who also is a professor of microbiology and immunology and medicine. http://www.iu.edu

T Nef could be

suppressed on the molecular level to prevent it from translating into

protein

Mutant host cell protein sequesters critical HIV-1 element Scientists have identified a new way to inhibit a molecule that is critical for HIV pathogenesis. The research, published by Cell Press in the January 16th issue of the journal Molecular Cell, presents a target for development of antiretroviral therapeutics that are likely to complement existing therapies and provide additional protection from HIV and AIDS. Infection of human cells with HIV-1 requires multiple events that involve complex interactions between viral elements and cellular proteins. The virus must copy key parts of its DNA as mRNA molecules through a process called transcription. The mRNA molecules must be properly "spliced", or rearranged, and then transported out of the cell nucleus and into the cytoplasm where the mRNAs can be "translated" into viral proteins. Little known about transitional control "Although there has been a great deal of effort directed at understanding HIV-1 transcription, mRNA splicing and nuclear export, little is known about the translational control of HIV-1 RNA in the cytoplasm," says senior study author, Dr. Johnny J. He from the Centre for AIDS Research at Indiana University School of Medicine. Dr. He and colleagues examined a protein called HIV-1 Nef that is translated from completely spliced HIV-1 RNA. Nef is very important for HIV pathogenesis and AIDS disease. "It is highly conceivable that intervention with Nef expression may complement the current anti-HIV therapies that are mainly targeted at HIV-1 protease and reverse transcriptase, providing a better treatment outcome," explains Dr. He. The researchers found that a mutant form of Src-associated protein in mitosis of 68kDa (Sam68), a host cellular protein involved in HIV-1 pathogenesis, specifically interacts with nef mRNA and directly suppresses Nef expression. This particular Sam68 mutant was previously shown to inhibit HIV-1 replication by overriding its wild-type counterpart's function in nuclear export of unspliced and incompletely spliced HIV RNA. However, the mutant Sam68 was present in the cytoplasm, suggesting that it may serve some function in the cytoplasmic stage of the HIV-1 life cycle. The ability of the Sam68 cytoplasmic mutant to interfere with Nef correlated with its ability to induce stress granules in the cytoplasm. Stress granules regulate gene expression at the translational level in response to a variety of external stimuli. Importantly, nef mRNA was targeted to and enriched in the stress granules. "Taken together, these results demonstrate that stress granule induction and nef mRNA sequestration account for this translational suppression of Nef expression and offers a new strategy for development of anti-HIV therapeutics to buttress our fight against HIV/AIDS," concludes Dr. He. http://www.cellpress.com

‘Little is known about the

translational control of HIV-1 RNA in the cytoplasm’

MALARIA

Researchers find essential proteins for final stage of malaria transmission cycle Researchers at the Johns Hopkins Malaria Research Institute (JHMRI) have identified, for the first time, the molecular components that enable the malaria-causing parasite Plasmodium to infect the salivary glands of the Anopheles mosquito-a critical and final stage for spreading malaria to humans.

ccording to the researchers, saglin, a mosquito salivary protein, is a receptor for the Plasmodium protein Thrombospondin-Related Anonymous Protein (TRAP). The two proteins bind together to allow invasion of the salivary gland by

Plasmodium sporozoites, which can be transmitted to a human when bitten by an infected mosquito. The findings are published in the January 16 edition of PLoS Pathogens. Through a series of experiments, JHMRI researchers found that saglin bound with the artificial peptide SM1. The team then developed an antibody to find a protein similar to SM1 that existed naturally in the parasite, which they identified as TRAP. To further prove the interaction between saglin and TRAP, the team conducted experiments to down-regulate, or switch off, saglin expression, which greatly diminished salivary gland invasion in the mosquito. "This work is the culmination of a decade-long research project in which peptide libraries were used to understand the mechanisms that the parasite uses to develop in its obligatory mosquito host," explained Marcelo Jacobs-Lorena, PhD, an author of the study and professor with the Johns Hopkins Bloomberg School of Public Health's W. Harry Feinstone Department of Molecular Microbiology and Immunology. "Identification of molecular recognition mechanisms between the parasite and mosquito vector provides novel targets for further investigation aimed at interrupting malaria transmission," said co-author Nirbhay Kumar, PhD, also a professor in the Bloomberg School W. Harry Feinstone Department of Molecular Microbiology and Immunology. Using different methods, Kumar and his colleagues had previously identified the saglin protein and suggested it could potentially be a sporozoite receptor. Malaria is estimated to infect 300 to 500 million people worldwide resulting in over a million deaths each year. JHMRI was established in 2001 at the Bloomberg School of

A

‘Identification of molecular recognition mechanisms between the parasite and mosquito vector

provides novel targets for further investigation aimed at interrupting malaria transmission’

Public Health to mount a broad program of basic-science research to treat and control the deadly disease. Additional authors of "Malaria Parasite Invasion of the Mosquito Salivary Gland Requires Interaction Between the Plasmodium TRAP and the Anopheles Saglin Proteins" are Anil K. Ghosh, Martin Devenport, Deepa Jethwaney, Dario E. Kalume, Akhilesh Pandey, Vernon E. Anderson and Ali A. Sultan. The research was supported by the National Institutes of Health, the Johns Hopkins Malaria Research Institute and the Bloomberg Family Foundation. http://www.jhsph.edu

The retina reveals deadly secrets of malaria Looking at the retina in the eyes of patients with cerebral malaria has provided scientists with a vital insight into why malaria infection in the brain is so deadly. n a study funded by the Wellcome Trust and Fight for Sight and published in the Journal of Infectious Diseases, researchers in Malawi have shown for the first time in patients that the build-up of infected blood cells in the narrow blood vessels of the

brain leads to a potentially lethal lack of oxygen to the brain.

I

Malaria is one of the world's biggest killers, killing over a million people every year, mainly children and pregnant women in Africa, and adults in South-east Asia. Malaria parasites enter the bloodstream from bites by infected mosquitoes and live in red blood cells, making them stick to the inside of narrow blood vessels and causing blockages. Most deaths occur as a result of cerebral malaria, where red blood cells infected by malaria parasites build up into the brain, leading to coma and convulsions and, if not treated swiftly, death. Scientists have known for some time that cerebral

malaria is accompanied by changes in the retina, known as malarial retinopathy which can be seen by examining the eye. Because the retina can be considered as an extension of the central nervous system, it has been used previously as a "window into the brain", allowing for swifter diagnosis of cerebral malaria. However, until now it was not clearly understood why the disease should be so deadly. In new research, Dr Nick Beare of the Royal Liverpool University Hospital, together with colleagues at the Queen Elizabeth Central Hospital in Blantyre, Malawi, examined the retinas of 34 children admitted to the hospital with cerebral malaria. They used a technique known as fluorescein angiography, which involves injecting a special dye into the arm intravenously and photographing its passage through the blood vessels of the retina. It is used to identify fluid leakage or blockages in the small blood vessels at the back of the eye. More than four in five of the children examined by Dr Beare and colleagues were found to have impaired blood flow in the blood vessels of their eyes. Three-quarters had whitening to areas of the retina where blood did not appear to reach, implying that the parasites were disrupting the supply of oxygen and nutrients. "We have previously used the retina to accurately diagnose severe malaria, but now this window into the brain has opened up our knowledge of what makes cerebral malaria so deadly," says Dr Beare. "This is the first study to clearly show impaired blood flow in the eyes of patients with cerebral malaria. It has provided strong evidence to support what, until now, had been merely hypothesised: that cerebral malaria causes inadequate blood

flow to the brain, depriving it of oxygen and causing potentially life-threatening damage." Many deaths could be prevented If caught in time, the effects of cerebral malaria can be reversed with no lasting damage to the patient's cognitive functions or vision. Dr Beare believes

these new findings point to new therapeutic measures for treating cerebral malaria more effectively, particularly in comatose children.

More than four in five of the children examined

by Dr Beare and colleagues were found to have impaired blood

flow in the blood vessels of their eyes

Drugs that improve circulation and limit the

damage caused by the lack of oxygen could help

prevent many deaths

"Many children are dying across Africa with cerebral malaria because we don't understand how to help them whilst the anti-malarial drugs have an affect," he says. "Drugs that improve circulation and limit the damage caused by the lack of oxygen could help prevent many deaths." The research has been welcomed by Michele Acton, Chief Executive of Fight for Sight, who comments: "The findings of Dr Beare's work on malaria are incredibly important. Fight for Sight is delighted to have helped to fund such progress towards better therapies to prevent children dying from cerebral malaria." http://www.wellcome.ac.uk

Will we be able to take the malaria card test? Small disposable cards could serve as malaria tests for developing countries. New wallet-sized disposable cards with dehydrated chemical contents could be used to detect malaria in developing countries, according to researchers from the University of Washington, PATH, Micronics and Nanogen, the Seattle Times "Business of Giving" blog reports. The researchers developed the cards using funds from the Bill & Melinda Gates Foundation's Grand Challenges in Global Health Initiative, which aims to develop inexpensive and easy-to-use diagnostic tools for developing countries. According to "Business of Giving," diagnostic tools in resource-limited settings must be fast and easy to use, in part because many health workers must diagnose and treat a patient in a single visit. The new diagnostic system, called the DxBox, contains malaria tests printed on disposable Mylar cards with chemical reagents stabilized in a dry form using sugar. The DxBox also contains a portable, automatic reader developed by Micronics to process the cards. According to the university, evaluations of the tests demonstrated that the cards retained 80% to 96% of their activity after 60 days of storage at high temperatures. The team hopes these cards will lead to the development of a system in which an instrument can read a card containing a drop of a patient's blood and provide diagnostic results for a series of infectious diseases in 20 minutes or less. Paul Yager, a bioengineering professor at the university, said creating tests that are "storable for long periods of time at ambient temperatures" is a "pivotal issue" in creating successful diagnostic tools for developing countries. Yager added that the researchers dried the chemical reagents so that the tests would not require refrigeration.

The cards retained 80% to 96% of their activity after 60 days of storage at high temperatures

TUBERCULOSIS

New avenue for TB therapy Masses of immune cells that form as a hallmark of tuberculosis (TB) have long been thought to be the body's way of trying to protect itself by literally walling off the bacteria.

owever, a new study in the January 9th issue of the journal Cell, a Cell Press publication, offers evidence that the TB bacteria actually sends signals that encourage the growth of those organized granuloma structures, and for good

reason: each granuloma serves as a kind of hub for the infectious bugs in the early stages of infection, allowing them to expand further and spread throughout the body. "This fundamentally turns our understanding of granulomas all topsy turvy," said Lalita Ramakrishnan of the University of Washington, Seattle. "Scientists thought they were protective, but they are not - at least not in early infection. The bacteria use them to reproduce and disseminate themselves." Not only do the bacteria expand themselves within the first granuloma to form, she added, but some of the immune cells in that initial mass leave to start new granulomas elsewhere. Those new granulomas then also serve as breeding grounds for the bacteria. The finding suggests a new avenue for TB therapy at an important time in the struggle against TB infection. "We might think about ways to prevent granulomas that might be therapeutic," Ramakrishnan said. That might be done either by intercepting the bacterial signal that spurs granulomas' formation or by manipulating the human immune system in some other way. "Finding a new way to intervene in the infection is particularly relevant now because there is a horrible epidemic of drug-resistant TB," she added. "Many of the bugs are resistant to practically everything." At the outset of human pulmonary tuberculosis, the inhaled bacteria (Mycobacterium tuberculosis) is gobbled up by immune cells known as macrophages and transported into the lung. There, infected macrophages recruit additional macrophages and other

H

immune cells to form granulomas. Under the classical view, those granulomas help protect against the bacteria, even if they don't successfully contain the infection. They were also thought to form only after the adaptive immune system shifts into gear. But Ramakrishnan's team began to find evidence calling that classical view into question by studying the disease in zebrafish embryos. Because zebrafish embryos are transparent, they allowed the team to literally watch the infection take hold and spread in real time. Their initial studies showed that, contrary to the classical view, granulomas form well before adaptive immunity comes into play, within days of infection. Indeed, granulomas' formation coincides with the bacteria's expansion. In addition, in embryonic fish infected with a less-virulent, mutant strain of bacteria, which lacked a secretion system known as ESX-1/RD1, granulomas didn't form nearly as well. Together, those findings suggested to Ramakrishnan's team that granuloma formation actually works not as a protective manoeuvre on the part of the infected host, but rather as a bacterial tool for expanding infection. To further investigate in the new study, the researchers observed and quantified the events in zebrafish embryos infected with normal TB bacteria and the mutant bacteria lacking the ESX-1/RD1 system. They found that, once transported inside of cells by macrophages, the bacteria use the RD1 signal to call on new macrophages to come and move in to the growing granuloma. As multiple macrophages arrive, they efficiently find and consume infected and dying macrophages to become infected themselves. That process leads to a rapid, iterative expansion of infected macrophages and thereby bacterial numbers, they report. The primary granuloma also seeds secondary granulomas as infected macrophages leave for other parts of the body. "In summary," the researchers wrote, "we propose that the pathway of granuloma formation and subsequent bacterial dissemination is based upon macrophage responses that are of themselves generally protective and that work reasonably well against less virulent (i.e., RD1-deficient) infection. Rather than block these host responses, RD1-competent mycobacteria appear to accelerate them to turn the granuloma response into an effective tool for pathogenesis. The initiation of the adaptive immune response then may halt bacterial expansion not by forming granulomas as suggested by the classical model but by altering the early granuloma into a form of stalemate between host and pathogen." http://www.cellpress.com

Tuberculosis commandeers body's defences to gain foothold Tuberculosis bacteria can commandeer the body's defences in the early stages of infection and redirect them for their own offensive strategies, according to results reported in the scientific journal, Cell.

he dense granulomas characteristic of TB were originally thought to thwart infection by walling-off newly invading tuberculosis bacteria and preventing their spread. These published findings suggest that these structures do just the T

opposite, at least in the early stages of infection. "Tubercles or granulomas have long been considered host-protective. What we observed completely overturns the fundamental dogma on their role, at least early in infection," said Dr. Lalita Ramakrishnan, University of Washington (UW) associate professor of microbiology, medicine, and immunology, who conducted the study with Dr. J. Muse Davis of the Immunology and Molecular Pathogenesis Graduate Program at Emory University and a visiting scholar at the UW. Granolomas are dense, complex clusters of immune cells, some of which are infected with TB bacteria. The outer edges are granulomas are surrounded by tightly interlocked white blood cells. Evidence from Ramakrishnan's and Davis' latest research suggests they might be created when newly arrived TB bacteria grow and emit signals to recruit macrophages -- the body's germ-eating and clean-up cells -- to the initial infection site, then pirate the macrophages to truck fresh bacteria to other spots and replicate themselves there to establish more granulomas. The granulomas form within days of infection. This occurs during the period when the body is trying to launch its first, generalized response to infection, called innate immunity. Later, when the body targets its fight, called adaptive immunity, Ramakrishnan says that the host and the bacteria usually reach a stalemate. "One of the reasons we are studying the mechanisms of early TB infection," Ramakrishnan said, "Is to see where medical science might be able to intervene to stop the disease with new treatments without the problem of creating antibiotic resistance." For example, she said, if scientists can figure out how TB bacteria signal to recruit and exploit macrophages and usurp the body's immune processes to gain a foothold, perhaps researchers could then find a way to block this takeover. By comparing fully virulent wild strains of bacteria that have a secretion system called ESX-1/RD1 with less virulent, mutant strains without this system, Ramakrishnan and Davis found that RD1 appears to encourage macrophages to arrive quickly at the site of infection. These macrophages moved five times faster than macrophages heading to the mutant bacteria, and covered greater areas with their haphazard movements. The researchers saw that the fast macrophages took on the striking appearance of white cells racing to the scene after a chemical alarm: they had elongated centres, a ruffled front edge, and a trailing rear extension. The roundness of the slower macrophages going to the mutant bacteria indicated that they weren't getting the same "hurry up" chemical signal. Soon after arriving at the site of the wild-type, virulent bacteria, the macrophages became infected by engulfing the remains of other, previously infected macrophages, the researchers noted. RD1 is suspected to hasten the death of infected macrophages. The macrophages had collapsed like deflated balloons, but the waxy TB rods inside them were safe in the intact macrophage cell membrane. Several macrophages would help dispose of a single dead partner, thereby resulting in more infected cells for the bacteria

This re-engulfing of virulent bacteria from dying macrophages is

likely a major mechanism for

granuloma expansion

to grow in. In contrast, the dying macrophages infected with mutant bacteria did not summon even nearby macrophages to come to them. "This re-engulfing of virulent bacteria from dying macrophages is likely a major mechanism for granuloma expansion," Ramakrishnan noted. The researchers observed that some of the newly infected macrophages left the original granuloma. The fluorescent-labelled bacteria inside them were later found at new granulomas elsewhere in the host. "The bacteria in all the exiting macrophages remained fully viable after departure and had the potential to initiate new granulomas," Ramakrishnan observed. "The macrophages exiting the original granuloma were leaving to seed distant granulomas to spread the infection." The role of RD1 in nascent granulomas revealed by this study, the researchers said, is likely a critical factor in the irrevocable early bacterial expansion that establishes the infection. Bacteria producing the RD1 virulence factor actually accelerate parts of the body's innate immune response of macrophage recruitment, macrophage movement, and macrophage collapse and death, the researchers wrote. Instead of enhancing the body's ability to halt a dangerous pathogen, the acceleration of these parts of the immune response is directed by a bacterial virulence factor and promotes bacterial growth, they concluded. This study was supported by grants from the National Institutes of Health and the Burroughs Wellcome Foundation, as well as an American Society for Engineering Education predoctoral fellowship. http://www.washington.edu

PAEDIATRICS

All countries should offer universal infant immunization for hepatitis B All countries should offer universal infant immunization for hepatitis B, write Dr. Christopher Mackie from McMaster University and co-authors in a public health analysis in CMAJ.

pidemiological studies suggest that roughly one-third of chronic hepatitis B infections are acquired during infancy and early childhood.

In Canada, British Columbia, New Brunswick and Prince Edward Island are the only provinces to offer universal hepatitis B vaccination to infants. The incidence of acute hepatitis B in BC is now consistently below the national average, after years of having a

E

higher incidence rate. Globally, 98% of universal hepatitis B immunization programs are offered in infancy. While vaccination for adolescents offers protection, booster shots are unnecessary for those who were immunized as babies. "The few jurisdictions that continue to offer universal immunization in adolescence rather than infancy should consider changing to an infant program," write the authors. They advocate adequate national immunization registries and surveillance systems to monitor vaccine strategies. http://www.cma.ca/cmaj

Paediatric vaccine propels sharp drop in meningitis cases A paediatric vaccine with University of Rochester roots has proven to be highly successful at reducing cases of bacterial meningitis across all age groups. That is the conclusion of a seven-year study, the results of which appeared today in the New England Journal of Medicine. "This is a very effective vaccine and a textbook example of herd immunity," said Nancy M. Bennett, M.D., M.S., professor of Medicine, director of the Center for Community Health at the University of Rochester Medical Center, and deputy director of the Monroe County Department of Public Health. "Even though the vaccine is only given to infants, it has proven highly effective in reducing infections among people who don't get vaccine, as well as among those who do." The paediatric pneumococcal conjugate vaccine, which is marketed under the brand name Prevnar by Wyeth, was introduced in 2000, and a year later the CDC recommended that it be given to all children younger than 2 years. The vaccine was created using a "conjugate" vaccine platform that was developed by URMC paediatric researchers in the 1980s.The process makes a vaccine more effective by linking it to a protein that spurs an infant's immune system to fight an infection especially vigorously. Designed to provide immunity Prevnar is designed to provide immunity to 7 serotypes - or strains - of the bacteria streptococcus pneumoniae. While commonly associated with pneumonia and blood infections, pneumococcus is also the most common cause of bacterial meningitis - a potentially life threatening inflammation in the central nervous system. Bennett - a co-author of the study - oversees the Rochester Emerging Infections Program, one of several sites in a national surveillance and research network funded by the Centers for Disease Control and Prevention (CDC).The network tracks the

The process makes a vaccine more effective by linking it to a protein that spurs an infant's immune

system to fight an infection especially

vigorously

epidemiology of several bacterial and viral diseases that are preventable by vaccines and evaluates the effectiveness of new vaccines after they have been introduced. The other sites included in the study are Baltimore, Connecticut, Minnesota, Tennessee, San Francisco, Atlanta, and Oregon. Incidence declines The study included data on 1379 cases of pneumococcal meningitis between 1998 and 2006; 71 of the cases were from the 7-county Rochester region. By the end of the seven-year period, researchers found that incidence of meningitis caused by all serotypes had declined by more than 30% across all age groups. Meningitis caused by the 7 strains in the vaccine declined 73%. The vaccine even reduced infection rates in serotypes of the disease that were related to, but genetically different from the ones targeted by the vaccine. In a finding that was a cause for concern, the researchers also saw a small increase in disease caused by serotypes that are not included in Prevnar. However, the overall decline in disease far outweighed the small increase in the disease caused by the serotypes not included in the vaccine. Researchers also point out that there are new vaccines under development that may provide protection from these strains. http://www.urmc.rochester.edu

Magnesium sulphate protects babies against cerebral palsy Giving pregnant mothers magnesium sulphate when they are at risk of very preterm birth can help protect their babies from cerebral palsy, according to an international review of research involving the University of Adelaide, Australia.

he findings of this review - published today on the international research website The Cochrane Library - could help decrease the incidence of this disabling condition, which affects one in 500 newborn babies overall and one in 10 very

premature babies (less than 28 weeks gestation). Magnesium sulphate therapy involves giving doses of magnesium sulphate to pregnant women via injection. The potential for magnesium sulphate to decrease the risk of cerebral palsy in babies was first proposed in the early 1990s. The new Cochrane review, which supports this suggestion, was carried out by leading researchers from Australia (University of Melbourne and University of Adelaide), France (University Hospital, Rouen) and the United States (University of Alabama). The review involved data from 6145 babies included in five trials of antenatal magnesium sulphate therapy.

T

For infants born very premature, there is a high risk of cerebral palsy

"For infants born very premature, there is a high risk of cerebral palsy," says one of the researchers, Professor Caroline Crowther, Director of the University of Adelaide's Australian Research Centre for Health of Women and Babies (ARCH). "This new Cochrane review shows there is now evidence to support giving magnesium sulphate therapy to women at risk of very preterm birth to increase their unborn baby's chance of survival, free of cerebral palsy." The exact mechanism of magnesium sulphate in protecting the developing brain is not certain. However, magnesium is vital for normal cell function, may protect against destructive molecules that can harm cells, and in some circumstances improves blood flow. Side effects of the treatment include flushing, sweating, nausea, vomiting, headaches and palpitations. However, the researchers found no increase in major complications in mothers due to magnesium therapy. "Given the positive findings of the Cochrane review, further studies will need to be conducted to clarify exactly how magnesium sulphate works as a neuroprotective agent, who should receive the medication and how best the treatment should be given," Professor Crowther says. http://www.adelaide.edu.au

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