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The Star Online: Lifestyle: Health

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• The osteoarthritis puzzle
• Haemophilia: When you can't stop bleeding
• Workout for better digestion

The osteoarthritis puzzle Posted: 21 May 2014 09:00 AM PDT While people with osteoarthritis struggle to move, there's plenty of movement in research as scientists work through the biological puzzle of osteoarthritis to come up with potential treatments. HER foot pain began 15 years ago, leading to a 2002 diagnosis of osteoarthritis, which left her limping and unable to walk for extended periods of time. And it progressively worsened. In time, Deborah Cole Thomas, 60, would undergo surgeries to fuse joints in both feet along with a left-ankle replacement, all from the wear-and-tear form of arthritis. She endured shoulder pain and more recent problems with right-knee pain, which she likens to a knife stab. Round-the-clock pain medications are a must. Deborah Cole Thomas' arthritis has led to an ankle replacement and two mid-foot fusions. She works out in a gym to help her joints remain flexible. – MCT   "I try not to let it affect me," Thomas said, noting that her husband, Llewellyn, 82, has had both arthritic knees replaced. "It drives me to keep moving. I watched my mum give up, and her hands became so crippled she had to be fed." Thomas, now retired, worked as a Westinghouse computer engineer, spending hours at a desk that made her "feel like the Tin Man in The Wizard of Oz". She'd stand and struggle to flex stiffened joints. In coming years, she faces further surgeries, including knee-replacement surgery. But she's still walking, with the goal of 10,000 steps a day and an average of about 7,000. "I wouldn't go to climb Mount Washington – or Kilimanjaro," she said, adding that osteoarthritis can be immobilising if you let it. She also can't run and isn't allowed to jump. Doctor's orders. But she works around those limitations. "There's always something I can do just to keep moving." Innovative solutions While people with osteoarthritis struggle to move, there's plenty of movement in research as scientists work through the biological puzzle of osteoarthritis to come up with potential treatments. A University of Pittsburgh research team, led by Rocky S. Tuan – professor and executive vice chairman of the department of orthopaedic surgery and director of the Center for Cellular and Molecular Engineering – is making headway in understanding the complex stew of enzymes (histones), proteins and genes that cause osteoarthritis while identifying a potential treatment to slow the rate of cartilage destruction. There's further breaking news from the Tuan camp that sounds like science fiction: His team is using a 3-D printer, which makes structures one layer at a time, to make new joints. Using a solution containing the patient's stem cells, along with growth factors and scaffolding material, the 3-D printer constructs actual cartilage in the right shape to replace damaged cartilage. The stem-cell solution extruded through a catheter also could be used to create new cartilage, as guided by a 3-D printer, directly onto the joint bone. The team's tissue-engineered joints already have shown success in large animals, raising the promise of creating replacement joints for people now dependent on plastic and metal ones. The process could be particularly useful in repairing battlefield injuries. Tuan announced the success on April 27 at the Experimental Biology 2014 scientific sessions and meeting in San Diego. "We essentially speed up the development process by giving the cells everything they need, while creating a scaffold to give the tissue the exact shape and structure that we want," Tuan said, adding that his team continues working to develop cartilage more closely resembling human cartilage. "Total joint replacements involving plastic and metal joints work well, but they don't last long enough," Tuan said. "For someone who is 60, that's OK. But if you are in your 30s, that's not good because you may need revision after revision. "We are not in position to say that it will last a lifetime. Time is the true test," Tuan said of the tissue-engineered joints his team has created. "I can only say it's very promising and is looking good." Joints, the business end of bones, include a covering made of flexible and protective cartilage to prevent damage from friction. But chronic wear and tear from overuse, traumatic injury or bone misalignment, among other factors such as obesity, promotes a biological process, not yet fully understood, that degrades cartilage. A common condition Osteoarthritis represents 80% of all cases of arthritis, whose various forms plague 27 million Americans, making arthritis the nation's major form of physical disability. The disease burden is particularly acute in the aged population, with one out of two individuals older than 65 having at least one joint affected. In other promising University of Pittsburgh research, Tuan and Dr Veronica Ulici, an Arthritis Foundation-supported post-doctoral fellow at the university and medical doctor, are focusing on a method to prevent destruction of the cartilage, which would do away with the need to replace joints. "The joint is a very interesting organ," Tuan said. "There is no blood flow there, or nerves." The immune response in the joint that occurs from chronic wear and tear or injury increases the level of unhealthy inflammation, which eventually causes cartilage degradation. Tuan said, "It tries to repair itself, but in the end it fails." Tuan, a doctor of biochemistry and cell biology, and Ulici have investigated the process, which focused attention on the histone deactetylase enzymes, or HDAC. Injury to the joint activates certain genes to produce known inflammatory factors, which increase the activity of degradative enzymes. Genes activated by injury can be bad ones, initiating a vicious cycle of enzyme degradation that causes fibrillation on the cartilage surface while chewing up cartilage. The studies involving cow tissues show that injured cartilage appears to generate increased levels of HDAC enzymes, raising the specter that they play a key role in activating the changes leading to cartilage damage. But a pharmaceutical agent that inhibits HDAC, already being tested as a treatment for lymphoma, slows down the degradation of cartilage, the Pitt team has found. As such, it holds promise as a treatment, with the advantage of already being tested for safety in human clinical trials as a lymphoma treatment. It would take five or more years before any treatment is available, if all goes well with the research. "Once we know the effects, we can stop them with treatment," said Ulici, a key figure in the series of studies. "If we can do that, we can prevent osteoarthritis and its changes in the tissue." While the pharmaceutical agent doesn't stop cartilage degradation, "we do see good improvement", Ulici said. "The inflammatory molecules are going down." "Obviously, the goal is to prevent degradation from happening in the first place," Tuan said. "Based on Veronica's findings, if someone gets banged up one way or another, there's a way to make sure HDAC activity is involved, then use inhibitors that are injected to avoid degradation" of the cartilage. Cutting edge research There's even more news that could advance treatments for osteoarthritis. The Pitt team also is using tissue engineering to develop human tissue and cartilage in a laboratory dish that can be used to test the effect of drugs. The live model of human joint tissue is being heralded as the creation of "the first example of living human cartilage grown on a laboratory chip". For now, the engineered cartilage tissue on a computer chip will serve "as a test-bed for researchers to learn about how osteoarthritis develops" and to develop new drugs. "We hope that the methods we're developing will really make a difference, both in the study of the disease and, ultimately, in treatments for people with cartilage degeneration or joint injuries," said Tuan, who also serves as director of the McGowan Institute for Regenerative Medicine and director of the Center for Military Medicine Research at the Pitt School of Medicine. Osteoarthritis, the Arthritis Foundation website states, "leads to 632,000 joint replacements per year, with a total cost of US$128bil (RM422.4bil) in 2012 for medical care and indirect expenses, including lost wages and productivity. One in two people will develop a form of arthritis in their lifetime." It is distinct from rheumatoid arthritis, an autoimmune disease that causes chronic inflammation in flexible joints, with potential to lead to severe disability if left untreated. But it affects less than 1% of Americans. The foundation said trends suggest that "half of all adults will develop symptomatic osteoarthritis of the knee at some point in their lives and the risk increases with obesity to two of every three obese adults". Women older than 50 are more commonly affected by osteoarthritis than men, with it typically beginning after age 40. But arthritis is a tough opponent. Thomas, as board member of the foundation's regional chapter, says people must work to stave off immobility by walking and exercising. She's trying to avoid another round of foot surgery. That's why the Pitt research is stirring optimism for her and the Arthritis Foundation. "Replacing cartilage with extra good stuff would be fantastic," she said. "Oh, Lord, it's exciting. I can't wait." – Pittsburgh Post-Gazette/McClatchy-Tribune Information Services

Haemophilia: When you can't stop bleeding Posted: 21 May 2014 09:00 AM PDT Haemophilia is a group of hereditary genetic disorders that impair the body's ability to control blood clotting or coagulation. MY nephew recently had a swelling of his right knee after a fall during football practice. At first, we thought the swelling was due to the knee injury. But when the swelling did not subside, we took him to a doctor. After a series of tests, he was diagnosed with haemophilia. What is this? Haemophilia is a bleeding disorder in which blood does not clot normally. This means that if you have haemophilia, you may bleed for a longer time compared to someone who doesn't have haemophilia. You may bleed inside your body, especially in your knees, ankles and elbows. Sometimes, you may even bleed inside your organs. How did he get haemophilia? Is it due to an injury or infection? Haemophilia is mostly an inherited disease. This means that your nephew got it from his parents. However, there are some forms of haemophilia which are not inherited. These are called acquired haemophilia, but they are rare. You didn't inherit it, but over time, your body forms antibodies that attack clotting factors, and you present with symptoms of haemophilia. This is an autoimmune disease. Something to note is that inherited haemophilia is passed down through the X chromosome. We all have two sex chromosomes, the X and the Y. If you are a girl, you inherited one X chromosome from your mother and the other X from your father. If you are a boy, you inherited one X chromosome from your mother and a Y from your father. Because the gene for haemophilia is located on the X chromosome, it cannot be passed down from father to son, only from mother to son. Most women who inherited the haemophilia gene and have it on one of their X chromosomes are simply carriers, and they do not manifest signs or symptoms of haemophilia. Inherited haemophilia is predominantly a male disease. Why do haemophiliacs bleed? In haemophilia, you have little or no clotting factor in your blood. There are several types of clotting factors that every human being has. These work together with platelets in a complex clotting process to stop bleeding should you get an injury. This is how the clotting process works. When an injury occurs and one or more of your underlying blood vessels is traumatised, the walls of your blood vessels contract quickly to limit the flow of blood outside your body. The platelets, which are in your blood, come rushing to the site of injury. They stick there, plugging the area, to stop the bleeding. As they do so, they also release some chemicals to attract other cells to the area to make them stick and clump together. Then the clotting factors, which are also swimming in your blood, come to play. They work on the surface of these platelets to start a cascading reaction. This results in the formation of a fibrin clot, which is something like a mesh to permanently stop your bleeding. Normally, these clotting or coagulation factors are dormant. They only act when you are injured. So in haemophilia, which clotting factor is missing? There are 13 clotting factors altogether. They are all written in Roman numerals, like I, II, III and so on. They act in a certain cascade which I actually memorised in medical school, but granted, it's a complicated activation process. But there are several types of haemophilia. ·Haemophilia A: This one is caused by the lack of clotting factor 8 (VIII). It is the most common form of haemophilia, occurring in as many as eight out of 10 haemophiliacs. ·Haemophilia B: This one is caused by the lack of clotting factor 9 (IX). It is the second most common type. ·Haemophilia C: This one is caused by the lack of clotting factor 11 (XI), and it is a milder disease compared with the other two. How do we know if we have haemophilia? If your clotting factor levels are very low, you may experience spontaneous bleeding – which means you can bleed even without any injury. If your levels are mild to moderately low, you may bleed only after injury, or surgery. Do look out for: · Large or deep bruises · Joint pains and swellings caused by internal bleeding · Blood in your urine or stool · Prolonged bleeding from cuts or injuries or after surgery · Nose bleeds for no reason at all Can we treat haemophilia? There is no cure for haemophilia, but the bleeding can be controlled and you can actually live a fairly normal life. Treatments include infusions of clotting factors, injections of the hormone desmopressin (DDAVP) and antifibrinolytics. Dr YLM graduated as a medical doctor, and has been writing for many years on various subjects such as medicine, health, computers and entertainment. For further information, e-mail starhealth@thestar.com.my. The information contained in this column is for general educational purposes only. Neither The Star nor the author gives any warranty on accuracy, completeness, functionality, usefulness or other assurances as to such information. The Star and the author disclaim all responsibility for any losses, damage to property or personal injury suffered directly or indirectly from reliance on such information.

Workout for better digestion Posted: 21 May 2014 09:00 AM PDT Encourage better digestive health in children through various healthy activities. DIGESTIVE disorders are fairly common and may have a variety of causes. While it is true that your child's dietary intake plays an important role on digestive health, ensuring that she maintains a physically active lifestyle will have a positive impact on his digestive health. Getting regular exercise can help your child maintain a healthy body and also helps her digestive system work the way it should. As parents, it is important to keep two main things in mind: > Ensure your own lifestyle incorporates physical activity (children tend to follow their parents' lifestyle). > Keep a part of your child's daily schedule free for physical activity such as games, sports, or any form of unstructured play. Being physically active can work wonders for your child's digestive system: > Regular exercise stimulates intestinal muscles to contract, thus regulating bowel movements. > Helps relieve constipation by moving food through the digestive system. > Better absorption of nutrients. > Helps gas pass through the digestive tract quicker. One of the factors leading to higher levels of obesity among children in Malaysia now is a lack of physical activity. Don't let your child become another statistic in the current trend of obese children. There will be a World Digestive Health Day roadshow at 1Utama Old Wing Concourse in PJ from May 21 to May 25, 10am-10pm.

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