iblog

Thomas King: An 18-year-old British man has had his failing eyesight improved by cutting edge gene therapy. Steven Howard from Bolton, near Manchester, suffers from a rare form of blindness called Leber’s congenital amaurosis. The condition is the result of a faulty gene which prevents sufferers from manufacturing rhodopsin, a light-absorbing pigment which is a vital component of the human eye. Lack of this pigment has left Howarth with extremely poor night-vision since birth but his vision was progressively worsening and would have left him totally blind by his mid-to-late twenties. The treatment, pioneered by doctors at London’s Moorfields Eye Hospital, works by replacing the damaged gene. This rejuvenates the dying cells on the retina and restores vision as they recover. A healthy copy of the gene is inserted into the cells by injecting a fluid containing a modified virus which carries the healthy gene. When the virus ‘infects’ the retinal cells and copies its own genetic material across, it also copies the healthy gene and repairs the cells’ nuclei. The treatment has improved Howarth’s low-light vision 100-fold and has also improved his peripheral vision, allowing him to see out of the corner of his eye for the first time. Where once he could barely walk across a dimly lit room, Howarth now says he would ‘feel comfortable’ walking home at night. The study’s leader, Professor Robin Ali said that the result was "a major boost for the whole field". Professor Ali, who is the brother of Brick Lane author Monica Ali, admitted that he was surprised to see such a significant improvement but now felt that gene therapies for other vision-reducing conditions, such as macular degeneration, could soon be possible. He said “I find it difficult to remember being as excited as I am today about our science and what it might achieve.” The success is the second breakthrough by Moorfield’s Eye Hospital in just over a week. On the 21st of April, researchers at the hospital announced the trialling of a ‘bionic eye’ which could help sufferers of a degenerative eye disease, retinitis pigmentosa, to regain a basic level of vision. The ‘eye’ is actually a camera mounted on a pair of glasses. The camera picks up images and transmits them wirelessly to a receiver which is connected to the patient’s retina. The receiver sends a sequence of electrical impulses which the retina passes onto the brain. Here they are decoded as patterns of light and darkness to give subjects a vague outline of their surroundings. Researchers warned that it was ‘early days’ but said that they were hopeful for the trial’s success.

Thomas King: A new ‘smart drug’ for treating rheumatoid arthritis has received extremely positive results in two separate trials published this week in The Lancet. Medical schools at the University of Vienna and the University of Yokohama have studied rheumatoid arthritis sufferers over a wide age range being treated with tocilizumab, a drug developed by pharmaceutical giants Roche and Chugai. Both studies found that the treatment could massively reduce the severity of the symptoms which the patients had to suffer and could do so with fewer side effects than common treatments Rheumatoid arthritis is an autoimmune disorder which affects over 450,000 people in the UK and is far more common in women than men. The disease creates painful swellings in the joints and can even destroy the cartilage padding them, making the pain even worse. It can also lead to tiredness and other symptoms such as rashes and can increase the risk of heart disease. These symptoms are caused by the immune system mistakenly identifying cells of the sufferer’s own body as disease microbes. It attacks these cells by flooding them with white blood cells called T-lymphocytes The disease is usually treated with drugs called disease modifying antirheumatic drugs (DMARDs), the most common of which is called methotrexate. These drugs work by blocking the enzyme pathways needed to allow the T-lymphocytes to form and to attach to the sufferer’s cells. The major disadvantage of these treatments is that they are all extremely toxic and cannot be taken for a prolonged period of time, making them unsuitable for treating chronic sufferers. Tocilizumab works by attacking the problem from a different angle. It blocks the synthesis of a protein called interleukin-6 which is found in high concentrations in severely inflamed joints and, by doing so, claims to reduce the severity of the condition. It is also far less toxic as it blocks a less crucial pathway. The first study, by the University of Vienna, focussed on adult sufferers and says that the new drug, based on the structure of a human antibody, "significantly and rapidly improves the signs and symptoms of rheumatoid arthritis". In this trial, the drug was given to 623 patients with moderate to severe rheumatoid arthritis. A successful outcome for this study was defined as a 20% improvement in symptoms (under American College of Rheumatology criteria) Of the 623 patients, 205 were given 8mg of tocilizumab per kg of body weight, 214 patients received 4mg per kg of body weight and 204 received a placebo. The drugs and placebo were given intravenously every four weeks, along with methotrexate, at doses of 10-25mg per week. After 24 weeks, 59% of patients receiving the 8mg dose had shown a 20% decrease in symptoms. In those receiving 4mg, 48% recorded a response, compared with 26% in the placebo group. This, the study says, proves that tocilizumab could be “an effective agent for the treatment of patients with moderate to severe rheumatoid arthritis.” The second study, by the University of Yokohama, focussed on juvenile arthritis sufferers aged 2-19. It found an improvement in symptoms in 91% of the patients treated and hails tocilizumab as “a step forward in the control of a disease that has previously proved to be difficult to manage”. Both trials found adverse effects, such as gastric infections, in some subjects but, compared to the extreme side effects which traditional arthritis treatments can have, these were comparatively minor. Therefore, tocilizamub seems to represent a significant advance in the treatment of this painful and crippling disease.

Thomas King: Sales of Morrissey albums will soar, the poetry of Leonard Cohen will top the bestsellers lists, black will become (if possible) more fashionable. No, it's not the Eighties coming back, it's a new piece of research saying that, if you're depressed, you may need to live with it and not rely on pills to feel better because anti-depressants may not really work. The study, published yesterday in the journal PLoS Medicine and led by an academic from the University of Hull, took data from 35 clinical trials, covering the four most-prescribed anti-depressants in the US. The results from these studies were pooled and examined to see if, overall, there was any significant effect of anti-depressant. The research found that, overall, there was a improvement in mood when taking an anti-depressant. But it also found that an almost equal improvement in mood was seen when taking a sugar-pill that the subject was told was an anti-depressant. In fact, in two of the trials, patients reported feeling happier when taking the sugar-pill than they did when taking the actual drug. Interestingly, the trial found that the more depressed an individual was to begin with, the greater the benefit that they seemed to get from the drug. Severely depressed individuals were the group who reported the biggest difference in improvement of mood when taking the real drug and when taking the sugar pill. The study's authors say that this is a false result, "attributable to a decrease in responsiveness to placebo, rather than an increase in responsiveness to medication." More depressed people were no more likely to report an increase in mood with the anti-depressant, they were just less likely to report an improvement with the placebo. If these drugs have no real effect, then why are they still prescribed? In the year 2006/2007 there were over 31 million prescriptions for anti-depressants in the UK. Would so many people be taking them if they didn't make them feel better? According to the study's authors, any beneficial effects you might feel come down to a 'placebo effect'. We've probably all heard stories of people getting drunk on water because they believe it's vodka. This, in essence, is a 'placebo effect'; something affects you a certain way because you believe it should. Anti-depressants make you happier because you expect to be happier. After all, you're taking anti-depressants. So, should this finding be seen as a hammer-blow to depressives, one less way to scare away the black dog? No. If anything it should be seen as a hopeful message as it shows just how easily depression can be relieved if you're in the right frame of mind. They say "Let a smile be your umbrella" but an upbeat attitude could protect you from more than just rain.