SCOTTISH HOSPITAL NEWS
‘LINK BETWEEN CHOLESTEROL AND DIABETES’: STUDY
The slight increase in risk of developing type 2 diabetes during statin treatment may actually be a consequence of having lowered cholesterol, rather than a direct effect of the drug, according to Oxford University research funded by the British Heart Foundation. The genetic study found that people with genes predisposing them to having lower levels of low density lipoprotein (LDL) cholesterol, had a decreased risk of heart disease and an increased risk of diabetes.
The researchers, from UCL and the University of Oxford, used large data sets of genetic information to investigate the possible effects of two types of cholesterol, low density lipoprotein (LDL) cholesterol and high density lipoprotein (HDL) cholesterol, and a form of dietary fat known as triglycerides, on a person’s risk of developing heart disease and diabetes.
The researchers found that individuals with genetic variations that increase their LDL cholesterol or triglyceride levels were at an increased risk of heart disease. They also found that individuals with genetic variations increasing their LDL or HDL cholesterol, and possibly triglyceride levels, were at a slightly decreased risk of having diabetes.
The results of this study, published in the journal JAMA Cardiology, confirm findings from many previous studies which have shown that increased levels of LDL cholesterol increase a person’s likelihood of suffering from a heart attack or stroke.
NEW STUDY SHEDS LIGHT ON HUNTINGDON’S DISEASE GENE
As many as 1 in 400 people have the mutated gene that causes Huntington’s disease – far more than previously thought - according to researchers at the University of British Columbia, the University of Aberdeen, and the Coriell Institute for Medical Research.
The study, published in the June 22, 2016, issue of Neurology®, the medical journal of the American Academy of Neurology, is the first to reveal how common the genetic cause of Huntington’s disease is in the general population.
Huntington’s disease is an inherited condition typically diagnosed in adult life, which causes involuntary movements and psychiatric problems. The symptoms of the disease, which become evident years after specific brain cells start to die, steadily worsen and lead to death fifteen to 20 years later.
The gene which causes Huntington’s disease, HTT, was discovered in 1993. It contains a section where three letters of the DNA code are repeated. Most people have up to 27 repeats in the gene. People with more than 40 repeats develop the disease, as do some of those with 37 to 39 repeats. But, until now, it has remained unclear how many people in the general population have the additional repeat mutation that causes Huntington’s disease, and how many of them are at risk of developing it.
‘It has been a difficult question to answer, since no one has ever examined the gene repeats in large numbers of people outside the clinic,’ says Chris Kay from the University of British Columbia, lead author on the manuscript. ‘We had estimates based on how many patients we see, but our study in Canada, USA and Scotland found far more mutations than expected.’
The majority of these had between 37 and 39 repeats, which usually results in Huntington’s disease starting over the age of 60. The new results suggest that many people with the mutation may never actually develop the disease.
‘We have known for many years that older Huntington’s disease patients tend to have smaller numbers of repeats,’ says Dr Michael R Hayden from the University of British Columbia, who directed the study. ‘But the high frequency of these mutations in the general public shows that we may be underestimating the number of elderly patients with Huntington’s disease. Their symptoms may not be clearly recognised as Huntington’s disease. Likewise, it may be that only some of these people will ever go on to develop Huntington’s disease, and that others are protected in some way.’
POSITIVE SMC DECISION ON INNOVATIVE ASTHMA TREATMENT
The Scottish Medicines Consortium (SMC) has issued positive advice for Nucala (mepolizumab) for restricted use in adult patients with severe refractory eosinophilic asthma within NHS Scotland.
This evaluation by the SMC means Health Boards across Scotland now have advice that will allow appropriate adult patients access to this first-in-class medicine. Mepolizumab is the only licensed biologic therapy in Europe that targets interleukin-5 (IL-5) which plays an important role in regulating the production and survival of eosinophils, an inflammatory cell known to be important in asthma.
Of the 5.4 million people in the UK receiving treatment for asthma, 380,000 live in Scotland. About five per cent of people with asthma have severe ‘refractory’ asthma and cannot achieve symptom control with existing therapies.
‘Patients with severe, difficult to control asthma have limited options to control their significant, debilitating symptoms; they are often reliant on steroid tablets, and may suffer the short and long term side effects associated with them,’ said Dr Tom Fardon, Consultant Respiratory Physician at Ninewells Hospital. ‘The introduction of
mepolizumab for patients in Scotland provides a new method to control asthma symptoms, reduce hospital admissions, and, critically, reduce the burden of steroids our patients endure. Mepolizumab will offer more patients with severe asthma the opportunity to control their disease and improve their quality of life.’
The SMC decision follows marketing authorisation by the European Commission of mepolizumab in December 2015.
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64