London: Offering hope to thousands of people suffering from the psoriasis skin condition, a trail of a new drug has reported quick and extensive improvement of the disease.
The details published in The Lancet journal showed that 40 percent of people reported a complete clearance of psoriatic plaques after 12 weeks of treatment with the new drug and over 90 percent showed improvement.
People with psoriasis develop thick, red skin with flaky, silver-white patches called scales which can be itchy for sufferers.
“The visible effects of psoriasis can have a major and life-ruining impact on people’s confidence and self-esteem,” said lead researcher Chris Griffiths, professor of dermatology at University of Manchester in Britain.
The research tested 2,500 people with psoriasis. Half were given a new drug – ixekizumab – either once every two or four weeks. The other half were given a placebo or a widely used drug for psoriasis called etanercept.
“What we saw in this trial was not just the physical aspects of the disease clearing up, but people on the new drug also reporting a marked improvement in their quality of life as they felt more confident and suffered less from itching – far more than in the other two groups,” Griffiths added.
Around half of these patients in the trial showed improvement as early as week four of the trial and up to 71 percent had shown a high level of improvement, as measured using a scale called the Psoriasis Area and Severity Index, by week 12.
Ixekizumab is a monoclonal antibody – a cloned antibody – which neutralises the inflammatory effects of an interleukin (IL) a protein in the skin which carries signals to cells – known as (IL)-17A.
This protein is increasingly becoming recognised as one of the causes of the characteristic red, scaly plaques of psoriasis.
Human trial to assess efficacy of autism drug New York: A clinical trial to investigate the safety and efficacy of a drug therapy for autism has been launched in the US, University of California, San Diego School of Medicine has said in a statement.
The phase 1 clinical trial, which is recruiting 20 participants, will evaluate suramin — a century-old drug still used for African sleeping sickness — as a novel treatment for children with a diagnosis of Autism Spectrum Disorder (ASD).
ASD is characterised by social impairments, communication difficulties and restricted, repetitive and stereotyped patterns of behaviour.
“To date, there are no medications that can cure ASD, and very few that can improve its core symptoms,” said Robert Naviaux, professor of medicine, pediatrics and pathology at the UC San Diego School of Medicine.
Previous published research by Naviaux and colleagues reported that a single injection of suramin reversed symptoms of ASD in mouse models.
This trial is the first to test suramin in children with ASD.
It is also the first clinical investigation of a novel theory, advanced by Naviaux, that posits autism may be a consequence of abnormal cell communication resulting from abnormal activation of the cell danger response.
Cells threatened or damaged by microbes, such as viruses or bacteria, or by physical forces or by chemicals, such as pollutants, react defensively, a part of the normal immune response, Naviaux said.
Their membranes stiffen. Internal metabolic processes are altered – most notably mitochondria, the cells’ critical ‘power plants’ — resulting in activation of the cell danger response and reduced communications between cells.
Naviaux said the cell danger response theory does not contradict other research regarding the causes of autism.
Rather, it offers another perspective and, perhaps, a new therapeutic target.
The study will involve 10 to 12 clinical visits over three to four months for each child.
In the trial, suramin will be given as a single dose through an intravenous line. Half of the participating children will receive suramin, half will receive a placebo (saline infusion).
Behavioural and medical tests will be conducted before and after treatment, and include some blood and urine analyses, the statement said.