2º INTERNATIONAL MEXICO POLIO SYNDROME PPS SYMPOSIUM
PRESS RELEASE ON MEXICO'S
2ND INTERNATIONAL POST POLIO SYNDROME
Liliana Marasco Garrido, President and Co-Founder of Litaff
Shari Fiksdal, President & Co-Founder of International
Post Polio Support
THE LATEST NEWS ON POST POLIO SYNDROME (PPS)
Three important issues came from the symposium, we feel it is important that we share this latest news with everyone.
Some may already know there is a WHO Code for Post Polio Syndrome, that there is
a possible marker waiting for approval by the ...Journal
And that they are continuing to find IV Gamma globulin is helping those
of us with PPS! We apologize that this release has been delayed due to to ill health.
LATEST INVESTIGATIONS INTO THE CAUSE
OF POST POLIO SYNDROME
Dr. Brian Joseph, PhD. (Harvard) brought us up to date on IV Gamma Globulin Studies of
Dr. H. Gonzalez! Dr. Kristian Borg and Henrick Gonzalez in Sweden have been working for
many years testing the benefits of IV Gamma Globulin for PPS patients.
Dr. Joseph asked Dr. Henrik Gonzalez about their test results since their last release in 2008.
Dr. Joseph explained that the tests being done in Sweden by
Dr. Henrick Gonzalez and Dr. Kristian Borg had proven to be successful
and their research into the cause of PPS was “revolutionary
1. The study proved gamma helps PPS.
2. The study shows we have fragments of polio protein in our spinal cords, which causes our immune systems to continue to battle the polio virus that was there. This and not dying neurons is what is causing PPS by weakening our immune systems. Our body is still in the fight mode to kill off the tiny polio fragments in our bodies. This does not mean we still have polio, just remnants of the old virus our immune systems are still attacking, causing further degeneration.
3. And even more importantly, they have found a blood test to tell if you have PPS!
Dr. Brian Joseph
The details will all be released as soon as the peer review process is complete.
Here is a letter from Dr. Henrik Gonzalez to Liliana Marasco Garrido of Litaff confirming the statements above!
Pharmalink AB today announces positive results from a follow‐on Phase III study of Xepol®,
its candidate for the treatment of post‐polio syndrome (PPS). The data have shown the candidate to be effective an
d well tolerated with no serious adverse events attributed to the product being reported in the treated patients.
The Phase III study, involving 142 patients, is a placebo controlled, double blind trial designed to evaluate the efficacy
and safety of Xepol® in PPS, a neurological pain and weakness syndrome in patients that have survived poliovirus infection.
The original placebo controlled, double blind Phase III trial was six months
(Gonzalez et al (2006) Lancet Neurology 5:493‐500)
and this follow‐ up period was another six months.
The follow‐on results strengthen the position of this novel treatment modality for PPS by demonstrating a reduction of
inflammatory cytokines in the cerebrospinal fluid and a significant reduction of symptoms of PPS while also showing that Xepol®
is safe and well tolerated with few or no side‐effects. Endpoints studied were pain, walking ability and SF‐36 scores (a common self assessment scoring system that measures physical and psychological variables).
All showed significant and clinically meaning fulresults. Full results are to be published in a peer review journal. Xepol®, the first medical PPS treatment , is an injectable biologic product, administered once per 9‐12 months, which down
‐regulates the inflammatory process in the nervous system of PPS patients. The concept and medical hypothesis was first developed by Dr Henrik Gonzalez and Professor Kristian Borg, scientists at the Karolinska Institute (Sweden)
. Pharmalink licensed the invention and is now working to bring the candidate towards registration.
“We are very encouraged by the outcome of the follow‐up analysis as it is clear from the results that Xepol brings relief from pain and muscle weakness to PPS patients,” said Johan Häggblad, Managing Director of Pharmalink.
“We are very excited about this data as currently there is no medical treatment for PPS and patients in the treated group have experienced a reduction in disease symptoms after just 12 months.”
“It is very rewarding to see that Xepol is demonstrating efficacy and the potential to help PPS patients,” said inventor and principal investigator Professor Kristian Borg. “We are looking forward to expanding the Xepol treatment procedure following product registration.”
Pharmalink is actively seeking a partner to bring Xepol® to the market. More than 1000 PPS patients have been treated with the drug and many return on an annual basis for new treatment courses. Xepol® has already achieved Orphan Drug Designation in the US and is patented in the major markets.
APPLAC México a la vanguardia en el Síndrome de Post Polio
THE POLIO CRUSADE IN AMERICAN EXPERIENCE A GOOD VIDEO
THE STORY OF THE POLIO CRUSADE pays tribute to a time when Americans banded together to conquer a terrible disease. The medical breakthrough saved countless lives and had a pervasive impact on American philanthropy that ...
A 41-year-old man developed an acute illness at the age of 9 months during which, following a viral illness with headache, he developed severe weakness and wasting of the limbs of the left side. After several months he began to recover, such that he was able to walk at the age of 2 years and later was able to run, although he was never very good at sports. He had stable function until the age of 18 when he began to notice greater than usual difficulty lifting heavy objects. By the age of 25 he was noticing progressive difficulty walking due to weakness of both legs, and he noticed that the right calf had become larger. The symptoms became more noticeable over the course of the next 10 years and ultimately both upper as well as both lower limbs had become noticeably weaker.
On examination there was wasting of the muscles of upper and lower limbs on the left, and massively hypertrophied gastrocnemius, soleus and tensor fascia late on the right. The calf circumference on the right exceeded that on the left by 10 cm (figure1). The right shoulder girdle, triceps, thenar eminence and small muscles of the hand were wasted and there was winging of both scapulae. The right quadriceps was also wasted. The wasted muscles were also weak but the hypertrophied right ankle plantar flexors had normal power. The tendon reflexes were absent in the lower limbs and present in the upper limbs, although the right triceps was reduced. The remainder of the examination was normal.
The patient's legs, showing massive enlargement of the right calf and wasting on the left
What is that nature of the acute illness in infancy?
What is the nature of the subsequent deterioration?
What investigations should be performed?
What is the differential diagnosis of the cause of the progressive calf hypertrophy?
An acute paralytic illness which follows symptoms of a viral infection with or without signs of meningitis is typical of poliomyelitis. Usually caused by one of the three polio viruses, it may also occur following vaccination and following infections with other enteroviruses.1 Other disorders which would cause a similar syndrome but with upper motor neurone signs would include acute vascular lesions, meningoencephalitis and acute disseminated encephalomyelitis.
A progressive functional deterioration many years after paralytic poliomyelitis is well known, although its pathogenesis is not fully understood.2 It is a diagnosis of exclusion; a careful search for alternative causes, for example, orthopaedic deformities such as osteoarthritis or worsening scoliosis, superimposed neurological disorders such as entrapment neuropathies or coincidental muscle disease or neuropathy, and general medical causes such as respiratory complications and endocrinopathies.3
Investigations revealed normal blood count and erythrocyte sedimentation rate and normal biochemistry apart from a raised creatine kinase at 330 IU/l (normal range 60–120 IU/l), which is commonly seen in cases of ongoing denervation. Electromyography showed evidence of denervation in the right APB and FDI with polyphasic motor units and complex repetitive discharges, no spontaneous activity in the left calf and large polyphasic units in the right calf consistent with chronic partial denervation. Motor and sensory conduction velocities were normal. A lumbar myelogram was normal. Magnetic resonance imaging (MRI) scan of the calves is shown in figure2.
Axial T1 weighted MRI scan (TR 588 ms, TE 15 ms) of the calves, showing gross muscle atrophy and replacement by adipose tissue on the left, and hypertrophy of the muscles on the right, with only minor adipose tissue deposition
The differential diagnosis of the progressive calf hypertrophy is given in the box.
Causes of calf muscle hypertrophy
Chronic partial denervation
hereditary motor and sensory neuropathy
spinal muscular atrophy
following paralytic poliomyelitis
Neuromyotonia and myokymia
continuous muscle fibre activity due to: chronic inflammatory demyelinating polyradiculopathy, Guillain Barre syndrome, myasthenia gravis, thymoma, thyrotoxicosis, thyroiditis