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Internaf Newsletter May 2000 Issue Page 4Home Index Page1 Page2 Page3 Page4
Viagra
(sildenafil) may reduce levodopa-induced dyskinesia in Parkinson’s patients
by
Richard Robinson
SAN DIEGO, CA—May 3, 2000
--Sildenafil (Viagra) may provide a novel treatment for motor complications
in late-stage Parkinson’s disease, according to a study presented at the
52nd Annual Meeting of the American Academy of Neurology held
here May 2, 2000. While levodopa is the most effective medication for
Parkinson’s disease, its long-term use leads to dyskinesias, or abnormal
uncontrolled movements, in more than 50 percent of patients within five
years. Sildenafil has been used increasingly in Parkinson’s
patients to treat erectile dysfunction. David Swope, MD, a neurologist
at Loma Linda Medical School, in Loma Linda, CA, has begun to gather evidence
that sildenafil may be an effective treatment for dyskinesia, as well.
Dr. Swope became interested in this possibility when
one of his advanced PD patients reported that when he took 50 mg of sildenafil,
his dyskinesia nearly completely resolved. This patient later decreased
his daily dose to 25 mg, with continued benefit for over one year. Dr. Swope subsequently treated eight other PD patients,
five men and three women, with open-label sildenafil for moderate-to-severe
peak-dose dyskinesias. Each patient received 25 mg of sildenafil on two
consecutive days in addition to their previously optimized anti-parkinsonian
medications (including amantadine, an antiviral drug with some antidyskinetic
effects). Five of eight patients reported improvements, with
three reporting complete resolution. One of three non-responders went
on to try 50 mg, with noted improvement at the higher dose. All responding
patients reported benefit for the entire day, with dyskinesia returning
after treatment was discontinued. No patient reported worsening of parkinsonian
symptoms, and several reported improvements. “In small, open-label studies such as this, the placebo
effect always has to be considered,” cautioned Swope. “While recognizing
the limitations of this study, these results suggest that sildenafil may
be an effective treatment for drug-induced dyskinesias in Parkinson’s
disease.” Dr. Swope is currently beginning a double-blind trial.
Copyright © 2000 P\S\L Consulting Group Inc. Judith Richards, London, Ontario, Canada
SENT TO YOU FROM FARA- The Friedreich's Ataxia Research Alliance The ENTIRE articleVery Late-Onset Friedreich Ataxia Despite Large GAA Triplet Repeat Expansions is available at:http://archneur.ama-assn.org/issues/v57n2/full/nob8393.html#r20 Includes interesting background information on different ages of onset & severity, footnotes and links to other FRDA information and statistics.
SENT TO YOU FROM FARA- The Friedreich’s Ataxia Research Alliance Excerpt: It
should be noted that these proportions of positive test results are likely
to increase as additional disease mutations are discovered for relatively
common syndromes such as... ataxia, Archives of Neurology; March 2000 To
Test or Not to Test?
Thomas D. Bird, MD WHEN
DEALING with possible genetic diseases it is important to remember that
“familial is not always genetic and genetic is not always familial.” Familial
simply means more than 1 case of a disorder in a family. Familial instances
of a disease can certainly have toxic or infectious causes as a result
of common exposure. Alternatively, single cases of a disorder in a family
can have a primary genetic cause. Such single cases are often referred
to as isolated or sporadic. There are at least 5 explanations for the
sporadic occurrence of a possible genetic disorder. The first possibility
is that the cause is not genetic, but actually acquired or environmental,
a so-called phenocopy. Second, autosomal recessive genetic diseases often
occur only once in a family, especially in small sibships. Third, the case may represent a new mutation of an autosomal
dominant disease. Fourth, other family members may also carry the dominant
mutation, but not express obvious symptoms or signs of the disease. This
is called reduced penetrance. Finally, the biological father may not be
the social father as a result of adoption or false paternity. Note that
in the first 2 examples there is a very low recurrence risk to children
of the patient vs a high (50%) recurrence risk to children in the other
3 examples. Many direct DNA diagnostic tests are now available for neurogenetic
diseases, ... For full article, go to:
Sent to you from FARA -the Friedreich's Ataxia Research Alliance Hum Mol Genet 2000 Apr 12;9(6):887-892 Recent advances in the molecular pathogenesis of Friedreich ataxia.Puccio H, Koenig M Institut de Genetique et de Biologie Moleculaire et Cellulaire Strasbourg, France[Record supplied by publisher] Friedreich ataxia, the most frequent cause of recessive ataxia, is due in most cases to a homozygous intronic expansion resulting in the loss of function of frataxin. Frataxin is a mitochondrial protein conserved through evolution. Yeast knock-out models and histological data from patient heart autopsies have shown that frataxin defect causes mitochondrial iron accumulation. Biochemical data from patient heart biopsies or autopsies have revealed a specific deficiency in the activities of aconitases and of mitochondrial iron-sulfur proteins. These results suggest that frataxin may play a role either in mitochondrial iron transport or in iron-sulfur cluster assembly or transport. Iron abnormalities suggest a pathogenic mechanism involving free radical production and oxidative stress, a process that might be sensitive to antioxidant therapies. PMID: 10767311
Sent to you from FARA- the Friedreich's Ataxia Research Alliance Genetic disorders affecting proteins of iron metabolism: clinical implications.Sheth S, Brittenham GM Department of Pediatrics, [Medline record in process] Remarkable progress is being made in understanding the molecular basis of disorders of human iron metabolism. Recent work has uncovered unanticipated relationships with the immune and nervous systems, intricate interconnections with copper metabolism, and striking homologies between yeast and human genes involved in the transport of transition metals. This review examines the clinical consequences of new insights into the pathophysiology of genetic abnormalities affecting iron metabolism. The proteins recently found to be involved in the absorption, transport, utilization, and storage of iron are briefly described, and the clinical manifestations of genetic disorders that affect these proteins are discussed. This chapter considers the most common inherited disorder in individuals of European ancestry (hereditary hemochromatosis), a widespread disease in sub-Saharan populations for which the genetic basis is still uncertain (African dietary iron overload), and several less frequent or rare disorders (juvenile hemochromatosis, atransferrinemia, aceruloplasminemia, hyperferritinemia with autosomal dominant congenital cataract, Friedreich's ataxia, and X-linked sideroblastic anemia with ataxia). PMID: 10774476, UI: 20236291
Internaf Newsletter May 2000 Issue Page 4 |