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Hepatolenticular Degeneration: more detail

Studies of protein metabolism in hepatolenticular degeneration (Research report) by Frank L Iber, 1956
Diseases of the Nervous System described for Practitioners and Students with Chapters on the Neurological Complications of Liver Disease and Hepatolenticular Degeneration. by Francis Martin Rouse ; Walshe, John Michael Walshe, 1956-01-01
Wilson's Disease: A Clinician's Guide to Recognition, Diagnosis, and Management by George J. Brewer, 2001-05-31
Orphan Diseases and Orphan Drugs (Fulbright Papers, Proceedings of Colloquia, Vol 3) by I. Herbert Scheinberg, 1986-12
Wilson's Disease by Tjaard Hoogenraad, 1996-07-15
Wilson's Disease for the Patient and Family: A Patient's Guide to Wilson's Disease and Frequently Asked Questions about Copper by George J. Brewer M.D., 2002-04-09
Liver-brain relationships by Ian A Brown, 1957
Die Wilson'sche Krankheit (Westphal-StruÌˆmpell'sche Pseudosklerose): Eine UÌˆbersicht uÌˆber die humangenetischen Forschungsergebnisse der Jahre 1967-1977 : Inaugural-Dissertation by Susanne Dworak, 1980
Wilson's disease: Familial presentatin by Ying-tung Kung, 1983

lists with details

Entrez PubMed
OBJECTIVE To describe the course of depression in a patient with hepatolenticular degeneration (Wil
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9
Entrez PubMed
hepatolenticular degeneration*/diagnosis hepatolenticular degeneration*/etiology hepatolenticular degeneration*/metabolism hepatolenticular degeneration*/
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=5
INVESTIGATION OF THE AMINOACIDURIA IN WILSON'S DISEASE (HEPATOLENTICULAR DEGENER
INVESTIGATION OF THE AMINOACIDURIA IN WILSON S DISEASE (hepatolenticular degeneration) DEMONSTRATION OF A DEFECT IN RENAL FUNCTION 1
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=439748
Studies On Copper Metabolism. XIII. Hepatolenticular Degeneration1
Tissue copper determinations in a case of hepatolenticular degeneration treated with BAL Metabolism of copper in hepatolenticular degeneration.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1072574
LRCP - Jim Koropatnick, PhD
Experimental model for Wilson s disease hepatolenticular degeneration. Role of metallothionein in cellular drug resistance and metaldependent protein
http://www.lrcc.on.ca/research/staff/jkoropatnick/current_projects.xml

Extractions: How to contact LRCP MORE TOPICS Research at LRCP - Cancer Research Laboratory Program - Radiation physics - Translation Breast Cancer Research Unit - Clinical Research Unit - Transgenic Core Facility Research Staff - Biological research - Radiation physics - Jerry Battista - Ann Chambers - Fred Dick - Gabriel DiMattia - Kevin Jordan - Jim Koropatnick - Joe Mymryk - Nathalie Berube - David Rodenhiser - Richard Rozmahel - Joe Torchia - Eva Turley - Jake Van Dyk - Siu-Pok Yee Education and training opportunities - Medical physics residency program Library and Information Services News and events - Recent news - Upcoming events - Innovation and discovery Donating Search: Research Research Staff RESEARCH AT LRCP
Wilson's Disease -- Encyclopædia Britannica
also called hepatolenticular degeneration, a hereditary defect associated with the metabolism of copper and characterized by the progressive degeneration of
http://www.britannica.com/eb/article?tocId=9077137
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So far, the institute has cured hepatolenticular degeneration patients for about 3000 from Taiwan, Hong Kong and other parts of China, the hospital is
http://www.lifesciences.cn/enshanghai/SPT--FullRecord.php?ResourceId=2254
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Translate this page ??, Mental Derangement/Research/hepatolenticular degeneration So far, the institute has cured hepatolenticular degeneration patients for about
http://www.lifesciences.cn/SPT--FullRecord.php?ResourceId=2254
MDVU Resource Library - Movement Disorders
Corticobasal degeneration (CBD) is a rare neurological disease in which parts of the brain Wilson disease, also known as hepatolenticular degeneration,
http://www.mdvu.org/library/disease/

Extractions: Resource Library Resource Library Special Events Classrooms Movement Disorders Corticobasal degeneration (CBD) is a rare neurological disease in which parts of the brain deteriorate. CBD is also known as corticobasal ganglionic degeneration, or CBGD. Paroxysmal dyskinesias are neurologic conditions characterized by sudden episodes of abnormal involuntary movements or hyperkinesias. Dystonia is a movement disorder characterized by sustained muscle contractions, usually producing twisting and repetitive movements or abnormal postures or positions. Cervical dystonia (CD) is a focal dystonia characterized by abnormal movements or postures of the neck and head. Essential tremor or ET is a common movement disorder characterized by involuntary, rhythmic oscillatory movements resulting from alternating or irregularly synchronous contractions of antagonist muscles.
MDVU Resource Library - Wilson Disease
Wilson disease, also known as hepatolenticular degeneration, is a rare inherited systemic disorder of copper metabolism.
http://www.mdvu.org/library/disease/wd/

Extractions: Resource Library Movement Disorders Latest Wilson Disease News from E-MOVE Resource Library Wilson Disease Description Wilson disease, also known as hepatolenticular degeneration, is a rare inherited systemic disorder of copper metabolism. In patients with this disease, copper initially accumulates in the liver. When the liver's storage capacity is eventually exceeded, copper is then released from the liver and begins to collect in other organs of the body, particularly the brain, eyes, and kidneys. Please see the following topics related to Wilson disease below, and available on the left side of this page. WE MOVE makes every effort to present medical information that is up-to-date and accurate. The material provided has undergone rigorous medical review. Information regarding the authors, editors, publisher, and medical reviewers of this material of the WE MOVE Web site is listed below. Medical science is constantly changing. Therefore, the authors, editors, and publisher do not warrant that the information in this text is complete, nor are they responsible for omissions or errors in the text or for the results of the use of this information. This information does not replace consultation with a physician. All medical procedures, drug doses, indications, and contraindications should be discussed with your personal physician.
Directory Of Open Access Journals
Abstract, AIMTo compare the longterm effect of succimer (Suc) with that of penicillamine (Pen) in treating hepatolenticular degeneration (HLD).
http://www.doaj.org/abstract?id=92209&toc=y
IWFmediacatalogue - Details For "Hepatolenticular Degeneration - Late Pseudoscle
Translate this page hepatolenticular degeneration - Late Pseudosclerosis (44), Manifestation about 16 Years before. (Original title Degeneratio hepato-lenticularis - Späte
http://mkat.iwf.de/medien/katalog/Kat_Details.asp?Signatur=W 1078&Language=en
1910-1919 By George K York, MD & David Steinberg, MD
published his classical description of hepatolenticular degeneration. to SA Kinnier Wilson s description of familial hepatolenticular degeneration.
http://www.aneuroa.org/html/c20html/1910_1919.htm

Extractions: David A. Steinberg, MD The world of neurology began the decade 1910-1919 optimistically, in the conviction of the primacy of science. It ended the decade discouraged and uncertain. In between it participated in a war unparalleled in futility. Wassily Kandinsky, Untitled (1911) Kandinsky's paintings matched his writings on the spiritual aspects of modern art. This watercolor, often considered the first completely abstract painting, expresses the daring and confidence of the golden age of modernism. The avant garde opened new vistas in art, music, science and medicine. Pencil, watercolor and India ink, 49.6 x 64.8 cm. Inscription on verso: Watercolor, 1911. Musee National d'Art Moderne, Centre Georges Pompidou, Paris. In the beginning of the decade, amid studies of neurosyphilis and brain tumors, the American Neurological Association engaged in a contentious debate about the place of Freudian psychoanalysis in the practice of neurology. As practical physicians, many neurologists found the time required for couch therapy onerous. Harvey Cushing, Ramsay Hunt, Bernard Sachs, Foster Kennedy and Charles Dana presented important papers at nearly every annual meeting of the ANA. Title page of the 1910 edition of the Transactions of the American Neurological Association The concentration of neurologists in Boston, New York, Philadelphia and Cincinnati was reflected in the officers of the ANA. At the Washington meeting, Harvey Cushing spoke on eye signs in patients with brain tumors, James J. Putnam presented his personal experiences as a practitioner of Freudian psychoanalysis, and Charles K. Mills discussed his cases of spinal cord tumors. Dementia praecox was the subject of three presentations, and Burt G. Wilder described a man with average intelligence whose brain was half the normal size.
Wilson? (,hepatolenticular Degeneration) Wilson
Translate this page The summary for this Japanese page contains characters that cannot be correctly displayed in this language/character set.
http://brain.bri.niigata-u.ac.jp/~stsuji/resrc/disease/metab/Wilson/wilson.htm

Extractions: Wilsona (ÌYjÏ«ÇChepatolenticular degeneration) WilsonaÌðj WilsonaÌTO WilsonaÌÕ° pxÆµÄÍ3lÉ1löxÆÜêÈíõFÌò«â`«¾³Å éD 10ÎãæèÌ×EÉºª¾µCÌdÏÉis·éDNîÆµÄÍCÌáQÅÇ·éêÍ8-16Ë±ëC_oÇóÅÇ·éÌÍ12ËÈ~Ì±Æª½¢D@ ÌáQÉæéÇóÆµÄÍC©átCSgÓ´ÈÇª½CÇóÍÉðÄ·é±Æà éD áÇóÆµÄCKayser-FleischerpÖªdvÅ éDpÌüÓÉÉo»·éÎFCÎÂFÈÇðæ·éFÖÅCpüÓÌDescemetÉºª¾µ½àÌÅ éDWilsonaÉÁÙIÅff¿lª¢D tÅÍA×ÇáQÌ½ßCAâñ«FanconiÇóQðæµÄéD eé ÇCÖßÔÌ·»CaIÜCéaCî»ÇCÏ`«ÖßÇÈÇÌ¹ÇàæÝçêéD ff Kayser-Fleischer pÖ, CT XLÅC¼¤ÌíkÌázûæð¦·D MRI ÅÍ¼¤YjiÁÉíkjÉCî»CXE`¬COI[VXÈÇÌaÏð½fµÄCT1²æÅáMCT2²æÅMÆÈéD½¾µCT2²æÅÍCáMÆMª¬ÝµÄÝçêé±Æà èCYjÖÌºCSÌ¾ð½fµÄ¢éÆl¦çêéD ÓÊff ´ºÌálCZvX~ÌálÆ¢¤_ÅÍC Menkesa C ZvX~¹Ç ÈÇÆÓÊ·éKvª éDÌOHÇóÆ¢¤_ÅÍC Hallervorden-Spatza Cn`gaCchorea-acanthocytosisC¬l^ (type 3) GM1 KOIVh[VXàÓÊ·éKvª éD
Copper
Wilson s disease, or hepatolenticular degeneration, is an autosomal recessive disorder that results from pathological accumulation of copper, principally in
http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/cop_0083.shtml

Extractions: //This is the Top Banner OAS_AD('Top'); Copper CU-5 (Bio-Tech Pharmacal), Coppermin (The Key Company) Copper is an essential trace mineral in animal and human nutrition. Anemia, neutropenia and osteoporosis are found with frank copper deficiency. Copper deficiency in humans is rare but it does occur under certain circumstances, such as in patients receiving long-term total parenteral nutrition (TPN). Mild copper deficiency due to marginal copper intake over a long period may also occur. In addition to possible anemia, neutropenia and osteoporosis, manifestations of mild copper deficiency may include abnormal glucose tolerance, hypercholesterolemia, arthritis, myocardial disease, arterial disease, cardiac arrhythmias, loss of pigmentation and neurological problems. Copper is a transition metal with atomic number 29 and an atomic weight of 63.55 daltons. Its symbol is Cu. Copper participates in metabolism as a component of many metalloenzymes, including ceruloplasmin or ferroxidase I, cytochromecoxidase, copper/zinc superoxide dismutase, dopamine beta-hydroxylase, tyrosinase, monoamine oxidase, diamine oxidase, lysyl oxidase (protein-lysine 6-oxidase), peptidylglycine-alpha-amidating monoxygenase and ferroxidase II. Copper essentiality for humans was first demonstrated in malnourished children in Peru. The children had an anemia that was not responsive to iron therapy, as well as neutropenia and bone abnormalities. The anemia, neutropenia and bone abnormalities were responsive to copper supplementation. Copper is required for normal infant development, red and white blood cell maturation, iron transport, bone strength, cholesterol metabolism, myocardial contractility, glucose metabolism, brain development and immune function, among other things.
Denny-Brown Bibliography
DennyBrown, D., Hereditary chorea; hepatolenticular degeneration; Familial spastic Denny-Brown, D., hepatolenticular degeneration (Wilson s Disease).
http://users.ipfw.edu/vilensk/Dennybib.htm
Final Diagnosis -- Case 47
Leigh AD, Card WI (1949) hepatolenticular degeneration A case associated with posterolateral column degeneration. J Neuropathol Exp Neurol 8 318-346
http://path.upmc.edu/divisions/neuropath/bpath/cases/case47/dx.html

Extractions: FINAL DIAGNOSIS: Acquired (Non-Wilsonian) hepatocerebral degeneration with "shunt myelopathy" DISCUSSION: It is well known that patients with severe liver disease may suffer from a reversible neurologic condition known as hepatic encephalopathy [1,6]. Some of these patients suffer from a more permanent neurologic disorder, particularly if they have surgically induced or spontaneous porto-systemic shunts and experience episodes of severe hepatic encephalopathy with coma. Victor, Adams, et al. reported the features of AHCD in detail in a series of 27 cases [14]. These symptoms and signs included progressive dementia, dysarthria, involuntary movements (including tremor, asterixis, and choreoathetosis), ataxia of limb and gait, and mild pyramidal tract signs, typically in a patient with severe hepatic disease and recurrent episodes of coma. Less commonly reported is a progressive spastic myelopathy in association with AHCD [4,12]. Only about 15 cases have been reported in the world literature with detailed pathological descriptions [2,3,7,9,13]. The present case report has several distinctive features. Whereas most reported cases resulted from a surgically created porto-systemic shunt as a treatment for cirrhosis, a few other cases, including this one, are thought to result from spontaneously created shunts (e.g., varices) with the same functional consequences. The published cases usually had Alzheimer II cells in the brain, but only a few had the severe spongy degeneration in the deep cortex illustrated here. Recently, hepatocerebral degeneration has occasionally been documented in vivo by MRI [8,9]. Few electron microscopic studies of human Alzheimer II cells and hepatocerebral degeneration have been published [5,11]. The present report suggests that the vacuolation results from the disruption of astrocytes.
Atypical Presentation Of Wilson's Disease
hepatolenticular degeneration/DI; hepatolenticular degeneration/DT; Liver Failure/CO; Bilirubin; Human; Male; Adolescents; Case Report. References 5
http://medind.nic.in/imvw/imvw586.html

Extractions: Extracted from IndMED Jain A; Bhatnagar MK Department of Medicine, Lady Harding Medical College and associated SK Hospital, New Delhi - 110001 Atypical presentation of Wilson's Disease Journal, Indian Academy of Clinical Medicine. 2002 Jul-Sep; 3(3): 300-1 ABSTRACT: Wilson's disease is an uncommon inherited disorder, which is characterised by low serum ceruloplasmin levels, low copper levels, Kayser-Fleischer rings, and hypercupriuria. Here we describe the case of a young boy who did not have classical features as mentioned above, rather presented with fulminant hepatic failure, normal serum ceruloplasmin levels, absent Kayser-Fleischer rings, and diagnosis was confirmed by high 24 hr. urinary copper levels. This is an uncommon presentation of Wilson's disease. KEYWORDS: Hepatolenticular Degeneration/DI; Hepatolenticular Degeneration/DT; Liver Failure/CO; Bilirubin; Human; Male; Adolescents; Case Report References: 5 Record Identifier: NI207845
Karger Publishers
19 Walshe JM Wilson s disease (hepatolenticular degeneration); in Vinken PJ, Bruyn GW, Klawans HL (eds) Handbook of Clinical Neurology, vol 27.
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ProduktNr=
Revista Brasileira De Ginecologia E Obstetrícia - Pregnancy And Wilson's Diseas
hepatolenticular degeneration) is a rare autosomal recessive disorder that usually occurs between the first and third decades.
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-72032001000500009

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