Hepatitis Symptoms Due to altered liver functions, the brain reacts in a way that istermed portalsystemic encephalopathy, or mental confusion. In http://mcss.mcmaster.ca/~ghoshh/hepsymptoms.html
Extractions: SYMPTOMS OF HEPATITIS C There are various stages of Hepatits C virus (HCV), including the initial, acute phase and prodromal (early) phase. In this phase, the effects of the virus are mild, in terms of symptoms. Some common symptoms of this stage are: jaundice, muscle aches, headaches (which are due to the virus itself and due not to liver failure), lethargy, irritability, myalgia, arthralgia, anorexia, nausea, vomiting, abdominal pain, diarrhea or constipation, fever, and other flulike manifestations. In the chronic form of HCV, the effects are usually mild and asymptomatic. Although, many patients do complain of fatigue, poor stamina and an inability to concentrate. In the later stages of HCV, internal homeostasis is effected. Albumin levels may decrease, which will lead to a decrease in clotting ability. Albumin is a water soluble, heat-coagulable protein. Bilirubin levels may rise, which leads to jaundice. Bilirubin is the orange, yellow pigment of bile, formed mainly by the breakdown of hemoglobin in RBCs after termination of their normal lifespan. When bilirubin levels rise, as in HCV, jaundice is caused by the accumulation of bilirubin in the blood and in the tissues of the skin. Prothrombin (Factor II) time increases, which is also an indication of suffering blood clotting, as prothrombin time (PT) is a test for detecting certain plasma coagulation degects. A prolonged PT indicates deficiency in one of the factors. These above conditions occur because the liver is becoming less able to make its usual quota of substances the body needs.
Extractions: Clinical Resources by Topic: Gastroenterology Hepatic Encephalopathy Clinical Resources Pediatrics Clinical Guidelines News Miscellaneous Resources See also: Family Practice Handbook 4th Ed.-2001: Table of contents Medicine, Ob/Gyn, Psychiatry, and Surgery (eMedicine): Table of contents Pediatrics Resources See also General Pediatrics Resources The New Children's Hospital Handbook 1999 Ed.: Table of contents Clinical Guidelines News Resources Miscellaneous Hepatic Encephalopathy Clinical Resources Health Reviews for Primary Care Providers on the Internet:
Arch Neurol -- Abstracts: Norenberg 33 (4): 265 Norenberg MD. , Contact me when this article is cited. Histochemicalstudies in experimental portalsystemic encephalopathy. MD Norenberg. http://archneur.ama-assn.org/cgi/content/abstract/33/4/265
Extractions: Vol. 33 No. 4, April 1976 Featured Link E-mail Alerts ARTICLE Article Options Send to a Friend Readers Reply Submit a reply Similar articles in this journal Literature Track Add to File Drawer Download to Citation Manager PubMed citation Articles in PubMed by Norenberg MD Contact me when this article is cited M. D. Norenberg Results of a histochemical study of glutamic dehydrogenase in experimental portal-systemic encephalopathy with hyperammonemia indicate that the enzyme's activity in brain was increased in all stages of the encephalopathy, and this increase appeared to be localized exclusively in astrocytes. The results are consistent with the view that the astrocyte has a critical role in ammonia metabolism in brain, probably in ammonia detoxification. The findings, moreover, indicate that one pool of
Nolte Et Al.: Bright Basal Ganglia In T1-weighted... Overt portalsystemic encephalopathy was not noted prior to or at the timeof evaluation. Normal EEG results were recorded in all patients. http://www1.elsevier.com/gej-ng/10/26/38/74/29/40/abstract.html
Extractions: Full-text PDF files should be viewed and printed using Adobe Acrobat Reader version 3.01 or higher ( download here ). Further details about PDF and Adobe Acrobat Reader can be found on our "PDF FAQ " page. Search PubMed for: Wilhelm Nolte Jens Wiltfang Christian G. Schindler Knut Unterberg ... Giuliano Ramadori d Received 9 February 1998; received in revised form 8 April 1998; accepted 27 April 1998 Background/Aims: Deposition of paramagnetic substances in basal ganglia, resulting in increased signals in T1-weighted magnetic resonance images (bright basal ganglia), is frequently seen in liver cirhrosis. The present study describes the prevalence of bright basal ganglia and its clinical significance in patients with long-standing portal vein thrombosis in the absence of liver cirrhosis. Methods: Six patients with angiographically proven complete portal vein thrombosis and cavernomatous transformation without signs of acute or chronic liver disease were studied by magnetic resonance imaging of the brain, neuropsychiatric evaluation, psychometric tests, electroencephalography, and determination of arterial ammonia levels and of serum manganese concentrations from peripheral venous blood.
Radiology -- Abstracts: Inoue Et Al. 179 (2): 551 America. ARTICLES. portalsystemic encephalopathy presence of basalganglia lesions with high signal intensity on MR images. E Inoue http://intl-radiology.rsnajnls.org/cgi/content/abstract/179/2/551
Extractions: Department of Diagnostic Radiology, Center for Adult Diseases, Osaka, Japan. Sixteen patients with cirrhosis of the liver underwent cranial magnetic resonance (MR) imaging and transarterial portography to evaluate the relationship between basal ganglia lesions and portal-systemic collateral vessels. No neuropsychiatric disturbance was observed in any of the patients at the time of the MR examination, but four patients with portal-systemic encephalopathy were included in the study. Basal ganglia
Entrez PubMed B.Alexander@kcl.ac.uk The pathogenesis of portalsystemic encephalopathy (PSE) andhepatic encephalopathy (HE), disorders of the brain attributed to abnormal http://www.biomedcentral.com/pubmed/10715601
Extractions: Summary Brief Abstract Citation ASN.1 MEDLINE XML UI List LinkOut Related Articles Cited in Books CancerChrom Links Domain Links 3D Domain Links GEO DataSet Links Gene Links Genome Links GEO Links HomoloGene Links Nucleotide Links OMIM Links PMC Links Cited in PMC PopSet Links Protein Links SNP Links Structure Links UniSTS Links Show: Sort Author Journal Pub Date Text File Clipboard E-mail Order
Extractions: Nutritional Disorders Chapters: A Collection of High Quality Online Resources for Health Professionals Toxicology Carbon Monoxide Poisoning Carbon monoxide poisoning - Postgraduate Medicine, January 1999 A Noninvasive Method For Rapid Diagnosis Of Carbon Monoxide Poisoning Identifying and managing adverse environmental health effects: 6. Carbon monoxide poisoning Canadian Medical Association Journal, June Ethanol/Alcohol Alcohols - eMedicine/Emergency Alcoholism - eMedicine/Medicine Alcohol and the CNS - University of Vermont Acute care for alcohol intoxication - Postgraduate Medicine, December
Veröffentlichungen 2001 E, Wiltfang J. Quantification of the electroencephalographic theta/alpha ratio forthe assessment of portalsystemic encephalopathy following implantation of http://wwwuser.gwdg.de/~egogoll/PubGesamt.htm
Extractions: Veröffentlichungen 2003 Nolte W, Ramadori G. Albumin for refractory ascites. Gastroenterology 2003; 125: 1283-4. Saile B, Eisenbach C, El Armouche H, Neubauer K, Ramadori G. Antiapoptotic effect of interferon-alpha on hepatic stellate cells (HSC): a novel pathway of IFN-alpha signal transduction via Janus kinase 2 (JAK2) and caspase-8. Eur J Cell Biol 2003; 82: 31-41. Chen Y, Jurgens K, Hollemann T, Claussen M, Ramadori G, Pieler T. Cell-autonomous and signal-dependent expression of liver and intestine marker genes in pluripotent precursor cells from Xenopus embryos. Mech Dev 2003; 120: 277-88. Schafer G, Schenk U, Ritzel U, Ramadori G, Leonhardt U. Comparison of the effects of dried peas with those of potatoes in mixed meals on postprandial glucose and insulin concentrations in patients with type 2 diabetes. Am J Clin Nutr 2003; 78: 99-103. Immenschuh S, Baumgart-Vogt E, Tan M, Iwahara S, Ramadori G, Fahimi HD. Differential cellular and subcellular localization of heme-binding protein 23/peroxiredoxin I and heme oxygenase-1 in rat liver. J Histochem Cytochem 2003; 51: 1621-31. Dudas J, Saile B, El Armouche H, Aprigliano I, Ramadori G.
Abstract 1PO-92 TREATMENT OF portal-systemic encephalopathy WITH OCTREOTID AND L-ORNITHINE-L-ASPARTATE.TE Kodua 4 , NN Kipshidze 1 , VI Bakhutashvili 2 , FI Todua 3. http://www.knt-ec.com/event/icim/abstract/1-PO-14.html
Extractions: ABSTRACTS 1-PO: Gastroenterology: liver disease 3 May 29 (Wed.), 2002 1-PO-81: PROGNOSTIC EFFECT ON GRAFT-VERSUS HOST DISEASE(GVHD) FROM ALLOGENEIC BONE MARROW TRANSPLANTATION BY URSODEOXYCHOLIC ACID N. Iwata , Y. Seto , T. Yamamoto , Y. Amuro , H. Hada , E. Kakishita Dept. of Internal Medicine, Hyogo College of Medicine, Hyogo, Japan The usefulness of ursodeoxycholic acid (UDCA) for treatment of hepatic lesions such as PBC has been reported. Since histological findings of hepatic GVHD is similar to that of PBC, we have reported that UDCA has a prophylactic effect on acute hepatic GVHD. UDCA has an immunomodulating effect, so it may induce some severe infections such as interstitial pneumonia (IP) by cytomegalovirus. Here, we studied the usefulness and side effects of UDCA for the treatment of complications in bone marrow transplantation(BMT). METHODS: Seventy-one patients who had received BMT were used in this study. Thirty-six patients, randomly chosen, were given UDCA 600mg/day orally 4 weeks before BMT (group U). Another 35 patients were started on UDCA just after the onset of acute hepatic GVHD, along with the usual combination of immunosuppressive agents( group C). The rate of acute hepatic GVHD of more than stage 2, based on the classification scale of Thomas et al., was compared between groups U and C. The survival rate and cause of death were compared for one year after BMT.
Extractions: PDF - Requires Adobe Acrobat Reader or other PDF viewer. Nutritional support to hepatic failure patients is challenging and requires experience, skill, careful planning and meticulous follow-up. It is indeed an attempt to replenish the lost power of one of the most vital organs we possess. Keywords: Hepatic failure, diet Subjects: JOURNALS Online Journal of Health and Allied Sciences ID Code: Deposited By: Kakkilaya Bevinje, Dr. Srinivas Deposited On: 17 October 2003 Alternative Locations: http://www.ojhas.org/issue1/2002-1-2.htm Select the SEEK icon to attempt to find the referenced article. If it does not appear to be in cogprints you will be forwarded to the paracite service. Poorly formated references will probably not work. 1. Cabre, E, Abad-Lacruz, A, Nunez, M.C etal: The relation of plasma polyunsaturated fatty acid deficiency with survival in advanced liver cirrhosis: a multivariate analysis. Am J Gastr. 1993; 88:718. 2. James, J.H, Jeppson, B., Ziparo, V. and Fisher, J.E.: Hyperammonemia, plasma aminoacid imbalance and blood-brain aminoacid transport: a unified theory of portal-systemic encephalopathy. Lancet. 1979; 2:772.
Portal-Systemic Shunts portalsystemic Shunts. Portosystemic Shunt The shunt may lead to episodic developmentof hepatic encephalopathy (seizures or bizarre behavior) associated with http://www.cah.com/library/ps.html
Extractions: Portosystemic Shunt Congenital Portal Shunts are due to a defect in the circulation around the liver-instead of blood entering the liver to be de-toxified it is bypassed. The liver usually eliminates toxins derived from the gut. There is a bridging between the veins around the liver and the toxic material bypasses the liver causing an elevation of ammonia in the circulation. This defect may be within the liver (intrahepatic) or occur outside of the liver (extrahepatic)- most are single vessels Acquireddevelops subsequent to portal hypertension (high blood pressure); typically multiple-This occurs due to a lack of valves in the portal vein permits circulatory accommodation through the shunt. Portal hypertensionusually associated with liver scarring or cirrhosis) The shunt may lead to episodic development of hepatic encephalopathy (seizures or bizarre behavior) associated with ingestion of high- protein food, and administration of certain drugs. Another effect of the shunt is the development of bladder stones due to inability of the liver to delete uric acid from the blood. SYSTEMS AFFECTED Nervous system signs include episodic hepatic encephalopathy (seizures).
Extractions: WWW Medical.WebEnds.com Encephalopathy, Hepatic; Portosystemic Encephalopathy; Encephalopathy, Hepatocerebral; Encephalopathy, Portal-Systemic; Encephalopathy, Portosystemic; Fulminant Hepatic Failure with Cerebral Edema; Hepatic Coma; Hepatic Stupor A syndrome characterized by central nervous system dysfunction in association with LIVER FAILURE , including portal-systemic shunts. Clinical features include lethargy and CONFUSION (frequently progressing to COMA ); asterixis; NYSTAGMUS; brisk oculovestibular reflex es; decorticate and decerebrate posturing; MUSCLE SPASTICITY ; and bilateral extensor plantar reflex es (see REFLEX , BABINSKI ELECTROENCEPHALOGRAPHY may demonstrate triphasic waves. (From Adams et al., Principles of Neurology Diagnosis of Stupor and Coma , 3rd ed, p222-5)
AUTISM-PHYSIO Archives -- July 1999 portal systemic encephalopathy portal systemic encephalopathy (27lines) From William Shaw Williamsha@AOL.COM . portalsystemic http://maelstrom.stjohns.edu/CGI/wa.exe?A1=ind9907&L=autism-physio
