Extractions: What are some common liver disease symptoms? When diagnosing liver disease, the physician looks at the patient's symptoms and conducts a physical examination. In addition, the physician may request a liver biopsy, liver enzyme tests, an ultrasound, or a CT scan (computed tomography scan). Some common liver disease symptoms include the following, each of which are described briefly below: What is jaundice? Jaundice is a yellow discoloration of the skin and whites of the eyes due to an abnormally high level of bilirubin (bile pigment) in the bloodstream, which is then excreted through the kidneys. High levels of bilirubin may be attributed to inflammation or other abnormalities of the liver cells, or blockage of the bile ducts. Sometimes jaundice is caused by the breakdown of a large number of red blood cells, which can occur in newborns. Jaundice is usually the first sign, and sometimes the only sign, of liver disease. What is cholestasis?
Extractions: When diagnosing liver disease, the physician looks at the patient's symptoms and conducts a physical examination. In addition, the physician may request a liver biopsy, liver function tests, an ultrasound, or a CT scan (computerized tomography scan). Some common liver disease symptoms include the following, each of which are described briefly below: What is jaundice? Jaundice is a yellow discoloration of the skin and eye whites due to abnormally high levels of bilirubin (bile pigment) in the bloodstream. Urine is usually dark because of the bilirubin excreted through the kidneys. High levels of bilirubin may be attributed to inflammation or other abnormalities of the liver cells or blockage of the bile ducts. Sometimes jaundice is caused by the breakdown of a large number of red blood cells, which can occur in newborns. Jaundice is usually the first sign, and sometimes the only sign, of liver disease. What is cholestasis?
SpringerLink: Neuroradiology - Abstract Volume 39 Issue 5 (1997) Pp 326-328 Abstract We report MRI in a patient with portalsystemic encephalopathy, in whichthe high signal in the basal ganglia on T1-weighted images showed marked http://link.springer-ny.com/link/service/journals/00234/bibs/7039005/70390326.ht
Extractions: Received: 21 June 1996 Accepted: 26 July 1996 Abstract We report MRI in a patient with portal-systemic encephalopathy, in which the high signal in the basal ganglia on T1-weighted images showed marked resolution after successful embolization of the intrahepatic portal-systemic venous shunt. Key words Article in PDF-Format Last change: May 16, 1997
SpringerLink: Neuroradiology - Abstract Volume 39 Issue 3 (1997) Pp 171-174 report three patients who had highsignal lesions in the globus pallidus on T1-weightedimages, a finding seen in patients with portal-systemic encephalopathy. http://link.springer-ny.com/link/service/journals/00234/bibs/7039003/70390171.ht
Extractions: Received: 26 January 1996 Accepted: 1 April 1996 Abstract Most reports of MRI in Wilson's disease have been of abnormal low-signal lesions on T1-weighted images and high signal intensity on T2-weighted images. In contrast, we report three patients who had high-signal lesions in the globus pallidus on T1-weighted images, a finding seen in patients with portal-systemic encephalopathy. The possible causes include the paramagnetic effect of copper or iron and accumulation of Alzheimer type II glial cells. Key words Article in PDF-Format Last change: April 3, 1997
MEDLINE Abstract TI Comparison of lactulose and neomycin in the treatment of chronicportal-systemic encephalopathy. A double blind controlled trial. http://www.uptodate.com/patient_info/topicpages/abstrcts/Abstrx24/733777.htm
Extractions: Allergy and Asthma Arthritis Alternative Medicine Blood Disorders Bone Disorders Breast Health Cancer Cardiovascular Diseases Childbirth and Pregnancy Dermatology Diabetes Digestive Disorders Drug Information Ear, Nose and Throat Endocrinology Environmental Medicine Eyecare Glossary Gynecology: Health/Oncology Home Health Care Household/Common Emergency Infectious Diseases Men's Health Mental Health Nervous System Disorders Oral Health Orthopaedics Pathology Pediatrics Plastic Surgery Pregnancy and Childbirth Prostate Health Radiology Respiratory Disorders Skin Cancer Spine, Shoulder and Pelvis Surgical Care Travel Medicine Urology Women's Health Liver Transplantation Common Characteristics of Liver Disease What are some common liver disease symptoms? When diagnosing liver disease, the physician looks at the patients symptoms and conducts a physical examination. In addition, the physician may request a liver biopsy, liver function tests, an ultrasound, or a CT scan (computerized tomography scan). Some common liver disease symptoms include the following, each of which are described briefly below:
Congenital Porto-Systemic Shunt As The Major Cause Of Galactosemia FULL TEXT; Raskin NH, Price JB, Fishman RA. portalsystemic encephalopathydue to congenital intrahepatic shunts. N Engl J Med. 1964;270225-229. http://www.int-pediatrics.org/newip/volumes/16,2,3,4/16-4/review/sakura/sakura.h
Extractions: International Pediatrics Volume 16, Number 4 Review Article Congenital Porto-Systemic Shunt as the Major Cause of Galactosemia Nobuo Sakura, MD, PhD; Nobuyuki Mizoguchi, MD; Hiroaki Ono, MD, PhD; Yutaka Nishimura, MD; Kumiko Naito, MD From the Department of Pediatrics (Dr Sakura, Dr Mizoguchi, Dr Ono, Dr Nishimura), and the Department of Radiology (Dr Naito), Hiroshima University School of Medicine, Hiroshima, Japan Address reprint requests to the Department of Pediatrics, Hiroshima University School of Medicine, Kasumi 1-2-3, Minami-ku, Hiroshima, 734-8551, Japan (Dr Sakura). Please give Japanese version time to download. Click on Japanese characters. Abstract Introduction It is well known that inherited deficiencies of galactose-metabolizing enzymes resulted in hereditary galactosemias, but increasing evidence has accumulated that porto-systemic (PS) shunts caused hypergalactosemia. In our screening programs, the most common cause of persistent hypergalactosemia is PS shunts rather than hereditary galactosemias. To date we have identified 15 cases with PS shunts detected by neonatal mass-screening for galactosemia. In this report, we have reviewed the clinical manifestations and outcome of these cases, and insisted that mass-screening for galactosemia by Paigen method is useful for the early diagnosis of PS shunts during the neonatal period.
P Subject headings liver cirrhosis; portalsystemic encephalopathy; nutritionalstatus; albumin; somatosensory evoked potentials Yang SS,Wu CH,Chen LL,Mi SC http://www.wjgnet.com/1007-9327/4/380.htm
Extractions: METHODS Fifty-one non-alcoholic patients with cirrhosis without PSE were studied prospectively and compared with 20 healthy volunteers. The nutritional evaluation included serum prealbumin, albumin, transferrin, body mass index (BMI), mid-arm muscle circumference (MAMC), and grip power. The occurrence of subclinical PSE (SPSE) was defined when N20-N65 inter-peak latencies of median nerve-stimulated somatosensory evoked potentials were 2.5 standard
Bulletin Of Russian Peoples Friendship University PORTAL SYSTEMIC ENCEPHALOPATHY AND DIURETIC THERAPY IN PATIENTS WITH ALCOHOLICLIVER CIRRHOSIS. portalsystemic encephalopathy were in 34,1% of patients. http://www.med.pfu.edu.ru/_new/english/win/library/vestnik/v991e/09.htm
Extractions: Bulletin of Russian Peoples Friendship University. "Medicine" PORTAL SYSTEMIC ENCEPHALOPATHY AND DIURETIC THERAPY IN PATIENTS WITH ALCOHOLIC LIVER CIRRHOSIS N.D.KISLIY, M.MULLA OSMAN, N.N.OMELCHUK, G.R.ZLATINSKAJA Department of Hospital Therapy RPFU. Moscow. 117198. M-Maklaya st 8. Medical faculty P.N.POPOV, S.A.AZEVICH, S.M.SCHEMILCHANOVA Municipal Hospital N 53. Moscow. 109432. Trofimova st 26. 357 patients (216 men and 141 women) with alcoholic liver cirrhosis were studied. Their mean age was 50,5 0,6 years. Portal-systemic encephalopathy were in 34,1% of patients. Diuretic therapy complicated with portal-systemic encephalopathy in 25,9% of patients with alcoholic liver cirrhosis. Grade of portal-systemic encephalopathy correlate with quantity of hemoglobin, red cells, albumin, urea, creatinine and bilirubin.
Hep C Vets, Fibrosis & Cirrhosis, Signs And Symptoms hypertension. The initial presentation may occasionally be that of hepatocellularfailure with ascites or portalsystemic encephalopathy. http://hepcvets.com/cirrhosis/signs.html
Extractions: What's New? Our Latest Additions Hepatitis C Books On Liver Disease (Recommended) Clinical Trials Depression Drugs Used In Treatment Fibrosis/Cirrhosis Genotypes Hepatitis B HEPC INFO Only List Sign Up HEPC INFO Only Full Text Medical Articles Herbs/Alternative Medicine Insurance Issues Liver Disease Glossary Miscellaneous Vaccine Information Veterans Table Of Contents Viral Loads What The Heck Is....VERY INFORMATIVE 2002 NIH Hepatitis C Consensus Hep C Vets Bulletin Board Hepatitis C Bulletin Board Poetry/Short Stories Symptoms and Signs Of Cirrhosis People with cirrhosis often have few symptoms at first. Symptoms generally present themselves after two major problems occur: the loss of functioning liver cells and the distortion of the liver caused by scarring. Among the findings of cirrhosis are: Fatigue, weakness, and exhaustion. Gallstones . Gallstones often form in persons with cirrhosis. Intense itching . Some people with cirrhosis experience intense itching. Jaundice . In the later stages of cirrhosis, jaundice (yellow skin) may occur. Loss of appetite, nausea, and weight loss.
Postgraduate Medicine: Hepatic Encephalopathy Often, the term portalsystemic encephalopathy is used to emphasize thefailure of the liver to detoxify toxins that escape from the intestine. http://www.postgradmed.com/issues/2001/02_01/assi.htm
Extractions: Souheil Abou-Assi, MD; Z. Reno Vlahcevic, MD* VOL 109 / NO 2 / FEBRUARY 2001 / POSTGRADUATE MEDICINE CME learning objectives The authors disclose no financial interests in this article. Supported by a grant from the National Institutes of Health and a grant from the Department of Veterans Affairs. *Deceased. This is the first of three articles on cirrhosis This page is best viewed with a browser that supports tables. Preview : Hepatic encephalopathy is characterized by neuropsychiatric manifestations ranging from a slightly altered mental status to coma, and neuromuscular symptoms may be present. This complication of chronic or acute liver disease is a result of the failure of the liver to detoxify toxins originating in the intestine. The pathogenesis probably is multifactorial, although the predominant causative agent appears to be ammonia. In this article, Drs Abou-Assi and Vlahcevic discuss the timely recognition and correction of factors contributing to this often reversible condition.
CV: Vemuganti RM and Butterworth RF (1995) Selective alterations of extracellular brain amino acidsin relation to function in portalsystemic encephalopathy Results of an http://www.neurosurg.wisc.edu/cvvem.htm
CCHS Clinical Digital Library portalsystemic encephalopathy Access document; Other Symptoms andSigns of Liver Disease Access document. Chapter 43. Drugs and http://cchs-dl.slis.ua.edu/clinical/gastroenterology/general.htm
Extractions: Clinical Resources by Topic: Gastroenterology General Gastroenterology Clinical Resources Pediatrics Geriatrics Atlases Radiology ... Miscellaneous Resources See also: Feldman: Sleisenger and Fordtran's Gastrointestinal and Liver Disease 7th Ed.-2002 (MD Consult): Table of contents Health Sciences Library subscription INFO Chapter 2 - Mucosal Immunology and Mechanisms of Gastrointestinal Inflammation: Access document Chapter 3 - Cellular Growth and Neoplasia:
Federico2 Acta Neurologica Scandinavica. 2001;103198200 portal-systemic encephalopathymay be seen with hyperammonemia that complicates chronic liver disease. http://www.brain.org.au/publications/abstracts2001/federico2.html
Extractions: Portal-systemic encephalopathy may be seen with hyperammonemia that complicates chronic liver disease. We report an unusual case of reversible parkinsonism associated with hyperammonemia and portal vein thrombosis. An active 90-year-old male developed motor slowing and resting hand tremor over 6 months. Examination showed asterixis, bradykinesia, cogwheel rigidity, rest tremor, and a parkinsonian gait. Serum venous ammonia was elevated at 145 microM. The next day, the patient became comatose and serum ammonia was 178 microM. With lactulose therapy,serum ammonia level normalized and examination showed only minimal parkinsonismafter 1 week. An abdominal CT scan identified portal vein thrombosis withporto-systemic shunting that reversed after 7 months of treatment. Examination 2 years later showed no signs of parkinsonism. Parkinsonism can dominate the clinical picture of patients with hyperammonemia before the onset of encephalopathy.
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.
ILM - Klinisk Farmakologi Bergqvist, PBF, Hjort, S., Apelqvist, G. Bengtsson, F. Potassiumevoked neuronalrelease of serotonin in experimental chronic portal-systemic encephalopathy. http://www.klinfarm.lu.se/publikationer.html
Extractions: Apelqvist G., Wikell C., Hindfelt B., Bergqvist P.B.F., Andersson G., and Bengtsson F. (1999) Altered open-field behavior in experimental chronic hepatic encephalopathy after single venlafaxine and citalopram challenges. Psychopharmacology 143(4), 408-416. Bergqvist P.B.F., Bouchard C., and Blier P. (1999) Effect of long-term administration of antidepressant treatments on serotonin release in brain regions involved in obsessive-compulsive disorder. Biol. Psychiatry, 45(2), 164-174. Bergqvist P.B.F., Dong J., and Blier P. (1999) Effect of atypical antipsychotic drugs on 5-HT2 receptors in the rat orbito-frontal cortex: an in vivo electrophysiological study. Psychopharmacology 143(1), 89-96. Bergqvist P.B.F., Carpenedo R., Apelqvist G., Moroni F., and Bengtsson F. (1999) Plasma and brain levels of oxindole in experimental chronic hepatic encephalopathy: effects of systemic ammonium acetate and L-tryptophan. Pharmacol. Toxicol. 84 .
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
Hepatic Encephalopathy to West Nile virus.) Chronic hepatitis C patients with advanced liver disease maydevelop hepatic encephalopathy, also called portalsystemic encephalopathy. http://www.hcvadvocate.org/hepatic_encephalopathy.htm
Extractions: By Liz Highleyman Print this page The liver carries out many important bodily functions including filtering toxic metabolic byproducts from the blood. Normally blood coming from the intestines flows through the liver, where it undergoes detoxification. In people with decompensated cirrhosiswhen the damaged liver is unable to carry out its normal metabolic processes or when blood bypasses the liverthese toxins can build up in the bloodstream. Blood may bypass or be shunted around the liver when blood flow through the liver is blocked by scar tissue (causing portal hypertension) or when an artificial shunt is surgically inserted (a procedure sometimes done to control bleeding varices or ascites). High levels of toxins can affect the central nervous system (the brain and spinal cord), although how they do so is not well understood. Increased levels of ammonia are believed to be most responsible for hepatic encephalopathy. Ammonia is a byproduct of the digestion of proteins by bacteria in the intestines; normally ammonia is metabolized into urea by the liver and excreted by the kidneys as urine. High levels of ammonia appear to alter the balance of neurotransmitters (chemicals that carry messages between neurons) in the brain . This theory is supported by the fact that reducing ammonia usually improves encephalopathy symptoms; however, some people with hepatic encephalopathy do not have elevated blood ammonia levels.
Extractions: Changes in cerebral hemodynamics and metabolism associated with anesthesia and liver transplantation may present particular hazards for patients with cirrhosis. Fifteen patients undergoing liver transplantation were studied, 7 of whom had encephalopathy. Cerebral blood flow (CBF) was measured at the start of surgery, during veno-venous bypass and post reperfusion, using a method based on the Kety-Schmidt method. Cerebral metabolism was assessed by measuring the cerebral metabolic rate for oxygen (CMRO2) and the lactate oxygen index (LOI). The cerebral vascular reactivity to carbon dioxide (CO2) was studied during the preanhepatic and post reperfusion phases. During the preanhepatic period, the median CBF was 44 mL/100 g/min at an arterial carbon dioxide tension (PaCO2) of 3.8 kPa. After reperfusion the CBF increased (P < .02) to 102 mL/100 g/min, the arterial hydrogen ion concentration increased from 39 nmol/L to 53 nmol/L (P
