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Relevant bibliographies by topics / Sub clinical hepatic encephalopathy

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Academic literature on the topic 'Sub clinical hepatic encephalopathy'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "Sub clinical hepatic encephalopathy"

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Dr., Abdul Haque Khan* Dr. Muhammad Adnan Bawany Dr. Mukhtiar Hussain Jaffery Dr. Aida Nasar Dr. Hamid Nawaz Ali Memon Dr. Abdul Subhan Talpur and Dr. Muhammad Ayyaz and Dr. Zulfiqar Ali Qutrio Baloch. "EVALUATION OF SUB-CLINICAL HEPATIC ENCEPHALOPATHY BY PSYCHOMETRIC TESTS." Indo American Journal of Pharmaceutical Sciences 04, no. 10 (2017): 3698–701. https://doi.org/10.5281/zenodo.1036536.

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Objective: To evaluate the sub-clinical hepatic encephalopathy by psychometric tests. Patients and Methods: The cross sectional study of six months was conducted at the tertiary care hospital Hyderabad. The inclusion criteria were the patients of ≥12 years of age, either gender, diagnosed to have cirrhosis of liver by history, clinical examination, laboratory findings, ultrasonography and liver biopsy and spare from the medications the impaired the cognitive function. A detailed clinical history, physical examination including neuropsychological tests [NCT and DST] and the baselines and specif

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Kato, Akinobu, Yuki Watanabe, Kei Sawara, and Kazuyuki Suzuki. "Diagnosis of sub-clinical hepatic encephalopathy by Neuropsychological Tests (NP-tests)." Hepatology Research 38 (November 2008): S122—S127. http://dx.doi.org/10.1111/j.1872-034x.2008.00437.x.

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Ushapadmini, Dr V., Dr Akila Md, and Dr C. Vignesh. "Evaluation of the Prevalence of Sub-Clinical Hepatic Encephalopathy in Compensated Cirrhotics." IOSR Journal of Dental and Medical Sciences 15, no. 08 (2016): 144–47. http://dx.doi.org/10.9790/0853-150806144147.

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Gajender, Kumar Kumawat, Pipliwal P.S., Kumar Kasana Rajendra, and Ishran Rohit. "Altered Mental Status Patients Associated Evaluations in the Medicine Department." International Journal of Pharmaceutical and Clinical Research 15, no. 1 (2023): 1082–89. https://doi.org/10.5281/zenodo.13155044.

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<strong>Background: </strong>Altered mental status (AMS) comprises a group of clinical symptoms rather than a specific diagnosis, and includes cognitive disorders, attention disorders, arousal disorders and decreased level of consciousness. Patients often manifest vague symptoms, thus, AMS diagnosis and treatment are highly challenging for general medicine physicians. <strong>Material & Methods: </strong>Within the Department of General Medicine, SMS Medical College and the attached group of hospitals, Jaipur, our research team explored patterns in 150 AMS patients from June

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Hamed, Amr, Reda Elwakil, Eman Gawish, Walid Kamel, and Ahmed Elbaz. "Sub-Clinical Hepatic Encephalopathy in Cirrhotic Patients Subjected to Sedation with either Propofol or Midazolam‎." Afro-Egyptian Journal of Infectious and Endemic Diseases 13, no. 3 (2023): 190–96. http://dx.doi.org/10.21608/aeji.2023.219593.1298.

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Williams, Mary-Jane OU, Hossein Akhondi, and Omar Khan. "Primary Hepatic Follicular Lymphoma Presenting as Sub-acute Liver Failure: A Case Report and Review of the Literature." Clinical Pathology 12 (January 2019): 2632010X1982926. http://dx.doi.org/10.1177/2632010x19829261.

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Sub-acute liver failure is a term that describes the relatively sudden loss of liver function, usually >21 days and <26 weeks, with impaired synthetic function and associated encephalopathy in a person with no pre-existing liver disease or cirrhosis. It is commonly caused by viruses and drugs, less so by malignancy. Our patient is a 71-year-old Japanese man who presented with signs of sub-acute liver failure. A subsequent liver biopsy demonstrated involvement by B-cell non-Hodgkin lymphoma. Evaluation of the bone marrow demonstrated significant marrow involvement by B-cell lymphoma. The

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Abdelhalim, Boucaid, Rafik Anis, and Rhorfi Abderahman Ismail. "ACUTE SUB FULMINANT HEPATITISINDUCED BY ANTI-TUBERCULOSIS DRUGS." International Journal of Advanced Research 12, no. 11 (2024): 1169–71. https://doi.org/10.21474/ijar01/19931.

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Introduction :Hepatotoxicity is a prominent adverse effect of anti-tuberculosis drugs, with a frequency of up to 20%, but it is often reversible on cessation of treatment, and fatal outcome is exceptional. We report an observation of acute subfulminant hepatitis induced by antituberculosis treatment. Observation : A 60-year-old patient with a three-year history of insulin-dependent diabetes was started on anti-tuberculosis treatment for smear-positive pulmonary tuberculosis. After two months of treatment, the patient complained of asthenia, epigastric pain, and conjunctival jaundice. Physical

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Kullmann, Frank, Stephan Hollerbach, Guntram Lock, Axel Holstege, Thomas Dierks, and Jürgen Schölmerich. "Brain electrical activity mapping of EEG for the diagnosis of (sub)clinical hepatic encephalopathy in chronic liver disease." European Journal of Gastroenterology & Hepatology 13, no. 5 (2001): 513–22. http://dx.doi.org/10.1097/00042737-200105000-00009.

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Hollerbach, S., G. Lock, F. Kullman, et al. "Assessment of functional cognitive impairment in patients with (sub)clinical hepatic encephalopathy (HE) by brain topographic evoked P300-potentials." Gastroenterology 108, no. 4 (1995): A1085. http://dx.doi.org/10.1016/0016-5085(95)28640-3.

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Miwa, Takao, Tatsunori Hanai, Kayoko Nishimura, et al. "A simple covert hepatic encephalopathy screening model based on blood biochemical parameters in patients with cirrhosis." PLOS ONE 17, no. 11 (2022): e0277829. http://dx.doi.org/10.1371/journal.pone.0277829.

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Aim Covert hepatic encephalopathy (CHE) adversely affects clinical outcomes in patients with liver cirrhosis, although its diagnosis is difficult. This study aimed to establish a simple CHE screening model based on blood-related biochemical parameters. Methods This retrospective study enrolled 439 patients who were assessed for CHE using a neuropsychiatric test between January 2011 and June 2019. A simple CHE (sCHE) score was calculated with hypoalbuminemia (≤ 3.5 g/dL) and hyperammonemia (≥ 80 μg/dL) as 1 point each. The association between sCHE score and CHE or overt hepatic encephalopathy (

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Dissertations / Theses on the topic "Sub clinical hepatic encephalopathy"

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石原, 哲郎, and Tetsuro Ishihara. "Clinical and radiological impact of liver transplantation for brain in cirrhosis patients without hepatic encephalopathy." Thesis, 2013. http://hdl.handle.net/2237/19059.

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Books on the topic "Sub clinical hepatic encephalopathy"

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Balzano, Tiziano, ed. Experimental and Clinical Methods in Hepatic Encephalopathy Research. Springer US, 2025. https://doi.org/10.1007/978-1-0716-4354-9.

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Patel, Sameer, and Julia Wendon. Pathophysiology and causes of acute hepatic failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0194.

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Acute liver failure (ALF) is a rare, life-threatening clinical syndrome, resulting in loss of hepatic metabolic and immunological function, in a person with no prior history of liver disease. Mortality can still exceed 50%. ALF is characterized by hepatic encephalopathy (HE) and coagulopathy, occurring within days or weeks. Establishing aetiology is essential for treatment, prognostication, and liver transplantation consideration. Viral hepatitis and drug-induced liver failure are the two commonest causes worldwide. Aetiology and time of onset of encephalopathy determines prognosis. Disease pr

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Keshav, Satish, and Palak Trivedi. Chronic liver failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0210.

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Chronic liver failure is the functional syndrome resulting from cirrhosis. Clinical features of chronic hepatic decompensation include encephalopathy, coagulopathy, and hepatocellular jaundice. Cirrhosis is the final common pathway for a variety of chronic liver diseases and is characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules. There often exists a poor correlation between biopsy findings and the clinical presentation. Some individuals with cirrhosis are asymptomatic and have a reasonably good life expectancy, while others have severe

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Irani, Zubin, and Sara Zhao. Adjustable Small-Diameter TIPS. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0081.

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Transjugular intrahepatic portosystemic shunt (TIPS) was first described by Rosch et al. in 1969, and in 1982, Colopinto et al. described its first clinical application in a patient with cirrhosis and variceal hemorrhage. It was not until 1988 that the first metal-lined shunt was created, and in 1997 the first polytetrafluoroethylene (PTFE)-lined stent was used in humans for shunt revision after stenosis, created by pinning the Gore PTFE graft material between two metal stents. Introduced in 2000, the Viatorr stent graft is now the most commonly used device for TIPS. One of the major side effe

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Rosenblatt, Elizabeth. Peritonitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0032.

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Peritonitis, or inflammation of the serosal membranes lining the abdominal cavity, is used predominately to describe primary peritonitis (spontaneous bacterial peritonitis [SBP]) and secondary peritonitis—two conditions with distinct pathophysiologies that require different diagnostic and therapeutic approaches. Tertiary peritonitis is characterized by persistent symptoms or signs of infection despite appropriate treatment of primary or secondary peritonitis. Patients undergoing peritoneal dialysis are at risk for catheter-associated peritonitis, which is sometimes considered an additional cat

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Book chapters on the topic "Sub clinical hepatic encephalopathy"

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Mavilia, Marianna G., and George Y. Wu. "Hepatic Encephalopathy." In Clinical Gastroenterology. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72592-1_11.

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Bath, Roopjeet K. "Hepatic Encephalopathy." In Clinical Gastroenterology. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33317-5_11.

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Ellul, Mark A., and Tim Cross. "Hepatic Encephalopathy." In In Clinical Practice. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43126-0_4.

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Tarter, Ralph E., Kathleen L. Edwards, and David H. Van Thiel. "Hepatic Encephalopathy." In Advances in Clinical Neuropsychology. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2211-5_8.

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Mehtani, Rohit, Akash Roy, and Virendra Singh. "Hepatic Encephalopathy." In Clinical Rounds in Hepatology. Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8448-7_10.

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Brown, Thomas A., and Kevin D. Mullen. "Hepatic Encephalopathy." In Textbook of Clinical Gastroenterology and Hepatology. Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118321386.ch102.

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Johansen, Kaj. "Partial Portal Decompression: Initial Clinical Experience with Small-Stoma Portacaval Shunt." In Hepatic Encephalopathy. Humana Press, 1989. http://dx.doi.org/10.1007/978-1-4612-4506-3_37.

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Ellul, Mark A., and Tim Cross. "Erratum to: Hepatic Encephalopathy." In In Clinical Practice. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-43126-0_20.

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Moriya, Kei, Tadashi Namisaki, Kosuke Kaji, and Hitoshi Yoshiji. "Diagnosis of Hepatic Encephalopathy." In Clinical Investigation of Portal Hypertension. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-10-7425-7_54.

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Kaji, Kosuke, Norihisa Nishimura, Kei Moriya, and Hitoshi Yoshiji. "Treatment of Hepatic Encephalopathy." In Clinical Investigation of Portal Hypertension. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-10-7425-7_55.

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Conference papers on the topic "Sub clinical hepatic encephalopathy"

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Erjavec, Vladimira, and Barbara Lukanc. "Portosystemic Shunts in Cats." In Socratic Lectures 8. University of Lubljana Press, 2023. http://dx.doi.org/10.55295/psl.2023.ii6.

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The portosystemic shunt (PSS) is an abnormal communicating vessel between the portal and systemic vasculature. The liver is underdeveloped due to decreased blood flow. The PSS may be congenital (intrahepatic or congenital) or acquired (extrahepatic). Ammonia and intestinal toxins are not cleared in the liver, causing various clinical signs of hepatic encephalopathy. Medical treatment is aimed at minimising clinical signs and stabilising the cat prior to surgical treatment. Surgical treatment is currently the method of choice; however, the best method of occluding the shunts has yet to be found

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Lorenz, R., M. Holweger, GE Vogel, and M. Classen. "SUBSTITUTION THERAPY WITH ANTITHROMBIN III: CLINICAL EXPERIENCE WITH DECOMPENSATED LIVER CIRRHOSIS AND HEMORRHAGIC COMPLICATIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643069.

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In patients with decompensated liver cirrhosis, the coagulation disorder requires therapy only when bleeding complications occur. As therapy involves the risk of triggering a consumption coagulopathy, the discussion here examines the beneficial effect of boosting the inhibitor Potential by supplementing the administration of fresh plasma with substitution of AT III concentrate. To investigate this question, we conducted a retrospective study on the clinical course in 19 patients with decompensated liver cirrhosis, hepatic encephalopathy and bleeding complications.The following treatment scheme

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Ferro, D., F. Violi, C. Alessandri, C. Quintarelli, M. Saliola, and C. Cordova. "FOLLOW UP OF PREKALLIKREIN AND FA3T0R VII IN PATIENTS WITH LIVER FAILURE (LF)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644801.

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Life expectancy of patients with liver cirrhosis (LC) is dependent upon thepresence of haemodinamic and metabolic complications.Patients with ascites, hepatic encephalopathy and bleeding have lower survival than patients in compensated state. Neverthless the clinical signs of decompensated state are not useful in the individual assessment of LF. Recently we showed that some coagulation factors such as factor VII and prekallikrein (prekk) are good indexes of LF.In fact they clearly differentiate decompensated LC from compensated one and, in a short term follow up. survivors from non survivors.

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Shearer, M., K. Andrassy, H. Bechtold, P. McCarthy, J. Koderisch, and H. Koderisch. "CEPHALOSPORIN-INDUCED HYPOPROTHROMBINAEMIA: RELATION TO CEPHALOSPORIN SIDE CHAIN, VITAMIN K METABOLISM AND VITAMIN K STATUS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643076.

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An increased incidence of bleeding episodes due to hypopro-thrombinaemia has been associated with several cephalosporins especially those which contain an N-methyl-thio-tetrazole (NMTT) side chain. To study the etiology of cephalosporin-induced hypo-prothrombinaemia in the clinical situation we have investigated the ability of different cephalosporins to alter the metabolism of vitamin K and the relationship between hypoprothrombinaemia and vitamin K status as assessed from plasma levels of vitamin K. Cephalosporins containing an NMTT side chain (latamoxef, cefmenoxime, cefoperazone, cefotetan

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