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עמוד בית
Sat, 02.03.24

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January 2023
Itai Kalisky MD, Yaakov Maor MD, Lilach Goldstein MD, Yael Inbar MD, Ziv Ben-Ari MD

Background: Acquired hepatocerebral degeneration (AHD) is a neurologic complication of severe chronic liver disease (CLD) with portosystemic shunts. The proposed etiology is manganese accumulation in the brain tissue, especially in the basal ganglia. Combination of clinical manifestation, mostly extrapyramidal movement disorders, and hyperintensities on T1-weighted brain magnetic resonance imaging (MRI) is diagnostic. Although liver transplantation controversial, it is suggested for AHD.

Objectives: To depict clinical and neuroimaging characteristics and response to treatments in patients diagnosed with AHD at Sheba Medical Center.

Methods: Review of patients with AHD diagnosis at the Liver Diseases Center at Sheba Medical Center between 2012 and 2017, data of clinical and neuroimaging, follow-up, and response to treatments, including liver transplantation were recorded.

Results: Five patients with diagnosis of AHD were identified, median age at diagnosis 55 years (range 45–64 years). Four patients had cirrhosis at the time of AHD diagnosis. The main risk factor for AHD was the presence of portosystemic shunts. The most prevalent clinical manifestations were movement disorders, specifically a combination of extrapyramidal and cerebellar signs including instability, rigidity, tremor, bradykinesia, and cognitive impairment. Brain MRI revealed hyperintensities on T1-weighted images in the basal ganglia in all patients. Administration of antiparkinsonian drugs showed clinical improvement, whereas liver transplantation performed in two patients was not associated to neurological improvement.

Conclusions: AHD is related to portosystemic shunts. The combination of Parkinsonism and cerebellar signs and MRI pallidal lesions should alert physicians to the diagnosis. The role of liver transplantation in AHD is still controversial.

September 2019
September 2018
Keren Cohen-Hagai MD, Dan Feldman MD, Tirza Turani-Feldman BOT, Ruth Hadary MD, Shilo Lotan MD and Yona Kitay-Cohen MD

Background: Magnesium is an essential intracellular cation. Magnesium deficiency is common in the general population and its prevalence among patients with cirrhosis is even higher. Correlation between serum levels and total body content is poor because most magnesium is intracellular. Minimal hepatic encephalopathy is a subclinical phase of hepatic encephalopathy with no overt symptoms. Cognitive exams can reveal minor changes in coordination, attention, and visuomotor function, whereas language and verbal intelligence are usually relatively spared.

Objectives: To assess the correlation between intracellular and serum magnesium levels and minimal hepatic encephalopathy.

Methods: Outpatients with a diagnosis of compensated liver cirrhosis were enrolled in this randomized, double-blinded study. Patients were recruited for the study from November 2013 to January 2014, and were randomly assigned to a control (placebo) or an interventional (treated with magnesium oxide) group. Serum and intracellular magnesium levels were measured at enrollment and at the end of the study. Cognitive function was assessed by a specialized occupational therapist.

Results: Forty-two patients met the inclusion criteria, 29 of whom were included in this study. Among these, 83% had abnormal cognitive exam results compatible with minimal hepatic encephalopathy. While only 10% had hypomagnesemia, 33.3% had low levels of intracellular magnesium. Initial intracellular and serum magnesium levels positively correlated with cognitive performance.

Conclusions: Magnesium deficiency is common among patients with compensated liver cirrhosis. We found an association between magnesium deficiency and impairment in several cognitive function tests. This finding suggests involvement of magnesium in the pathophysiology of minimal hepatic encephalopathy.

May 2018
Ido Laish MD, Amir Mari MD, Batya Mannasse MSc, Ruth Hadary MD, Fred Meir Konikoff PhD, Aliza Amiel PhD and Yona Kitay-Cohen MD

Background: Shortened telomeres were found in patients with cirrhosis, probably reflecting chronic liver injury, continuous regeneration, and destruction of hepatic nodules.

Objectives: To test whether telomere shortening is a general marker of cirrhosis, independent of disease etiology.

Methods: We evaluated telomere length in patients with cryptogenic cirrhosis (largely a late sequela of steatohepatitis) compared to patients with cirrhosis caused by chronic hepatitis B and C (HBV/HCV). We also evaluated telomere aggregates, a sensitive parameter of telomere dysfunction and genetic instability. We analyzed peripheral lymphocytes from 25 patients with cryptogenic cirrhosis, 15 patients with cirrhosis due to chronic viral hepatitis, and 20 age-matched controls. Telomere length was analyzed using quantitative fluorescence in situ hybridization. Aggregate size was divided into three fusion groups of 2–5, 6–10, and 11–15 telomeres, relative to the size of a single telomere.

Results: Shorter telomere length was found in patients with cirrhosis from all three etiologies (mean 121.3 ± 24.1) compared to controls (mean 63.5 ± 23.5). In contrast, there was significantly more fusion of > 5 telomeres only in the HBV/HCV cirrhosis group compared to healthy controls (P = 0.023), but not in the cryptogenic cirrhosis group.

Conclusions: While shortened telomeres in peripheral lymphocytes are a general marker of liver cirrhosis, telomere aggregates may signify a more sensitive genetic instability parameter for the diverse, etiology-based malignant potential of cirrhosis. This finding is in agreement with the well-known higher tendency toward developing hepatocellular carcinoma with cirrhosis caused by chronic hepatitis relative to steatohepatitis.

May 2017
Abdel-Rauf Zeina MD, Saif Abu-Mouch MD and Amir Mari MD
March 2015
Eilon Krashin MD, Michael Lishner MD, Michal Chowers and Sharon Reisfeld MD
February 2015
Attila Kovacs MD PhD, Adelina G. Siminischi MD, Beáta Baksay MD, Andras Gall MD, Maria Takacs MD and Zoltan Szekanecz MD PhD
December 2014
Eilon Krashin MD, Michael Lishner MD, Michal Chowers MD and Sharon Reisfeld MD
March 2011
E. Yefet, M. Gershovich, E. Farber and S. Soboh
January 2011
G.M. Hirschfield and M.E. Gershwin

Primary biliary cirrhosis is considered a model autoimmune disease because of the similarities between patients, their relative homogeneous presentation and natural history, and the presence of the signature autoantibody, the anti-mitochondrial antibodies. PBC[1] also illustrates the potential role of genetic and environmental influence and is unique in having several well-defined animal models that recapitulate distinct features of the disease. The pathogenesis of the disease includes genetic predisposition, the production of both innate and adaptive immune responses, and cholangiocyte-specific biology that addresses the specificity of disease. In this review we highlight these features of PBC in comparison to other autoimmune diseases.






[1] PBC = primary biliary cirrhosis


November 2010
Y. Goykhman, M. Ben-Haim, G. Rosen, M. Carmiel-Haggai, R. Oren, R. Nakache, O. Szold, J. Klausner and I. Kori

Background: Inserting a transjugular intrahepatic portosystemic shunt by means of interventional radiology has become the procedure of choice for decompression of portal hypertension. The indications and criteria for patient selection have been expanded and refined accordingly.

Objectives: To review our experience with TIPS[1] and analyze the results with emphasis on patient selection and indication (conventional vs. atypical).

Methods: In this retrospective analysis in a single center all cases were managed by a multidisciplinary team (comprising liver surgery and transplantation, hepatology, imaging, interventional radiology and intensive care).

Results: Between August 2003 and December 2009, 34 patients (mean age 51, range 27–76 years) were treated with TIPS. The cause of portal hypertension was cirrhosis (23 cases), hypercoagulabilty complicated by Budd-Chiari syndrome (n=6), and acute portal vein thrombosis (n=5). Clinical indications for TIPS included treatment or secondary prevention of variceal bleeding (10 cases), refractory ascites (n=18), mesenteric ischemia due to acute portal vein thrombosis (n=5), and acute liver failure (n=1). TIPS was urgent in 18 cases (53%) and elective in 16. Three deaths occurred following urgent TIPS. The overall related complication rate was 32%: transient encephalopathy (6 cases), ischemic hepatitis (n=2), acute renal failure (n=2) and bleeding (n=1). Long-term results of TIPS were defined as good in 25 cases (73%), fair in 4 (12%) and failure in 5 (15%). In three of five patients with mesenteric ischemia following acute portal vein thrombosis, surgery was obviated. Revision of TIPS due to stenosis or thrombosis was needed in 7 cases (20%).

Conclusions: TIPS is safe and effective. While its benefit for patients with portal hypertension is clear, the role of TIPS in treatment of portal-mesenteric venous thrombosis needs further evaluation. Patient selection, establishing the indication and performing TIPS should be done by a multidisciplinary dedicated team.






[1] TIPS = transjugular intrahepatic portosystemic shunt


February 2009
N. Agmon-Levin, B. Porat Katz and Y. Shoenfeld

Primary biliary cirrhosis is an autoimmune cholestatic liver disease characterized by humoral and cellular response directed at mitochondrial autoantigens, mainly the E2 component of the pyruvate dehydrogenase complex. The etiology of PBC[1], like most polygenic autoimmune diseases, belongs to the "complex" category, including genetic elements and environmental factors. Many environmental factors, such as xenobiotics, smoking, hormonal therapy, toxins, oxidative stress and recurrent urinary tract infections, are associated with PBC. Infectious agents can trigger autoimmunity via several mechanisms and are associated with various autoimmune diseases. A relationship between PBC and several infectious agents, and a possible role for Escherichia coli in the pathogenesis of PBC has been suggested. The identification of a culprit agent that induces or exacerbates PBC might have diagnostic and therapeutic implications. This review evaluates the evidence for an infectious agent role in the pathogenesis of PBC.






[1] PBC = primary biliary cirrhosis


January 2008
Y. Shoenfeld, M. Blank, M. Abu-Shakra, H. Amital, O. Barzilai, Y. Berkun, N. Bizzaro, B. Gilburd, G. Zandman-Goddard, U. Katz, I. Krause, P. Langevitz, I.R. Mackay, H. Orbach, M. Ram, Y. Sherer, E. Toubi and M.E. Gershwin
March 2007
A. Brautbar, Y. Esyag, G.S Breuer, Y. Wiener-Well and G. Nesher

The human papillomavirus family of viruses causes a variety of benign, premalignant and malignant lesions in men and women. All cervical cancers are caused by HPV[1]. It is the leading cause of death from cancer in women in developing countries; every year some 493,000 women develop cervical cancer and 230,000 women die every year of this disease. The vaccine against HPV includes virus-like particles, composed of the major viral capsid protein of HPV without the carcinogenic genetic core. Large-scale studies have shown that the vaccine is tolerated well, leads to high antibody levels in both men and women, and prevents chronic HPV infection and its associated diseases. To achieve effective coverage the vaccine should be given prior to sexual debut. Introduction of the vaccine into specific countries, particularly Israel, should take into account the local incidence of cervical cancer as well as the increasing incidence of precancerous cervical lesions and genital warts, which reduce quality of life and are associated with considerable costs.

 

 







[1] HPV = human papillomavirus


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