scholarly journals Management of liver disease patients in different clinical situations during COVID-19 pandemic

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Samy Zaky ◽  
Mohamed Alboraie ◽  
Mohamed El Badry ◽  
Mohamed A. Metwally ◽  
Ahmed Abdelaziz ◽  
...  

AbstractChronic liver diseases are common worldwide, especially in developing countries. The rapid spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)/(COVID-19) leads to the infection of many patients with underlying chronic liver diseases. As a relatively new disease, management of COVID-19, in the context of chronic liver disease, is mainly based on the experience of the treating physician and the available data. In this review, we summarize the available evidence about the management of liver disease patients, in the context of COVID-19 infection, which can increase the severity of viral hepatitis B. Also, its clearance in HBV patients is delayed. A sixfold increased severity of COVID-19 was reported in obese patients with metabolic associated fatty liver disease (MAFDL). In patients with autoimmune liver disease (AILD), it is not recommended to change their immunosuppressive therapy (as long as they are not infected with COVID-19), in order to avoid a flare of liver disease. However, immunosuppressant drugs should be modified, in the case of infection with COVID-19. To date, no data suggest an increased risk or severity in metabolic liver diseases, such as hemochromatosis, Wilson’s disease, or alpha-1 antitrypsin deficiency. Patients with liver cirrhosis should be carefully managed with minimum exposure to healthcare facilities. Basic investigations for follow-up can be scheduled at wider intervals; if patients need admission, this should be in COVID-19-clean areas. Patients with hepatocellular carcinomas may have a poor prognosis according to preliminary reports from China. The course of COVID-19 in liver transplant recipients on immunosuppression seems to have a benign course, based on few reports in children and adults. The hepatotoxicity of COVID-19 drugs ranges from mild liver enzyme elevation to a flare of underlying liver diseases. Therefore, the decision should be customized. Telemedicine can minimize the exposure of healthcare workers and patients to infection with COVID-19 and decrease the consumption of personal protective equipment.

1991 ◽  
Vol 44 (10) ◽  
pp. 855-858 ◽  
Author(s):  
E T Littleton ◽  
L Bevis ◽  
L J Hansen ◽  
M Peakman ◽  
A P Mowat ◽  
...  

2010 ◽  
Vol 47 (12) ◽  
pp. 1015-1023 ◽  
Author(s):  
Narendra K. Arora ◽  
Shivali Arora ◽  
Anjali Ahuja ◽  
Prashant Mathur ◽  
Meenu Maheshwari ◽  
...  

2001 ◽  
Vol 38 (1) ◽  
pp. 63-68 ◽  
Author(s):  
Adriana Maria Alves De TOMMASO ◽  
Cláudio Lúcio ROSSI ◽  
Cecília Amélia Fazzio ESCANHOELA ◽  
Heliane Guerra SERRA ◽  
Carmen Sílvia BERTUZZO ◽  
...  

Background - Alpha-1-antitrypsin deficiency is a genetic disorder which is transmitted in a co-dominant, autosomal form. Alpha-1-antitrypsin deficiency affects mainly the lungs and the liver leading, in the latter case, to neonatal cholestasis, chronic hepatitis or cirrhosis. A precise diagnosis of Alpha-1-antitrypsin deficiency may be obtained by biochemical or molecular analysis. Objective - The purpose of this study was to use DNA analysis to examine the presence of an alpha-1-antitrypsin deficiency in 12 children suspected of having this deficiency and who showed laboratory and clinical characteristics of the disease. Patients and Methods - Twelve patients, aged 3 months to 19 years, who had serum alpha-1-antitrypsin levels lower than normal and/or had hepatic disease of undefined etiology were studied. The mutant alleles S and Z of the alpha-1-antitrypsin gene were investigated in the 12 children. Alpha-1-antitrypsin gene organization was analyzed by amplification of genoma through the polymerase chain reaction and digestion with the restriction enzymes Xmnl (S allele) and Taq 1 (Z allele). Results - Seven of the 12 patients had chronic liver disease of undefined etiology and the other five patients had low serum levels of alpha-1-antitrypsin as well as a diagnosis of neonatal cholestasis and/or chronic liver disease of undefined etiology. Five of the 12 patients were homozygous for the Z allele (ZZ) and two had the S allele with another allele (*S) different from Z. Conclusion - These results show that alpha-1-antitrypsin deficiency is relatively frequent in children with chronic hepatic disease of undefined etiology and/or low alpha-1-antitrypsin levels (41.6%). A correct diagnosis is important for effective clinical follow-up and for genetic counseling.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Andrew S. Chu ◽  
David H. Perlmutter ◽  
Yan Wang

Alpha-1-antitrypsin deficiency (ATD) is one of the most common genetic causes of liver disease and is a prototype of liver diseases caused by the pathologic accumulation of aggregated mutant alpha-1-antitrypsin Z (ATZ) within liver cells. In the case of ATD-associated liver disease, the resulting “gain-of-function” toxicity can lead to serious clinical manifestations, including cirrhosis and hepatocellular carcinoma. Currently, the only definitive therapy for ATD-associated liver disease is liver transplantation, but recent efforts have demonstrated the exciting potential for novel therapies that target disposal of the mutant protein aggregates by harnessing a cellular homeostasis mechanism called autophagy. In this review, we will summarize research advances on autophagy and genetic liver diseases. We will discuss autophagy enhancer strategies for liver disease due to ATD and another genetic liver disease, inherited hypofibrinogenemia, caused by the proteotoxic effects of a misfolded protein. On the basis of recent evidence that autophagy plays a role in cellular lipid degradation, we also speculate about autophagy enhancer strategies for treatment of hepatic lipid storage diseases such as cholesterol ester storage disease.


1987 ◽  
Vol 22 (1) ◽  
pp. 98-98 ◽  
Author(s):  
G Mieli-Vergani ◽  
D G Doherty ◽  
P T Donaldson ◽  
A P Mowat ◽  
D A Hopkinson ◽  
...  

1995 ◽  
Vol 30 (11) ◽  
pp. 1108-1112 ◽  
Author(s):  
A. Propst ◽  
T. Propst ◽  
D. Ofner ◽  
H. Feichtinger ◽  
G. Judmaier ◽  
...  

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