scholarly journals COVID-19 and Liver Dysfunction

Cureus ◽  
2022 ◽  
Nour Ibrahim ◽  
Jad Hosri ◽  
Yara Bteich ◽  
Alfred Dib ◽  
Antoine Abou Rached
2013 ◽  
Vol 51 (05) ◽  
RE Stauber ◽  
W Spindelböck ◽  
C Putz-Bankuti ◽  
H Pock ◽  
T Stojakovic ◽  

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 548-P

Seong Kyu Kang ◽  
Jae Yeon Jang ◽  
Kyung Yong Rhee ◽  
Ho Keun Chung

Blood ◽  
2014 ◽  
Vol 123 (15) ◽  
pp. 2302-2307 ◽  
Kate Gardner ◽  
Abid Suddle ◽  
Pauline Kane ◽  
John O’Grady ◽  
Nigel Heaton ◽  

Abstract Sickle cell disease (SCD) has evolved into a debilitating disorder with emerging end-organ damage. One of the organs affected is the liver, causing “sickle hepatopathy,” an umbrella term for a variety of acute and chronic pathologies. Prevalence of liver dysfunction in SCD is unknown, with estimates of 10%. Dominant etiologies include gallstones, hepatic sequestration, viral hepatitis, and sickle cell intrahepatic cholestasis (SCIC). In addition, causes of liver disease outside SCD must be identified and managed. SCIC is an uncommon, severe subtype, with outcome of its acute form having vastly improved with exchange blood transfusion (EBT). In its chronic form, there is limited evidence for EBT programs as a therapeutic option. Liver transplantation may have a role in a subset of patients with minimal SCD-related other organ damage. In the transplantation setting, EBT is important to maintain a low hemoglobin S fraction peri- and posttransplantation. Liver dysfunction in SCD is likely to escalate as life span increases and patients incur incremental transfusional iron overload. Future work must concentrate on not only investigating the underlying pathogenesis, but also identifying in whom and when to intervene with the 2 treatment modalities available: EBT and liver transplantation.

2021 ◽  
Vol 51 (5) ◽  
pp. 812-813
Michael J. Hoskins ◽  
Stephen Richards

2021 ◽  
Vol 11 (1) ◽  
Takumi Noda ◽  
Kentaro Kamiya ◽  
Nobuaki Hamazaki ◽  
Kohei Nozaki ◽  
Takafumi Ichikawa ◽  

AbstractAlthough heart failure (HF) and liver dysfunction often coexist because of complex cardiohepatic interactions, the association between liver dysfunction and physical dysfunction, and between coexistence of both and prognosis in HF patients remains unclear. We reviewed 895 patients with HF (mean age, 69.4 ± 14.2 years) who underwent liver function test using model for end-stage liver disease excluding international normalized ratio (MELD-XI) score and physical function test (grip strength, leg strength, gait speed, and 6-min walking distance [6MWD]). In the multiple regression analysis, MELD-XI score was independently associated with lower grip strength, leg strength, gait speed, and 6MWD (all P < 0.001). One hundred thirty deaths occurred over a median follow-up period of 1.67 years (interquartile range: 0.62–3.04). For all-cause mortality, patients with high MELD-XI scores and reduced physical functions were found to have a significantly higher mortality risk even after adjusting for several covariates (grip strength, hazard ratio [HR]: 3.80, P < 0.001; leg strength, HR: 4.65, P < 0.001; gait speed, HR: 2.49, P = 0.001, and 6MWD, HR: 5.48, P < 0.001). Liver dysfunction was correlated with reduced physical function. Moreover, the coexistence of lower physical function and liver dysfunction considerably affected prognosis in patients with HF.

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