Concomitant diverticulosis among patients undergoing liver transplantation. Does it influence the length of hospitalization after the procedure?

Aim of the study: We tried to assess the influence of concomitant diverticulosis and other factors, e.g., Child-Pugh (C-P) and MELD scores, viral etiology, and presence of alcoholic disease, on short-term results of liver transplantation (LT) with an emphasis on duration of patient's hospitalization. Material and methods: This prospective study was performed on 206 cirrhotic patients who were selected for LT. In order to assess the presence of diverticculosis we performed colonoscopy. Results: The duration of hospitalization after LT did not differ significantly between patients with and without diverticulosis (27.5 [21.0-33.5] vs. 24.0 [18.0-32.0] days, p = 0.28). Patients with C-P class C were hospitalized longer in comparison to the class B patients. It is reflected in the positive correlation between C-P score and days of hospitalization (r = 0.22, p = 0.002). Patients with diverticulosis were significantly older (59.6 [51.1-63.3] vs. 52.9 [43.8-59.2] years, p = 0.03). Alcoholic liver disease (ALD) was associated with a greater risk of diverticulosis (OR = 3.89, 95% CI [1.13-15.87], p = 0.04). Conclusions: Presence of diverticulosis among subjects undergoing LT did not influence the duration of hospitalization after the procedure. Significantly longer hospitalization was observed in patients with the most advanced liver disease according to C-P score. To determine the exact impact of diverticulosis on short-term results of LT additional studies are required.

Anti-inflammatory adipokines: chemerin, vaspin, omentin concentrations and SARS-CoV-2 outcomes.

Coronavirus disease 2019 (COVID-19) is associated with systemic inflammation. A wide range of adipokines activities suggests they influence pathogenesis and infection course. The aim was to assess concentrations of chemerin, omentin, and vaspin among COVID-19 patients with an emphasis on adipokines relationship with COVID-19 severity, concomitant metabolic abnormalities and liver dysfunction. Serum chemerin, omentin and vaspin concentrations were measured in serum collected from 70 COVID-19 patients at the moment of admission to hospital, before any treatment was applied and 20 healthy controls. Serum chemerin and omentin concentrations were significantly decreased in COVID-19 patients compared to healthy volunteers (271.0 vs. 373.0 ng/ml; p < 0.001 and 482.1 vs. 814.3 ng/ml; p = 0.01, respectively). There were no correlations of analyzed adipokines with COVID-19 severity based on the presence of pneumonia, dyspnea, or necessity of Intensive Care Unit hospitalization (ICU). Liver test abnormalities did not influence adipokines levels. Elevated GGT activity was associated with ICU admission, presence of pneumonia and elevated concentrations of CRP, ferritin and interleukin 6. Chemerin and omentin depletion in COVID-19 patients suggests that this adipokines deficiency play influential role in disease pathogenesis. However, there was no relationship between lower adipokines level and frequency of COVID-19 symptoms as well as disease severity. The only predictive factor which could predispose to a more severe COVID-19 course, including the presence of pneumonia and ICU hospitalization, was GGT activity.

Fetuin-A Deficiency but Not Pentraxin 3, FGF-21, or Irisin, Predisposes to More Serious COVID-19 Course.

Analysis of liver biopsy specimens showed that SARS-CoV-2 might have led to liver damage. This study aimed to evaluate the role of selected hepatokines and myokines in the development and progression of COVID-19. Seventy patients with laboratory-confirmed COVID-19 and 20 healthy volunteers were enrolled in the study. Irisin, pentraxin 3, fetuin-A, and FGF-21 serum concentrations and biochemical parameters were assessed using an immunoenzymatic method with commercially available enzyme immunoassay (EIA) or enzyme-linked immunosorbent assay (ELISA) kits. Serum fetuin-A concentrations were significantly decreased in COVID-19 patients compared to healthy volunteers. The serum concentration of FGF-21 was significantly increased in obese COVID-19 patients compared to overweight ones. Moreover, the FGF-21 level was higher in COVID-19 patients diagnosed with metabolic syndrome than in patients without metabolic syndrome. PTX3 concentration was higher in COVID-19 patients with higher HOMA-IR values than those with lower HOMA-IR values. COVID-19 patients with HOMA-IR ≤ 3 and >3 had significantly lower fetuin-A levels than the control group. Irisin concentration was significantly decreased in the HOMA-IR ≤ 3 COVID-19 subgroup when comparing with the control group. Lower levels of fetuin-A observed in COVID-19 patients despite higher HOMA-IR, CRP, and ferritin levels, pneumonia, patients requiring ICU care suggests that fetuin-A deficiency predisposes to more severe COVID-19 course. Upregulated pentraxin 3 may be used as a potential predictor of COVID-19 severity.

Influence of ursodeoxycholic acid therapy on levels of fibroblast growth factor 21, adiponectin and biochemical parameters in intrahepatic cholestasis of pregnancy.

The aim was to assess whether fibroblast growth factor 21 (FGF-21) and adiponectin influence intrahepatic cholestasis of pregnancy (ICP) pathogenesis and whether ursodeoxycholic acid (UDCA) has an impact on their levels. 50 pregnant women with ICP (ICP PW), 50 with uncomplicated pregnancy (HPW) and 50 healthy nonpregnant women (HW) were included. In ICP PW the first blood sample was drawn at the time of diagnosis, while in HPW it was drawn in the 28th week of pregnancy. The next blood samples were drawn in the 32nd and 36th week of pregnancy and one day after delivery. UDCA was administered when ICP was diagnosed. In ICP PW serum FGF-21 concentration was the lowest at the time of diagnosis with an evident increase after UDCA administration. Serum FGF-21 levels were significantly higher in ICP PW than in HPW from the first to the last measurement. There was a negative association between adiponectin and bile acids (BAs) levels in the later stage of pregnancy in ICP PW. Up-regulated FGF-21 serum levels in ICP patients compared to HPW persisted after delivery, suggesting its role in disease pathophysiology. The negative association between serum adiponectin and BAs of the later stage of pregnancy may suggest its role in regulation of BAs concentration. UDCA exerts a beneficial effect on insulin sensitivity and up-regulates FGF-21 in ICP.

Irisin in Liver Cirrhosis.

BACKGROUND: Sarcopenia is a prevalent muscle abnormality characterized by progressive and generalized loss of skeletal muscle mass and strength, common among patients with decompensated advanced chronic liver disease (dACLD). Irisin is a recently identified myokine, which is mainly expressed and secreted by skeletal muscle. Pointing to the essential role of irisin in metabolic regulation and energy expenditure we hypothesize that it plays an important role in cirrhosis development and progression. AIM: To assess irisin serum levels in patients with dACLD, with different cirrhosis stage and etiology. To analyze relationship between sarcopenia and irisin serum levels. METHODS: Serum irisin concentrations were measured with commercially available ELISA kits in 88 cirrhotic patients. Recorded parameters of muscle mass were hand-grip strength (HGS), mid-arm muscle circumference (MAC), and transversal psoas muscle index (TPMI). RESULTS: There was no difference in serum irisin levels between cirrhotic patients with different Child-Pugh (CTP) and model of end-stage liver disease (MELD) score, and those with and without ascites. The Liver Frailty Index (LFI) was significantly higher in patients with more advanced liver disease according to CTP and MELD. There was no association between serum irisin level with MAC (r = 0.04, p = 0.74) nor with TPMI (r = 0.20, p = 0.06). We observed significant negative correlation between serum irisin level and age (r = -0.35, p < 0.001). CONCLUSIONS: Serum irisin levels did not correlate with sarcopenia. There was no difference in serum irisin levels between cirrhotic patients with and without diabetes. There was no difference in serum irisin levels among patients with more severe dACLD, although we observed significant LFI increase among patients with more advanced liver disease.

Serum visfatin and vaspin levels in hepatocellular carcinoma (HCC).

Hepatocellular carcinoma (HCC) is the most common liver cancer, accountable for 90% cases. Visfatin and vaspin are adipocytokines with various suggested functions and proven significant correlations between BMI and percentage of body fat. The aim was to assess visfatin and vaspin serum levels in HCC patients and controls, compare their levels in patients with different cancer etiology and grade assessed according to the Barcelona-Clinic Liver Cancer (BCLC) staging system. The additional aim was to analyze relationship between analyzed adipokines and metabolic abnormalities and liver disfunction severity. The study was performed on 69 cirrhotic patients (54 males/15 females) with HCC, aged 59.0 ± 12.1 years, and with BMI 29.0 ± 4.5 kg/m2 compared to 20 healthy volunteers. Serum visfatin and vaspin concentrations were significantly increased in HCC patients compared to controls (p = 0.01 and p = 0.02, respectively). Serum vaspin was significantly higher in HCC patients with viral compared to those with non-viral etiology (p = 0.02), with more evident increase in chronic hepatitis C patients (CHC). Serum visfatin levels were significantly higher in patients with higher insulin resistance (p = 0.04) and with platelets count > 100 000/mm3 (p<0.001). Patients with BMI >30 kg/m2 had markedly up-regulated vaspin levels (p = 0.04). There was no difference in vaspin and visfatin serum levels with respect to liver dysfunction and BCLC classification. In conclusion, our study revealed serum vaspin and visfatin to be significantly increased in HCC patients independently of cancer etiology compared to controls. Additionally, serum vaspin was elevated in viral disease, especially in CHC. Vaspin up-regulation can be a compensatory mechanism against IR in HCC patients. Serum visfatin and vaspin, although up-regulated, seem not to be associated with cancer grade and cirrhosis severity.

Underrated enemy - from nonalcoholic fatty liver disease to cancers of the gastrointestinal tract.

Nonalcoholic fatty liver disease (NAFLD) is intrahepatic ectopic lipid deposition which is present despite a lack of other causes of secondary hepatic fat accumulation. It is the most common chronic liver disorder in the welldeveloped countries. NAFLD is a multidisciplinary disease that affects various systems and organs and is inextricably linked to simple obesity, metabolic syndrome, insulin resistance and overt diabetes mellitus type 2. The positive energy balance related to obesity leads to a variety of systemic changes including modified levels of insulin, insulin- like growth factor-1, adipokines, hepatokines and cytokines. It is strongly linked to carcinogenesis and new evidence proves that NAFLD is associated with higher risk of all-cause mortality and cancer-specific mortality among cancer survivors. This article focuses on the association between NAFLD and extrahepatic gastrointestinal tract cancers, aiming to shed light on the pathomechanism of changes leading to the development of tumors.

The role of metabolic disorders in the pathogenesis of intrahepatic cholestasis of pregnancy.

Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific liver disorder which typically commences in the late second or third trimester and resolves within 48 hours after delivery. It is characterized by mild to severe pruritus, without any specific dermatologic features, elevated liver enzymes and increased serum bile acids (BA). The etiology of ICP is still not completely explicit. Pathogenesis includes a combination of hormonal and environmental factors superimposing on a genetic predisposition. During recent years increasingly ICP is recognized to be associated with an abnormal metabolic profile, including glucose intolerance and dyslipidemia, although it is considered to be secondary to maternal aberrant BA homeostasis. This article reviews the recent literature data and current concepts for ICP, with emphasis on a possibility of metabolic disorders being primary causative factors in ICP pathogenesis.