Direct Exposure to Outdoor Air Pollution Worsens the Functional Status of Stroke Patients Treated with Mechanical Thrombectomy.

Background The effect of air pollutants on the functional status of stroke patients in short-term follow-up is unknown. The aim of this study was to evaluate the effect of air pollution occurring in the stroke period and during hospitalization on the functional status of patients undergoing mechanical thrombectomy (MT). Methods Our study included stroke patients for which the individual-level exposure to ambient levels of O3, CO, SO2, NO2, PM2.5, and PM10 during the acute stroke period was assessed. The correlations between the air pollutants' concentration and the patients' functional state were analyzed. A total of 499 stroke patients (mean age: 70) were qualified. Results The CO concentration at day of stroke onset was found to be significant regarding the functional state of patients on the 10th day (OR 0.014 95% CI 0-0.908, p = 0.048). The parameters which increased the risk of death in the first 10 days were as follows: NIHSS (OR 1.27; 95% CI 1.15-1.42; p < 0.001), intracranial bleeding (OR 4.08; 95% CI 1.75-9.76; p = 0.001), and SO2 concentration on day 2 (OR 1.21; 95% CI 1.02-1.47; p = 0.03). The parameters which increased the mortality rate within 90 days include age (OR 1.07; 95% CI 1.02-1.13; p = 0.005) and NIHSS (OR 1.37; 95% CI 1.19-1.63; p < 0.001). Conclusions Exposure to air pollution with CO and SO2 during the acute stroke phase has adverse effects on the patients' functional status. A combination of parameters, such as neurological state, hemorrhagic transformation, and SO2 exposure, is unfavorable in terms of the risk of death during a hospitalization due to stroke. The risk of a worsened functional status of patients in the first month of stroke rises along with the increase in particulate matter concentrations within the first days of stroke.

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.