Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease worldwide and affects nearly 30% of the adult population and 10% of the pediatric population. It is estimated that this number will double by 2030. MASLD is one of the leading causes of hepatocellular carcinoma, cirrhosis, and liver transplantation, as well as a significant risk factor for cardiovascular disease and mortality. Due to the ever-increasing number of patients, the long-term asymptomatic course of the disease, serious complications, and lack of preventive programs, as well as insufficient awareness of the disease among patients and doctors themselves, MASLD is a growing interdisciplinary problem and a real challenge for modern medicine. The main cause of MASLD is an inappropriate lifestyle—inadequate nutrition and insufficient physical activity, which lead to various components of metabolic syndrome. Lifestyle changes—appropriate diet, weight reduction, and systematic physical activity—are also the basis for the prevention and treatment of MASLD. Hence, in recent years, so much importance has been attached to lifestyle medicine, to non-pharmacological treatment as prevention of lifestyle diseases. The narrative review presents possible therapeutic options for non-pharmacological management in the prevention and treatment of MASLD. The best documented and available diets used in MASLD were discussed, focusing on the benefits and drawbacks of the Mediterranean, high-protein, ketogenic, and intermittent fasting diets. In addition, the most recent recommendations regarding physical activity are summarized.

Background: There are three main methods of mechanical thrombectomy (MT): using a stent retriever (SR) only (SO), aspiration catheter (AC) only (AO) and the combined method (CM) using both the SR and AC. This paper describes a real-life, single-center experience using SO, AO and CM during 276 consecutive MTs. Methods: The primary endpoint was the frequency of first-pass complete (FPE TICI3). The secondary endpoints were final mTICI 2b-3, procedure duration, clinical outcome and the total number of device passes. The third aim of this study was to test the association between the clinical outcomes in patients treated with each method and various factors. Results: There was a significant difference (p = 0.016) between the groups’ FPE TICI3 rates with 46% mTICI 3 in the AO group, 41% in the CM group and 21% in the SO group. AO resulted in procedure time shortening to a mean duration of 43 min, and the scores were 56 min for CM and 63 min for SO (p < 0.0001). There were no significant differences in clinical outcomes or in-hospital mortality. The analysis showed a correlation between good clinical outcomes and the administration of IVT: OR 1.71 (1.03–2.84) p = 0.039. Patients ≥66 years old had higher odds of a bad outcome compared to younger patients in general (OR, 1.99 95% CI, 1.17–3.38; p = 0.011). FPE TICI3 was associated with good functional outcomes in the whole treated cohort (OR, 1.98; 95% CI, 1.21–3.25; p = 0.006). Conclusions: In our series, AO proved to be the best starting point in most cases. It demonstrates good technical efficacy regarding FPE, it is fast and clinical outcomes seem to be the least age- and FPE TICI3-dependent. It can be easily converted into the combined method, which had the second-best outcomes in our cohort.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease worldwide and affects nearly 30% of the adult population and 10% of the paediatric population. It is estimated that this number will double by 2030. MASLD is one of the leading causes of hepatocellular carcinoma, cirrhosis and liver transplantation, as well as a significant risk factor for cardiovascular disease - heart attack or stroke being the leading cause of death in this group of patients. Due to the ever-increasing number of patients, the long-term asymptomatic course of the disease, serious complications and lack of preventive programmes, as well as insufficient awareness of the disease among patients and doctors themselves, MASLD is a growing interdisciplinary problem and a real challenge for modern medicine. The main cause of MASLD is an inappropriate lifestyle - inadequate nutrition and too little physical activity, which lead to metabolic disorders - overweight and obesity, pre-diabetes and diabetes, hypertension, lipid disorders. Lifestyle changes - appropriate, diet, weight reduction and systematic physical activity - are also the basis for the prevention and treatment of MASLD. Hence, in recent years, so much importance has been attached to lifestyle medicine, to non-pharmacological treatment as prevention of lifestyle diseases. This paper presents methods of non-pharmacological management in the prevention and treatment of MASLD.

Wstęp. W ostrej fazie udaru mózgu zaobserwować można rozwój stanu zapalnego w obrębie ogniska udarowego. W związku z powyższym w odpowiedzi na proces zapalny w mózgu, dochodzi do reakcji zapalnej we krwi obwodowej. Cel. Celem pracy była ocena parametrów stanu zapalnego we krwi obwodowej w grupie chorych z udarem krwotocznym. Materiał i metody. Do badania włączono 64 chorych z udarem krwotocznym hospitalizowanych w Centrum Udaru Mózgu Kliniki Neurologii Szpitala Uniwersyteckiego nr 1 w Bydgoszczy. Typ i lokalizację udaru weryfikowano badaniem KT głowy wykonywanym w pierwszej dobie hospitalizacji. W pierwszej dobie udaru wraz z rutynowymi badaniami laboratoryjnymi oznaczano poziom CRP1, WBC1, PCT, OB oraz fibrynogenu1. Badanie poziomu CRP2, WBC2 i fibrynogenu2 powtarzano w 14 dobie udaru. Z badania wyłączono pacjentów z infekcją. W analizie zastosowano nieparametryczne metody statystyczne: test Manna–Whitneya, test Kruskala–Wallisa oraz współczynnik korelacji Spearmana. Wyniki. U większości chorych stwierdzono podkorową lokalizację ogniska krwotocznego. Zarówno wyjściowe, jak i kontrolne wartości CRP i WBC przekraczały zakres normy laboratoryjnej. Nie stwierdzono istotnych statystycznie różnic pomiędzy wyjściowymi i kontrolnymi wartościami CRP i WBC, natomiast kontrolny poziom fibrynogenu był istotnie wyższy od wartości wyjściowych (p<0,041). Pacjenci, którzy zmarli oraz osoby z zaburzeniami przytomności mieli istotnie statystycznie wyższe wartości parametrów stanu zapalnego (z wyjątkiem OB, PCT i FIBR1) w porównaniu z chorymi, którzy przeżyli i byli przytomnymi. Wnioski. W naszym badaniu obserwowaliśmy istotny wzrost poziomu fibrynogenu po 14 dniach od początku udaru. Dodatkowo kontrolny poziom fibrynogenu korelował z wielkością ogniska krwotocznego i stanem klinicznym chorych. Niezbędne jest dalsze prowadzenie badań w tym obszarze. (PNN 2023;12(1):3–8)

Metabolic dysfunction-associated steatotic liver disease -MASLD, is the most common chronic liver disease worldwide, one of the leading causes of cirrhosis, hepatocellular carcinoma and liver transplantation in developed countries, and an important cardiovascular risk factor. It affects about 30% of the adult population and about 10% of the paediatric population. These figures may be underestimated due to the long-standing asymptomatic or sparse course of the disease, the lack of nationwide screening for MASLD in patients with risk factors for its development and the low awareness of both patients and physicians themselves. According to projections, this number could double by 2030 due to the growing obesity epidemic and the associated development of other weight-dependent metabolic complications, such as insulin resistance, pre-diabetic state, type 2 diabetes, lipid disorders and hypertension. The basis for prevention and treatment of MASLD is weight reduction with diet and regular physical activity and modern pharmacotherapy for obesity-related disease, as well as treatment aimed at reducing the cardiometabolic factors - diabetes, hyperlipidaemia and hypertension. Pharmacological treatment of hepatic steatosis, steatohepatitis or liver fibrosis alone is limited, and many drugs are currently in clinical trials. This article presents the current pharmacological options and potential pharmacotherapy pathways for the hepatic complications of MASLD - steatosis, steatohepatitis and incipient liver fibrosis.