Metabolic dysfunction-associated steatohepatitis (MASH) is increasingly recognized as a leading cause of hepatocellular carcinoma (HCC), the third-leading cause of cancer mortality worldwide, driven by the global obesity epidemic. Projected to become the primary cause of HCC by 2030, MASH-HCC presents unique clinical challenges. This review examines its clinical management, including surveillance strategies and treatment advances, and discusses prospects to overcome existing challenges. MASH-HCC accounts for 10%–20% of HCC cases, particularly in Western countries, with a rising incidence due to obesity. Risk factors include cirrhosis, diabetes, obesity, alcohol, smoking, genetic polymorphisms (e.g., PNPLA3), and microbiome alterations. The pathogenesis involves fibrosis, immune dysfunction (e.g., T-cell impairment), and molecular changes. Prevention focuses on lifestyle modifications. Surveillance in patients with MASH cirrhosis is crucial but is hindered by poor ultrasound sensitivity in obese patients, necessitating alternative methods. Treatment mirrors that of other HCC types, but comorbidities and potentially reduced efficacy of immunotherapy necessitate tailored approaches. MASH is becoming the leading cause of HCC, necessitating lifestyle interventions for prevention. Improved surveillance and early detection are critical but challenging due to obesity-related factors. Treatments align with those for other HCC types, but comorbidities and potential differences in immunotherapy efficacy due to T-cell dysfunction require careful consideration. Key needs include identifying molecular drivers in non-cirrhotic metabolic dysfunction-associated steatotic liver disease, developing preventive therapies, refining surveillance methods, and tailoring treatments. Trials should specifically report MASH-HCC outcomes to enable personalized therapies. Further research is needed to understand T-cell dysfunction, optimize immunotherapies, and identify predictive biomarkers.
Metabolic syndrome (MetS) is a cluster of metabolic abnormalities that include hypertension, altered glucose metabolism, dyslipidemia, and abdominal obesity and is strongly associated with an increased risk for diabetes and cardiovascular disease onset in obese adults and children. A progressively greater number of children and adolescents are being affected by this syndrome due to the constant increase in the prevalence of obesity. Like obesity, childhood MetS highly tracks to adulthood. The pathogenesis of MetS includes the interaction between obesity, insulin resistance, and inflammation. Early diagnosis and intervention are important in order to conduct lifestyle modification. In this article, we review the definition and pathophysiology of MetS, the importance of screening, and prevention and treatment options for MetS in childhood.
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, Dong Hyeon Lee, Kwang Hyun Kim, Dong-Ryeol Ryu, Seung-Jung Kim, Duk-Hee Kang, Kyu Bok Choi, Shina Lee Metabolic acidosis frequently develops in patients after neobladder reconstruction. However, the incidence of metabolic acidosis in patients with neobladder and the factors associated with the development of metabolic acidosis have not been well elucidated. We aimed to investigate the incidence and the potential predictors for the development of metabolic acidosis after neobladder reconstruction with intestinal segment.
We included patients who underwent neobladder reconstruction using intestinal segment at Ewha Womans University Mokdong Hospital between January 1, 2005 and December 31, 2014. A subgroup of patients according to the time of metabolic acidosis occurrence was further analyzed in order to characterize predictors for metabolic acidosis.
Metabolic acidosis was encountered in 79.4% of patients with neobladder during follow up period. When patients were divided into 2 groups according to anion gap (AG), total CO2 (18.9±2.1 mEq/L vs. 20.0±1.3 mEq/L, P=0.001) and chloride (106.6±4.9 mE/L vs. 109.4±3.6 mEq/L, P<0.001) were significant different between groups with AG>12 and AG≤12. Furthermore, when patients were divided into 3 groups; patients with metabolic acidosis at postoperative day (POD) 1; from POD 2 to 14 days; after 14 days, there was significant difference among those subgroups.
Our study showed the rate of metabolic acidosis in patients underwent neobladder reconstruction and the difference between patients with metabolic acidosis and those without metabolic acidosis for the first time in Korea. In the future, well designed prospective study will be needed to prevent metabolic acidosis after neobladder reconstruction.
, Jin Hwa Lee, Sook Hui Kim, Hyang Woon Lee Women with epilepsy(WWE) are at risk for reproductive and metabolic disorders. This study was performed to investifate whether WWE are more likely to have menstual or metabolic abnormalities, and whether some antiepileptic drugs(AEDs) more likely provoke those problems.
WWW aged 15-50 years old, taking one or more AEDs for at least 6 months, were recruited. Subjucts checked their oral temperature each morning. Body mass index(BMI : kg/m2) and waist to hip (W/H) ratio were calculated as obesity markers. Hirsutism index, as a marker of polycystic ovary syndrome, was calculated by Ferriman-Gallwey score(hirsutism if score>8). Serum tests ofr gonadotrophins, steroid hormones, sex hormone binding globulins (SHBG), lipid profiles, insulin were performed on menstrual cycle days 3 to 5.
Among 54 patients, 18 women were diagnosed as primary generalized epilepsy(PGE) and the other 36 were localoization-related epilepsy(LRE). Also, 21 women(38.9%) were treated with carbamazepine(CBZ), 14 women(25.9%) with valproate(VPA), and 19(35.2%) with lamotrigine(LTG) or topiramate(TPM). Menstrual disturbance was found in 60.0% of PGE versus 30.6% of LRE patients(p=0.050), while 64.3% of VPA and 28.6% of CBZ-treated patients(
WWE are more likely to experience menstrual and metabolic alterations. WWE with VPA tend to have abdominal obesity and alterations in lipid metabolism.
Tumor lysis syndrome(TLS) has been broadly defined as the metabolic abnormalities that occur after rapid tumor breakdown. The purpose of this study was to evaluate the types or degrees of metabolic abnormalities and clinical characteristics in patients with high-grade non-Hodgkin's lymphoma(NHL) who developed clinical TLS.
Patients were considered to have 'clinical TLS' if two of the following metabolic abnormalities occurred within 4 days of treatment : a 25% increase in the serum phosphate, potassium, uric acid, urea nitrogen concentrations, or a 25% decline in the serum calcium concentration and one of the following : a serum potassium level greater than 6.0mEq/L, a creatinine level greater than 2.5mg/dL, a calcium level less than 6.0mg/dL, the development of a life-threatening arrhythmia, or sudden death.
Clonical TLS occurred in 15 patients with advanced high-grade NHL, and these patients were associated with elevated lactate dehydrogenase(LDH) and β2-mivtonlonulin(MG)levels. Pre-treatment TLS occurred in 10 patients(66.7%) and post-treatment TLS in 5 patients(33.3%). Most of these patients showed metabolic abnormalities including hyperuricemia, hyperphosphatemia, hypocalcemia, or acute renal insufficiency. They were treated with adequate hydration combined with allopurinol and recovered in 4 patients. In remained 11 patients, hemodialysis was required and the metabolic parameters returned to normal levels without any significant complications.
It is important to remember that patients with advanced high-grade NHL who have more increased serum LDH or β2-MG level be carefully monitored. Further investigations of elucidating risk factors and diagnostic criteria on clinical TLS will be required.
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