AimThis study aimed to evaluate the age‐specific characteristics, prognosis, and complications of patients with lean nonalcoholic fatty liver disease (NAFLD).MethodsBackground factors (age, sex, diabetes, dyslipidemia, hypertension, and PNPLA3 gene polymorphism), blood test results, liver histology findings, muscle mass, and grip strength were investigated in 782 patients with NAFLD who underwent liver biopsy. Prognosis and complications were compared among 549 patients with nonlean or lean NAFLD who were followed up for 6.5 years. Additionally, background factors, blood test results, liver histology findings, prognosis, and complications were compared according to age (≥60 years vs. <60 years) in patients with lean NAFLD.ResultsLean NAFLD patients showed lower aspartate aminotransferase, alanine aminotransferase, homeostasis model assessment–insulin resistance, high‐sensitivity C‐reactive protein, ferritin, and leptin but higher adiponectin and hemoglobin A1c (HbA1c) levels than patients with nonlean NAFLD. Furthermore, lean NAFLD patients showed less liver fibrosis, inflammation, steatosis, and ballooning. Among lean NAFLD patients, those aged 60 years and older were more frequently female, showed higher rates of hypertension, diabetes, and dyslipidemia, had higher HbA1c and type IV collagen 7S levels, lower platelet count, higher liver fibrosis and inflammation grades, and lower muscle mass and grip strength. Lean NAFLD was associated with a worse prognosis in patients aged 60 years and over than in those younger than 60 years of age and with a higher incidence of liver‐related disease, cerebrocardiovascular events, and nonliver cancer.ConclusionsAge is an important consideration in patients with lean NAFLD. Compared with nonlean NAFLD, lean NAFLD was associated with a worse prognosis and higher risk of complications in patients aged 60 years and older.
Background Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. The serum level of soluble CD163 (sCD163), a macrophage activation marker, is associated with liver tissue changes; however, its prognostic value is unknown. Here, we determined the utility of sCD163 as a marker for hepatocellular carcinoma (HCC) and prognostic marker for NAFLD. Methods This retrospective study obtained data regarding serum sCD163 levels, liver histology, and background factors associated with NAFLD in 287 patients (men/women, 140/147; average age, 53 ± 14 years) with NAFLD who underwent liver biopsy. Repeated liver biopsies of 287 patients with NAFLD (5.0 ± 2.7 years) were compared regarding serum sCD163 levels and liver tissue changes (stage, grade, steatosis, and NAFLD activity score). Results Serum sCD163 levels increased with the progression of liver fibrosis and inflammation (both P < 0.05) and were particularly helpful in distinguishing cases of Grade 4 fibrosis (P < 0.001). Levels of sCD163 significantly decreased in patients with NAFLD exhibiting alleviated fibrosis and inflammation (P < 0.05). We could also predict the development of HCC and associated mortality based on serum sCD163 levels at the time of NAFLD diagnosis. Serum sCD163 levels were higher in patients with HCC than in patients without HCC (1074 ± 379 ng/ml vs. 669 ± 261 ng/ml; P < 0.0001), and the same trend was observed for mortality. Conclusions The serum sCD163 level reflects the progression of fibrosis and inflammation in liver tissues, showing much promise as a noninvasive biomarker for nonalcoholic steatohepatitis and NAFLD as well as a possible predictor of HCC development and patient prognosis.
Type 2 diabetes mellitus patients are immunocompromised, particularly under poorly controlled conditions, and thereby they could develop rare inflammatory diseases, such as spontaneous discitis, pyogenic psoas abscess, spinal epidural abscess and bacterial meningitis. Herein we report a pyogenic psoas abscess on the dorsal side, and bacterial meningitis and spinal epidural abscess on the ventral side, both of which were induced by spontaneous discitis in a patient with poorly controlled type 2 diabetes mellitus. This case was very rare and interesting, because we successfully treated various infections with antibiotics over a long period of time, complicated by hyperglycemic crises, although the patient suffered severe bone destruction and required rehabilitation for a long time.
Background and Aim Percutaneous drainage of intra‐abdominal abscesses is often uncomfortable for the patient and may result in prolonged hospital stays. Recent studies have shown that endoscopic ultrasound‐guided abscess drainage (EUS‐AD) could effectively treat various abscesses and fluid collections. However, no indications or procedures have been established for EUS‐AD treatments, and studies on its usefulness and safety are insufficient. The present study aimed to evaluate the efficacy and safety of EUS‐AD for treating non‐pancreatic abscesses. Methods This retrospective study included 20 patients, aged ≥20 years, who underwent EUS‐AD for an abscess or fluid accumulation in the abdomen or mediastinum, but not the pancreas. Patients were treated at the Kawasaki University General Medical Center between March 2013 and June 2021. All EUS‐AD procedures were performed prior to a percutaneous drainage or surgical drainage. Results Among the 20 patients who underwent an EUS‐AD for abscess, 8 (40%) had liver abscesses, 6 (30%) had intraperitoneal abscesses, 3 had (15%) splenic abscesses, 1 (5%) had a mediastinal abscess, 1 (5%) had an iliopsoas abscess (n = 1, 5%), and 1 (5%) had an abdominal wall abscess. The technical success rate was 95% (n = 19/20). We inserted nasobiliary catheters in 4/20 patients (20%). The clinical success rate was 90% (n = 18/20). Two clinical failures required reintervention, and both were treated with percutaneous drainage. Adverse events were observed in 2/20 patients (10%). One patient experienced fever after the procedure, and the other experienced localized peritonitis. Conclusion EUS‐AD was effective and safe for abscess removal, particularly when approached from the upper gastrointestinal tract.
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