Necrotising myositis – learnings for a plastic surgeon

BackgroundNecrotising myositis (NM) is a life-threatening emergency. Prompt treatment is associated with more favourable outcomes, but early diagnosis is challenging. The initial absence of cutaneous signs and symptoms coupled with delayed recognition commonly result in higher rates of morbidity and mortality.ObjectivesAnalyse data regarding demographics, epidemiology, aetiology, clinical manifestations, diagnosis and treatment of previously reported cases. This publication is intended for plastic surgeons in training to help them look out for this disease.Search methods/criteriaPublications reporting necrotising myositis between 1974 to January 2020 were identified from Embase, Medline All, Web of Science Core Collection, Google Scholar and Cochrane Central Register of Controlled Trial.Data collection and analysis: Identified studies were exported to an end note library. In animal studies, studies relating to statin-induced myotoxicity and auto-immune myositis were excluded. The quality of included case reports was assessed using JBI Critical Appraisal Checklist for Case Reports.Main resultsThe most common initial presentation was a few days of antecedent prodromal flu-like symptoms associated with muscle pain. The mean age was 43.3 years and 82% had no significant medical history. The most frequent misdiagnoses were muscle strain (11%), deep vein thrombosis (10%) and viral illness (9%). Seventy-four per cent of presentations were due to Group A Streptococcus infections and only 3.5% of cases were polymicrobial. The most common clinical course following the initial presentation was rapid deterioration into profound sepsis and progression into multi-organ failure. The overall mortality rate was 36.5%.ConclusionsNM is a life-threatening muscle infection. It is a diagnostic conundrum as initial presentation is often only myalgia without features of preceding trauma. We propose that a high index of suspicion and increased awareness will reduce morbidity.OtherPROSPERO (registration number CRD42018087060). Nil funding/conflict of interest.     

The largest western experience on salvage hepatectomy for recurrent hepatocellular carcinoma: propensity score-matched analysis on behalf of He.RC.O.Le.Study Group

BackgroundWe aimed to evaluate, in a large Western cohort, perioperative and long-term oncological outcomes of salvage hepatectomy (SH) for recurrent hepatocellular carcinoma (rHCC) after primary hepatectomy (PH) or locoregional treatments.MethodsData were collected from the Hepatocarcinoma Recurrence on the Liver Study Group (He.RC.O.Le.S.) Italian Registry. After 1:1 propensity score-matched analysis (PSM), two groups were compared: the PH group (patients submitted to resection for a first HCC) and the SH group (patients resected for intrahepatic rHCC after previous HCC-related treatments).Results2689 patients were enrolled. PH included 2339 patients, SH 350. After PSM, 263 patients were selected in each group with major resected nodule median size, intraoperative blood loss and minimally invasive approach significantly lower in the SH group. Long-term outcomes were compared, with no difference in OS and DFS. Univariate and multivariate analyses revealed only microvascular invasion as an independent prognostic factor for OS.ConclusionSH proved to be equivalent to PH in terms of safety, feasibility and long-term outcomes, consistent with data gathered from East Asia. In the awaiting of reliable treatment-allocating algorithms for rHCC, SH appears to be a suitable alternative in patients fit for surgery, regardless of the previous therapeutic modality implemented.     

夫西地酸乳膏联合丙酸氟替卡松乳膏治疗湿疹52例临床观察

目的观察夫西地酸乳膏联合丙酸氟替卡松乳膏治疗湿疹的临床疗效及安全性。方法通过随机数字表法将入选的102例湿疹患者随机分为两组,治疗组52例,用夫西地酸乳膏和丙酸氟替卡松乳膏交替外涂于皮疹处,间隔时间约为1h,早、晚各一次。对照组50例,单用丙酸氟替卡松乳膏外搽,疗程14d。结果治疗组治疗第7天和第14天时有效率分别为50.00%为80.76%;对照组分别为46.00%和62.00%。仅治疗第14天时差异有统计学意义(P0.05)。治疗过程中均未出现严重的不良反应,未经特殊处理均于1~5d消失。结论夫西地酸乳膏联合丙酸氟替卡松乳膏治疗湿疹效果较好,且无明显不良反应。     

miR-122 Inhibits Hepatocarcinoma Cell Progression by Targeting LMNB2

In the present study, we investigated the role of miR-122 in hepatocarcinoma progression and explored the mechanism. In hepatocarcinoma tissues and cells, we used qRT-PCR to validate the miR-122 expression level. Next, we used colony formation by crystal violet staining assay to compare cell proliferation ability, and we used scratch test or Transwell assay to compare cell migration or invasion ability. We then conducted bioinformatics or luciferase reporter gene assay to prove the regulation effect of miR-122 on lamin B2 (LMNB2), and the biological function of LMNB2 was analyzed. We used nude mouse tumorigenicity assay to test the inhibition effect of miR-122 ASO therapy against hepatocarcinoma. miR-122 was reduced in hepatocarcinoma tissues compared to the paracarcinoma tissues, which was relatively low or high in hepatocarcinoma cell line SMMC7721 or Hep3B, and overexpressed miR-122 inhibited proliferation, migration, and invasion in hepatocarcinoma cells. Additionally, some reports showed that LMNB2 was regulated by miR-122, which inhibited the expression of LMNB2. Moreover, LMNB2 functioned to promote cell proliferation, migration, and invasion. We could achieve the inhibition of hepatocarcinoma using miR-122 therapy through decreasing LMNB2 expression in vivo. Our data indicated that miR-122 could inhibit hepatocellular carcinoma cell progression by targeting LMNB2 and as a therapeutic target for hepatocarcinoma treatment.     

Sappanone A protects mice against cisplatin-induced kidney injury

Cisplatin (CP) is an anti-cancer drug that often causes nephrotoxicity due to enhanced inflammatory response and oxidative stress. Sappanone A (SA), a homoisoflavanone isolated from the heartwood of Caesalpinia sappan, has been known to have antioxidant and anti-inflammatory effects. In this study, we aimed to investigate the protective effects and mechanism of SA on CP-induced kidney injury in mice. The results showed that treatment of SA improved CP-induced histopathalogical injury and renal dysfunction. SA also inhibited CP-induced MPO, MDA, TNF-α and IL-1β production and up-regulated the activities of SOD and GSH-PX decreased by CP. SA significantly inhibited the apoptosis rate of kidney tissues induced by CP. Furthermore, SA was found to inhibit CP-induced NF-κB activation. Treatment of SA up-regulated the expression of Nrf2 and HO-1 in a dose-dependent manner. In vitro, SA dose-dependently inhibited CP-induced TNF-α and IL-1β production and NF-κB activation in HK-2 cells. In conclusion, these results suggested that SA inhibited CP-induced kidney injury through activating Nrf2 and inhibiting NF-κB activation. SA was a potential therapeutic drug for treating CP-induced kidney injury.