Angina bullosa haemorrhagica: a systematic review and proposal for diagnostic criteria

The aim of this study was to perform a critical review of published data on the epidemiological, aetiological, clinical, histological, biological, and therapeutic characteristics of patients with angina bullosa haemorrhagica (ABH). A literature search was conducted in the PubMed, Science Direct, Web of Science, and Cochrane Library databases. All publications fulfilling the selection criteria were included in the eligibility assessment according to the PRISMA statement. The full texts of 54 retrieved articles were screened. Forty articles published between 1985 and 2016 describing 225 cases of ABH were finally selected. The mean age of the patients was 55.4 years; the male to female ratio was 0.7. The predominant localization was the palate (66%). A third of patients had no medical history. When specified, a triggering event or promoting factor was frequently found (82%). Biological tests were normal. A biopsy was performed on 35% of the patients. Treatment was symptomatic with a favourable outcome. Recurrences were frequent (62%). In conclusion, ABH is poorly documented and only by studies of low-level evidence. This review did not allow any aetiopathogenic association to be made with a general pathology or treatment. On the basis of this systematic review of the literature, diagnostic criteria aiming to improve the care of patients presenting with ABH are proposed.     

乙型肝炎肝硬化程度与胃黏膜组织病理改变的相关性

〔摘 要〕 目的：探讨乙型肝炎肝硬化程度与胃黏膜组织病理改变的相关性。方法：回顾性分析 2019 年 1 月至 2020 年 1 月河南科技大学第一附属医院收治的 92 例乙型肝炎肝硬化患者的临床资料，根据病情程度将患者分为轻度组 42 例、中 度组 30 例、重度组 20 例，同时采取自愿方式选取体检健康人群 30 例作为健康组，比较四组研究对象的血清肝纤维化指 标、胃黏膜炎症情况以及胃黏膜病变程度，并分析其与乙型肝炎肝硬化病情程度的关系。结果：轻度组、中度组、重度组 层粘连蛋白（LN）、透明质酸（HA）、Ⅲ型前胶原肽（PC Ⅲ）和Ⅳ型胶原（Ⅳ C）水平均高于健康组，胃黏膜炎症率均 高于健康组，胃黏膜病变程度均高于健康组，且以上指标均为重度组＞中度组＞轻度组＞健康组，差异均具有统计学意义 （P ＜ 0.05）；Spearman 相关性分析结果显示，乙型肝炎肝硬化程度与胃黏膜组织病理改变呈正相关（r = 0.539，P ＜ 0.01）。 结论：乙型肝炎肝硬化患者易合并胃黏膜炎症病变，且病变程度与肝硬化程度密切相关。     

ICU经口气管插管患者口腔黏膜压力性损伤研究进展

对ICU经口气管插管患者口腔黏膜压力性损伤发生率、高发部位、影响因素、评估方法及防护策略进行综述,以期使临床医护人员了解及重视ICU经口气管插管患者口腔黏膜压力性损伤,为采取有效防护措施提供参考。     

p53 Overexpression in Oral Mucosa in Relation to Shisha Smoking in Syria and Lebanon

Introduction: Shisha (waterpipe) smoking is becoming a very prevalent form of tobacco consumption in the Middleeast and use is growing over the world. Smoking-related malignancies have a high genome-wide burden of mutations,including examples in the gene encoding p53. Aims: To investigate alterations in p53 immunohistochemical expressionin the normal, pre-malignant, malignant oral mucosa in relation to Shisha smoking habits. Materials and Methods:A total of 105 paraffin embedded tissue sections of OSCCs (52 smokers,53 non-smokers), 96 of premalignant lesions(48 smokers,48 non-smokers) and 60 normal oral mucosa. Some 30 patients with a history of Shisha smoking dailyfor more than 5 years were also investigated for mutant expression of p53. Tissue samples were considered positivefor p53 staining when any positive cells of epithelial origin could be detected. Results: The majority (74.3%) of oralsquamous cell carcinomas showed positive staining for p53 expression (83.1% and 65.5% with Shisha smokers andnon-smokers, respectively). In the 96 premalignant lesions, about 23% from non-smokers and 41.7% from smokersshowed p53 positivity. In normal epithelium, P53 positive cells were noted in 6.6% of non-smokers and 16.6% ofsmokers. Positive correlations with Shisha smoking were evident for the following groups: WDOSCC, MDOSCC,mild dysplasia G1, moderate dysplasia G2 and in normal mucosa using Student’s t- test, P valueThese results strongly suggest that p53 mutations are associated with Shisha smoking in OSCC, pre-malignant lesionsand normal mucosa of the oral cavity.     

胃康复冲剂对胃癌前病变脾虚证胃粘膜超微结构的影响

目的：观察胃康复冲剂对胃粘膜组织超微结构的影响。方法：应用胃康复冲剂治疗６１例脾虚证胃粘膜肠上皮化生（ＩＭ）和不典型增生（ＡＴＰ）患者，治疗前后均作胃镜检查，取胃窦部粘膜作组织病理和超微结构检查。结果：脾气虚证与脾阳虚证病理疗效优于脾阴虚证和脾虚气滞证（Ｐ〈０．０５，Ｐ〈０．０１）；４组脾虚证胃窦部病灶区组织病理、肠化生亚型和非病灶区粘膜超微结构 的“背景病变”，在治疗后均有改善，趋向接近于健康对     

Age-related susceptibility to 3,3'-iminodipropionitrile-induced olfactory mucosal damage

3,3′-Iminodipropionitrile (IDPN) causes degeneration of the olfactory mucosa (OM) in rodents following systemic exposure. Approximately 30% of the OM degenerates in 21-day- and 10-week-old rats following a single 200 or 400 mg/kg intraperitoneal (i.p.) dose of IDPN, whereas 100% olfactory mucosal degeneration occurred in 21-month-old rats. Age-related changes in the flavin-containing monooxygenases (FMOs) or heat shock protein 70 (HSP70) were hypothesized to be responsible for altered olfactory mucosal susceptibility to IDPN. FMO activity in OM was higher than in liver in rats up to 40 weeks of age. Western blots of OM and liver revealed no change in FMO1 protein; however, FMO2, 3, and 5 decreased in olfactory microsomes with age. FMO3 and FMO5 increased in liver microsomes with age. Heat shock protein 70 did not differ between 10-week- and 10-month-old rats in either tissue. The mechanism underlying the increased susceptibility of older rats is likely a complex interaction between the activities of one or more of the enzymes involved in IDPN metabolism in OM and liver.