刮除加冷冻治疗牙源性角化囊肿(附30例报告)

刮除加冷冻治疗牙源性角化囊肿（附３０例报告）１５９医院口腔科（河南驻马店４６３００８）付新国刘杨刘霜印任云壮肖斌赵翠梅牙源性角化囊肿（ｏｄｏｎｔｏｇｅｎｉｃｋｅｒａｔｏｃｙｓｔ，ｏｋｃ）是一种比较常见的颌骨内囊性病变。因其独特的组织学特征，单纯刮治后...     

颌骨囊肿148例临床分析

目的介绍颌骨囊肿的诊治体会。方法回顾分析148例经手术及病理证实的颌骨囊肿的临床资料。结果148例颌骨囊肿病例经手术切除治愈。结论颌骨囊肿的早期确诊主要靠肿物部位、质地、病变牙、缺失牙和不愈的瘘口,X线检查简便易行,且能确诊大多数颌骨囊肿,颌骨囊肿的治疗以手术切除为主。     

牙源性颌骨囊肿38例疗效分析

颌骨囊肿是与成牙组织或与牙有关的囊肿，现就牙源性颌骨囊肿38例临床手术治疗结果分析报告如下。     

牙源性颌骨囊肿的诊断和治疗进度

牙源性颌骨囊肿是由成牙组织或牙的上皮或上皮剩余演变而来的,可以分为根尖周囊肿（radicalcyst,Rc）、始基囊肿（primordial cyst,Pc）、含牙囊肿（dentigerous cyst,Dc）、牙源性角化囊肿（odontogenic keratocyst,OKC）等。牙源性颌骨囊肿多发生于青壮年．可发生于颌骨任何部位。     

392例颌骨角化囊肿临床分析

颌骨牙源性角化囊肿临床较多见,由于其发生发展早期较难发现,对颌骨及牙齿破坏较大。本文对我院1993—2007年1月收治经病理确诊的颌骨牙源性角化囊肿392例的临床表现、治疗方式作一回顾性分析。     

3例牙源性腺样瘤的临床病理学观察

牙源性腺样瘤比较少见,仅占牙源性肿瘤的2%-7%,主要是位于颌骨内的一种独立的肿瘤,患者男女比例为1：1.9,多发生于10-19岁的青少年,几乎都位于骨内,上下颌骨均可发生,但以上颌骨多见,好发于颌骨前部[1]。肿瘤生长缓慢,致颌骨膨大,可引起面部变形,病变处可引起牙齿移位或松动。X线片显示颌骨为单房或多房边界清晰的透明区,常含有钙化斑或牙齿,临床常误诊为含牙囊肿而进行手术[1]。本研究回顾性分析3例牙源性腺样瘤的临床表现和组织学特点,以期加深临床医师及病理医师对该肿瘤的了解,从而减少误诊的几率,有利于对患者进行合理治疗、更准确的评估患者的预后情况。     

医用硫酸钙和磷酸钙修复颌骨囊性病变骨缺损的疗效评价

目的评价生物材料医用硫酸钙和磷酸钙在颌骨囊肿刮除后修复骨缺损的效果。方法共选取30名牙源性颌骨囊肿患者,20例采用囊肿刮除术加人工生物材料充填术治疗。其中,10例角化囊性瘤刮除后填充硫酸钙材料;10例单纯性囊肿刮除后填充磷酸钙。10例只进行囊肿刮除术但不填充生物材料设为对照组。术后随访观察患者情况并结合影像学方法评估骨缺损的修复情况。结果术后无1例出现感染和材料排斥反应。术后1、3、6、12个月患者复诊检查并拍摄颌骨曲面断层片。术后6个月的颌骨曲面断层片显示:生物材料颗粒全部溶解吸收,低密度影像基本消失,新骨形成,与正常骨组织无明显差别。对照组病例骨缺损修复时间大于6个月。结论医用硫酸钙和磷酸钙材料可作为理想的骨移植替代材料用于颌骨囊肿的治疗。     

颌骨囊肿开窗术治疗42例体会

目的探讨开窗治疗在颌骨囊肿中的临床疗效及其应用价值。方法对42例颌骨囊肿患者实行开窗术,吸出囊内容物,不刮除囊壁,使囊腔与口腔相通呈开窗状态,碘仿纱条填塞,术后换药,并定期复查和随访。结果所有病例均未出现反复感染,颌骨形态良好,未出现神经及邻近重要结构损伤。术后6个月至3年随访,X线片示骨质再生情况良好,未见有囊肿复发。结论囊肿开窗术具有手术简单,术后复发率低,能最大限度地保留牙颌的完整性,并发症少等优点。     

37例替牙期颌骨囊性病变开窗引流术的临床效果观察

目的评价开窗引流术治疗替牙期颌骨囊性病变的治疗效果。方法 37例替牙期颌骨囊性病变均采用开窗引流术进行治疗。术后放置囊肿塞持续引流。结果 25例囊腔消失,12例囊腔缩小行二期手术刮除,所有病例均达到保存恒牙,颌骨改建的治疗目的。结论开窗引流术是治疗替牙期颌骨囊性病变的理想方法。     

颌骨囊肿34例临分析

目的提高颌骨囊肿的诊治水平。方法回顾分析我科2003年1月至2009年12月收治的34例经病理证实的颌骨囊肿的临床资料。结果大多数颌骨囊肿,通过X线检查就可明确诊断。颌骨囊肿的治疗我科以手术切除为主,随访观察取得较为满意的效果。结论颌骨囊肿应根据其性质、大小、部位,选择不同的术式。     

胃肠道间质瘤90例的临床诊治及病理分析

目的 探讨胃肠道间质瘤的发病年龄及部位、临床表现、诊断、免疫组化特点及治疗现状.方法 回顾性分析本院近9年来住院病人资料,分析经过病理和免疫组化检查确诊的90例胃肠道间质瘤病人的发病部位、临床表现、诊治方法、病理及免疫组化特点.结果 胃肠道间质瘤男女发病比例为1.5∶1.发病年龄范围为21 ～ 86岁,60岁以上患者比例最高.所有患者的胃肠道间质瘤主要起源于胃（55.6％）和小肠（27.8％）.临床表现缺乏特异性,首发症状主要为呕血、黑便或便血,腹痛、腹胀等.间质瘤的临床诊断是困难的,其正确诊断依赖于手术或活检标本的病理组织学和免疫组化检查确定,免疫组化检测CD117阳性率94.05％（79/84）,CD34阳性率92.86％（78/84）,两者同时为阳性者78例（92.86％）.本病的治疗以手术彻底切除病变为唯一有效的方法,格列卫对不能手术者或对预防术后复发有一定的作用.结论 胃肠道间质瘤是一种未定的多潜能的间叶源性肿瘤,其临床表现缺乏特异性,确诊须依赖大体标本或免疫组化病理结果,CD117和CD34对诊断有重要价值,手术切除是唯一有效的治疗方法.     

头颈部皮肤钙化上皮瘤17例临床分析

目的　探讨头颈部皮肤钙化上皮瘤的诊疗方法 ,提高临床诊断的正确率。方法　对 17例头颈部皮肤钙化上皮瘤病人的临床资料进行回顾分析。结果　 5 2 9% (9例 )钙化上皮瘤病人年龄小于 15岁 ,病变部位多样化 ,临床误诊率较高 ;B超诊断具有较高的符合率 (6 / 7) ;手术切除后无复发。结论　增强临床医生对钙化上皮瘤的临床特征的认识 ,必要时结合B超检查有利于提高头颈部钙化上皮瘤诊断的正确率。     

Fatal venous thromboembolism associated with different combined oral contraceptives: a study of incidences and potential biases in spontaneous reporting.

BACKGROUND: Fatal venous thromboembolism (VTE) is a rare complication of combined oral contraceptive (COC) treatment. This study aims to determine incidences of fatal VTE in relation to the type of COC and the percentage of cases reported to the Swedish Adverse Drug Reactions Advisory Committee (SADRAC). A further aim is to compare the characteristics of reported and not reported cases. METHODS: This retrospective study is a separate analysis using data from a larger study that included women aged 15-44 years between 1990 and 1999 with VTE coded as the underlying or contributory cause of death in the Swedish Cause of Death Register. COC use within 2 months of the date of symptom onset or death was identified in 28 cases. Sales data were obtained from the National Corporation of Swedish Pharmacies. Reported cases were identified in the SADRAC database. RESULTS: After excluding two cases where the type of COC was unknown, the crude incidences of fatal VTE were 5.1 (95% CI 2.3, 9.6), 8.6 (95% CI 4.3, 15.4) and 9.1 (95% CI 3.3, 19.8) cases per million women per year for levonorgestrel-, desogestrel- and norethisterone-containing COCs, respectively. Age-adjusted incidences were approximately twice as high for desogestrel- and norethisterone-containing COCs compared with levonorgestrel-containing COCs, although differences were not statistically significant. Thirty-six percent of cases were reported. Reporting was positively associated with information in medical records relevant to the VTE diagnosis that the patient was a COC user and was significantly higher in northern Sweden. CONCLUSION: Results from this study support a higher incidence of fatal VTE with desogestrel-containing COCs than with levonorgestrel-containing COCs.     

Immunomodulation by cocaine and ketamine in postnatal rats

The abuse of cocaine (COC) in combination with ketamine (KET) among pregnant women was shown to be high. Transplacental exposure is not the only route by which a newborn may be exposed to these agents, but they can also distribute into breast milk. Chronic COC exposure is associated with immunological modulation in human and animal models. The effect of sub-chronic exposure to COC and KET alone and in combination on the developing immune system was assessed in neonatal male Sprague-Dawley (SD) rats. To simulate the route of exposure during lactation, newborn male rats were treated orally with saline, COC alone (20 mg/kg), KET alone (50 mg/kg), or KET (50 mg/kg) followed 15 min later by COC (20 mg/kg) from days 1 to 21 of life. Pups were sacrificed 30 min following the last treatment. Total circulating leukocyte and lymphocyte counts were decreased with relative neutrophilia, while spleen/body weight ratio and IgM antibody response to sheep red blood cells (SRBCs) were increased in animals treated with COC. Moreover, treatment with COC alone increased serum interleukin 10 (IL-10) concentration; however, it did not affect serum interferon gamma (IFN-gamma) concentration. On the other hand, KET treatment did not produce any significant change of any of these parameters. However, when co-administered with COC, the immunomodulatory effects of COC were prevented. COC caused a significant increase in serum corticosterone concentration that KET effectively prevented. Lack of significant change of plasma and tissue concentrations of norcocaine (NC) suggested no role for COC metabolism in COC-induced immunomodulation. However, the results of this study indicate that COC-induced immunomodulatory reactions and their prevention by KET most likely occurred through neuroendocrinal mechanisms.     

Pharmacokinetics of etonogestrel and ethinylestradiol released from a combined contraceptive vaginal ring

OBJECTIVE: To assess the pharmacokinetics of etonogestrel and ethinylestradiol released from a novel combined contraceptive vaginal ring (NuvaRing) releasing etonogestrel 120microg and ethinylestradiol 15 microg per day and compare them with those of a combined oral contraceptive containing desogestrel 150 microg/ethinylestradiol 30 microg (DSG/EE COC). DESIGN AND SETTING: This was a nonblind, randomised, crossover study in 16 healthy women. METHODS: All volunteers received one cycle of DSG/EE COC before being randomised to 1 of 2 treatment groups. The participants in group 1 received 1 cycle of DSG/EE COC, a treatment period with NuvaRing and an intravenous bolus injection of etonogestrel/ethinylestradiol (150 microg/30 microg). Those in group 2 received a NuvaRing treatment period, 1 cycle of DSG/EE COC and the same intravenous bolus injection. RESULTS AND CONCLUSIONS: After the insertion of NuvaRing, maximum serum concentrations of etonogestrel and ethinylestradiol were achieved in approximately 1 week. The concentrations subsequently showed a gradual linear decrease in time. The maximum serum concentrations of etonogestrel and ethinylestradiol were approximately 40 and 30%, respectively, of those for the DSG/EE COC. In comparison with the DSG/EE COC, the absolute bioavailability for NuvaRing was higher for etonogestrel (102.9 vs 79.2%) and similar for ethinylestradiol (55.6 vs 53.8%). Taking the difference in daily doses into account, systemic exposure to etonogestrel was similar for NuvaRing and the DSG/EE COC, whereas systemic exposure to ethinylestradiol with NuvaRing was only approximately 50% of that for the DSG/EE COC.     

Nicotine exposure suppresses hyperinsulinemia and improves endothelial dysfunction mediators independent of corticosteroids in insulin-resistant oral contraceptive-treated female rats

Estrogen-progestin oral contraceptives (COC) or tobacco smoking has been associated with hypertension and endothelial dysfunction resulting in increased risk of cardiovascular diseases (CVD). Contrasting effects of nicotine exposure on endothelial function have been reported. The effect of non-smoking nicotine exposure on endothelial dysfunction during COC treatment remains to be fully elucidated. We therefore, sought to determine the effects of nicotine exposure during COC treatment on endothelial dysfunction mediators and circulating corticosteroids. Female Wistar rats aged 10?weeks were given (po) vehicle, nicotine (1.0?mg/kg) with or without COC steroids (1.0?µg ethinylestradiol and 5.0?µg levonorgestrel) daily for 6?weeks. Nicotine exposure caused 113.3% increase in insulinemia whereas COC treatment led to 76.9% increased insulinemia compared with control. Furthermore, COC treatment or nicotine exposure led to glucose deregulation, insulin resistance, reduced nitric oxide bioavailability, elevated plasminogen activator inhibitor-1, uric acid, oxidative stress, atherogenic dyslipidemia, and corticosteroids. However, COC?+?NIC treatment led to 41.2% decrease in insulemina compared with COC-treated rats. Furthermore, all other alterations were alleviated by nicotine exposure in COC-treated female rats with the exception of corticosteroids.     

Hemostatic effects of a novel estradiol-based oral contraceptive: an open-label, randomized, crossover study of estradiol valerate/dienogest versus ethinylestradiol/levonorgestrel

Background: A novel estradiol-based combined oral contraceptive (COC) is currently available in many countries worldwide, including Europe and the US. Based on previous studies, it is expected that this estradiol-based COC will have a reduced hepatic effect compared with COCs containing ethinylestradiol with regard to proteins controlling the hemostatic balance.Objective: The aim of this study was to compare the hemostatic effects of the estradiol valerate/dienogest COC with a monophasic low-estrogen dose COC containing ethinylestradiol/levonorgestrel.Study Design: Healthy women aged 18–50 years were randomized to receive a COC containing estradiol valerate/dienogest (2 days estradiol valerate 3 mg, 5 days estradiol valerate 2mg/dienogest 2 mg, 17 days estradiol valerate 2mg/dienogest 3 mg, 2 days estradiol valerate 1 mg, 2 days placebo) or ethinylestradiol 0.03mg/levonorgestrel 0.15mg in a crossover study design. Women received each treatment for three cycles, with two washout cycles between treatments. The primary efficacy variables were the intra-individual absolute changes in prothrombin fragment 1 + 2 and D-dimer from baseline to cycle three.Results: Data from 29 women were assessed. Intra-individual absolute changes in prothrombin fragment 1 + 2 and D-dimer from baseline to cycle three were less pronounced with estradiol valerate/dienogest than with ethinylestradiol/ levonorgestrel.Conclusion: The novel COC containing estradiol valerate/dienogest had similar or less pronounced effects on hemostatic parameters than ethinylestradiol/ levonorgestrel.     

穿琥宁对COC1/DDP顺铂耐药性的逆转作用

 目的：建立人卵巢癌顺铂耐药细胞株COC1/DDP,探讨穿琥宁对COC1/DDP顺铂耐药性的逆转作用及其机制。方法：采用逐步递增顺铂浓度、体外间歇诱导法建立COC1/DDP;CCK-8试剂盒（Cell Counting Kit-8）检测穿琥宁对COC1/DDP顺铂耐药性的逆转作用;GSH和GSSG试剂盒检测细胞内GSH的水平;高效液相色谱测定细胞内顺铂的含量。结果：历时5个月建立的COC1/DDP细胞株对顺铂耐药性稳定,耐药指数为9.44,对卡铂、长春新碱和阿霉素有不同程度的交叉耐药性。穿琥宁对COC1/DDP的顺铂耐药性有逆转作用,逆转倍数达到5.63倍。与COC1比较,COC1/DDP细胞内GSH水平增高,顺铂含量下降,但经穿琥宁干预后,COC1/DDP胞内的GSH水平降低,顺铂的含量增加（P<0.01）。结论：穿琥宁对COC1/DDP的顺铂耐药性有逆转作用,其机制可能与干预COC1/DDP细胞内GSH/GST-π 解毒系统,增加COC1/DDP细胞内顺铂的含量有关。     

Cocaine and salicylate: documentation of hydroxyl radical formation in hearts and brains of 18-day-old chick embryos and unexpected interactive toxicity

RATIONALE: Multiple low doses of cocaine (COC) may cause intermittent vasoconstriction and reperfusion, leading to elevations in damaging reactive oxygen species, such as hydroxyl free radicals (*OH). Salicylate may offer protection because it reacts with *OH and/or because of its anti-inflammatory actions. OBJECTIVE: To measure *OH concentrations in hearts and brains of chicken embryos exposed to multiple, small doses of COC, and to determine if otherwise non-toxic doses of sodium salicylate (NaSal) protected against the marginal but significant reduction in hatchability caused by a model of "binge" COC exposure. METHODS: Three experiments were carried out. In the first, 67.5 mg COC/kg egg was administered as five doses of 13.5 mg/kg egg or 0.675 mg/egg every 1.5 h, injected just beneath the shell, on day 18 of development (E18), 1 h after NaSal (25 or 100 mg/kg egg) was injected as a bolus. Hearts and brains taken shortly afterward were analyzed for *OH. In experiment 2, the dose of COC was reduced to 56.5 mg/kg egg so as to achieve a small but significant reduction in hatchability in order to determine if NaSal protected against or enhanced COC's toxicity, manifest as an increase or decrease in hatchability. The doses of NaSal for this experiment were 50, 100 or 200 mg/kg egg, all devoid of effects upon hatchability when injected alone. Experiment 3 was done to confirm the presence of vascular disruptions/hemorrhages observed on COC-exposed embryos while harvesting hearts and brains for chemical analyses and to quantify what appeared to be enhanced COC-related vascular accidents associated with NaSal pretreatment. The dose of NaSal used in experiment 3 was 200 mg/kg egg and COC was injected again at 5x13.5 mg/kg egg. RESULTS: COC increased *OH in hearts and brains of chicken embryos on E18, and non-toxic doses of NaSal (i.e. 100 or 200 mg/kg egg) enhanced COC's toxicity in a dose-related manner. The lowest NaSal dose (50 mg/kg egg) may have offered some protection against the effects of COC, as the reduction in hatchability caused by 56.5 mg COC/kg egg was no longer significant. Vascular disruptions/hemorrhages were associated with and most likely responsible for the interactive toxicity. CONCLUSIONS: Our unexpected findings may be of clinical relevance because of the use of aspirin for treatment of misdiagnosed "preeclamptic" COC-abusing pregnant women and its possible use for COC abusers at risk for reduced cerebral blood flow and stroke.     

Effect of ketamine pretreatment on cocaine-mediated hepatotoxicity in rats

Cocaine (COC) produces hepatotoxicity by a mechanism, which remains undefined, but has been linked to its oxidative metabolism. Ketamine (KET) is also a potentially hepatotoxic agent. The abuse of KET with COC is currently popular among young abusers therefore; this study was conducted to investigate the possible potentiation of COC-mediated hepatotoxicity (CMH) by KET. Male Sprague Dawley (SD) rats were administered oral KET hydrochloride for three consecutive days at a dose of 100 mg/kg with and without a single dose of COC (5 mg/kg, i.v.) administered 18 h after the last KET dose. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured as markers of liver injury. Liver reduced glutathione (GSH) levels were determined as well as the activities of glutathione peroxidase (GPx) and catalase (CAT). In addition, the activity of liver glutathione reductase (GRx) was measured. The results demonstrate that KET pretreatment potentiated the hepatotoxicity of COC. Serum ALT and AST were significantly elevated with the combined KET and COC treatment versus all other treatments. While COC alone resulted in focal inflammatory cell infiltration, COC administration after KET pretreatment produced sub-massive hepatic necrosis. Hepatic GSH content was significantly reduced in KET-pretreated COC group compared to the other treatment groups, rendering the liver more susceptible to oxidative stress. Moreover, there was a significant decrease in the activities of hepatic GPx and CAT, particularly with the KET-pretreated COC group. In addition, norcocaine (NC) was only detected in the plasma of rats received COC after KET pretreatment. In conclusion, this study demonstrates that KET pretreatment potentiates the hepatotoxicity of COC as revealed by an array of biochemical and morphological markers most probably due to increase in COC oxidative metabolism.