阴茎异常勃起的鉴别诊断及急诊处理

目的:提高阴茎异常勃起的诊治水平。方法:对18例阴茎异常勃起患者的诊断和治疗进行了回顾性分析。结果:发病原因:白血病1例,海绵体注射罂粟碱16例,原因不明1例。发病至就诊时间4~18 h,平均7 h。均为低流量异常勃起。海绵体穿刺血液行血气分析3例,海绵体动脉血流彩色多普勒检查2例。17例经阴茎海绵体内注射缩血管药物、海绵体穿刺放血以及肝素化盐水冲洗后异常勃起消失。1例白血病诱发勃起的患者经上述治疗无效,后经化疗后恢复正常。结论:海绵体内注射罂粟碱诱发的阴茎异常勃起和白血病诱发的异常勃起均为低流量型异常勃起。阴茎海绵体内注射缩血管药物,海绵体穿刺放血冲洗可解除异常勃起。白血病诱发的异常勃起应强调原发病的治疗。     

12例阴茎异常勃起临床分析

目的 提高阴茎异常勃起的诊断和治疗水平.方法 阴茎异常勃起患者12例,均诊断为低流量型.12例患者中2例保守治疗有效;10例保守治疗无效后行海绵体内药物注射,其中2例注射美蓝20mg,8例注射间羟胺2～10mg;2例保守治疗、海绵体内药物注射后依然复发的患者行手术分流.随访2～117个月,平均48个月.结果 12例患者中10例保守治疗患者未复发;2例手术患者手术后也未再复发,但并发阴茎勃起功能障碍.2例白血病患者分别死于随访第4个月和第12个月.结论 完整的病史、仔细体检对阴茎异常勃起的诊断非常重要,治疗应以保守治疗为主,尽可能减少创伤.     

使用间羟胺无效的阴茎异常勃起4例

报告了４例使用间羟胺阴茎海绵体注射治疗无效的阴茎异常勃起，分别采用抽吸放血法或海绵体穿刺灌洗法，以及阴茎－尿道海绵体分流术，白血病确诊后采用化学疗法。结果２例持续勃起时间在１３ｈ内的阴茎异常勃起恢复正常，１例慢性粒细胞白血病经化疗后，２７ｄ后疲软，但功能未能恢复，１例勃起７２ｈ以上未能恢复，出现海绵体纤维化。讨论了阴茎异常勃起的治疗效果同其类型、勃起持续时间、病因有密切关系，以及应当选择的治疗方法     

阴茎异常勃起的诊断和治疗(附7例报告)

目的根据不同原因,区分低流量型和高流量型阴茎异常勃起,提高阴茎异常勃起的诊治水平。方法7例阴茎异常勃起患者年龄20~46岁,平均35岁。持续勃起时间4~68h,平均22h。其中服用两地那非后性交勃起异常1例,膀胱癌转移至阴茎1例,白血病1例,有外伤史者1例,不明诱因者3例。对异常勃起分型,治疗及预后进行分析。结果7例患者中1例为高流量型,6例为低流量型。1例高流量型患者行选择性阴部内动脉栓塞后治愈,6例低流量型患者,均先行肝素盐水及肾上腺素盐水龟头-阴茎海绵体冲洗,但效果不理想,随后改行龟头——阴茎海绵体分流术,5例患者术后1至5天恢复正常,1例患者术中行病理活检为膀胱癌转移至阴茎,有阴茎全切术。结论详细询问病史、阴茎海绵体血气分析、彩色多谱勒检查、阴部内动脉造影等是区分高流量型和低流量型阴茎异常勃起的重要方法。阴茎异常勃起如保守治疗无效,应立刻进行手术治疗。     

阴茎异常勃起的诊断和治疗(附10例报告)

目的提高急诊处理阴茎异常勃起的能力。方法回顾10例阴茎异常勃起患者的临床资料、诊疗过程及随访结果,结合文献资料进行分析。结果10例患者中8例为低流量型,2例为高流量型。8例低流量型患者行海绵体灌洗或阴茎头-海绵体分流术治愈;2例高流量型患者海绵体灌洗同样有效。结论阴茎海绵体血气分析、彩色多谱勒检查、阴部内动脉造影等是区分高流量型和低流量型阴茎异常勃起的重要方法,治疗阴茎异常勃起首选海绵体药物灌洗,如无效应进行手术治疗。     

以阴茎异常勃起为首发症状的慢性粒细胞性白血病一例报告

慢性粒细胞性白血病(慢粒)以阴茎异常勃起为首发症状者在临床上较少见,最近我院收治1例报告如下。患者男,19岁,1987年5月11日入院。入院前6个月,患者每天晨起时阴茎异常勃起伴轻度胀痛,持续10分钟左右自行缓解。入院前4天,突然出现阴茎持续性异常勃起伴胀痛,阵发性加剧。体检:轻度     

阴茎异常勃起的诊断和治疗(附12例报告)

阴茎异常勃起是指无性欲刺激情况下 ,阴茎呈持续痛性勃起状态 ,临床较少见。我院自１９９０年１月至２０００年１０月共收治１２例 ,报告如下。１资料与方法１ １临床资料本组１２例均为已婚患者 ,年龄２７～６０岁 ,平均４１ ８岁 ,５０岁以上者１人。患者均表现为在无性欲刺激情况下 ,阴茎海绵体呈持续勃起状态。阴茎持续勃起状态病程２０ｈ～１５ｄ。动脉高流入性异常勃起１例 ,阴茎皮肤颜色正常 ,无阴茎疼痛。静脉阻塞低流入性异常勃起１１例 ,阴茎坚硬 ,疼痛 ,阴茎皮肤青紫。发病诱因 :服用复方降压片后阴茎勃起３例 ,输注血塞通后阴茎…     

阴茎异常勃起临床研究

目的　探讨阴茎异常勃起的诊断与治疗。方法　对 13例阴茎异常勃起的诊治进行回顾性分析。结果　低血流量型 12例 ,保守治疗治愈 7例 ,行改良的Winter分流术治愈 5例 ,高血流量型 1例保守治疗治愈。结论　早期区分异常勃起的类型对确定治疗方案至关重要 ;低血流量型发病时间 <12h治疗以保守为主 ,12～ 2 4h者保守治疗无效者行改良的Winter分流术 ,>2 4h者主张及时行Winter分流术 ,高血流量型首选保守治疗。     

海绵体抽吸冲洗法治疗阴茎异常勃起的临床观察

阴茎异常勃起是指缺乏性刺激的阴茎持续勃起或在性高潮后仍不能转入疲软状态,勃起持续时间超过4～6h。阴茎异常勃起分为2种类型:低血流量阴茎异常勃起是因静脉流出量减少和静脉血液滞留;高血流量阴茎异常勃起是因海绵体动脉损伤引起血流灌注量过度增加[1]。高血流量阴茎异常勃起非常少见。笔者自1994年1月-2006年11月应用海绵体抽吸冲洗法治疗阴茎异常勃起18例,获得较满意治疗效果,现报道如下。1临床资料1.1一般资料选取阴茎异常勃起患者18例,年龄20～47     

阴茎异常勃起8例报告

阴茎异常勃起以往比较少见 ,近年来随着临床药物治疗与男性性功能障碍诊疗工作的开展 ,阴茎异常勃起作为泌尿男科临床急症越来越多见 ,正确及时的诊断与治疗 ,才能使患者的性功能得以恢复。我院 1992年～ 2 0 0 0年共收治 8例 ,现报告如下。1　临床资料本组年龄 2 4～ 5 6岁 ,平均 34岁。发病至就诊时间最短 6ｈ ,最长 4ｄ。发病原因 :药物性假体 3例 ,白血病 1例 ,外伤性 1例 ,特发性 3例。治疗方法 :单纯阴茎海绵体穿刺抽吸术 3例 ,阴茎海绵体尿道海绵体分流术 4例 ,阴茎头阴茎海绵体分流术 +阴茎背动脉结扎术 1例。治疗后 5例出现ＥＤ ,3…     

CTA指导下介入治疗外伤性阴茎异常勃起

目的探讨在CT三维血管成像指导下进行动脉栓塞治疗外伤性阴茎异常勃起的临床价值。方法 3例外伤性阴茎异常勃起,术前行CT三维血管成像检查,根据CT结果行阴部内动脉栓塞治疗,术中选用明胶海绵颗粒栓塞出血动脉,术后1周行CT三维血管成像检查了解阴茎血供情况。结果 3例术前CT检查提示阴茎海绵体假性动脉瘤,行选择性阴部内动脉栓塞后,阴茎异常勃起消退,术后1周复查CT检查提示出血消失,随访两年阴茎勃起正常。结论 CT三维血管成像对外伤性阴茎异常勃起诊断有很高的价值,同时可用于指导介入治疗及术后随访。     

Inhibitory effect of curcumin onWT1 gene expression in patient leukemic cells

Leukemias are common worldwide. Wilms' tumor1 (WT1) protein is highly expressed in leukemic blast cells of myeloid and lymphoid origin. Thus, WT1 mRNA serves as a tumor marker for leukemias detection and monitoring disease progression. Curcumin is well known for its anti-cancer property. The objective of this study was to investigate the effect of curcumin on WT1 gene expression in patient leukemic cells. The leukemic cells were collected from 70 childhood leukemia patients admitted at Maharaj Nakorn Chiang Mai Hospital, Chiang Mai, Thailand, in the period July 2003 to February 2005. There were 58 cases of acute lymphoblastic leukemia (ALL), 10 cases of acute myeloblastic leukemia (AML), and 2 cases of chronic myelocytic leukemia (CML). There were 41 males and 29 females ranging from 1 to 15 years old. Leukemic cells were cultured in the presence or absence of 10 mM curcumin for 48 h. WT1 mRNA levels were determined by RT-PCR. The result showed that curcumin reduced WT1 gene expression in the cells from 35 patients (50%). It affected the WT1 gene expression in 4 of 8 relapsed cases (50%), 12 of 24 cases of drug maintenance (50%), 7 of 16 cases of completed treatment (44%), and 12 of 22 cases of new patients (54%). The basal expression levels of WT1 gene in leukemic patient cells as compared to that of K562 cells were classified as low level (1-20%) in 6 of 20 cases (30%), medium level (21-60%) in 12 of 21 cases (57%), and high level (61-100%) in 17 of 23 cases (74%). In summary, curcumin decreased WT1 mRNA in patient leukemic cells. Thus, curcumin treatment may provide a lead for clinical treatment in leukemic patients in the future.     

Bone marrow fibroblasts-conditioned medium regulates the proliferation of leukemic cells

The effect of normal human bone marrow fibroblasts-conditioned medium (BMF-CM) was studied on the proliferation of K562 cells, and on leukemic cells from patients with acute myelocytic leukemia at the time of diagnosis and chronic myelogenous leukemia (CML) at chronic phase. BMF-CM was obtained from normal human bone marrow fibroblasts by using long-term liquid cultures. BMF-CM suppressed the proliferation of K562 cells and leukemic cells from patients with undifferentiated type of leukemia (M1 in FAB classification). However it stimulated the proliferation of leukemic cells from patients with differentiated type of leukemia (M2 in FAB classification), and it slightly stimulated that from patients with CML. These results suggest that normal human BMF regulate the proliferation of leukemic cells in their various stages of differentiation in the bone marrow by releasing a humoral factor.     

Inhibitory effect of curcumin onMDR1 gene expression in patient leukemic cells

When patients with cancers are treated with chemotherapeutic agents a long time, some of the cancer cells develop the multidrug resistance (MDR) phenotype. MDR cancer cells are characterized by the overexpression of multidrug resistance1(MDR1) gene which encodes P-glycoprotein (Pgp), a surface protein of tumor cells that functions to produce an excessive efflux and thereby an insufficient intracellular concentration of chemotherapeutic agents. A variety of studies have sought potent MDR modulators to decrease MDR1 gene expression in cancer cells. Our previous study has shown that curcumin exhibits characteristics of a MDR modulator in KB-V1 multidrug-resistant cells. The aim of this study was to further investigate the effect of curcumin on MDR1 gene expression in patient leukemic cells. The leukemic cells were collected from 78 childhood leukemia patients admitted at Maharaj Nakorn Chiang Mai Hospital, Chiang Mai, Thailand, in the period from July 2003 to February 2005. There were 61 cases of acute lymphoblastic leukemia (ALL), 14 cases of acute myeloblastic leukemia (AML), and 3 cases of chronic myelocytic leukemia (CML). There were 47 males and 31 females ranging from 1 to 15 years old. Bone marrows were collected. The leukemic cells were separated and cultured in the presence or absence of 10 microM curcumin for 48 hours. MDR1 mRNA levels were determined by RT-PCR. It was found that curcumin reduced MDR1 gene expression in the cells from 33 patients (42%). Curcumin affected the MDR1 gene expression in 5 of 11 relapsed cases (45%), 10 of 26 cases of drug maintenance (38%), 7 of 18 cases of completed treatment (39%), and 11 of 23 cases of new patients (48%). The expression levels of MDR1 gene in leukemic patient cells as compared to that of KB-V1 cells were classified as low level (1-20%) in 5 of 20 cases (25%), medium level (21-60%) in 14 of 32 cases (44%), and high level (61-100%) in 14 of 20 cases (70%). In summary, curcumin decreased MDR1 mRNA level in patient leukemic cells, especially in high level of MDR1 gene groups. Thus, curcumin treatment may provide a lead for clinical treatment of leukemia patients in the future.     

A phase II study of mitoxantrone in acute leukemia

Summary A phase II study of mitoxantrone (Novantrone®; dihydroxyanthracenedione) was conducted in 35 patients (22 male: 13 female) with acute leukemia. There were 35 evaluable cases with a mean age of 34 (range 8–61). Twenty-eight patients had acute non-lymphocytic leukemia (ANLL) and seven had acute lymphocytic leukemia (ALL). Mitoxantrone was administered intravenously 2–4 mg/m² daily for five days and after the nadir a further 2–3 doses were added if necessary. All previously treated cases (22 patients) had been treated with anthracyclines; 13 had no previous treatment. Out of the 13 untreated cases there were six complete remissions (CRs) (46.2%) and five partial remissions (PRs) (38.5%), while out of 22 pretreated cases, four CRs (18.2%) and five PRs (22.7%) were obtained. In seven of the untreated cases the decrease of leukemic cells and neutrophil leukocytes were analysed. Mitoxantrone showed a longer duration of decrease and higher log decrease of leukemic cells in the bone marrow than daunorubicin or cytosine arabinoside. Seventy-three percent of patients showed gastrointestinal disturbances such as nausea or loss of appetite. In 38.1% SGPT elevation and in 8.8% abnormal ECG findings were observed. All side-effects were mild and reversible. From this data mitoxantrone seems a very promising agent in the treatment of acute leukemia and a phase III study is now being carried out.     

Selective sensitivity to tiazofurin of human leukemic cells

This study reports the selective sensitivity to tiazofurin (2-beta-D-ribofuranosylthiazole-4-carboxamide, NSC-286193) of human leukemic leukocytes as compared to normal ones in bone marrow and peripheral blood samples by comparing the production of the active metabolite, thiazole-4-carboxamide adenine dinucleotide (TAD), from labeled tiazofurin and the depression of GTP concentration. When labeled tiazofurin was incubated with leukocytes obtained from healthy volunteers or from leukemic patients (acute non-lymphocytic leukemia or acute lymphoblastic leukemia), the TAD production was 27.0 +/- 8.3, 551.3 +/- 71.8 and 755.9 +/- 94.1 pmoles/10(9) cells per hr, respectively. Thus, the leukemic cells produced over 20-fold higher concentrations of TAD than the normal leukocytes. Incubation with tiazofurin in leukemic leukocytes decreased the GTP pools (to 48-79%), whereas there was no change in the normal leukocytes. These results indicate a selectivity of response to tiazofurin in human normal and leukemic leukocytes. The procedure reported in this work may be suitable as a rapid predictive test for the sensitivity of leukemic leukocytes to tiazofurin. Such a diagnostic test should be helpful in identifying neoplastic cells sensitive to tiazofurin in the Phase II trials now being developed.