23例脾脏原发性恶性淋巴瘤临床分析

目的 提高临床对少见的脾原发性恶性淋巴瘤诊断和治疗的水平。方法 对1956年1月至1999年8月收治的23例脾原发性恶性淋巴瘤临床资料进行回顾性分析。结果 23例均行手术探查,22例获切除,术后均行COP或CHOP方案化疗。23例均为术后病理确诊,病理类型均为NHL,其中B细胞源性21例,T细胞源性2例。按Ahman脾恶性淋巴瘤临床分期,I期9例、Ⅱ期8例、Ⅲ期6例,5年生存率分别为50％、40％、16％。结论 脾恶性淋巴瘤的诊断主要依靠B超和CT,病期的早晚影响其预后,以手术为主的综合治疗是本病的主要治疗方法。     

胃淋巴瘤的诊治经验——附36例临床分析

目的 探讨提高原发性胃淋巴瘤的诊治水平。方法 回顾性分析36例胃淋巴瘤病例。结果 在本组资料中,病理分期(Arbor标准)为ⅠE期15例．ⅡE期7例,ⅢE期8例,ⅣE期6例;术前误诊率为22．2％,手术切除率为72．2％。手术加化疗5年生存率,低度恶性胃淋巴瘤为87.4％,高度恶性胃淋巴瘤为52．1％;单纯化疗时高度恶性胃淋巴瘤5年生存率仅为17．6%。结论 早期诊断、切除胃的原发病灶加术后联合化疗是提高原发性胃淋巴瘤生存率的主要因素。     

21例胃原发恶性淋巴瘤的诊治体会

为总结胃原发恶性淋巴瘤的诊治经验。回顾分析21例胃原发恶性淋巴瘤的临床情况。胃原发性恶性淋巴瘤的诊断依赖于上消化道造影、胃镜和活检；治疗采用手术加化疗。21例患者中ⅠE，ⅡE期术后5，10年生存率分别为100％，83．3％和84．6％，74．2％。早期诊断，采用手术加化疗是提高胃原发恶性淋巴瘤生存率的关键。     

原发性胃肠道淋巴瘤的诊断与治疗

目的探讨原发性胃肠道淋巴瘤的诊治经验。方法回顾性分析12例原发性胃肠道淋巴瘤,均行剖腹探查,其中行根治性切除7例,姑息性手术3例,肿块活检术2例。结果胃淋巴瘤5例,肠淋巴瘤7例。病理分类:弥漫性非何杰金氏淋巴瘤9例,粘膜相关性淋巴瘤2例,高度恶性淋巴瘤1例。Ann Arbor临床分期:ⅡE期3例,ⅢE期7例,ⅣE期2例。平均随访18(6~72)月,6例存活,死亡6例。结论内镜和消化道造影是淋巴瘤主要诊断手段,手术切除为主的综合治疗为最佳治疗方案。     

原发性脾脏恶性淋巴瘤21例的临床分析

目的 研究原发性脾脏恶性淋巴瘤（SPL）的临床和病理特征与治疗方法。方法 对1975-2000年收治的21例原发性脾脏恶性淋巴瘤患者的临床资料进行回顾性分析。结果 21例均行手术治疗，14例行COP或CHOP方案化疗，7例未行化疗，术后5年生存率分别为35．7％和28．6％。21例均为术后病理确诊，其中B细胞源性20例，T细胞源性1例。按Ahman脾恶性淋巴瘤临床分期，Ⅰ期9例，Ⅱ期7例，Ⅲ期5例，5年生存率分别为55．6％、42．9％、20％。结论 原发性脾脏恶性淋巴瘤的诊断主要依靠B超和CT，病期的早晚影响其预后，手术治疗联合化疗是本病的主要治疗方法。     

原发性胃恶性淋巴瘤的诊断与治疗

目的　探讨原发性胃恶性淋巴瘤的诊断、治疗及预后问题。方法　回顾性分析我院 41例的临床、病理及随访资料。生存率用寿命表法计算 ,显著性检验用卡方检验。结果　本组病例主要症状为腹部疼痛不适 (37/4 1)、消化道出血 (13/4 1)和腹部肿块 (12 /4 1)。 41例均为非何杰金氏淋巴瘤 ,其中MALT淋巴瘤 8例。术前诊断率2 9.3% ,手术切除率 90 % ,病例随访率 82 .9% ,1年、5年、10年生存率分别为 70 .6 %、5 2 .9%、38.2 %。临床分期(P <0 .0 1)、肿瘤大小 (P <0 .0 1)、组织学分级 (P <0 .0 5 )、浆膜累及 (P <0 .0 5 )和手术切除 (P <0 .0 5 )与预后有关。结论　手术切除是诊断、临床分期和治疗的主要方法 ;临床分期、恶性程度和根治手术是患者的预后因素 ;巨块型和浆膜累及者预后较差     

原发性直肠恶性淋巴瘤诊治分析

目的探讨原发性直肠恶性淋巴瘤的诊断和治疗方法。方法回顾性分析1994～2011年我院收治的7例原发性直肠恶性淋巴瘤诊断、治疗的临床资料。结果ⅡE期1例因患有肾功能衰竭放弃治疗并于1个月后死于急性肾衰外。ⅠE期2例经肛门手术,ⅡE期2例行根治手术,其无病生存期均达5年以上。ⅡE期1例仅做化疗,生存43个月。ⅣE期1例行姑息性手术加化疗,生存20个月。结论原发性直肠恶性淋巴瘤误诊率高、早期诊断对改善预后十分重要,手术切除加规范放、化疗,可明显延长生存期。     

胃粘膜相关淋巴组织淋巴瘤的外科治疗

目的 探讨胃粘膜相关淋巴组织淋巴瘤外科治疗经验。方法 回顾性复习1984－1996年手术治疗的69例胃粘膜相关淋巴组织淋巴瘤患者的临床资料。结果 69例中I期26例Ⅱ期21例、Ⅲ期13例、Ⅳ期9例,全组病例均经手术及理证实。病变完全切除者61例,部分切除者4例,未切除者4例。单纯手术切除者5例,手术加放疗25例,手术加化疗19例,手术加放疗、化疗20例。全组总的5年生存率71％（49／69）,10年生存率31．9％（22／69）。结论 临床分期及治疗方法是影响预后的主要因素,年龄与性别与预后无关。外科手术在胃粘膜相关淋巴组织淋巴瘤治疗中是重要治疗手段。     

原发性小肠恶性淋巴瘤的诊治分析

目的　提高对原发性小肠恶性淋巴瘤的认识和诊治水平。方法　回顾分析我院 1 983年 1月～ 2 0 0 0年 5月收治的 1 3例原发性小肠恶性淋巴瘤患者的临床资料。结果　 1 3例患者中 ,接受手术者 1 1例。 1 1例平均病程 2 1 .8个月 ;腹痛和体重下降是最常的症状 ;其中ⅡE 期 2例 ,ⅢE 期 6例 ,ⅣE 期 3例 ;肿瘤平均大小为 4 .85cm。肿瘤部位 :回盲部 7例 ,空肠 3例 ,十二指肠 1例。术后病理结果均为非何杰金恶性淋巴瘤 ,其中B细胞型 8例 ,混合细胞型 2例 ,T细胞型 1例。淋巴结转移率平均为 4 .2 /7.1。结论　本病病程较长 ,但确诊或手术时多数已属晚期 ,提高认识、早期诊断并选择以手术为主的综合治疗是提高本病疗效的关键。     

原发性结直肠非霍奇金淋巴瘤的诊治和预后分析

目的　总结原发性结直肠非霍奇金淋巴瘤的诊断和治疗经验。方法　对 33年来收治的 6 8例原发结直肠非霍奇金淋巴瘤的临床资料进行回顾性分析。结果　患者中位年龄 4 6岁 ,男女比例 1 8∶1。腹痛、腹部包块、腹泻、体重下降、便血、恶心呕吐是主要临床表现。肿瘤部位以回盲部最为常见 (49% ,33/ 6 8)。肿瘤最大平均径为 (8 3± 3 6 )cm ,以B细胞来源为主 (94 % ,6 4 / 6 8) ,多为中低度分化 (84 % ,5 7/ 6 8)。ⅠE、ⅡE、ⅢE、ⅣE期患者分别占 4 9%、2 7%、9%、16 %。 6 8例中 4 2例接受根治性手术 ,2 1例为姑息性切除 ,5 9例作了化疗 ,14例接受放射治疗。本组患者累积 1、3、5年生存率分别为 6 3%、4 7%、4 4 %。结论　原发性结直肠的非霍奇金淋巴瘤好发于青壮年男性 ,手术切除和临床分期是影响患者预后的主要因素。     

21. Wasser-Elektrolyte

Zusammenfassung Störungen des Wasser- und Elektrolythaushaltes können bei chirurgischen Patienten aus anamnestischen Angaben und bestimmten Symptomen vermutet werden. Nur die Messung der Elektrolyte in Serum und Urin gibt zusammen mit anderen Parametern (besonders Säure-Basenhaushalt) die Grundlage für eine rationale, quantitative Substitution (Bilanzierungsprinzip). Auf die hierbei möglichen Fehler wird hingewiesen.Die Ätiologie und Symptomatik der Magnesiumstörungen werden beschrieben, deren Bedeutung bei chirurgischen Patienten (besonders bei chronischen Erkrankungen des Magen-Darmtraktes oder Stoffwechselerkrankungen) kann nicht mehr vernachlässigt werden.Die Fortschritte der letzten Jahre in Diagnostik und Therapie des Elektrolytund Wasserhaushaltes werden kurz erwähnt.

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Water and electrolyte metabolism in surgical patients

Summary The clinical diagnosis of water and electrolyte imbalance can be made from the case history and certain symptoms. Only the measurements of electrolyte in blood and urine can give the basic information for a rational substitution with consideration of other parameters (e.g. acid-base-balance). The possible mistakes are shown.Etiology, symptoms and importance of magnesium abnormalities are described; they can be neglected no longer for surgical patients.The progress in diagnosis and therapy of electrolyte-water-metabolism is mentioned.

     

Ring chromosome 21 and monosomy 21 mosaicism in a patient with azoospermia

In this report, we describe a patient with azoospermia in conjection with de novo ring chromosome 21 and monosomy 21 mosaicism. Inter‐phase fluorescence in situ hybridisation (FISH) studies on uncultured peripheral blood and epithelial cells obtained by buccal smear revealed that 25% of the uncultured blood cells and 11% of the epithelial cells were monosomic for chromosome 21. Y chromosome microdeletion analysis ruled out the presence of any genomic deletions in the azoospermic factor a,b,c regions on the long arm of chromosome Y. Additionally, through subtelomeric FISH analysis, it was found that there was no deletion in the subtelomeric region of ring chromosome 21. Our results indicate that ring chromosome 21 is a rare, but recurrent chromosomal abnormality in male factor infertility. Furthermore, in individuals with ring chromosome 21, defective spermatogenesis is not associated with the deletion of any gene or genes located in the subtelomeric region of chromosome 21.     

Fibroblast growth factor 21 (FGF21) in human cerebrospinal fluid: relationship with plasma FGF21 and body adiposity

OBJECTIVE

Reports of increased circulating fibroblast growth factor 21 (FGF21) levels in obesity indicate that FGF21 may be implicated in body weight homeostasis. We sought to investigate the existence of FGF21 in human cerebrospinal fluid (CSF) and, if present, the relationship between CSF FGF21 with body adiposity and metabolic parameters.

RESEARCH DESIGN AND METHODS

CSF and corresponding plasma FGF21 were measured by an enzyme-linked immunosorbent assay (18 men and 20 women, aged 19–80 years, and BMI 16.2–38.1 kg/m²) and correlated to body adiposity and metabolic parameters.

RESULTS

CSF and plasma FGF21 increased in particular with rising BMI and fat mass. In CSF, FGF21 was detectable at concentrations ~40% that of plasma levels. CSF and plasma FGF21 levels were significantly positively correlated with BMI and fat mass, body weight, plasma insulin, and homeostasis model assessment of insulin resistance. Plasma FGF21 levels were significantly negatively correlated with plasma adiponectin. When subjected to multiple regression analysis, only fat mass was predictive of plasma FGF21 (β = 0.758; P = 0.004) and CSF FGF21 (β = 0.767; P = 0.007). The CSF-to-plasma FGF21 ratio was significantly negatively correlated with BMI, fat mass, and plasma FGF21. Subjects in the highest plasma FGF21 quintile had a lower CSF-to-plasma FGF21 ratio (12.7% [9.7–14.9%]) compared with those in the lowest plasma FGF21 quintile (94.7% [37.3–99.8%]) (P < 0.01).

CONCLUSIONS

Our observations have important implications with respect to the potential central actions of FGF21. Future research should seek to clarify whether FGF21 would be beneficial in the management of obesity and its metabolic complications.The fibroblast growth factor (FGF) family has 22 members that exert a wide range of biological effects (1). In addition to its role in regulating cell growth and differentiation (2), three members of the FGF family, specifically, FGF19, FGF21, and FGF23 (members of the same FGF subfamily), have been shown to have significant metabolic functions (3). FGF19 is produced by the intestinal epithelium and has been implicated in regulating cholesterol and bile-acid synthesis (4). FGF23, on the other hand, is produced by the bone and regulates phosphate absorption and vitamin D biosynthesis via its actions on the kidneys (5). FGF21, in contrast, is predominantly produced in the liver as well as adipose tissue and has been shown to be an important factor in the homeostatic mechanisms regulating glucose and lipid metabolism (6).FGF21 recently has been described as a metabolic regulator and a key hormonal mediator of the adaptive starvation response; FGF21 levels were positively associated with obesity and the metabolic syndrome and increased in type 2 diabetes (7–11). Of relevance, FGF21 has been reported to alleviate obesity in mice (12).The hypothalamus is the key regulatory center for energy balance and is abundant with peptides that regulate satiety (13). Many of these peptides also are produced in peripheral sites, in the case of FGF21, as mentioned above, the liver, and adipose tissue. Recently, an elegant study by Hsuchou et al. (14) demonstrated that FGF21 crosses the blood-brain barrier (BBB) in mice and affirmed that peripheral FGF21 could reach the brain directly and thus potentially exert its central effects (14,15).Given the above, we investigated the presence of FGF21 in human cerebrospinal fluid (CSF) and examined the potential contribution of circulating FGF21 to the brain by studying the CSF concentrations of FGF21 in relation to corresponding plasma levels, body adiposity, and metabolic parameters within the same cohort of subjects.Thirty-eight Caucasian subjects participated in the study (18 men and 20 women, aged 19–80 years, and BMI 16.2–38.1 kg/m²). Fourteen participants had normal body weight, 14 subjects were overweight (BMI 25 to <30 kg/m²), and 10 subjects were obese (BMI ≥30 kg/m²). Exclusion criteria included a history of diabetes, congestive heart failure, liver or kidney disease, or malignancy or signs of inflammation, pregnancy, and any drugs influencing body weight such as corticosteroids or contraceptives. During the study, three subjects (two men and one woman) were diagnosed with type 2 diabetes (fasting plasma glucose levels >7 mmol/L), as per the American Diabetes Association criteria. After an overnight fast, subjects undertook simultaneous sampling of blood and CSF (1 mL) via a lumbar puncture after local anesthesia (2 mL mepivacaine–HCL 1%). Blood samples immediately were centrifuged. Plasma and CSF samples were prepared within 1 h and stored at −80°C until assayed. All patients underwent anthropometric measurements. Body composition was measured by standard bioelectrical impedance analysis (BIA 2000-M, Data Input, Hofheim, Germany). Frequencies of 1, 5, 50, and 100 Hz were used; also, Eurobody software (Data Input) was used to analyze body fat mass. The study was approved by the local research ethics committee, and written informed consent was obtained from all participants, in accordance with the guidelines in the Declaration of Helsinki 2000.