广东东莞地区中老年非暴力性骨折107例及无骨折求诊者392例超声骨密度测定

目的:应用超声骨密度/骨质量测量仪对东莞地区中老年非暴力性骨折患者进行检测,探讨各参数的变化规律及临床意义,并确立骨折的骨密度阈值。方法:①实验对象:选择2003-09/2006-08在东莞石龙人民医院进行超声骨密度测定的非暴力性骨折东莞地区中老年患者107例,男30例,女77例;同期同龄进行超声骨密度测定的无骨折求诊者392例,作为对照组,男83例,女309例。②实验分组:根据年龄分为3个时期:46～60岁为老年前期、61～75岁为老年期、76岁以上为高龄期,以及相应男女组及骨折与非骨折组。③实验方法:采用法国DMS公司UBIS5000型超声骨密度/骨质量测量仪对中老年非暴力性骨折者、无骨折就诊者进行超声骨密度测量。④实验评估:比较两组男女及不同年龄段超声振幅衰减平均值、超声传播速度、骨硬度指数、T值(代表患者测量值如超声振幅衰减平均值和20岁正常人的测量值之间的差异)、Z值(代表患者测量值如超声振幅衰减平均值和同龄正常人的测量值之间的差异)。结果:两组499例患者全部进入结果分析。①总体比较:男、女性骨折组与非骨折组比较,除超声传播速度差别无统计学意义外(P>0.05),其余指标(超声振幅衰减、骨硬度指数、T值、Z值)非骨折组高于骨折组(P<0.01)。②分年龄组比较:老年前期组与总体一致,老年组、高龄组主要指标无统计学意义。应用方差分析对女性骨折组各年龄组之间进行比较,除骨硬度指数外(P<0.05),其余指标差异无显著性;男性骨折组各年龄组之间比较得出与女性一样结果。③男性与女性骨折组比较:除T值男性组高于女性组外(P<0.01),其余指标(超声振幅衰减、超声传播速度、骨硬度指数、Z值)差异均无统计学意义。结论:①中老年人群骨质下降至一定程度(相应测量参数为骨折阈值)时容易发生脆性骨折。②致脆性骨折的骨质量条件与性别、年龄因素无明显相关性。③东莞地区步入老年期后不论男女骨质疏松现象相当普遍,是否会出现骨折关键在于有否外力作用,对其预防性诊断很有价值。     

Transvaginal and transabdominal sonography: prospective comparison

Transvaginal (TV) and transabdominal (TA) sonography were compared in a prospective study. A total of 230 examinations (126 pelvic, 104 pregnancy) were performed on 215 patients, ranging in age from 14 to 80 years. The improved anatomic detail on TV scans yielded new information in 138 (60%) examinations and better visualization of pelvic structures in 51 (22%) examinations. There was no important difference in diagnostic information provided by the two imaging modalities in 36 (16%) cases, and TV images were worse in five (2%). The clinical diagnosis was altered on the basis of TV sonographic findings in 54 (24%) cases and confirmed with certainty in 166 (72%). Diagnostic problems posed by TA scanning were not resolved by TV scanning in ten (4%) instances. Statistical analysis indicated that TV scanning was significantly better than TA scanning in the visualization of gestational sac contents (P less than .005), detection of fetal heart motion (P less than .001), and evaluation of the endometrial canal in the retroverted or retroflexed uterus (P less than .001). TV scanning was significantly better than TA scanning in visualization of the ovaries in patients with uterine leiomyomas (P less than .005) but not significantly better in peri- and postmenopausal patients (P greater than .05).     

Heterogeneity of drug-dependent platelet antigens and their antibodies in quinine- and quinidine-induced thrombocytopenia: involvement of glycoproteins Ib, IIb, IIIa, and IX

The molecular nature of platelet receptors for quinine- and quinidine- dependent antiplatelet antibodies (Q.Ab and Qd.Ab) was studied by immunoblotting. One Q.Ab caused quinine-dependent IgG binding to platelet proteins with molecular weights (mol wts) of 174 Kd and 93 Kd and another to only a 93-Kd protein. A third Q.Ab caused binding to 174- , 140-, 93-, and 57-Kd proteins, while a fourth Q.Ab and a Qd.Ab caused IgG binding to 174- and 18-Kd proteins. Using platelets from patients with Glanzmann's thrombasthenia or Bernard Soulier syndrome and purified GPIIIa, these proteins were shown to be GPIb, GPIIb, GPIIIa, GPIX, and an unidentified 57-Kd protein missing in Bernard Soulier syndrome. Binding to the 93-Kd protein was independent of the PIA1 antigen. Absorption of one Q.Ab with Glanzmann's thrombasthenia platelets revealed different populations of antibodies with different specificities within the one patient. Thus Q.Ab and Qd.Ab are heterogeneous and may be directed toward different epitopes on major platelet glycoproteins.     

Platelet modulation of polymorphonuclear leukocyte shear induced aggregation

A cone and plate viscometer and Coulter Counter were used to study platelet modulation of polymorphonuclear leukocyte (PMNL) aggregation caused by controlled shear stress. As an index of aggregation, the large-particle percentage (LPP) was calculated. This represents the ratio of aggregated cell count to total cell count. PMNL suspensions in buffer (1.0 X 10(7) cells per milliliter, final concentration) did not show any aggregate formation at shear stresses below 150 dynes/cm2 for one minute exposure time (LPP less than 3%). However, there was PMNL aggregation in mixed PMNL and platelet-rich plasma suspensions in this shear stress range. Supernatant plasma from sheared platelets initiated PMNL aggregation at moderate shear stress (150 dynes/cm2 for one minute; LPP, 20.3% +/- 2.5%). In contrast, platelet release factors, such as adenosine diphosphate (2 mumol/L) and serotonin (2 mumol/L) did not cause PMNL aggregation (LPP, 2.9% +/- 1.2% and 3.3% +/- 0.8%, respectively). The use of a cyclo-oxygenase inhibitor (acetylsalicylic acid, 50 mumol/L) did not suppress the aggregation of PMNLs after shear (LPP, 20.1% +/- 2.4%). However, preincubation with nordihydroguaiaretic acid (10 mumol/L), an inhibitor of C-5 and C-12 lipoxygenase, and 6,9- deepoxy-6,9-(phenylimino)-6,8-prostaglandin I1 (U-60257, 10 mumol/L), an inhibitor of C-5 lipoxygenase in human leukocytes, suppressed this aggregation (LPP, 9.1% +/- 2.5% and 10.4% +/- 3.2%, respectively). Also, the formation of lipoxygenase products (5-HETE, 12-HETE, 15-HETE, and LTB4) activated by shear stress was documented by reversed phase- high-performance liquid chromatography (RP-HPLC). These data support the possibility of a cooperation between platelets and leukocytes in shear-induced PMNL aggregation that is dependent on C-12 or C-5 lipoxygenase activity, or both.     

Platelet refractoriness and alloimmunization in pediatric oncology and bone marrow transplant patients

BACKGROUND: The purposes of this study were to determine the overall incidence of platelet refractoriness and alloimmunization among multiply transfused children on a medical oncology and bone marrow transplant service and to evaluate the effect of routine white cell reduction in blood components on that incidence. STUDY DESIGN AND METHODS : The platelet transfusion records of 128 consecutive children admitted to the hospital and requiring blood component support for the treatment of disease were evaluated retrospectively. Mean corrected count increments (CCIs) for each patient were calculated for all random- donor platelet transfusions given within 7 days of the routine weekly testings of the patient's serum for lymphocytotoxic antibodies (LCTAbs). Mean CCIs for HLA-matched platelet transfusions were calculated separately for the patients receiving them. RESULTS : Thirty- one patients (24%) had or developed persistently positive LCTAbs (patient's serum reacted with > or = 3/10 panel lymphocytes); 22 (71%) of these patients had a mean CCI < 7.5 to random-donor platelet transfusions. In contrast, of the 97 patients with negative or transiently positive LCTAbs, only 25 (26%) had a mean CCI < 7.5. The overall incidence of platelet refractoriness (CCI < 7.5) was 37 percent. Patients with acute myelogenous leukemia had a significantly (p < 0.01) reduced incidence (17%) of low CCIs, with or without positive LCTAbs, as compared to patients with other malignant or nonmalignant disorders (41%). No difference in the incidence of LCTAbs or low CCIs was seen in patients undergoing allogeneic or autologous bone marrow transplant or receiving drug therapy only. Among the 24 patients who received HLA-matched platelets, only those with positive LCTAbs showed a significant improvement in CCIs over that achieved with random-donor platelet transfusions. Routine white cell reduction in red cell and platelet components with third-generation white cell filters was performed prior to transfusion in 73 of the patients. There was no significant difference between the incidence of LCTAbs and/or low CCIs in this group and that in the 55 children receiving unfiltered transfusions. CONCLUSION : Alloimmunization and platelet refractoriness occur in pediatric oncology and bone marrow transplant patients, but the incidence-particularly in children with acute myelogenous leukemia- -appears to be low. The detection of LCTAbs predicts a poor response to random-donor platelet transfusion, but most such patients show improved CCIs with HLA-matched platelets. Routine use of white cell-reduction filters has thus far failed to eliminate alloimmunization in children requiring prolonged blood component support.     

Natural kinds, natural history and the clinician-researcher

Recent medical research has been based on a flawed rationale of clinical innovation (here termed the 'basic-to-mega model') which neglects the human organism as a vital focus of clinical scientific study. The consequent over-concentration upon cellular and population levels of analysis has probably damaged the rate of therapeutic progress. The key role in medical research should be acknowledged to lie with clinician-researchers whose 'experimental animal' is the patient and whose 'end-points' are health and disease. The distinctive strength of the clinician-researcher derives from an ability to combine understanding of the 'natural kinds' (i.e. true biological categories) relevant to human disease, with experience of the 'natural history' of disease (i.e. its longitudinal pattern, including the response to interventions). Such knowledge is explicitly formalized by the activities of clinical science and clinical epidemiology. A sufficient supply of active clinician-researchers is the catalyst of innovation, and an insufficient supply is currently a rate-limiting factor in therapeutic progress.      

Myeloma bone marrow acid phosphatase staining: a correlative study of 38 patients

Acid phosphatase (AP) activity of plasma cells was studied in 38 patients with multiple myeloma (MM). The average activity per cell was strong (mean score = 2.42; maximum score = 4) and the percentage of positive cells was greater than 90% in over 71% of patients. The average AP activity per cell was higher prior to treatment (3.06 +/- 0.53) compared to relapse (2.48 +/- 0.77) and remission (1.81 +/- 1.02 (p less than 0.05 and p less than 0.01, respectively). In correlation of AP activity with clinical features at the time of the study, the only significant difference was between kappa and lambda subtype. Patients with lambda MM had a higher average AP activity per cell in remission (2.71 +/- 0.43) as opposed to kappa MM (1.17 +/- 1.06, p less than 0.05 for difference). AP activity was not significantly correlated with degree of bone involvement. However, activity seemed to be a good marker of disease activity.