Resurgence of bedbugs in southern France: a local problem or the tip of the iceberg?

Background Bedbugs (Cimex lectularius) have been feeding on sleeping human beings since prehistory. In Europe, bed bugs were common and endemic until World War II when improved body and home hygiene, and widespread use of insecticides led to almost complete eradication. Current evidence indicates that bedbugs are making a comeback in Europe, USA, Canada and Australia. In our practice in Southern France, we observed several cases within a period of only 1 year. Objectives Based on this experience, we conducted an epidemiological study to evaluate the status of bedbugs in France. Methods During summer 2009, we mailed a short questionnaire to all hospital professors in the CEDEF (Collège des Enseignants de Dermatologie de France) asking four questions: number of suspected diagnosis of bedbugs in the year 2009, and number of certain positive diagnosis, difficulties in treatment, use of a pest control professional for treatment, and finally personal opinion on actual incidence of bedbugs, compared with past years. Results Of the 84 questionnaires sent, there were only 26 responses despite two reminders. The responses were predominantly southern France, probably as a result of intensive immigration and increased travel and trade. Difficulties encountered during diagnosis and treatment are also mentioned. Utilizing the services of entomological experts and pest control professionals is essential. Conclusions France has the same experience regarding the resurgence of bedbugs as several European countries, USA, Canada and Australia, especially the southern regions. This emerging health problem has to be known by dermatologists. A national programme has been launched in France to assess actual incidence and study C. lectularius‐ related diseases.     

Primary headache care delivery by nonspecialists in Brazil

Headaches are common disorders usually examined by nonneurologists. In order to assess how primary headache patients (IHS groups 1, 2, and 3) are generally managed by nonspecialists, 414 patients were asked about their previous headache care. Correct diagnosis had previously been made in only 44.9%, 6.7%, and 26.7% of the migraine, tension-type headache, and cluster headache patients, respectively. The patients underwent 501 investigative procedures motivated by the headache, averaging 1.21 examinations per patient, mostly EEGs. Preventive treatment was largely overlooked irrespective of the headache type. It is concluded that scientific improvements in headache care may be ineffective unless educational programs improve headache knowledge in general.     

Amplatzer封堵器的生物学性能及经导管介入治疗房间隔缺损

目的:评价经导管置入Amplatzer封堵器治疗继发孔房间隔缺损的治疗效果。方法:①选择2002-08/2006-04在兰州市第一人民医院心外科住院的继发孔型房间隔缺损65例,男26例,女39例;平均年龄(18±8)岁;平均房间隔缺损直径(19.3±7.2)mm。纳入患者对手术方案知情同意。②手术所用封堵器为美国公司的Amplatzer房间隔缺损封堵器,是一种新型的适于关闭二孔型房间隔缺损的装置,它由具有自膨胀性的双盘及连接双盘的腰部三部分组成。双盘状结构恢复记忆形状后可以稳定封堵房间隔缺损的边缘部分,降低残余分流的发生率。③根据选择封堵器大小的方式(即球囊测量或经胸超声心动图直接观察)将患者分为球囊测量组38例和经胸超声心动图测量组27例。均在透视及经胸超声心动图监视下经导管置入Amplatzer封堵器封堵房间隔缺损。同时测量患者缺损扩张直径、封堵器大小,记录X射线透视时间和手术时间。④术后即刻、24h、3个月及1年分别行经胸超声心动图、心电图及X射线检查评价治疗效果。⑤超声心动图显示完全无分流为无分流;残余分流血流宽度≤1mm为微量分流;血流宽度1.0～2.0mm为少量残余分流;血流宽度2～4mm为中量残余分流;血流宽度>4mm为大量残余分流。⑥组间计量资料差异比较采用两个独立样本t检验,组间手术效果比较采用两个独立样本的等级资料秩和检验。结果:①技术成功率:65例房间隔缺损患者,64例封堵器置入成功,技术成功率为98%。②选择封堵器直径:球囊测量组缺损扩张直径为(20.4±6.1)mm,选择的封堵器直径为(21.6±5.7)mm,与经胸超声心动图测量组相近[(22.5±4.3),(25.1±4.9)mm,P>0.05]。③术后残余分流情况:术后即刻经胸超声心动图显示,球囊测量组35例完全无分流,经胸超声心动图组有23例,差异不明显(P>0.05);术后24h,球囊测量组36例完全无分流,经胸超声心动图组有24例,差异不明显(P>0.05);术后3个月,球囊测量组37例完全无分流,经胸超声心动图组有25例,差异不明显(P>0.05);术后1年完成随访的52例患者均未见封堵器移位及房间隔缺损再通。④X射线平片检查:全部显示肺血减少,右心房、室缩小。结论:封堵器直径比球囊测量的房间隔缺损扩张直径大1.0～2.0mm,比超声心动图测量的大2～6mm封堵效果好,成功率高。     

CVA3 Adherence to Hypertension Therapy: The Effect of Initial Drug Choice

Health-care case management places pressure on decision makers to adopt treatment strategies that promote economic efficiency and hence profitability. Traditional costeffectiveness analysis (CEA), where the objective is to calculate cost-effectiveness ratios, can better inform decision making in markets where prices and efficacy vary widely. However, the threshold at which a given therapy becomes economically efficient relative to competing therapies is not evident from cost-effictiveness ratios alone.
OBJECTIVE: To illustrate the use of spatial techniques for identifying efficient treatment options, using statin therapy in secondary prevention of coronary heart disease (CHD) as a case study.
METHODS: We used a Markov model of CHD epidemiology and treatment to estimate cost-effectivness of 13 statin regimens versus no therapy in secondary prevention of CHD. Comparative efficacy was assessed using data from a recent trial (CURVES) that included these regimens. Patients were assumed to have a history of CHD with risk factors similar to those observed in the trial. CHD event risk was estimated using new subsequent-event risk equations from the Framingham Heart Study. Effectiveness was measured alternatively as gain in life expectancy and CHD events averted.
RESULTS: At usual starting doses, atorvastatin therapy provided the largest life expectancy gain and CHD event avoidance at the lowest cost per life-year gained ($12,900 and $23,400 for men and women, respectively), followed by simvastatin ($17,700 and $31,700), lovastatin ($18,800 and $33,700), pravastatin ($22,600 and $40,200), and fluvastatin ($23,800 and $42,000). Any desired level of effectiveness can be obtained at lowest cost with atorvastatin.
CONCLUSION: Economic efficiency is enhanced when atorvastatin is used to treat some or all patients requiring statin therapy in secondary prevention of CHD.     

Ambulatory blood pressure monitoring

Ambulatory blood pressure monitoring (ABPM) in adults is proving to be useful. The aim of this study was to determine if ABPM is accurate in the lower blood pressure range encountered in children and, equally important, whether it is acceptable to children. Thirty one children, between the ages of 6 and 18 years, were assessed using an ambulatory blood pressure monitor that uses an auscultatory method. Blood pressure was measured in the contralateral arm with a mercury sphygmomanometer and an oscillometric device at the beginning and end of the study for comparison. Over a blood pressure range of 90-130 mm Hg systolic and 40-80 mm Hg diastolic, a close agreement was found with the sphygmomanometer; the limits of agreement (+/- 2 SD) were 11.6 mm Hg for systolic blood pressure and 13.6 mm Hg for diastolic blood pressure. The bias was less than 1.0 mm Hg. The ambulatory device was worn by all patients for at least 16 hours with an average of 52 recordings per patient. The majority found the device comfortable to wear and were not woken from sleep.     

HMGB1 as a predictor of organ dysfunction and outcome in patients with severe sepsis

OBJECTIVE: To study the predictive value of high mobility group box-1 protein (HMGB1) and hospital mortality in adult patients with severe sepsis. STUDY DESIGN: Prospective observational cohort study in 24 ICUs in Finland. PATIENTS: Two hundred and forty-seven adult patients with severe sepsis. MEASUREMENTS AND MAIN RESULTS: Blood samples for HMGB1 analyses were drawn from 247 patients at baseline and from 210 patients 72 h later. The mean APACHE II and SAPS II scores were 24 (SD 9) and 44 (SD 17), respectively. The hospital mortality was 26%. The serum HMGB1 concentrations were measured first by semi-quantitative Western immunoblotting (WB) analysis. The median HMGB1 concentration on day 0 was 108% (IQR 98.5-119) and after 72 h 107% (IQR 98.8-120), which differed from healthy controls (97.5%, IQR 91.3-106.5; p=0.028 and 0.019, respectively). The samples were re-analysed by ELISA (in a subgroup of 170 patients) to confirm the results by WB. The median concentration in healthy controls was 0.65 ng/ml (IQR 0.51-1.0). This was lower than in patients with severe sepsis (3.6 ng/ml, IQR 1.9-6.5, p< 0.001). HMGB1 concentrations (WB and ELISA) did not differ between hospital survivors and non-survivors. In ROC analyses for HMGB1 levels (WB) on day 0 and 72 h with respect to hospital mortality, the areas under the curve were 0.51 and 0.56 (95% CI 0.40-0.61 and 0.47-0.65). CONCLUSIONS: Serum HMGB1 concentrations were elevated in patients with severe sepsis, but did not differ between survivors and non-survivors and did not predict hospital mortality.     

The molecular basis of renal amyloidosis in Irish-American and Polish- Canadian kindreds

Hereditary amyloidosis of an unusual form has been reported in two separate kindreds; one was Polish-Canadian and the other was Irish- American (Am J Med 1975; 59:121 and Trans Assoc Am Physicians 1981; 94:211). In both kindreds, affected members developed hypertension and nephrotic syndrome due to amyloidosis in their forties or fifties, but the genetic background responsible for the condition has been left undetermined. To identify the genetic defect in these kindreds, a portion of exon 5 of the fibrinogen alpha-chain gene in members of these kindreds was examined for a mutation by single-strand conformation polymorphism analysis and direct DNA sequencing. DNA analyses revealed an A-->T transversion at the second base of codon 526 of the fibrinogen alpha-chain gene in both of these kindreds. Analysis of DNA polymorphisms in the fibrinogen alpha-chain gene locus (TCTT repeat in intron 3, Rsal site in exon 5, and Taql site in the 3' flanking region of the gene) showed the haplotype B5-Rsal(+)-Taql(-) for the Val 526 mutant gene in both kindreds studied here, as well as in two kindreds previously described (J Clin Invest 1994; 93:731). The fibrinogen alpha-chain gene mutation (Val 526) is the genetic defect responsible for hereditary renal amyloidosis in these two kindreds, and the mutant genes in the Val 526 kindreds may have been derived from a single founder.      

SELECTIVE IgA DEFICIENCY PRESENTING WITH HYPERSPLENISM

SUMMARY A young patient presenting with splenomegaly and hypersplenism was inadvertently found to have selective IgA deficiency. There were no symptoms of immunodeficiency and the patient responded well to splenectomy, with return of blood counts to normal without adverse effects. No other cause for the hypersplenism was found. We postulate selective IgA deficiency as a cause of splenomegaly and hypersplenism.