Association between palmoplantar pustulosis and cigarette smoking in Brazil: a case–control study

Background  Palmoplantar pustulosis (PPP) discloses some differences compared to vulgar psoriasis (PV) in terms of age of onset, female predominance and low occurrence of psoriasis lesions elsewhere. Cigarette smoking has been associated to PPP in international studies; nevertheless, these studies were never performed among Brazilian.
Objectives  To compare prevalence of smoking among PPP, PV and other dermatologic patients (NPD).
Methods  Case–control study involving 25 PPP patients from a reference psoriasis centre. Two control groups were matched according to gender and age: 50 patients with PV and 50 NPD. Confounders were adjusted by conditional multiple logistic regression.
Results  Among cases, 84.0% were female and PPP age of disease onset (41.4 years) was greater than PV (34.5 years). Prevalence of ever smoking was higher among cases (92.0%) than PV (52.0%) and NPD (30.0%). Adjusted odds ratio of PPP ever smoking compared to PV and NPD was 9.5 and 36.2, respectively. All smokers reported the onset of their habit before the development of PPP.
Conclusions  There was significant association between PPP and smoking. However, the impact of giving it up in the clinical course of the disease remains to be established.     

Intradiscal electrothermal treatment for chronic discogenic low back pain: a prospective outcome study with minimum 1-year follow-up. (SOAR, Physiatry Medical Group, Menlo Park, CA) Spine 2000;25:2622–2627.

This prospective case series study was to determine the outcome of patients with chronic low back pain whose symptoms did not improve with aggressive nonoperative care and who chose intradiscal electrothermal anuloplasty (IDET) as an alternative to chronic pain management or interbody fusion surgery. Sixty‐two patients who had chronic low back pain unresponsive to nonoperative care, no evidence of compressive radiculopathy, and concordant pain reproduction at one or more disc levels on provocative discography were enrolled in the study. Visual analog scale (VAS) pain scores Short Form (SF)‐36 Health Status Questionnaire Physical Function subscale, and SF‐36 Bodily Pain subscale scores were assessed at baseline and at least 1 year later. Mean follow‐up was 16 months, and mean preoperative duration of symptoms was 60 months. Baseline and follow‐up outcome measures demonstrated a mean change in VAS score of 3.0, mean change in SF‐36 physical function of 20, and mean change in SF bodily function of 17. Symptoms improved in 44 (71%) of 62 of the study group on the SF‐36 physical function subscale, in 46 (74%) of 62 on the SF‐36 Bodily Pain subscale, and in 44 (71%) of 62 on the VAS scores. Twelve (19%) of 62 did not show improvement on any scale. Conclude a cohort of patients with chronic unremitting low back pain of discogenic origin whose symptoms had failed to improve with aggressive nonoperative care demonstrated a statistically significant and clinically meaningful improvement on the SF‐36 and the VAS scores at a minimum follow‐up of 1 year after IDET. The positive results should be validated with placebo‐controlled randomized trials and studies that compare IDET with alternative treatments. Comment by Gabor B. Racz, M.D. This is a report on 62 patients from a single practice where the diagnosis of discogenic pain was made. Prior to and at the end of 12‐months, visual analog pain scores and short form (SF‐36 Health Status Questionnaire Physical Function subscale and SF‐36 Bodily Pain subscale scores were assessed. The results indicate a VAS score reduction of 3.0 and a change in SF‐36 physical function of 20 and mean change in SF‐36 bodily pain of 17. Nineteen percent of the 62 patients did not show improvement on any scale. There are significant problems with this study in that there are no controls and no randomization, no reasonable alternatives to heat lesioning the disc was offered as the patient was given the only alternative of interbody fusion surgery. The materials and methods describe the practice as 1,116 patients with chronic low back pain referred to the authors. This must be an unbelievably unique practice as anybody that works with chronic patients would find it almost impossible to have patients with chronic low back pain with no leg pain. It is the rule rather than the exception that patients come to us with back and leg pain. Discogenic pain can give rise to back spasm. The pathways for discogenic stimulation leading to paraspinal spasm have been beautifully outlined by Indahl. Injury to the disc can lead to leaking of disc material causing epidural scar formation involving the sinovertebral system nerves and nerve root or nerve roots. Simultaneously, there may be facet involvement and back spasm originating from the same process. The pathway for discogenic back spasm as suggested by Indahl is likely from the lateral branch of the posterior primary ramus and can also be interrupted by diagnostic nerve block followed by radiofrequency thermocoagulation. The patients in this study supposedly have failed all therapeutic modalities, yet, there is absolutely no mention of caudal lysis of adhesions or transforaminal lysis of adhesions and/or diagnostic and radiofrequency thermocoagulation of the pathways for discogenic back spasm. In our clinical experience, it is extremely rare where patients described in this series would have exclusive solitary disc problem necessitating electro‐thermo‐lesioning of the disc. We certainly find that a great deal of the problem is located in the spinal canal rather than exclusively in the disc or facets. Freeing up the ventral and lateral epidural space by the lysis of adhesions technique, followed by addressing the sino vertebral nerve and facet joint innervation can lead to excellent pain relief for 5 years or longer when the problem is looked at in a nonrandomized, noncontrolled study environment. Furthermore, the pain relief is prompt and does not necessitate the rather elaborate precautions outlined in this paper that clearly are different than the conservative therapy offered to these patients prior to disc lesioning. In the very rare instance, where clearly there is no spinal canal pathology and there is no facet and discogenic back spasm, we do believe an appropriately carried out discogram with monitoring of facial expressions and pressure recordings had resulted in clear rapid response pain relief. I just find a great deal of difficulty in understanding the physiological process of burning the structures within the disc that can take months to lead to pain relief. The rational expectation is that if you thermocoagulate a nerve that is involved in propagating pain, that you should have prompt and lasting pain relief until those nerves or pain pathways regenerate. Clearly, one needs to clarify the issues involved in exposing patients to discitis and osteomyelitis by interventional lesioning with no clear‐cut evidence of reasonable results. The studies need to be carried out with appropriate controls and randomization. Our clinical experience with intradiscal electrothermal treatment comes from two sources. One source is patients who have had the treatment elsewhere and failed to respond and the second source is where we have ruled out any other explanation for the patient's back pain and the patient responds to diagnostic and therapeutic disc procedures, but more commonly without a favorable outcome. These patients then are offered the option of various neuromodulation pain relieving procedures rather than interbody fusion surgery. Richard North has rather convincingly shown documented evidence that spinal cord stimulation gives better outcome than back surgery.     

Zinc transfer among proteins in rat duodenum mucosa

Duodenums from freshly killed stock colony rats were incubated in Krebs buffer containing carrier-free 65ZnCl2 for periods of time between 5 and 60 s. Mucosa cytosol was separated and fractionated by gel filtration on Sephadex G-75. 65Zn was present in two main bands of protein with molecular weights of about 45,000 and 6,500, but the ratio between them rose progressively with time of exposure to the isotope. Addition of metabolic inhibitors greatly lowered the 45,000/6,500 ratio for 65Zn. It is concluded that when zinc enters the mucosal cytoplasm during absorption, it rapidly binds to the 6,500 protein in a passive way and is then transferred to the protein of molecular weight 45,000 by an active process.     

Controlled trial of chemical disinfection of urinary drainage bags. Reduction in hospital-acquired catheter-associated infection

A controlled, prospective trial was conducted on an orthopaedic ward to test the use of peroxide disinfection of drainage bags as the only measure taken to affect the rate of hospital-acquired, catheter-associated urinary tract infection (UTI). A significant reduction (P less than 0.05) in the number of patients with catheter-associated UTI occurred with the use of bag disinfectant when compared with patients in whom this technique was not used. We consider this technique to be suitable for the management of catheterised patients on general hospital wards to reduce catheter-associated UTI and environmental spread of their bacteria.     

Failure of Dietary Protein and Phosphate Restriction to Retard the Rate of Progression of Chronic Renal Failure: A Prospective, Randomized, Controlled Trial

SUMMARY Ninety-five patients (63 male, 32 female), age 45±2 years(mean±SEM) with chronic renal failure of varied aetiologywere randomized to receive either a conventional low proteindiet (0.6 g/kg/day protein, 800 mg phosphate; n=33), a low phosphatediet (providing approximately 1000 mg phosphate plus an orallyadministered phosphate binder, minimum protein intake 0.8 g/kg/day;n=30) or to control (minimum protein intake 0.8 g/kg/day, nophosphate restriction; n=32). Patients were reviewed for a minimumof 6 months before randomization and were withdrawn from thestudy if plasma creatinine exceeded 900 µmol/1, plasmaphosphate was > 2.0 mmol/1 or at the onset of uraemic symptoms. Following randomization patients were studied for an averageof 19±3 months. Mean plasma creatinine rose from 398±33to 600±50 µmol/1. Dietary protein intake was estimatedat 0.69±0.02 g/kg/day in the low protein group, 1.02±0.05in the low phosphate and 1.14±0.05 in the controls, phosphateintake was 815±43, 1000± 47, and 1315±57mg/day, respectively. Urinary urea excretion and protein catabolicrates were significantly reduced (p<0.01) only in those onprotein restriction, at 213±9 mmol/24 hours and 0.71g/kg/day, respectively. Phosphate excretion was significantlylower (p<0.05) in both the low protein group (17.9±0.8mmol/24 hours) and the low phosphate group (18.6±1.0mmol/24 hours) compared to controls. Changes in body weight,muscle mass and serum transferrin, albumin and immunoglobulinswere comparable between the groups. Mean blood pressure followingrandomization was 150/89±3/1 (low protein), 148/87±3/1(low phosphate) and 146/87±3/1 (controls). Progression of renal failure was analysed by rate of fall ofcreatinine clearance (ml/min/ 1.73 m²/month), by rate of deteriorationderived from reciprocal plasma creatinine against time plots(1/mmol/year) and to assess individual patient's response totreatment by two phase linear regression (‘breakpoint’)analysis of reciprocal plasma creatinine/time plots. Progressionwas analysed only in patients seen for at least 3 months followingrandomization. The rate of fall of creatinine clearance was not significantlydifferent between the groups (ANOVA): 0.56±0.08 ml/min/1.73m2/month (low protein, n=28), 0.44±0.07 (low phosphate,n=23) and 0.69±0.11 (control, n=27). In 50 patients (18low protein, 16 low phosphate and 16 control) whose rate ofprogression could be calculated before and after randomization,there was a fall in rate of progression averaging 0.18 ml/min/1.73m2/month in those on low protein diet and those on low phosphatediet, but a rise of 0.08 in the controls. These differenceswere, however, not statistically significant. Similar resultswere obtained when the rates of deterioration were calculatedfrom plasma creatinine. Significant individual improvements(p<0.01) in rates of progression by ‘breakpoint’analysis occurred in 17 patients: six on low protein, sevenon low phosphate and in four controls. Sixty-one (72 per cent)of the patients examined by this method showed no significantchange in the rate of progression while seven patients had acceleratedprogression. There was no difference in the requirement formaintenance dialysis facilities between groups. No significant benefit of protein and phosphate restrictionwas therefore demonstrated.     

神经生长因子对局灶性脑缺血神经干细胞巢蛋白表达及细胞类型的影响

目的:实验于2006-02/07在锦州医学院科学实验中心完成。将72只健康SD大鼠按随机数字表法分为假手术组、模型组、神经生长因子治疗组,每组24只。采用Logna等改良法复制大脑中动脉血栓模型,动物清醒2h后进行功能评价,动物神经功能达到2级的纳入实验。假手术组除不进行大脑中动脉线栓外,其余同模型组。神经生长因子治疗组于缺血后立即腹腔注射神经生长因子1000μg/kg,1次/d。于缺血后1,3,7,14d处死动物,运用免疫组化和免疫荧光双标的方法观察神经生长因子对脑缺血后神经干细胞巢蛋白的表达及其细胞类型的影响。结果:72只大鼠均进入结果分析。①神经生长因子治疗组和模型组大脑皮质均可见巢蛋白阳性细胞,细胞呈圆形或椭圆形。与模型组相比,除缺血后1d外,神经生长因子治疗组其他时间点的巢蛋白阳性细胞数均明显高于模型组,两组缺血后各时间点的巢蛋白阳性细胞数均高于假手术组[模型组:(3.47±0.51),(5.13±1.14),(13.95±3.56),(8.97±2.08)个;神经生长因子治疗组:(3.81±0.66),(9.88±2.08),(19.87±3.86),(26.17±2.90)个,假手术组:0,P<0.05,P<0.01]。②模型组和神经生长因子治疗组3d时缺血皮质巢蛋白阳性突起主要与胶质纤维酸性蛋白共存,14d时巢蛋白与神经元特异性烯醇化酶共存明显增多。结论:神经生长因子能增加局灶性脑缺血后巢蛋白的阳性细胞的数目,并促进其分化为神经元和神经胶质细胞。     

Kidney transplants in mice. An analysis of the immune status of mice bearing long-term, H-2 incompatible transplants

Kidney transplants between strains of mice which are incompatible at either the K or the D end of the H-2 complex usually function for prolonged periods supporting the lives of nephrectomized recipients. This occurs with no recipient treatment. With multiple H-2 and non-H-2 determined incompatibilities, transplants may be rejected but more slowly than skin grafts. In the strain combination studied most extensively in these experiments (B10.D2 to B6AF(1)) in which the incompatibility was confined to the K end of the H-2 region, about 70 percent of recipients survived for many weeks with normal blood urea nitrogen levels. Skin grafts between untreated members of these strains were rejected promptly (mean survival time of 13.5 +/- 1.1 days) as were kidney transplants to recipients of prior skin grafts. Donor strain skin grafts to recipients of kidney transplants after kidney transplantation enjoyed greatly prolonged survival whereas skin grafts from a third party (A.SW) were rejected normally. If kidney tissue was transferred in the form of free grafts without primary vascular union, it was rejected promptly leaving its recipient highly immunized. Cellular and humoral immunity to donor antigens declined over the first few weeks after transplantation, and the spleens of long-term recipients contained no “killer cells.” Recipient lymphoid cells could mount active graft versus host reactions to donor strain antigens on transfer to neonatal mice. Nevertheless, they were distinctly less able to respond specifically by the production of killer cells to donor strain antigens after sensitization in vitro. No evidence that this defect was associated with the presence of suppressor cells was forthcoming from several types of in vivo and in vitro tests.     

Defining sepsis on the wards: results of a multi‐centre point‐prevalence study comparing two sepsis definitions

Our aim was to prospectively determine the predictive capabilities of SEPSIS‐1 and SEPSIS‐3 definitions in the emergency departments and general wards. Patients with National Early Warning Score (NEWS) of 3 or above and suspected or proven infection were enrolled over a 24‐h period in 13 Welsh hospitals. The primary outcome measure was mortality within 30 days. Out of the 5422 patients screened, 431 fulfilled inclusion criteria and 380 (88%) were recruited. Using the SEPSIS‐1 definition, 212 patients had sepsis. When using the SEPSIS‐3 definitions with Sequential Organ Failure Assessment (SOFA) score ≥ 2, there were 272 septic patients, whereas with quickSOFA score ≥ 2, 50 patients were identified. For the prediction of primary outcome, SEPSIS‐1 criteria had a sensitivity (95%CI) of 65% (54–75%) and specificity of 47% (41–53%); SEPSIS‐3 criteria had a sensitivity of 86% (76–92%) and specificity of 32% (27–38%). SEPSIS‐3 and SEPSIS‐1 definitions were associated with a hazard ratio (95%CI) 2.7 (1.5–5.6) and 1.6 (1.3–2.5), respectively. Scoring system discrimination evaluated by receiver operating characteristic curves was highest for Sequential Organ Failure Assessment score (0.69 (95%CI 0.63–0.76)), followed by NEWS (0.58 (0.51–0.66)) (p < 0.001). Systemic inflammatory response syndrome criteria (0.55 (0.49–0.61)) and quickSOFA score (0.56 (0.49–0.64)) could not predict outcome. The SEPSIS‐3 definition identified patients with the highest risk. Sequential Organ Failure Assessment score and NEWS were better predictors of poor outcome. The Sequential Organ Failure Assessment score appeared to be the best tool for identifying patients with high risk of death and sepsis‐induced organ dysfunction.