Effect of white cells on platelets during storage

White cells (WBCs) present in stored platelet concentrates have adverse effects on platelet function and on posttransfusion recovery. Although these effects have been attributed to the fall in pH that results from active WBC metabolism, platelets stored in gas-permeable storage bags still exhibit abnormalities, despite maintenance of a stable pH of greater than 6.0. The changes in platelet proteins and function brought about by storage with a controlled number of WBCs were studied. Twelve platelet-pheresis specimens were centrifuged at 180 x g to achieve a WBC count of less than 2 x 10(5) per mL (which contained less than 10% granulocytes). These specimens were split into two aliquots and placed in platelet bags for storage at 22 degrees C with constant horizontal agitation. Neutrophils, obtained from the same donor by centrifugation of 50 mL of whole blood through a discontinuous ficoll gradient, were added to one of the two platelet storage bags to achieve a final neutrophil count of 1 x 10(6) per mL. Platelet aliquots were removed and studied on Days 3 and 5. In platelets stored without neutrophils, the average response to ristocetin, using the mean slope as an index of platelet responsiveness, was 10.3 (n = 9, SD = 11) on Day 3, whereas for the platelets stored with neutrophils, it was 1.25 (n = 12, SD = 0.9, p less than 0.01). Significant differences were also seen on Day 5 (slope = 4.5 for platelets stored without neutrophils, slope = 0.3 for platelets stored with neutrophils, p less than 0.01). Platelet aggregation with 8 microM ADP and 1.5 mg per mL of collagen did not differ significantly.(ABSTRACT TRUNCATED AT 250 WORDS)     

白介素与溃疡性结肠炎

近年来对白介素(interleukin,IL)和溃疡性结肠炎(ulcerative colitis,UC)的研究取得了很大进展,我们通过总结整理以前有关IL和UC的文献,概括出IL的产生和在UC发病及病理变化中的作用机制:IL-1直接介导了UC初期阶段炎症的发生:IL-8、IL-6直接促进炎性细胞过度分泌和/或抑制了炎性细胞的凋亡,IL-2分泌减少导致免疫系统内细胞间网络调节失衡, 使局部炎症介质和自由基释放,引起细胞毒作用,IL主要通过影响机体整体和/或局部免疫系统的功能介导UC的产生,并与UC的迁延难愈和反复发作有关．     

Weight Loss After Laparoscopic Adjustable Gastric Banding is not Caused by Altered Gastric Emptying

Background  In order to know the role of gastric emptying in the mechanism of weight loss and early satiety after a restrictive surgical procedure for treatment of morbid obesity, a consecutive series of patients were scintigraphically investigated before and after laparoscopic adjustable gastric banding. Methods  Sixteen patients undergoing laparoscopic adjustable gastric banding underwent preoperatively, and at 6 months postoperatively, a gastric emptying study (solid meal and single isotope). Esophageal retention time, lag phase, peak activity time, gastric emptying rate, fundus emptying rate, and weight loss were recorded. Upper GI symptom assessment was carried out by using a standardized questionnaire. Gastric emptying parameters were correlated with the upper GI symptoms. Results  Gastric band placement showed no significant influence on postoperative gastric emptying rate [median % (interquartile range): 42 (23.3–59) preoperatively vs 38 (31–71) postoperatively and fundus emptying rate: 59(37–91) preoperatively vs 70 (53–89) postoperatively]; however, an increase in early satiety was found. Neither gastric emptying rate nor fundus emptying rate showed a relation with early satiety or weight loss. Furthermore, no correlation was found between early satiety and lag phase, esophageal retention time, start of activity, and peak activity time in proximal stomach. Conclusion  Laparoscopic adjustable gastric banding seems not to affect gastric emptying. Neither a relation between postoperative gastric emptying rate and weight loss nor between early satiety and weight loss was found. Therefore, it is unlikely that gastric emptying plays a role in the mechanism of weight loss following laparoscopic adjustable gastric banding. The authors disclose that there was no commercial interest and declare that there was no financial or material support.     

Anaesthesiological considerations in small-incision and laparoscopic cholecystectomy in symptomatic cholecystolithiasis: implications for pulmonary function. A randomized clinical trial

BACKGROUND: Upper abdominal surgery, including laparoscopic cholecystectomy (LC), is associated with post-operative pulmonary dysfunction. LC has, by consensus, become the treatment of choice for symptomatic cholecystolithiasis. Small-incision cholecystectomy (SIC), a procedure that does not require a pneumoperitoneum, threatens to be lost to clinical practice, even though there is evidence of equality. We hypothesized that the SIC technique should be equal, and might even be superior, to LC when considering post-operative pulmonary function because of the short incision length. METHODS: A single-centre randomized clinical trial was performed including patients scheduled for elective cholecystectomy. Pulmonary flow-volume curves were measured pre-operatively, post-operatively and at follow-up. Blood gas analyses were measured pre-operatively, in the recovery phase and on post-operative day 1. Anaesthesia, analgesics and peri-operative care were standardized by protocol. Post-operatively, patients and caregivers were blind to the procedure. RESULTS: Two hundred and fifty-seven patients were analysed. There was one pulmonary complication (pneumonia) in the LC group. In both groups, similar reductions of approximately 20% in pulmonary function parameters occurred, with complete recovery to pre-operative values. Patients in the SIC group consumed more analgesia when compared with the LC group, without any impact on blood gas analysis. Patients converted to a conventional open technique showed significant differences in six of the eight parameters in pulmonary function tests. CONCLUSION: When evaluated with strict methodology and standardization of care, no clinically relevant differences were found between SIC and LC with regard to pulmonary function. Our results suggest that the popularity of the laparoscopic technique cannot be attributed to pulmonary preservation.     

Oral refeeding after onset of acute pancreatitis: a review of literature

BACKGROUND: Oral refeeding in patients recovering from acute pancreatitis may cause pain relapse. Patients with pain relapse may be ill for prolonged periods, thereby consuming additional health care resources. We aimed to determine the incidence and risk factors of pain relapse on the basis of reviewing all studies on oral refeeding in acute pancreatitis. METHODS: Relevant literature cited in three electronic databases (Cochrane Central Register of Controlled Trials, EMBASE, and MEDLINE) as well as the abstracts of major gastroenterological meetings was reviewed. Outcome measures studied were the incidence of pain relapse and length of hospital stay. RESULTS: A total of three studies met the inclusion criteria. Sixty of 274 patients (21.9%) experienced pain relapse during the course of acute pancreatitis. In 47 of 60 (78.3%) patients pain relapse occurred within 48 h after commencement of oral refeeding. Two studies showed a significantly higher Balthazar's CT score on hospital admission in patients with pain relapse, whereas all three studies found no difference in the severity scores between patients with and without pain relapse. All three studies found a significant increase in the length of hospital stay in patients with pain relapse. CONCLUSIONS: The incidence of pain relapse after oral refeeding in acute pancreatitis is relatively high. Thereby, the quest for new therapeutical modalities that can prevent pain relapse is of current importance.     

Sexual and urinary functioning after rectal surgery: a prospective comparative study with a median follow-up of 8.5?years

Purpose  

The purpose of this study was to prospectively compare rectal resection (RR) with colonic resection on sexual, urinary and bowel function and quality of life in both short-term and long-term.     

Effect of amphotericin B and fluconazole on platelet membrane glycoproteins

BACKGROUND : Fever, chills, and reduced platelet recovery may result when platelets are transfused simultaneously with amphotericin B. Amphotericin B reportedly increases the pitting of membranes in stored platelets. STUDY DESIGN AND METHODS : The effects of amphotericin B and another antifungal agent, fluconazole, on platelet membrane glycoproteins (GP) were examined by the incubation of split aliquots of fresh and stored platelet concentrates (PCs) with these drugs for 3 days in storage bags. To determine the effect of storage, PCs were stored for 5 days, and aliquots removed on Days 1 through 5 were placed in platelet storage bags with 4 micrograms per mL of amphotericin B for 2 to 6 hours. Membrane glycoprotein expression was assessed by flow cytometry with fluorescein isothiocyanate-labeled monoclonal antibodies (MoAbs) directed against the following antigens: GPIb (CD42b), CD63 (an activation protein), P-selectin (CD62), and GPIIb/IIIa (CD41a). RESULTS : Amphotericin B produced a concentration-dependent decrease in the surface binding of CD42b MoAb with no consistent changes in the binding of CD41a, CD63, or CD62 MoAbs after a 3-day exposure. Stored but not fresh PCs showed decreased binding of MoAb CD42b after a 6-hour exposure to amphotericin B (4 micrograms/mL). Fluconazole produced no changes. When the binding of MoAb CD42b to permeabilized platelets was used to measure total platelet content, amphotericin B (4 micrograms/mL) decreased MoAb CD42b binding to a similar degree in fresh and stored platelets. Inhibition of aggregation to ADP and collagen and ADP and epinephrine was seen in stored but not fresh PCs. CONCLUSION : Therapeutic levels of amphotericin B resulted in partial loss of total platelet GPIb in fresh and stored PCs, but decreased surface expression of platelet membrane GPIb only in stored platelets. This difference between fresh and stored platelets may be related to the limited reservoir of GPIb available for redistribution to the membrane in the previously stored PCs and may account for the decreased recovery of transfused platelets observed in some patients receiving amphotericin B.     

Nutrition in acute pancreatitis: a critical review

Severe acute pancreatitis poses unique nutritional challenges. The optimal nutritional support in patients with severe acute pancreatitis has been a subject of debate for decades. This review provides a critical review of the available literature.

According to current literature, enteral nutrition is superior to parenteral nutrition, although several limitations should be taken into account. The optimal route of enteral nutrition remains unclear, but normal or nasogastric tube feeding seems safe when tolerated. In patients with predicted severe acute pancreatitis an on-demand feeding strategy is advised and when patients do not tolerate an oral diet after 72 hours, enteral nutrition can be started. The use of supplements, both parenteral as enteral, are not recommended. Optimal nutritional support in severe cases often requires a tailor-made approach with day-to-day evaluation of its effectiveness.