***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: The purpose of this investigation was to study risk factors for  Clostridium difficile infection ( CDI ) in an endemic setting . In a 34-month prospect i ve case – control study , we compared the risk factors and clinical characteristics of all consecutively diagnosed hospitalised CDI patients ( n = 93 ) with those of patients without diarrhoea ( n = 76 ) and patients with non-CDI diarrhoea ( n = 64 ) . The incidence of CDI was 17.5 per 10,000 hospital admissions .  C. difficile polymerase chain reaction ( PCR ) ribotype 014 was the most frequently found type ( 15.9 % ) , followed by types 078 ( 12.7 % ) and 015 ( 7.9 % ) . Independent risk factors for endemic CDI were the use of second-generation cephalosporins , previous hospital admission and previous stay at the intensive care unit ( ICU ) . The use of third-generation cephalosporins was a risk factor for diarrhoea in general . We found no association of CDI with the use of fluoroquinolones or proton pump inhibitors ( PPIs ) . The overall 30-day mortality among CDI patients , patients without diarrhoea and patients with non-CDI diarrhoea was 7.5 % , 0 % and 1.6 % , respectively . In this endemic setting , risk factors for CDI differed from those in outbreak situations . Some risk factors that have been ascribed to CDI earlier were , in this study , not specific for CDI , but for diarrhoea in general . The 30-day mortality among CDI patients was relatively high There is a lack of information about the effectof omeprazole or other antisecretory drugs onintraduodenal pH. Aim of the study was to document thevariation over time of intraduodenal pH during a 24-hr period and to simultaneously study the effectof omeprazole 40 mg once daily on intragastric and intraduodenal pH in healthy H. pylori-negative subjects . In a r and omized , placebo-controlled study , eight subjects ( five women , three men , mean age 22.7years ) received oral 40 mg omeprazole or placebo oncedaily for eight days . On day 7 , intragastric and intraduodenal pH was measured continuously for 24 hr , using two miniature glass-membrane electrodesplaced in the stomach ( fundus ) and in the distal thirdof the duodenum . The 24-hr median intraduodenal pH was5.95 with placebo and 5.85 with omeprazole .  Median intragastric pH was 1.68 without and 4.93 withomeprazole . During omeprazole therapy , intragastric pHfell below 4.0 in five of eight subjects . In the 2- and 3-hr postpr and ial periods , the percentage of time with pH < 5 was significantly reducedwith omeprazole . In healthy subjects , 24-hr median and postpr and ial pH in the distal part of the duodenum waslower than previously thought . Omeprazole significantly reduced the percentage of time with pH < 5postpr and ially . At night , intragastric pH fell below 4.0with omeprazole 40 mg once daily . Omeprazole does notchange 24-hr median intraduodenal pHsignificantly BACKGROUND Previous studies have examined the association between proton pump inhibitor ( PPI ) use and the risk of Clostridium difficile-associated disease ( CDAD ) , with conflicting results . Whether outpatient PPI use influences the risk of hospital admission for CDAD  among older patients who have recently been treated with antibiotics is unknown . METHODS We conducted a population -based , nested case-control study of linked health care data bases in Ontario , Canada , from 1 April 2002 through 31 March 2005 . We identified patients aged > or = 66 years who were hospitalized for CDAD within 60 days of receiving outpatient antibiotic therapy .  Each case patient with CDAD was matched with 10 control subjects on the basis of age , sex , and details of antibiotic use ( antibiotic class , timing , and number of antibiotics used ) . PPI use by case patients and control subjects was categorized as current ( within 90 days ) , recent ( 91 - 180 days ) , or remote ( 181 - 365 days ) . We used conditional logistic regression to estimate the odds ratio for the association between outpatient  PPI  use and risk of hospitalization for CDAD . RESULTS We identified 1389 case patients and 12,303 matched control subjects . Case patients were no more likely than control subjects to have received a PPI  in the preceding 90 days ( adjusted odds ratio , 0.9 ; 95 % confidence interval , 0.8 - 1.1 ) . Similarly , we found no association between hospitalization for CDAD and more remote use of PPIs . CONCLUSIONS Among community-dwelling older patients , PPI use is not a risk factor for hospitalization with CDAD Background —The effect of histamine H2receptor antagonists on gastric emptying is controversial . Aims —To determine the effects of ranitidine , famotidine , and omeprazole on gastric motility and emptying . Patients and methods —Fifteen normal subjects underwent simultaneous antroduodenal manometry , electrogastrography ( EGG ) , and gastric emptying with dynamic antral scintigraphy ( DAS ) . After 30 minutes of fasting manometry and EGG recording , subjects received either intravenous saline , ranitidine , or famotidine , followed by another 30 minutes recording and then three hours of postpr and ial recording after ingestion of a radiolabelled meal . Images were obtained every 10–15 minutes for three hours to measure gastric emptying and assess antral contractility . Similar testing was performed after omeprazole 20 mg daily for one week . Results —Fasting antral phase III migrating motor complexes ( MMCs ) were more common after ranitidine ( 9/15 subjects , 60 % ) , famotidine ( 12/15 , 80 % ) , and omeprazole ( 8/12 , 67 % ) compared with placebo ( 4/14 , 29 % ; p<0.05 ) . Postpr and ially , ranitidine , famotidine , and omeprazole  slowed gastric emptying , increased the amplitude of DAS contractions , increased the EGG power , and increased the antral manometric motility index . Conclusions —Suppression of gastric acid secretion with therapeutic doses of gastric acid suppressants is associated with delayed gastric emptying but increased antral motility The acid environment of the stomach serves as an important defense against intestinal colonization by potentially pathogenic bacteria . The purpose of this study was to examine the effect of increased gastric pH on bacterial translocation in a neonatal rabbit model . Fifty-nine rabbit pups were delivered by cesarean section and r and omly divided into normal acid ( NA ) and reduced acid ( RA ) groups . All were gavage fed and challenged with Enterobacter cloacae , 1 x 10(6 ) CFU/mL. The RA group received ranitidine , 20 mg/kg/d with all feeds . Gastric pH was measured by pH probe before and 4 hours after bacterial challenge . Mesenteric lymph node ( MLN ) , spleen , liver , midjejunum , and cecum were harvested for culture at 72 hours . Gastric pH in the RA group was significantly increased before and 4 hours after the bacterial challenge . The incidence of bacterial translocation to the MLN , spleen , and liver was significantly higher in the RA group . Log cecal and jejunal colony counts were significantly increased in the RA animals . The authors conclude that the gastric acidity is protective against intestinal colonization and translocation of potentially pathogenic bacteria in this neonatal rabbit model The extent of duodenal bacterial overgrowth during the pronounced inhibition of acid secretion that occurs with omeprazole treatment is unknown . The bacterial content of duodenal juice of patients treated with omeprazole  was therefore examined in a controlled prospect i ve study . Duodenal juice was obtained under sterile conditions during diagnostic upper endoscopy . Aspirates were plated quantitatively for anaerobic and aerobic organisms . Twenty five out patients with peptic ulcer disease were investigated after a 5.7 ( 0.5 ) weeks ( mean ( SEM ) ) treatment course with 20 mg ( nine patients ) or 40 mg ( 16 patients ) . The control group consisted of 15 out patients referred for diagnostic endoscopy without prior antisecretory treatment .  No patient in the control group had duodenal bacterial overgrowth . In the omeprazole group bacterial overgrowth ( > or = 10(5 ) cfu/ml ) was found in 14 ( 56 % ) patients ( p = 0.0003 ) . The number of bacteria ( log10 ) in duodenal juice in patients treated with omeprazole was distinctly higher ( median 5.7 ; range < 2 - 8.7 ) when compared with the control group ( median < 2 ; range < 2 - 5.0 ; p = 0.0004 ) . As well as orally derived bacteria , faecal type bacteria were found in seven of 14 and anaerobic bacteria in three of 14 patients . Bacterial overgrowth was similar with the two doses of omeprazole . These results indicate that duodenal bacterial overgrowth of both oral and faecal type bacteria occurs often in ambulatory patients treated with omeprazole . Further studies are needed to determine the clinical significance of these findings , particularly in high risk groups during long term treatment with omeprazole BACKGROUND The incidence and severity of Clostridium difficile infections are increasing . Acid-suppressive therapy has been suggested as a risk factor for C difficile , but this remains controversial . METHODS We conducted a pharmacoepidemiologic cohort study , performing a secondary analysis of data collected prospect ively on 101 796 discharges from a tertiary care medical center during a 5-year period . The primary exposure of interest was acid suppression therapy , classified by the most intense acid suppression therapy received ( no acid suppression , histamine(2)-receptor antagonist [ H(2)RA ] therapy , daily proton pump inhibitor [ PPI ] , and PPI more frequently than daily ) . RESULTS As the level of acid suppression increased , the risk of nosocomial C difficile infection increased , from 0.3 % ( 95 % confidence interval [ CI ] , 0.21%-0.31 % ) in patients not receiving acid suppressive therapy to 0.6 % ( 95 % CI , 0.49%-0.79 % ) in those receiving H(2)RA therapy , to 0.9 % ( 95 % CI , 0.80%-0.98 % ) in those receiving daily PPI treatment , and to 1.4 % ( 1.15%-1.71 % ) in those receiving more frequent PPI therapy . After adjustment for comorbid conditions , age , antibiotics , and propensity score-based likelihood of receipt of acid-suppression therapy , the association persisted , increasing from an odds ratio of 1 ( no acid suppression [ reference ] ) to 1.53 ( 95 % CI , 1.12 - 2.10 ) ( H(2)RA ) , to 1.74 ( 95 % CI , 1.39 - 2.18 ) ( daily PPI ) , and to 2.36 ( 95 % CI , 1.79 - 3.11 ) ( more frequent PPI ) . Similar estimates were found with a matched cohort analysis and with nested case-control techniques . CONCLUSIONS Increasing levels of pharmacologic acid suppression are associated with increased risks of nosocomial C difficile infection . This evidence of a dose-response effect provides further support for the potentially causal nature of iatrogenic acid suppression in the development of nosocomial C difficile infection In the period April-September 2005 , an outbreak of  Clostridium difficile infection ( CDI ) due to PCR ribotype 027 occurred among 50 patients in a 341-bed community hospital in Harderwijk , The Netherl and s. A retrospective case-control study was performed to identify risk factors specific for CDI , using a group of patients with CDI ( n = 45 ) , a group of r and omly selected control patients without diarrhoea ( n = 90 ) , and a group of patients with non-infectious diarrhoea ( n = 109 ) . Risk factors for CDI and for non-CDI diarrhoea were identified using multiple logistic regression analysis . Independent risk factors for CDI were : age above 65 years ( OR 2.6 ; 95 % CI 1.0 - 5.7 ) , duration of hospitalization ( OR 1.04 per additional day ; 95 % CI 1.0 - 1.1 ) , and antibiotic use ( OR 12.5 ; 95 % CI 3.2 - 48.1 ) . Of the antibiotics used , cephalosporins and fluoroquinolones were identified as the major risk factors for development of CDI . The risk of developing CDI was particularly high in people receiving a combination of a cephalosporin and a fluoroquinolone ( OR 57.5 ; 95 % CI 6.8 - 483.6 ) . The main factors affecting the risk of 
    Output:
    
RESULTS The use of PPIs increases gastric pH , encourages growth of the gut microflora , increases bacterial translocation and alters various immunomodulatory and anti-inflammatory effects .
Severe hypochlorhydria generated by PPI use leads to bacterial colonisation and increased susceptibility to enteric bacterial infection .