Potential Risk Factors For Development Research Articles

Does passive smoking induce sensorineural hearing loss in children?

ObjectivesSmoking plays major role in development of vascular and respiratory serious diseases. It has been reported that negative smoker children are prone for conductive hearing impairment due to repeated attacks of Eustachian tube dysfunction and middle ear effusion. This study aims to identify negative smoking as potential risk factor for development of sensorineural hearing loss. StudyThis study was done between January 2010 and November 2012. 411 children aged 5-11 years (8.2±1.5) participated in this study; they were children attending the Ear, Nose, and Throat clinic of a tertiary care hospital and their siblings. The inclusion criteria were: (i) normal speech and language, (ii) absence of any disease or condition that may cause sensorineural hearing loss, and (iii) normal middle ear function on the day of hearing assessment. They were divided into three groups according to the exposure to second-hand smoke at home; group of “no exposure” whereas no smoker in the family (131 children), group of ‘mild exposure” whereas the father was the only smoking parent and smoking was prohibited at home (155 children), and group of “heavy exposure”, whereas the mother was smoking, or the father was freely smoking at home and in the presence of his children (125 children). Audiological evaluation in the form of pure tone and speech audiometry and immitancemetry was done for the study group. ResultsAudiological evaluation revealed that the prevalence of hearing loss was 3.8%, 4.5% and 12% in the “no exposure”, “mild exposure”, and “heavy exposure” groups, respectively. Significant difference was only detected between the high exposure group and the other two groups. All children had minimal sensorineural hearing loss, i.e. threshold of frequencies showing hearing loss was 20 or 25dB HL. The risk ratios (95% confidence interval) for hearing loss in the study subgroups were 1.18 (0.38, 3.64) for mild exposure group (p>0.05), 3.14 (1.18, 8.3) for heavy exposure group (p<0.05). ConclusionsPassive smoking in childhood correlates with sensorineural hearing loss, and it is an important risk factor for development of minimal hearing loss. Strict prevention of children exposure to second-hand smoke should be encouraged by every mean.

Dental status, dental rehabilitation procedures, demographic and oncological data as potential risk factors for infected osteoradionecrosis of the lower jaw after radiotherapy for oral neoplasms: a retrospective evaluation

PurposeRetrospective evaluation of the dental status of patients with oral cancer before radiotherapy, the extent of dental rehabilitation procedures, demographic and radiotherapy data as potential risk factors for development of infected osteoradionecrosis of the lower jaw.MethodsA total of 90 patients who had undergone radiotherapy for oral cancer were included into this retrospective evaluation. None of them had distant metastases. After tumour surgery the patients were referred to an oral and maxillofacial surgeon for dental examination and the necessary dental rehabilitation procedures inclusive potential tooth extraction combined with primary soft tissue closure. Adjuvant radiotherapy was started after complete healing of the gingiva (> 7 days after potential extraction). The majority of patients (n = 74) was treated with conventionally fractionated radiotherapy with total doses ranging from 50-70Gy whereas further 16 patients received hyperfractionated radiotherapy up to 72Gy. The records of the clinical data were reviewed. Furthermore, questionnaires were mailed to the patients’ general practitioners and dentists in order to get more data concerning tumour status and osteoradionecrosis during follow-up.ResultsThe patients’ dental status before radiotherapy was generally poor. On average 10 teeth were present, six of them were regarded to remain conservable. Extensive dental rehabilitation procedures included a mean of 3.7 tooth extractions. Chronic periodontitis with severe attachment loss was found in 40%, dental biofilm in 56%. An infected osteoradionecrosis (IORN) grade II according to (Schwartz et al., Am J Clin Oncol 25:168-171, 2002) was diagnosed in 11 of the 90 patients (12%), mostly within the first 4 years after radiotherapy. We could not find significant prognostic factors for the occurrence of IORN, but a trendwise correlation with impaired dental status, rehabilitation procedures, fraction size and tumour outcome.ConclusionThe occurrence of IORN is an important long-term side effect of radiotherapy for oral cancers. From this data we only can conclude that a poor dental status, conventional fractionation and local tumour progression may enhance the risk of IORN which is in concordance with the literature.

RISK FACTORS, ANATOMICAL, AND VISUAL OUTCOMES OF INJURED EYES WITH PROLIFERATIVE VITREORETINOPATHY

To investigate potential risk factors for development of proliferative vitreoretinopathy (PVR) post trauma and evaluate the effect of PVR on anatomical and visual outcomes in injured eyes. Overall, 179 eyes with PVR and 221 eyes without PVR after injury were selected from the database of the Eye Injury Vitrectomy Study, a multicenter cohort study launched in 1997. Multivariate logistic regression was used to ascertain the independent risk factors for development of PVR and to evaluate the influence of PVR on anatomical and visual outcomes. An interval of injury and vitrectomy of more than 28 days (odds ratio, 139.25; confidence interval, 50.09-387.10), severe vitreous hemorrhage (odds ratio, 2.72; confidence interval, 1.13-6.52), and total retinal detachment (odds ratio, 12.67; confidence interval, 3.96-40.52) were important independent risk factors for PVR. One hundred and fifteen eyes (52.0%) and 49 eyes (27.4%) without and with PVR, respectively, were anatomically restored with ambulant visual acuity (≥4/200). Proliferative vitreoretinopathy, poor initial visual acuity, relative afferent pupillary defect, total retinal detachment, and retinal tear or retinal defect were unfavorable prognostic indicators. Proliferative vitreoretinopathy occurs frequently in injured eyes and is associated with poor outcomes. Its onset depends on interval of injury and vitrectomy, wound location, vitreous hemorrhage, and retinal detachment. Early vitrectomy (before 2 weeks) and aggressive therapy should be considered for specific high-risk cases.

Postoperative Prevertebral Soft Tissue Swelling Does Not Affect the Development of Chronic Dysphagia Following Anterior Cervical Spine Surgery

Prospective cohort study. To characterize the relation between postoperative soft tissue swelling and the development of chronic dysphagia after anterior cervical spine surgery. Chronic dysphagia was defined as dysphagia that persists more than 1 year. Dysphagia is commonly reported in the early postoperative period after anterior cervical spine surgery. Although prevertebral soft tissue swelling (STS) has been hypothesized as a potential risk factor for development of dysphagia, no studies have assessed STS' relation to dysphagia that persists more than 1 year. Sixty-seven patients who underwent elective anterior cervical spine surgery from 2008 to 2011 and completed a dysphagia questionnaire were included in the study. Prevertebral STS was measured at the caudal endplates of C2 and C6 on plain lateral cervical radiographs preoperatively, immediately after, and 6 and 12 weeks postoperatively. The presence and severity of chronic dysphagia was assessed using the Bazaz-Yoo Dysphagia Score. The prevalence of dysphagia in relation to STS was evaluated using the Wilcoxon rank-sum test. By 6 weeks after surgery, 89% of STS at C2 and 97% of STS at C6 had resolved, as compared with preoperative values. The overall dysphagia prevalence in our cohort was 73%, with 48% reporting no or mild symptoms. Moderate symptoms were present in 39% and severe symptoms were present in 13% of the patients. There was no relation between STS measured at all time points compared with the development of chronic dysphagia. Dysphagia did trend toward significance with higher cervical fusions (C4 and above) and as the number of levels fused increased, but STS did not seem to influence this. Postoperative STS is a self-limiting process. The magnitude of STS during the postoperative period does not seem to influence the development of chronic dysphagia.

New-Onset Diabetes After Transplantation: Assessment of Risk Factors and Clinical Outcomes

BackgroundNew-onset diabetes after transplantation (NODAT) is a serious complicatin of kidney transplantation (KT) with adverse impacts on graft and patient survivals. This study aims assess potential risk factors for development of NODAT and compare clinical outcomes of KT recipients with versus without NODAT. MethodsWe retrospectively evaluated 648 patients who underwent KT between 2005 and 2009. From the 83 (12.8%) subjects who developed NODAT, we selected 47 for comparison with controls free of diabetes. ResultsThe diagnosis of NODAT was made at 4.3 ± 8.5 months after transplantation in 47 patients, including 76.6% males, with an overall mean age of 54.5 ± 10.8 years. Patients with NODAT presented higher pretransplantation fasting plasma glucose levels (P < .001) as well as cyclosporine and tacrolimus trough levels (P = .003 and P < .001, respectively). On multivariate analysis, higher pretransplantation fasting plasma glucose and higher tacrolimus, but not cyclosporine concentrations were independent predictors of NODAT. No differences were found for other potential risk factors. Upon follow-up at 6, 12, 24, 36, 48, and 60 months, renal function (estimated Glomerular Filtration Rate using Modification of Diet in Renal Disease), 24 hour proteinuria and proportions of patients with hypertension were similar between groups. Patients with NODAT showed comparable numbers of hospitalizations and infections, as well as acute rejection episodes and acute cardiovascular events as their counterparts. Event-free survival (loss of graft function/death with functioning graft) was similar between the groups (P = .418; K-M). DiscussionIn our population, higher pretransplantation fasting plasma glucose levels and higher tacrolimus concentrations were independent predictors of NODAT. During a mean follow-up of 3 years, NODAT was not associated with worse clinical outcomes.

Staphylococcus aureus and topical fusidic acid use: results of a clinical audit on antimicrobial resistance

Fusidic acid (FA) resistance in Staphylococcus aureus poses a problem for treating systemic methicillin-resistant S. aureus infection, in which FA may otherwise remain a viable option. It can also result in treatment failure of common dermatological conditions such as impetigo and infected atopic eczema. Several studies have linked trends in prescribing medication and topical use of FA to development of resistance. However, few case-control studies have evaluated risk factors for developing FA resistance in S. aureus. A clinical audit for antimicrobial resistance was performed in dermatology patients from the National Skin Centre who were admitted for inpatient care from 2006 to 2008 and had positive bacterial cultures for S. aureus. Each FA-resistant S. aureus (FRSA) case was compared with four randomly selected FA-susceptible (FSSA) cases. Medical records were reviewed retrospectively, and potential risk factors for development of resistance were analyzed. Thirteen of 37 patients with FRSA (35.1%) had used FA topically compared with 11 of 148 patients with FSSA (7.4%). Findings from multivariate analysis indicate that previous use of topical FA was the only independent risk factor of FA resistance (adjusted OR 7.46, 95% CI [2.60-21.41], P<0.001). Patients' coexisting illnesses, recent hospitalization, or systemic antibiotic use were not significant risks. Previous recent topical FA use correlated positively with FA resistance in S. aureus. Prescribing physicians must be vigilant of the rise of FA resistance and its resultant problems and prescribe topical FA discerningly.

A Higher Glomerular Filtration Rate Predicts Low Risk of Developing Chronic Kidney Disease in Living Kidney Donors

The risk of developing chronic kidney disease (CKD) among living kidney donors (LKDs) is seldom included in evaluations of patients' outcomes. Potential risk factors and new criteria for estimating the glomerular filtration rate (eGFR) indexed for body surface area (BSA) were investigated with a view to prevent the development of CKD in LKDs. We conducted a retrospective study of LKDs from May 1983 to March 2011. The Mann-Whitney U test and χ(2) test were used to analyze the male versus female groups. Survival analysis was plotted as CKD-free survival and analyzed separately by different eGFR index classifications. The Cox regression model was used to identify potential risk factors for development of CKD. A total of 105 LKDs with a mean age of 46.3±12.5years had a mean eGFR indexed for BSA of 88.9±21.5ml/min per 1.73m(2). After a mean duration of 5.4±4.9years' follow-up, eGFR dropped to 61.4±16.4ml/min per 1.73m(2) (p=0.002). Median CKD-free survival was only 5.7years. The difference between eGFR≥80ml/min per 1.73m(2) and <80ml/min per 1.73m(2) was not statistically significant (p=0.980). Multivariate Cox regression analysis showed that higher eGFR at donation (HR=0.952, p=0.0199) could be a protective factor. The receiver operating characteristic (ROC) curve for initial eGFR with best sensitivity of 52.78% and specificity of 81.40% was obtained with a cutoff value of 90.2ml/min per 1.73m(2) for preoperative eGFR. An eGFR of 90ml/min per 1.73m(2) yielded a significant survival curve (p=0.0199) after 21years of follow-up. Further classifications of eGFR >90ml/min per 1.73m(2) into 90-99ml/min per 1.73m(2), 100-109ml/min per 1.73m(2), and ≥110ml/min per 1.73m(2) were examined, but this survival curve was not statistically significant (p=0.1247). Living kidney donors will develop CKD after a long duration of follow-up if there is insufficiently high eGFR at donation. An eGFR above 90ml/min per 1.73m(2) before donation is the only factor that predicts prevention of CKD. Larger studies with longer duration of follow-up are necessary to clarify the clinical outcome of this postoperative CKD group, especially for patients with eGFR between 80 and 90ml/min per 1.73m(2).

Показатели пищевого статуса как потенциальные факторы риска развития сердечно-сосудистых заболеваний (по результатам исследования среди жителей Москвы)

Показатели пищевого статуса как потенциальные факторы риска развития сердечно-сосудистых заболеваний (по результатам исследования среди жителей Москвы)

HER1 R497K and HER2 I655V polymorphisms are linked to development of breast cancer.

BACKGROUND: Polymorphism of the genes of Human Epidermal growth factor receptor1 (HER1) and receptor2 (HER2) have been reported to be linked to pathogenesis of several malignant tumors but still there is contradiction regarding their association with breast cancer.OBJECTIVE: In this case control study we aimed to analyze the frequency of HER1 R497K (rs 11543848) and HER2 I655V (rs 1136201) Polymorphisms in breast cancer.SUBJECT AND METHOD: The frequency of HER1 Arg(R) 497Lys (K) and HER2 Ile (I) 655Val (V) polymorphisms were tested in 64 breast cancer patients and 86 normal control by polymerase chain reaction followed by restriction fragment polymorphism detection. Immunohistochemical analysis was done for HER2 protein on the available 18 malignant tissue samples.RESULTS: HER1 497K and HER2 655V variant had significantly increased breast cancer risk (OR=2.6, 95% CI 1.6–4.2, OR=2.2, 95% CI 1.2–4.1, p< 0.05) respectively. Moreover, combined HER1 K497 and HER2 V655 variant was detected in 26.6% malignant in comparison to 8.14% of control group (OR=4.1, 95% CI 1.58–10.57), but, no significant association was noticed between both Polymorphisms and clinicopathological features of the disease. As regard HER2 immunohistochemical expression no significant correlation was revealed with HER2 655V polymorphism.CONCLUSIONS: Our findings suggest that HER1 497K and HER2 655V polymorphisms are potential risk factor for development of breast cancer.

HER1R497K andHER2I655V Polymorphisms Are Linked to Development of Breast Cancer

BACKGROUND: Polymorphism of the genes of Human Epidermal growth factor receptor1 (HER1) and receptor2 (HER2) have been reported to be linked to pathogenesis of several malignant tumors but still there is contradiction regarding their association with breast cancer.OBJECTIVE: In this case control study we aimed to analyze the frequency ofHER1R497K (rs 11543848) andHER2I655V (rs 1136201) Polymorphisms in breast cancer.SUBJECT AND METHOD: The frequency ofHER1Arg(R) 497Lys (K) andHER2Ile (I) 655Val (V) polymorphisms were tested in 64 breast cancer patients and 86 normal control by polymerase chain reaction followed by restriction fragment polymorphism detection. Immunohistochemical analysis was done for HER2 protein on the available 18 malignant tissue samples.RESULTS:HER1497K andHER2655V variant had significantly increased breast cancer risk (OR=2.6, 95% CI 1.6–4.2, OR=2.2, 95% CI 1.2–4.1, p&lt; 0.05) respectively. Moreover, combinedHER1K497 andHER2V655 variant was detected in 26.6% malignant in comparison to 8.14% of control group (OR=4.1, 95% CI 1.58–10.57), but, no significant association was noticed between both Polymorphisms and clinicopathological features of the disease. As regard HER2 immunohistochemical expression no significant correlation was revealed with HER2 655V polymorphism.CONCLUSIONS: Our findings suggest thatHER1497K andHER2655V polymorphisms are potential risk factor for development of breast cancer.

Can Early Onset of Disease Be One of the Risk Factors for Low Bone Mineral Density in Patients with Inflammatory Bowel Disease?

Can Early Onset of Disease Be One of the Risk Factors for Low Bone Mineral Density in Patients with Inflammatory Bowel Disease?

1417 Metabolic Syndrome and Insulin Resistance in Children and Adolescents

Overweight and obesity in children and adolescents have become a major public health problem in recent years. The prevalence of metabolic syndrome in childhood increases in parallel with the high...

Envolvimento sistêmico da doença periodontal – Quais as consequências?

The periodontal disease (PD) is triggered by a microbial aggression followed by a specific response with local and systemic repercussions. Several authors consider DP as a potential risk factor for development of systemic diseases such as stroke, diabetes, preterm birth, atherosclerosis and cardiovascular diseases. The study of how PD can influence a number of systemic disorders is called a periodontal medicine. The biofilm attached in teeth can release toxic bacterial products biologically active and the periodontum responds to these substances through the inflammation. There is a varied spectrum of periodontal inflammatory responses to microbial attack, from a slight gingivitis to a severe destructive PD. The bacterial products associated with inflammatory mediators can lead the patient to produce a series of systemic responses. The purpose of this review is to discuss the possible biological pathways by which the PD can influence the etiopathogenesis of some diseases and systemic disorders.

A review of equine sarcoid

SummaryEquine sarcoid is the most common tumour of horses and accounts for over half of all equine skin tumours. Six types of sarcoid based on gross appearance and clinical behaviour have been described including occult, verrucous, nodular, fibroblastic, mixed and malevolent. Common locations for sarcoid development include the periocular region, ear pinnae, lips, neck, extremities and ventrum (including groin region). Bovine papillomavirus (BPV) is causally associated with equine sarcoid with genetic haplotype, fly vectors and skin trauma identified as potential risk factors for development of the disease. Histopathology is required for definitive diagnosis of equine sarcoid but incomplete excision is thought to activate latent BPV and stimulate growth. Although there are no uniformly effective treatment options, several modalities have been successful in eliminating or managing equine sarcoid. Surgical excision, intratumoural chemotherapy, cryotherapy, hyperthermia, radiotherapy, immunotherapy and immune modulators are used with degrees of success relative to the accessibility and invasiveness of the tumour. Prevention of equine sarcoid may be facilitated by future development of vaccines against bovine papillomavirus.

Evaluation of the incidence and risk factors for development of fenofibrate-associated nephrotoxicity

Fenofibrate-associated nephrotoxicity has been described in two randomized controlled trials and several observational studies. However, little is known regarding its incidence and the population(s) at risk. This study aims to quantify the incidence and identify potential risk factors for development of nephrotoxicity in patients receiving fenofibrate. A retrospective, observational study was conducted in the South Texas Veterans Health Care System. Data were collected regarding baseline demographics, concurrent medical conditions, medications, laboratory results, and fenofibrate use. Within 6 months after initiation of fenofibrate in 428 patients, 115 (27%) experienced an increase in serum creatinine of ≥ 0.3 mg/dL. Any renal disease (P = .001), chronic kidney disease (P = .01), and diabetes (P = .02) were significantly more prevalent in patients with fenofibrate-associated nephrotoxicity. Patients with nephrotoxicity had significantly greater serum creatinine (1.2 [SD 0.3] vs. 1.1 mg/dL [SD 0.3], P = .0002) and lower estimated glomerular filtration rate (72 [SD 20] vs 81 mL/min/1.73 m² [SD 20], P < .0001) at baseline. These patients also had greater use of calcium channel blockers (P = .0003), furosemide (P = .02), and angiotensin-converting enzyme inhibitors (P = .02). The incidence of nephrotoxicity was significantly greater in patients initiated on high-dose versus those on low-dose fenofibrate (P = .002). In a multivariable regression model, renal disease (P = .02), high-dose fenofibrate (P = .001), and dihydropyridine calcium channel blocker use (P = .02) were determined to be independent predictors of development of increased serum creatinine on fenofibrate. This observational study suggests fenofibrate-associated nephrotoxicity occurs more frequently than previously reported, particularly in patients with renal disease and in those receiving high-dose fenofibrate or concomitant calcium channel blockers.

Epidemiological and genetic study of exertional rhabdomyolysis in a Warmblood horse family in Switzerland

Exertional rhabdomyolysis (ER) and its familial basis in Warmblood horses is incompletely understood. To describe the case details, clinical signs and management of ER-affected Warmblood horses from a family with a high prevalence of ER, to determine if histopathological signs of polysaccharide storage myopathy (PSSM) and the glycogen synthase (GYS1) mutation are associated with ER in this family, and to investigate potential risk factors for development of ER. A family consisting of a sire with ER and 71 of his descendants was investigated. History of episodes of ER, husbandry, feeding and use was assessed by interviewing horse owners using a standardised questionnaire. All horses were genotyped for GYS1. In 10 ER-affected horses, muscle histopathology was evaluated. Signs of ER were reported in 39% of horses and 51% of the entire family possessed the GYS1 mutation. Horses possessing the GYS1 mutation had a 7.1-times increased risk for developing ER compared to those with the normal genotype (95% confidence interval [CI] 2.37-21.23, P = 0.0005). All muscle samples from horses in the family with ER showed polysaccharide accumulation typical for PSSM, amylase-resistant in 9/10 cases. There was evidence (odds ratio 5.6, CI 1.00-31.32, P = 0.05) that fat or oil feeding improved clinical signs of ER. No other effects of environmental factors associated with clinical signs of ER were identified. PSSM associated with the GYS1 mutation is one identifiable cause of ER in Warmblood horses. Signs of ER are not always manifest in GYS1 positive horses and there are also other causes for ER in Warmblood horses. Breeding animals with the GYS1 mutation results in a high prevalence of ER due to its dominant mode of inheritance.

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The Editorial Comment raises an important concern about confounding of prostate-specific antigen (PSA) kinetics from biological variability in the PSA measurement. Surprisingly, we found that this was less of an issue than expected. In our community-based population, only ∼1% of PSAV values exceeded 0.4 ng/mL/y in healthy men with PSA levels <3 ng/mL. Thus, if this cutpoint were used to determine the need for prostate biopsy at low PSA levels, few men would be subjected to unnecessary biopsy on the basis of PSA variability alone. Furthermore, a PSAV >0.4 ng/mL/y substantially increased the probability of life-threatening prostate cancer, suggesting that the use of PSAV in men with low total PSA levels should increase the specificity of screening for clinically important prostate cancer. However, as pointed out in the Editorial Comment, well-designed prospective studies are necessary to confirm this assertion. Editorial CommentUrologyVol. 77Issue 1PreviewStudies looking at prostate-specific antigen (PSA) kinetics have emerged in the last two decades with the intent to better discern which PSAs are actually associated with prostate cancer and, more importantly, aggressive disease. Carter et al from Johns Hopkins were the first to assess PSA velocity (PSAV) as a potential risk factor for development of prostate cancer using the Baltimore Longitudinal Study of Aging (BLSA).1 The authors looked at the serum levels of PSA taken 7-25 years before the development of “prostate disease” (benign prostatic hyperplasia [BPH] or prostate cancer) and concluded that a rate of change of 0.75 μg/L/y was significantly greater in subjects with prostate cancer compared with control subjects and subjects with BPH, and therefore “may be a sensitive and specific early clinical marker for the development of prostate cancer.” Full-Text PDF

Editorial Comment

Studies looking at prostate-specific antigen (PSA) kinetics have emerged in the last two decades with the intent to better discern which PSAs are actually associated with prostate cancer and, more importantly, aggressive disease. Carter et al from Johns Hopkins were the first to assess PSA velocity (PSAV) as a potential risk factor for development of prostate cancer using the Baltimore Longitudinal Study of Aging (BLSA). 1 Carter H.B. Pearson J.D. Metter E.J. et al. Longitudinal evaluation of prostate specific antigen levels in men with and without prostate disease. JAMA. 1992; 267: 2215-2220 Crossref PubMed Scopus (929) Google Scholar The authors looked at the serum levels of PSA taken 7-25 years before the development of “prostate disease” (benign prostatic hyperplasia [BPH] or prostate cancer) and concluded that a rate of change of 0.75 μg/L/y was significantly greater in subjects with prostate cancer compared with control subjects and subjects with BPH, and therefore “may be a sensitive and specific early clinical marker for the development of prostate cancer.” Distribution of PSA Velocity by Total PSA Levels: Data From the Baltimore Longitudinal Study of AgingUrologyVol. 77Issue 1PreviewTo describe the distribution and implications of prostate-specific antigen velocity (PSAV) by prostate-specific antigen (PSA) in an unselected population. A PSAV >0.35 and >2.0 ng/mL/y have been associated with an increased risk of prostate cancer (CaP) death more than 10 years and 1 year before diagnosis, respectively. It is unknown how frequently PSAVs of this magnitude occur in community men. Full-Text PDF ReplyUrologyVol. 77Issue 1PreviewThe Editorial Comment raises an important concern about confounding of prostate-specific antigen (PSA) kinetics from biological variability in the PSA measurement. Surprisingly, we found that this was less of an issue than expected. In our community-based population, only ∼1% of PSAV values exceeded 0.4 ng/mL/y in healthy men with PSA levels <3 ng/mL. Thus, if this cutpoint were used to determine the need for prostate biopsy at low PSA levels, few men would be subjected to unnecessary biopsy on the basis of PSA variability alone. Full-Text PDF

Fulminant, Non-antibiotic Associated Clostridium difficile Colitis Following Salmonella Gastroenteritis

In the last decade there has been increasing awareness of the virulence and changing epidemiology of Clostridium difficile (C. difficile). While the vast majority of clinical cases of C. difficile are associated with antimicrobial or nosocomial exposure, this syndrome has been well described in the absence of antibiotic use. We present an unusual case of fatal, non-antibiotic associated C. difficile colitis following Salmonella serotype Saintpaul gastroenteritis in a previously healthy young person. We review the typical risk factors for C. difficile colitis and fulminant disease. We also review the epidemiology of community-acquired C. difficile-associated disease (CA-CDAD) and highlight Salmonella infection as a potential risk factor for development of CA-CDAD.

Molecular detection and antibacterial susceptibility of enteropathogenic Escherichia coli (EPEC) and shigatoxigenic Escherichia coli (STEC) strains isolated from healthy and diarrhoeic dogs

Animal contacts have been regarded as an emerging rout of Shiga toxin-producing Escherichia coli (STEC) infection in humans. Diarrhoeic and asymptomatic dogs have been recognised as a reservoir of atypical enteropathogenic Escherichia coli (EPEC), and STEC in some investigations. In this study E. coli isolates from 100 faecal samples of healthy (n = 50) and diarrhoeic (n = 50) dogs were screened by polymerase chain reaction (PCR) for the presence of determining virulence genes of STEC and EPEC pathotypes including stx and eaeA. The confirmed virulence-positive strains were subjected to antimicrobial susceptibility testing against 12 antibacterial using disc diffusion method. Resistance profiles were also determined for the STEC and EPEC strains. Ten isolates from 10 dogs (10%) were shown to possess at least one of the tested virulence genes. Six of these isolates (6%) harboured only the eaeA gene and were considered as EPEC. Four isolates (4%) were stx+ and regarded as STEC, of which two were stx+/eae+. The resistance was specially observed against penicillin, ampicillin, sulfomethoxazole, streptomycin and oxytetracyclin. Altogether, nine resistance profiles were observed among 10 isolates. In conclusion, dogs can act as a reservoir for EPEC and STEC strains, and close contacts of children with companion animals can be a potential risk factor in development of diarrhoea and haemolytic uremic syndrome. In rural areas shepherd dogs can also be a transient carrier of STEC strains that they may acquire from ruminants. To our knowledge this is the first study which reports the faecal shedding of STEC and EPEC from dogs in Iran.