8 research outputs found

    E. coli

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    Escherichia coli meningitis is a frequent pathology in children younger than 3 years old, but is an uncommon disease in adults. E. coli infection is the main cause of intrahospital bacteremia as a consequence of the employment of different medical procedures. Our patient, male, 69 years old, presented with fever, progressive difficulty in breathing, and shivers 24 h after transrectal prostate biopsy, with an absence of any other symptoms. He received prophylactic treatment with ciprofloxacin and later empirical treatment with ampicillin and tobramicin. After that, the patient presented with fever, headache, behavioral changes, somnolence, disorientation, a fluctuating level of conscience, cutaneous widespread pallor, and acute urinary retention. On physical exploration, we observed generalized hypoventilation, Glasgow 10, stiffness of the neck, inconclusive Kernig; the remaining neurological exploration was normal. Systematic of blood: leukocytes = 8,510/mm3 (94.5% polymorphonuclear), platelet = 87,000/mm3, pH = 7.51, pCO2 = 28.8 mmHg, pO2 = 61 mmHg, O2 saturation = 93.8%, and remaining values were normal. Chest X- ray, cranial CT scan, urine cultures were normal. Blood culture: E. coli. CSF: glucose <0.4 g/l, total proteins = 3.05 g/l, PMN = 7 cells. Microscopic examination of the CSF: Gram-negative bacilli; CSF's culture: abundant E. coli. The case of acute meningitis by multiresistant E. coli after transrectal prostate biopsy presented demonstrates that antibiotic prevention with ciprofloxacin is not absolutely risk free. Besides the use of antibiotic prevention for multiresistant microorganisms, the urologist and other physicians involved in the procedure must not forget that the rate of major complications of transrectal prostate biopsy is 1%, especially when it is performed in patients who will not benefit from that biopsy

    Interleukin-10 haplotypes in Celiac Disease in the Spanish population

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    BACKGROUND: Celiac disease (CD) is a chronic disorder characterized by a pathological inflammatory response after exposure to gluten in genetically susceptible individuals. The HLA complex accounts for less than half of the genetic component of the disease, and additional genes must be implicated. Interleukin-10 (IL-10) is an important regulator of mucosal immunity, and several reports have described alterations of IL-10 levels in celiac patients. The IL-10 gene is located on chromosome 1, and its promoter carries several single nucleotide polymorphisms (SNPs) and microsatellites which have been associated to production levels. Our aim was to study the role of those polymorphisms in susceptibility to CD in our population. METHODS: A case-control and a familial study were performed. Positions -1082, -819 and -592 of the IL-10 promoter were typed by TaqMan and allele specific PCR. IL10R and IL10G microsatellites were amplified with labelled primers, and they were subsequently run on an automatic sequencer. In this study 446 patients and 573 controls were included, all of them white Spaniards. Extended haplotypes encompassing microsatellites and SNPs were obtained in families and estimated in controls by the Expectation-Maximization algorithm. RESULTS: No significant associations after Bonferroni correction were observed in the SNPs or any of the microsatellites. Stratification by HLA-DQ2 (DQA1*0501-DQB1*02) status did not alter the results. When extended haplotypes were analyzed, no differences were apparent either. CONCLUSION: The IL-10 polymorphisms studied are not associated with celiac disease. Our data suggest that the IL-10 alteration seen in patients may be more consequence than cause of the disease

    Imaging of bronchial pathology in antibody deficiency: Data from the European Chest CT Group

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    Studies of chest computed tomography (CT) in patients with primary antibody deficiency syndromes (ADS) suggest a broad range of bronchial pathology. However, there are as yet no multicentre studies to assess the variety of bronchial pathology in this patient group. One of the underlying reasons is the lack of a consensus methodology, a prerequisite to jointly document chest CT findings. We aimed to establish an international platform for the evaluation of bronchial pathology as assessed by chest CT and to describe the range of bronchial pathologies in patients with antibody deficiency. Ffteen immunodeficiency centres from 9 countries evaluated chest CT scans of patients with ADS using a predefined list of potential findings including an extent score for bronchiectasis. Data of 282 patients with ADS were collected. Patients with common variable immunodeficiency disorders (CVID) comprised the largest subgroup (232 patients, 82.3%). Eighty percent of CVID patients had radiological evidence of bronchial pathology including bronchiectasis in 61%, bronchial wall thickening in 44% and mucus plugging in 29%. Bronchiectasis was detected in 44% of CVID patients aged less than 20 years. Cough was a better predictor for bronchiectasis than spirometry values. Delay of diagnosis as well as duration of disease correlated positively with presence of bronchiectasis. The use of consensus diagnostic criteria and a pre-defined list of bronchial pathologies allows for comparison of chest CT data in multicentre studies. Our data suggest a high prevalence of bronchial pathology in CVID due to late diagnosis or duration of disease

    Pancreatic autoimmunity: An unknown etiology on patients with assisted reproductive techniques (ART)-recurrent reproductive failure.

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    Pancreatic Autoimmunity is defined as the presence of autoantibodies and more frequent need for insulin treatment. Affected women presenting recurrent implantation failure (RIF) or recurrent miscarriage (RM) are often misdiagnosed. The objective of thestudy was to describe clinical and metabolic profiles suggestive of Pancreatic Autoimmunity and therapeutic strategy in patients with RIF/RM. We analyzed retrospectively 735 patients, and have identified a subset (N = 20) with similar metabolic characteristics. At the same time, we included a control group (n = 39), with similar demographic characteristics and negative for pancreatic, thyroid or celiac disease autoimmunity. The patients identified with autoimmune metabolic problem (N = 20) had relatives with diabetes mellitus. At 120 minutes after Oral Glucose Tolerance Test (OGTT) low level of insulin secretion (<2 IU/ml) was found in 70% of patients. Glutamic acid decarboxylase 65 (GAD 65) antibodies, with or without other autoantibodies, were positive in80% of patients and anti-IA2 alone were positive I the rest. Since pregestational period, insulin administration was recommended for 10 patients, metformin for 4 patients and exclusively diet control in 5 of them. Significantly increased live bith rates (LBR) per cycle were observed after metabolic control (52%) compared with live birth rate (LBR) after cycles without control (7.5%) (p<0.0001). We noticed 2 cases of pre-eclampsia and 6 low-birth weights. Insulin administration was needed during the pregnancy in 68% of patients and after childbirth in 31.57% of them. In our control group, all of patients (n = 39) underwent ART (53.8% SET and 46.1% DET) with a 50% (SET) and 61.9% (DET) live birth rate (LBR) per cycle. Patients with RIF/RM, normal BMI, low insulin levels after OGTT could benefit from additional metabolic immune testing. A correct diagnosis and treatment could have a positive impact on their reproductive results and live birth rate

    A review of the pathophysiology of recurrent implantation failure

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    Implantation is a critical step in human reproduction. The success of this step is dependent on a competent blastocyst, receptive endometrium, and successful cross talk between the embryonic and maternal interfaces. Recurrent implantation failure is the lack of implantation after the transfer of several embryo transfers. As the success of in vitro fertilization has increased and failures have become more unacceptable for patients and providers, the literature on recurrent implantation failure has increased. While this clinical phenomenon is often encountered, there is not a universally agreed-on definition—something addressed in an earlier portion of this Views and Reviews. Implantation failure can result from several different factors. In this review, we discuss factors including the maternal immune system, genetics of the embryo and parents, anatomic factors, hematologic factors, reproductive tract microbiome, and endocrine milieu, which factors into embryo and endometrial synchrony. These potential causes are at various stages of research and not all have clear implications or immediately apparent treatment
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