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Pauci-immune GN constitutes one-half of patients with crescentic GN at this center. Patients with pauciimmune GN, chiefly ANCA negative, show higher risk of disease progression. Renal loss is related to severity of initial presentation and extent of glomerular involvement.

Dilatation and oesophageal body aperistalsis in achalasia can lead to stasis which in turn can induce repeated microaspiration. It is therefore conceivable that patients with achalasia may also have abnormalities in lungs secondary to repeated episodes of microaspiration. There is a lack of systematic study on involvement of lungs in patients with achalasia. Thirty patients with achalasia underwent pulmonary function tests (spirometry, and carbon mono-oxide diffusion capacity) and high resolution computerized tomography (HRCT) of the chest. The mean age of patients and mean duration of disease were 33.5 +/- 10.9 years and 28.1 +/- 27.3 months respectively. Regurgitation was present in 22 (73.3%) of them. Respiratory symptoms in them were dry cough in 17 (56.6%), and chest pain in 18 (60%). The oesophagus was dilated in 26 (86.6%) and 13 (43.3%) had residue in oesophagus. Sixteen (53.3%) patients had either anatomical changes as seen on HRCT or functional changes as observed on pulmonary function tests. Of those with functional abnormalities, five (16.6%) and one (3.3%) had restrictive and obstructive airways disease respectively. While evidence of tracheo-bronchial compression by dilated oesophagus was present in eight (26.6%), 10 (33.3%) patients had parenchymal lung disease [nodular opacities in five (16.6%), ground glass appearance six (20%), patchy pulmonary fibrosis five (16.6%), air trapping two (6.6%), consolidation and bronchiectasis one (3.3%) each]. There was a significant association between presence of regurgitation and dilatation of oesophagus (P = 0.032). More than half (53.3%) of patients with achalasia have structural and/or functional abnormalities in lungs.

BackgroundThe growth trajectories of common measurements, including estimated fetal weight (EFW), head circumference (HC), and abdominal circumference (AC), in fetuses with congenital heart disease (CHD) have not been described for different cardiac lesions. We hypothesized that (i) fetuses with CHD have differential growth in utero, and (ii) different categories of CHD demonstrate different in utero growth curves.MethodsWe performed a retrospective observational cohort study of pregnancies with known fetal CHD seen from January 2000 to June 2013. For analysis, the infants were divided into single ventricle (SV), biventricular conotruncal, d-transposition of great arteries (d-TGA), biventricular septal defects (SD; including atrial, ventricular, and atrioventricular SD), and all others (Other).ResultsA total of 194 newborns met inclusion criteria. There was significant differential growth of EFW in all CHD types, except d-TGA, starting with low z-scores before 25 weeks gestation, improving toward normal around 30-32 weeks gestation, and then again differential growth with advancing gestation. SV and SD groups had significant differential growth of HC starting early in gestation and linearly progressing negative z-scores with advancing gestation.ConclusionWe observed differences in the fetal growth curves throughout gestation for the major categories of CHD, including significant differential growth in even "simple" CHD, such as SD.

Sequential testing combination of VIA and HPV, followed by colposcopy and directed biopsy for diagnosis, combines economic viability with high scientific fidelity. The high specificity and negative predictive value reduce referral and treatment rates, as well as number of visits required for diagnosis. HPV (P) followed by reflex Pap is a suitable option for high resource situations with access to liquid-based cytology.

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ObjectiveChorioamnionitis (inflammation of the placenta and fetal membranes) and abnormal gastrointestinal colonization have been associated with an increased risk of sepsis and death in preterm infants, but whether chorioamnionitis causes abnormal pioneering gastrointestinal colonization in infants is not known. We determined the relationship between chorioamnionitis, altered infant fecal microbiome indicating abnormal gastrointestinal colonization, and adverse outcomes.Study DesignPreterm infants ≤ 28 weeks at birth were enrolled from 3 level III NICUs in Cincinnati, Ohio and Birmingham, Alabama. Sequencing for 16S microbial gene was performed on stool samples in the first 3 weeks of life. Chorioamnionitis was diagnosed by placental histology. Late onset sepsis and death outcomes were analyzed in relation to fecal microbiota and chorioamnionitis with or without funisitis (inflammation of the umbilical cord).ResultsOf the 106 enrolled infants, 48 infants had no chorioamnionitis, 32 infants had chorioamnionitis but no funisitis (AC), and 26 infants had chorioamnionitis with funisitis (ACF). The fecal samples from ACF infants collected by day of life 7 had higher relative abundance of family Mycoplasmataceae (phylum Tenericutes), genus Prevotella (phylum Bacteroidetes) and genus Sneathia (phylum Fusobacteria). Further, AC and ACF infants had higher incidence of late-onset sepsis/death as a combined outcome. Presence of specific clades in fecal samples, specifically, order Fusobacteria, genus Sneathia or family Mycoplasmataceae, were significantly associated with higher risk of sepsis or death.ConclusionThe results support the hypothesis that specific alterations in the pioneering infant gastrointestinal microbiota induced by chorioamnionitis predispose to neonatal sepsis or death.