What is the difference between ipf and uip

We recognize this pattern by the patchy distribution and lack of other abnormal lung findings. Serial imaging if performed will show that these areas of scarring do not change over time.

Pulmonary function testing is usually only mildly abnormal and does not worsen with time. I often worry about recurrent gastro-esophageal reflux GER and recurrent aspiration of stomach contents into the lungs.

Patients that have had radiation therapy for cancer that included some lung tissue in the treatment field can have areas of scarring in the lungs. Tertiles were used to stratify on age and percentage pre-dicted total lung capacity TLC ; the median time before biopsy wa.

Differences between the study groups were evaluated by Student's t-test. Horizontal bars indicate the mean value of each study group. Idiopathic pulmonary fibrosis IPF is type of interstitial lung disease of unknown etiology.

If the pathology has nonclassifiable fibrosis -- the pathologist is not able to distinguish between the UIP and the nonclassifiable fibrosis -- it requires much more than the multidisciplinary discussion to.

A total of 47 Patient characteristics of the whole cohort at baseline are. Idiopathic pulmonary fibrosis IPF , the most common of the idiopathic interstitial pneumonias, is a devastating condition that carries a prognosis worse than that of many cancers. As such, it represents one of the most challenging diseases for chest physicians.

The aim of this study was to evaluate the pathologic and radiologic differences between the two conditions and their relationship with clinical outcome. The difference between A normal lungs and B lungs with idiopathic pulmonary fibrosis, which show damaged bronchioles, alveoli and fibrosis, leading to reduced gas exchange.

Risk factors Although it is not known what factors directly cause IPF, there are several inherited and environmental factors that have been linked with an increased risk. Eating becomes more difficult with IPF. It takes more energy to breathe between bites. For this reason, people with the disease sometimes lose their appetites and in turn, lose weight unintentionally. Pathophysiology YUCK! Cox proportional hazards ratios compared the survival.

A pulmonary pathologist explains how to tell the difference. In this video, Sanjay Mukhopadhyay, MD, staff pulmonary pathologist in the Department of Anatomic Pathology, presents an interesting case of Nonspecific Interstitial Pneumonia lung disease. Usually, due to the more extensive involvement of the lower lobes, the major fissure is shifted inferiorly which is best seen on the lateral chest radiograph. Similar to the pathology specimen, cross-sectional imaging also reveals heterogeneity, with patchy areas of fibrosis alternating with areas of normal lung 5.

In recent times some authors have suggested certain signs within a UIP pattern more suggestive of it being due to connective tissue disorder interstitial lung disease over IPF In patients with UIP, areas of ground-glass attenuation tend to increase in extent or progress to fibrosis despite treatment 8, In those with more active inflammation involving the pulmonary interstitium, there is a faster progression of honeycombing in long-term follow-up The average rate of progression of honeycombing in patients with idiopathic usual interstitial pneumonia according to one study was 0.

Please Note: You can also scroll through stacks with your mouse wheel or the keyboard arrow keys. Updating… Please wait. Unable to process the form. Check for errors and try again. Thank you for updating your details. Log In. Sign Up. Become a Gold Supporter and see no ads. Log in Sign up. Articles Cases Courses Quiz. About Recent Edits Go ad-free. Try out PMC Labs and tell us what you think. Learn More. The usual interstitial pneumonia UIP pattern of lung injury may occur in the setting of connective tissue disease CTD , but it is most commonly found in the absence of a known cause, in the clinical context of idiopathic pulmonary fibrosis IPF.

Our objective was to observe and compare longitudinal changes in pulmonary function and survival between patients with biopsy-proven UIP found in the clinical context of either CTD or IPF. Despite no significant differences in changes in pulmonary function over time, patients with CTD-UIP at least those with certain classifiable CTDs live longer than patients with IPF—an observation that we suspect is due to an increased rate of mortal acute exacerbations in patients with IPF.

The usual interstitial pneumonia UIP pattern of lung injury is nonspecific, occurring in a number of clinical contexts, including underlying connective tissue disease CTD. Over the last decade, a groundswell of research has advanced understanding of the pathogenesis of UIP. Equally elusive is a precise understanding of how measures of pulmonary function change over time in patients with UIP and whether the slopes of these changes vary with the clinical context.

We selected patients who had undergone surgical biopsy and were found to have UIP by an NJH pulmonary pathologist using standard criteria. Pulmonary function was performed as previously described. All statistical analyses were conducted with SAS, version 9. Summary statistics were generated for baseline characteristics. Initial models were developed using linear and cubic splines to account for nonlinearity of the data; number and location of knots were selected to minimize the Akaike Information Criterion.

Subsequent models categorized subjects into groups based on time of last observation in relation to biopsy, for which simple linear trends by time group were determined to be adequate. All models included a random intercept and random slope for time of observation relative to diagnosis for subjects to account for the longitudinal data. More detail is included in e-Appendix 1. Kaplan-Meier survival models were fit for life status of subjects as a function of time from biopsy.

The log-rank test was used to test for overall differences in survival curves between groups. Vital status was ascertained on October 12, Subjects were censored on the date of lung transplantation or on October 12, , if their death could not be confirmed in the Social Security Death Index.

Cox proportional hazards models were used to explore time to death between the two or, in exploratory analyses, five diagnosis groups, while controlling for potentially influential predictors.

The initial Cox models included only the diagnosis group variable. Baseline characteristics of the sample are presented in Table 1.

Physiologic values at diagnosis and median years of follow-up from diagnosis to vital status ascertainment did not differ significantly between the two groups. See e-Appendix 1 for more details.

A spatial power covariance structure was included in the model to account for repeated measures within subjects; random effect terms for subjects were also included, as described in e-Appendix 1. There were no significant differences between groups for segments between comparable time points. The plots demonstrate sharper declines near time of diagnosis for both groups. See Figure 1 legend for expansion of abbreviations. See Table 1 legend for expansion of abbreviations.