News about Health (Part 9)

The Overlap Between Respiratory Bronchiolitis and Desquamative Interstitial Pneumonia: Results Summary of the Two Index Cases

Correlations between the extent of RB/DIP-like changes (0 to 100% involvement of biopsy) and total pack-years smoked was performed using linear regression analysis and the Pearson correlation coefficient. Similarly, correlations between the extent of RB/DIP-like changes and pulmonary function variables total lung capacity [TLC], FEV1, and diffusion capacity of the lung for carbon monoxide [Dlco] was performed by linear regression and the Pearson correlation coefficient. Statistical analysis was performed using JMP software, version 4 (SAS Institute, Cary, NC) with p values < 0.05 considered statistically significant.
The first patient was a 52-year-old white woman (patient 1 in Tables 1, 2) with a 70 -pack-year smoking history referred for evaluation of dyspnea and cough. review

The Overlap Between Respiratory Bronchiolitis and Desquamative Interstitial Pneumonia: HRCT

The Overlap Between Respiratory Bronchiolitis and Desquamative Interstitial Pneumonia: HRCTWhen present, the distribution of the abnormalities such as adenopathy and emphysema was recorded. Surgical lung biopsy specimens were reviewed by a pathologist (T.V.C.) blinded to the findings on HRCT. Accumulation of pigmented macrophages in airspaces and around respiratory bronchioles was combined with more widespread airspace accumulation of macrophages (DIP-like change) as RB/DIP-like change. This score provided a rough quantification of the degree of airspace filling (both respiratory bronchiole and alveolar spaces) by macrophages. The extent of involvement of the biopsy by RB/DIP-like changes was classified by percentage (0 to 100%).

The Overlap Between Respiratory Bronchiolitis and Desquamative Interstitial Pneumonia: Materials and Methods

The medical record of two index patients with PLCH associated with marked RB/DIP-like changes on biopsy were reviewed and summarized. To further characterize the relationship between RB/DIP and PLCH, we searched the Mayo Clinic database and identified 10 additional cases for which both surgical lung biopsy specimens and HRCT scans were available for review. These 10 cases were part of a previously reported series. Patients with transbronchoscopic biopsy-proven PLCH were excluded from the study because the limited amount of tissue was believed to be inadequate for the purpose of the study. Two additional cases (with available lung biopsy and HRCT) were identified while conducting the study (during 1999). All lung biopsies were performed within 3 months of the CT scan. The diagnosis of PLCH was established by light microscopy in all cases. fully

The Overlap Between Respiratory Bronchiolitis and Desquamative Interstitial Pneumonia

The Overlap Between Respiratory Bronchiolitis and Desquamative Interstitial PneumoniaPulmonary Langerhans cell histiocytosis (PLCH) is an uncommon interstitial lung disorder that occurs almost exclusively in smokers. Cigarette smoking has also been implicated in the development of respiratory bronchiolitis (RB)-associated interstitial lung disease (ILD) [RB-ILD] and desquamative interstitial pneumonia (DIP), two uncommon ILDs with significant clinical and histopathologic overlap. These three ILDs are now often referred to as smoking-related ILDs, a term suggesting that PLCH, DIP, and RB-ILD may form a spectrum of patterns of interstitial lung injury that may occur in certain individuals who smoke. RB is a histologic lesion reported to occur in virtually all smokers. Since DIP is also etiologically linked to smoking, it is not unexpected that RB/DIP-like reactions frequently coexist in histologic specimens of PLCH, as reported in prior studies. review

Thrombin, Inflammation, and Cardiovascular Disease: Conclusions

Thrombin, Inflammation, and Cardiovascular Disease: ConclusionsThis statistical association may be mediated by the key proinflammatory cytokine (also an adipokine) TNF-a, which is a so-called first-wave cytokine influencing IL-6 production, as well as many other cellular functions. TNF-a receptor (TNFR) I signals programmed cell death, while TNFR II may signal survival or proliferation through cytoplasmic TNFR-associated proteins, which can both negatively regulate apoptosis and positively promote survival. Although the role (if any) of circulating TNF-a in humans remains uncertain, TNF-a induces insulin resistance in tissue culture and in animal models.’ Plasma levels are also elevated in the metabolic syndrome, and are associated with insulin resistance in humans. fully

Thrombin, Inflammation, and Cardiovascular Disease: Inflammatory cytokines

The exact mechanism for the association of CRP with coagulation status is not clear; however the work of Ritchie and colleagues suggests a possible pathway. Monocytes appear capable of binding FDPs and subsequently producing IL-6, which goes to the liver and affects the wide range of proteins known to be in the acute-phase response. This has been proposed to be the mechanism by which fibrinogen consumption is replaced, and may be an important mechanism connecting coagulation and inflammation. This theory may have far-reaching implications both in the general biology we have been discussing and in such areas as drug development, where the coagulation-inflammation connection in sepsis, as described by Esmon et al, has been recently exploited. Reading here

Thrombin, Inflammation, and Cardiovascular Disease: Metabolic Syndrome

Thrombin, Inflammation, and Cardiovascular Disease: Metabolic SyndromeIn some cases, there are significant differences in the strengths of association. Also, each marker may participate in the CVD process in a different way. In a side-by-side comparison, CRP had the strongest risk prediction, but a meta-analysis observed no real difference between CRP and fibrinogen in risk prediction.
Inflammation and the Metabolic Syndrome: an Important Relationship
It has been observed that markers of inflammation are associated with the components of the metabolic syn-drome; this finding is in addition to the known association of inflammation markers, as well as markers of coagulant activity, with diabetes status. there

Thrombin, Inflammation, and Cardiovascular Disease: Risk prediction to CRP

However, a wide variety of activities, such as innate immunity, coagulation, and others, fall under the term inflammation. Each of these activities plays an important role in our response to trauma and/or environmental challenge: coagulation and fibrinolysis in restricting blood loss and in wound repair; complement activation and T-cell differentiation as part of innate and adaptive immunity; endothelial cell, neutrophil, and monocyte activation in immunity and wound repair; antioxidation in response to oxidative challenge; and others. In addition, variances in the genes responsible for the overall regulation of this system may play important roles in disease susceptibility; eg, IL-6 and tumor necrosis factor (TNF)-a genes.

Thrombin, Inflammation, and Cardiovascular Disease: CRP or fibrinogen

Thrombin, Inflammation, and Cardiovascular Disease: CRP or fibrinogenWe should note that “inflammation” as the term is used here does not mean the full form of the condition (warmth, redness, swelling, and pain), but rather implies a “micro-inflammation.” A person with this condition is characterized by being in the upper part of the “normal” distribution for inflammation status, without the signs and symptoms of overt, clinical inflammation. Molecular epidemiology has played a key role in identifying the role of inflammation in CVD, and recently it has become clear that inflammation is connected to the metabolic syndrome in a complex and important manner. Link

Thrombin, Inflammation, and Cardiovascular Disease: Inflammation Markers and CVD Risk

PAI-1 levels are associated with insulin, suggesting that the role of PAI-1 may be particularly important in people with the metabolic syndrome or type 2 diabetes. The regulation of PAI-1 levels—at least in blood—is in part mediated by regulators of glycemic control and inflammation: insulin and proinsulin can stimulate endothelial cells and hepatocytes to produce PAI-1,’ and PAI-1 is believed to be a weak acute-phase reactant. In addition, adipocytes can directly synthesize and secrete PAI-1, helping to explain the known association of PAI-1 levels with body mass index. this

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