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At least 1,027 records · Page 57Linked to original sources
PubMed1996

[Serum CA 19-9 levels in rheumatic diseases with interstitial pneumonia].

Serum CA 19-9 (2-3 sialyl Le(a)) is a marker of malignant disorder such as pancreas or gall bladder cancers. It has been reported that sera from patients with interstitial pneumonia show elevated level of CA 19-9. To investigate the relationship between the elevation of serum CA 19-9 (sCA 19-9) and the presence of pulmonary fibrosis, we examined the level of sCA 19-9 in sera from patients with rheumatic diseases with or without interstitial pneumonia (IP). The sCA 19-9 level was determined by enzyme-linked immunosorbent assay (ELISA). Fourteen sera of 129 (10.9%) patients with rheumatic diseases without malignant disorders were positive for sCA 19-9 when normal range was determined as less than 100 U/ml (mean +/- 5 SD), and 26.7% of sera from poly/dermatomyositis (PM/DM) and 11.8% of systemic sclerosis (PSS) were positive for CA 19-9. Whereas only 8.0% of rheumatoid arthritis (RA) was positive. Twelve (28.6%) of 42 rheumatic patients with IP showed positive levels for sCA 19-9 (mean 142.5 +/- 363.0 U/ml), whereas only two (2.3%) of 87 without IP were positive (mean 33.9 +/- 65.8 U/ml; p < 0.05). The correlation between the level of sCA 19-9 and pulmonary diffusing capacity (%DLCO) revealed an inverse correlation in 32 rheumatic patients with IP (r = -0.43, p < 0.05). Furthermore, the elevated sCA 19-9 levels decreased after treatment with corticosteroid and/or cyclophosphamide or cyclosporin A. Therefore, elevation of the level of sCA 19-9 seems to be involved in the pathogenesis of IP and sCA 19-9 will be a useful parameter for IP. It has been reported that the CA 19-9 is produced from the bronchial glands and suggested that during chronic fibrotic process of the lung, the metaplastic change of the bronchial glandular cells occur and the cells produce CA 19-9.

Biomarkers↗
PubMed1983

Human converting enzyme.

Angiotensin I converting enzyme (kininase II, peptidyl dipeptidase, ACE) was purified by reverse immunoadsorption from a membrane fraction of the human kidney. ACE is very likely a transmembrane peptidase. Treatment of the membrane-bound enzyme with trypsin releases a low mol. wt. fragment (greater than 10,000), which is probably the anchor peptide inserted into the plasma membrane. Antibody to ACE was used to localize it in the CNS where it is bound to plasma membrane of neuroepithelial cells in structures such as the globus pallidus or substantia nigra. Radioimmunoassay indicated that ACEs of endothelial, epithelial and neuroepithelial origin are immunologically identical. Direct radioimmunoassay also showed that there is a strong negative correlation between plasma enzyme level and pulmonary diffusing capacity of sarcoid patients. Finally, in addition to various peptides, homogeneous human ACE cleaves fluorogenic substrates where the C-terminal amino acid is replaced with nitrobenzylamine.

Cell Membrane↗
PubMed2001

Hyperpolarised gases in magnetic resonance: a new tool for functional imaging of the lung.

In magnetic resonance imaging (MRI), nuclear spins are the source of the image signal. In the lung, low-proton spin density in alveolar gas and abundant gas-tissue interfaces substantially impair conventional native 1H-MRI. Spin polarisation can be increased in two non-radioactive noble gas isotopes, 3He and 129Xe, by exposure to polarised laser light. When inhaled, such "magnetized" gases provide high-intensity MR images of the pulmonary airspaces. Thus, hyperpolarised gas (HPG) MRI opens up new routes to a) morphologic imaging of airways and alveolar spaces, and b) analysis of the intrapulmonary distribution of inhaled aliquots of these tracer gases; c) diffusion-sensitive MRI-techniques allow mapping of the "apparent diffusion coefficient" (ADC) of 3He within lung airspaces, where ADC is physically related to local bronchoalveolar dimensions; d) also, 3He magnetisation decays in an oxygen-containing atmosphere at a rate proportional to ambient PO2. This property allows image-based determination of regional broncho-alveolar PO2 and its decrease during a breathhold. Currently, these modalities of functional lung imaging are being assessed by several European and American research groups in animal models, human volunteers and patients. First results show good imaging quality with excellent spatial and unprecedented temporal resolution, and attest to the reproducibility, feasibility and safety of the technique. Regionally impaired ventilation of both structural and functional origin is detected with high sensitivity, e.g. in smokers, asthmatics, patients with COPD or after lung transplantation. Studies into regional ADC and PO2 measurement demonstrate good agreement with reference methods and physiological predictions. The present limitations of HPG-MRI include the HPG production rate and the US and EU health authorities' still pending final approval for clinical use.

Adult↗
PubMed2004

Transfer factor for carbon monoxide: a glance behind the scene.

The transfer factor for carbon monoxide (TLCO) is widely used in pulmonary function laboratories because it represents a unique non-invasive window on pulmonary microcirculation. The TLCO is the product of two primary measurements, the alveolar volume (VA) and the CO transfer coefficient (KCO). This test is most informative when VA and KCO are examined, together with their product TLCO. In a normal lung, a low VA due to incomplete expansion is associated with an elevated KCO, resulting in a mildly reduced TLCO. Thus, in case of low VA, a seemingly "normal KCO" must be interpreted as an abnormal gas transfer. The most common clinical conditions associated with an abnormal TLCO are characterised by a limited number of patterns for VA and KCO: incomplete lung expansion, discrete loss of alveolar units, diffuse loss of alveolar units, emphysema, pulmonary vascular disorders, high pulmonary blood volume, alveolar haemorrhage.

Adult↗
PubMed1976

Idiopathic pulmonary fibrosis. Clinical, histologic, radiographic, physiologic, scintigraphic, cytologic, and biochemical aspects.

Idiopathic pulmonary fibrosis is a fatal disorder that starts as an alveolitis and progresses to interstitial fibrosis. Correlative morphologic, physiologic, and biochemical studies in 29 patients have shown that the inflammatory process in best followed by serial bronchoalveolar lavage and 67 Ga citrate scanning, and the fibrotic process is best followed by quantitation of the exercise-induced drop in arterial oxygen tension per unit of oxygen consumed. Although biopsies in idiopathic pulmonary fibrosis seem to show increased amounts of fibrotic tissue, biochemical studies suggest that the disease is probably one of collagen rearrangement rather than collagen increase. Perhaps becasue of this, peripheral lymphocytes of these patients recognize collagen as "non-self" and, when exposed to it in vitro, produce lymphokines and cell lysis. The fibrotic process is probably irreversible, but the inflammatory and immune processes that cause it may be amenable to therapy if diagnosed early.

Adult↗
PubMed1976

[Respiratory function in chronic obstructions of the large pulmonary arteries (study of 30 cases].

If diagnosis of chronic thromboses of pulmonary arteries is usually easy at the stage of confirmed chronic pulmonary heart, it is not so when dysponea is the only symptom of the disease. The authors report 30 cases of chronic thrombosis and remark that if respiratory alkalosis is very frequent, hipoxemia is often missing. On the other hand they observe 27 times out of 28 an increase of CO2 alveoloarterial difference; measuring the CO2 difference appears a safe and reliable test for detecting chronic thrombosis. It should take place in every systematic complete examination of unexplained dyspnoea.

Adult↗
PubMedDate not supplied

Emphysema as possible explanation for the alteration of expiratory PO2 and PCO2 curves.

The present explanation of the shape of deformed expiratory partial pressure curves of O2, CO2, N2 and foreign gases as being caused by sequential convective emptying of compartments with decreasing VA/Q is put into question, since the same deformation can be observed in healthy subjects during simultaneous breathing of helium and SF6, where the SF6 curve is deformed and the helium curve has a normal shape. The high molecular weight of SF6 causes a delay of its gaseous diffusion from the peripheral air spaces of the lung. A similar delay can be caused by emphysematous changes such as a longer distance for diffusion, an increased alveolar volume and a reduction of the number of small airways, where the gas has to pass through. Different data from cross-sectional and longitudinal studies, from induced changes of bronchomotor tone, from comparison of patients with relatively pure emphysema and patients with airway obstruction and from autopsy suggest that stratification and serial inhomogeneities, caused by emphysema, are at least a reasonable, if not a better explanation for the deformation than the VA/Q concept with sequential emptying of parallel units.

Adult↗
PubMed1978

Drug-induced lung disease.

Since there are no diagnostic studies to confirm the presence of a drug-induced lung reaction the physician will make a correct diagnosis only if he is aware of the drugs which have been identified to cause pulmonary reactions and their specific manifestations. Failure to recognize a drug-induced lung disease can lead to significant morbidity and in some cases mortality. The major drug-induced lung diseases are reviewed, the drugs being presented in the context of their clinical use and the reactions on the basis of common pathogenetic mechanisms.

Adult↗
PubMedDate not supplied

Transfer factor for the lung, airway obstruction and hyperinflation in chronic bronchitis and emphysema.

The interrelationships of breath holding lung transfer factor (TCO) and transfer coefficient (KCO) with ventilatory obstruction (FEV1.0) and FEV1.0/VC) and hyperinflation (RV and RV/TLC) were studied in 37 patients with chronic nonspecific lung disease with a FEV1.0 of 1.5 litre or less classified as "bronchitic", "emphysematous" or "intermediate" according to Nash, Briscoe and Cournand (1965). No relationships could be found between TCO and airway obstruction or hyperinflation. KCO tended to decrease as RV increased (r=-0.26) and was weakly related to the FEV1.0/VC ratio in "intermediate" (r=0.34) and "emphysema" (r=0.29) patients but these relationships were nonsignificant.

Adult↗