Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

NCPH is a result of obliteration of portal veins. Many inflammatory conditions may initiate the process by causing endothelial injury. As obliteration progresses, there is local stasis and low-grade portal hypertension. In many cases, superimposed PVT occurs before portal hypertension becomes clinically evident. Hypercoagulability is an important cofactor. Diagnosis requires the exclusion of cirrhosis. Focal atrophy and nodular hyperplasia on biopsy may be a clue to the presence of small vessel obliteration. The distribution of vascular disease should be documented with Doppler ultrasound of both portal and hepatic veins. Investigation of cause should include tests for myeloproliferative and other hypercoagulable disorders, systemic diseases associated with vascular injury (eg, autoimmune diseases and toxin exposure) and local portal tract inflammatory diseases (primary biliary cirrhosis and sarcoidosis). Advances in this field will likely be made with improved diagnosis of acute and recanalized PVT using MRI, the new Acuson Sequoia ultrasound technology, and intravascular ultrasonography. Advances in the cause of PVT await studies using new and improved tests for the diagnosis of hypercoagulable states.
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PMID:Noncirrhotic portal hypertension: recent concepts. 905 82

The association of large pituitary mass, lack of clinical syndromes of pituitary hypersecretion, hypopituitarism and visual field defects suggests the diagnosis of nonfunctioning pituitary adenoma, but the same characteristics can be present in patients affected by other tumorous lesions, cysts, inflammatory processes or vascular disease. The management of these patients depends on a correct diagnosis. A 53-year-old woman was admitted for nausea, vomiting and severe hypotension. For three months she had complained of weakness, sleepness, skin-dryness and loss of weight. Imaging and endocrine evaluations revealed an intra and extrasellar mass causing hypopituitarism without diabetes insipidus. Histological examination of the tissue obtained at transsphenoidal surgery showed a Rathke's cleft cyst, surrounded by areas of noncaseous granulomatous tissue with scattered multinucleated giant cells of foreign body type, similar to a sarcoid lesion. Other systemic sarcoidosis localizations were absent. After two years of full well-being, the patient reported a sudden visual impairment, due to sarcoidosis involvment of the prechiasmatic tract of the optic nerve, that promptly improved with corticosteroid treatment. This report emphasizes the overlap of signs and symptoms between non functioning tumors and nontumoral masses of hypothalamic-pituitary region and underlines the fact that a correct diagnosis is feasible only on histopathological basis. Although, occasionally, the coexistence of Rathke'cyst with pituitary adenoma has been reported, to the best of our knowledge, this is the first report of the association between Rathke's cleft cyst and noncaseating granuloma tissue. Finally, the remission of neurolgical symptoms following corticosteroid therapy confirms this treatment as a valid medical approach and suggests its use in a short therapeutic trial when the diagnosis is doubtful.
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PMID:Granulomatous sarcoidotic lesion of hypothalamic-pituitary region associated with Rathke's cleft cyst. 912 87

To clarify role of alveolar macrophages in the pathogenesis of idiopathic interstitial pneumonia (IIP), we studied (1) the localization and expression of monocyte chemoattractant protein-1 (MCP-1) in IIP by immunohistochemistry and in situ hybridization. (2) the role of MCP-1 in macrophage recruitment to be lung, and (3) the clinical usefulness of measuring MCP-1. (1) In IIP, MCP-1 was observed in cuboidal and flattened metaplastic epithelial cells, alveolar macrophages, and vascular endothelial cells. In contrast, no epithelial cells from patients without IIP stained positive for MCP-1, although alveolar macrophages and vascular endothelial cells were labeled. MCP-1 production by epithelial cells in IIP may be caused by the metaplastic nature of the epithelial cells and may be a main cause of the irreversible progression of IIP. (2) MCP-1 levels in bronchoalveolar lavage fluid (BALF) were significantly higher in the IIP, the interstitial pneumonia due to collagen vascular disease (IP-CVD) and sarcoidosis groups than in normal controls. In the IIP group, the MCP-1 level was significantly higher than in any other patient groups. In all three groups of patients, the monocyte chemotactic activity in BALF correlated positively with the MCP-1 levels in BALF, and were neutralized by anti-MCP-1. (3) BALF MCP-1 levels were significantly higher than serum MCP-1 levels in the IIP group, and they were lower in the IP-CVD and non-specific interstitial pneumonia groups. Serum MCP-1 levels reflected the activity of interstitial lung diseases, especially during treatment with corticosteroids. These results indicate (1) that MCP-1 plays a significant role in the recruitment of monocytes into the lung in IIP, (2) that measuring MCP-1 levels both in BALF and in serum may help discriminate IIP from other types of interstitial lung diseases, and (3) that monitoring the serum MCP-1 level may be useful in estimating the activity of interstitial lung diseases.
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PMID:[Role of alveolar macrophages in the pathogenesis of idiopathic interstitial pneumonia]. 921 11

The history of patients with idiopathic pulmonary fibrosis (IPF) shows that the disease may be preceded by a viral-like illness. Although viruses have not been demonstrated, it is possible that viruses were not detected in culture because they do not replicate during latency. We investigated the presence of adenovirus in IPF and interstitial pneumonia associated with collagen vascular disease (CVD-IP), using the nested polymerase chain reaction (PCR) and in situ hybridization (ISH) for the E1A region of the adenovirus genome. Studies were performed on lung tissues obtained by transbronchial lung biopsy from 19 patients with IPF, 10 patients with CVD-IP and, for comparison, from 20 patients with sarcoidosis. The E1A DNA was present in 3 out of 19 (16%) cases of IPF, in 5 of 10 (50%) cases of CVD-IP, and in 2 of 20 (10%) cases of sarcoidosis. The incidence of E1A DNA in CVD-IP was significantly higher than that in sarcoidosis (p<0.05). In patients with IPF and CVD-IP, E1A DNA was more prevalent in patients treated with corticosteroids (6 out of 9 cases; 67%) than in those without it (2 out of 20 cases; 10%) (p<0.01). ISH studies showed that 1 out of 8 cases of IPF and CVD-IP, in which E1A DNA was detected by PCR, was positive for E1A DNA. We conclude that adenovirus E1A is unlikely to be aetiologically involved in the pathogenesis of idiopathic pulmonary fibrosis or interstitial pneumonia associated with collagen vascular disease. However, a latent adenovirus infection may be reactivated or may newly infect the host following corticosteroid administration.
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PMID:Detection of adenovirus E1A DNA in pulmonary fibrosis using nested polymerase chain reaction. 923 Feb 25

The aim of this study was to determine whether latent viral infection is associated with idiopathic pulmonary fibrosis (IPF), an interstitial lung disease whose aetiology remains to be elucidated. Cytomegalovirus (CMV) immunoglobulin G (IgG) and complement fixation (CF), Epstein-Barr (EB) viral capsid antigen (VCA) IgG, herpes simplex virus (HSV) IgG, adenovirus CF, and parainfluenza 3 virus haemagglutinin inhibition (HI) titres were measured in the serum from patients with pulmonary diseases. The study included five subject groups: 35 normal controls (aged (mean +/- SD) 38 +/- 17 yrs); 43 IPF (63 +/- 10 yrs), seven collagen vascular disease-related interstitial pneumonitis (CVD-IP) (62 +/- 12 yrs); 22 sarcoidosis (36 +/- 14 yrs); and 17 emphysema (66 +/- 11 yrs). Levels of CMV IgG in IPF (87.6 +/- 51.7) and CVD-IP (101.2 +/- 69.9) were significantly elevated compared to those in the control (30.9 +/- 24.1), sarcoidosis (34.4 +/- 38.3) and emphysema groups (40.3 +/- 24.6), whereas CMV immunoglobulin M (IgM) was generally below the limit of detection. Similarly, CMV CF titres in IPF and CVD-IP were elevated compared to those in other diseases. EB VCA IgG titres in IPF, CVD-IP and emphysema and HSV IgG in IPF were also elevated. In contrast, adenovirus CF and parainfluenza 3 HI titres demonstrated no significant difference among all of the groups investigated. Increases in cytomegalovirus immunoglobulin G and complement fixation titres with negative cytomegalovirus immunoglobulin M suggest that latent cytomegalovirus infection may be more prominent in idiopathic pulmonary fibrosis or collagen vascular disease-related interstitial pneumonitis. Together with the elevation of Epstein-Barr virus viral capsid antigen and herpes simplex virus immunoglobulin G in idiopathic pulmonary fibrosis and/or collagen vascular disease-related interstitial pneumonitis, it is rational to assume that these viruses may be implicated in the development of pulmonary fibrosis. Further study is necessary to investigate the relationship between latent viral infection and pulmonary fibrosis.
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PMID:Elevation of antibodies to cytomegalovirus and other herpes viruses in pulmonary fibrosis. 931 99

Emphasis has recently been placed on the roles of chemotactic cytokines called chemokines to explain the accumulation of inflammatory cells in the lung that may precede or accompany pulmonary fibrosis in interstitial lung diseases. We hypothesized that RANTES, a member of the C-C chemokines, is one such chemokine. Bronchoalveolar lavage was done in 20 patients with sarcoidosis, 10 patients with interstitial pneumonia associated with collagen vascular disease (CVD-IP), 10 patients with idiopathic pulmonary fibrosis (IPF), and eight healthy volunteers (HV), all of whom were never-smokers. We semiquantitated the spontaneous RANTES mRNA expression by a competitive reverse transcription-polymerase chain reaction (RT-PCR) technique, and measured the levels of RANTES protein by enzyme-linked immunosorbent assay. In all disease groups the expression of RANTES mRNA by bronchoalveolar lavage fluid (BALF) cells and the levels of RANTES protein in BALF were significantly increased compared with those in HV. Patients with sarcoidosis and CVD-IP had a significant positive correlation between the expression of RANTES mRNA by BALF cells and BALF lymphocytosis. The amounts of RANTES mRNA expressed by peripheral blood mononuclear cells and the levels of RANTES protein in serum did not differ among all study groups. Our study demonstrates the adaptability of a semiquantitative RT-PCR method for determining cytokine mRNA expression in vivo. Our results suggest that RANTES may be one of the chemokines that are involved in the mechanism for the accumulation of inflammatory cells in the lung of some distinct interstitial lung diseases.
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PMID:Expression of RANTES by bronchoalveolar lavage cells in nonsmoking patients with interstitial lung diseases. 953 40

Excessive procoagulant activity in the alveolar space may play a relevant role in the pathogenesis of pulmonary fibrosis. Hypercoagulability results from the disruption of the balance between the procoagulant and anticoagulant factors. The aim of this study was to assess the levels of molecular markers of the anticoagulant protein C (PC) pathway in the bronchoalveolar lavage fluid (BALF) and plasma of 11 patients with idiopathic pulmonary fibrosis (IPF), 14 with sarcoidosis and 16 with collagen vascular disease (CVD)-associated interstitial lung disease (CVD-ILD). Six healthy nonsmoking volunteers served as control subjects. BALF concentrations of the marker of clotting activation, thrombin- antithrombin III complex (TAT), in patients with sarcoidosis and CVD-ILD were significantly greater than those in control subjects. PC levels in BALF were markedly higher in patients with IPF (610 +/- 150 ng/ml), sarcoidosis (680 +/- 170 ng/ml), and CVD-ILD (1,580 +/- 600 ng/ml) than in control subjects (230 +/- 140 ng/ml). BALF concentrations of activated PC-PC inhibitor (APC-PCI) complex were significantly decreased in IPF (0.46 +/- 0.16 ng/ml), sarcoidosis (0. 43 +/- 0.11 ng/ml), and CVD-ILD (0.50 +/- 0.15 ng/ml) patients as compared with control subjects (1.08 +/- 0.23 ng/ml). APC-PCI/PC ratios were significantly lower in patients with IPF (2.70 +/- 1.74 ng/microg), sarcoidosis (1.94 +/- 0.82 ng/microg), and CVD-ILD (1.89 +/- 0.68 ng/microg) than in control subjects (15.91 +/- 8.45 ng/microg). Plasma levels of APC- PCI and the APC-PCI/PC ratio were also significantly decreased in patients with CVD-ILD as compared with control subjects. Overall, these findings suggest that decreased PC activation with increased procoagulant activity occurs in patients with ILD.
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PMID:Protein C anticoagulant system in patients with interstitial lung disease. 962 Sep 17

Central serous retinopathy, a disorder of healthy young men, has also been reported to occur in patients with collagen vascular disease. This is the first report discussing the occurrence of central serous retinopathy in patients with sarcoidosis. It is critical to recognize the entity because corticosteroids, used in treating sarcoidosis, can have a disastrous effect on central serous retinopathy.
Sarcoidosis Vasc Diffuse Lung Dis 1998 Sep
PMID:Sarcoidosis and central serous retinopathy: a dangerous combination. 978 99

The history of patients with idiopathic pulmonary fibrosis (IPF) shows that the disease may be preceded by a viral-like illness. Although viruses have not been demonstrated, it is possible that viruses were not detected in culture because they do not replicate during latency. We investigated the presence of adenovirus in IPF and interstitial pneumonia associated with collagen vascular disease (CVD-IP), using the nested polymerase chain reaction (PCR) and in situ hybridization (ISH) for the E1A region of the adenovirus genome. Studies were performed on lung tissues obtained by transbronchial lung biopsy from 19 patients with IPF, 10 patients with CVD-IP and, for comparison, 20 patients with sarcoidosis. The E1A DNA was present in 3 out of 19 (16%) cases of IPF, in 5 of 10 (50%) cases of CVD-IP, and in 2 of 20 (10%) cases of sarcoidosis. The incidence of E1A DNA in CVD-IP was significantly higher than that in sarcoidosis (p < 0.05). In patients with IPF and CVD-IP, E1A DNA was more prevalent in patients treated with corticosteroids (6 out of 9 cases; 67%) than in those without it (2 out of 20 cases; 10%) (p < 0.01). ISH studies showed that 1 out of 8 cases of IPF and CVD-IP, in which E1A DNA was detected by PCR, was positive for E1A DNA. We conclude that adenovirus E1A is unlikely to be aetiologically involved in the pathogenesis of idiopathic pulmonary fibrosis or interstitial pneumonia associated with collagen vascular disease. However, a latent adenovirus infection may be reactivated or may newly infect the host following corticosteroid administration.
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PMID:In search of a cause of cryptogenic fibrosing alveolitis (CFA): one initiating factor or many? 1019 40

It has previously been reported that the expression of monocyte chemoattractant protein-1 (MCP-1) in the lung tissues of patients with idiopathic pulmonary fibrosis (IPF) was different from that in the tissues of patients with other interstitial lung diseases (ILDs). The aim of this study was to determine whether this difference reflects the amount of MCP-1 in the bronchoalveolar lavage fluid (BALF) or serum of patients with ILD, and whether such a correlation, if it exists, is clinically useful. MCP-1 concentrations in the BALF and sera were evaluated in 86 patients with ILDs including IPF, acute interstitial pneumonia, interstitial pneumonia with collagen vascular disease (IP-CVD), chronic interstitial pneumonia (CIP), bronchiolitis obliterans-organizing pneumonia, sarcoidosis, hypersensitivity pneumonitis, and in 10 normal healthy volunteers who were controls (NC). BALF MCP-1 levels were significantly elevated in the IPF, IP-CVD, CIP and sarcoidosis groups compared with the NC group. The level in the IPF group was significantly higher than that in any other patient group. Serum MCP-1 levels in the IPF, IP-CVD, CIP and sarcoidosis groups were significantly higher than the NC group. No statistical difference was found in serum MCP-1 levels between the IPF, IP-CVD and CIP groups. BALF MCP-1 levels were significantly higher than serum MCP-1 levels in the IPF group and lower than in the IP-CVD and CIP groups. Serum MCP-1 levels correlated with the clinical course of ILD treated with corticosteroid therapy. These results show that measurement of monocyte chemoattractant protein-1 levels in both bronchoalveolar lavage fluid and serum may be helpful in discriminating idiopathic pulmonary fibrosis from other types of interstitial lung disease and that monitoring of serum monocyte chemoattractant protein-1 may be useful for predicting the clinical course of interstitial lung diseases.
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PMID:Clinical significance of MCP-1 levels in BALF and serum in patients with interstitial lung diseases. 1051 17


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