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PubMed1988

Measures of the inflammatory response in cryptogenic fibrosing alveolitis.

Cryptogenic fibrosing alveolitis (CFA) is characterized by interstitial fibrosis and parenchymal inflammation. Eleven patients with CFA (10 proved by lung biopsy) were followed over 2 yr using clinical symptoms, radiographic change, and pulmonary function tests to adjust their treatment. Lung lavage, positron camera (PET) measurements of regional extravascular lung density (Dev), pulmonary blood volume (Vb), and the metabolic rate for 18F-deoxyglucose (MRglc), clearance of 99mTc-diethylenetriaminepentacetate (99mTc-DTPA) aerosol, and lung uptake of 67Ga were measured initially and at the end of the first year to give a profile of the inflammatory response. Compared with normal subjects, there was an increased percentage of neutrophils and eosinophils in the lung lavage, increased Dev (p less than 0.002) with no significant difference in Vb, increased MRglc (p less than 0.02), 99mTc-DTPA clearance (p less than 0.002), and 67Ga uptake (p less than 0.02). The smallest increases in Dev were seen in the two patients with most destruction shown by lung biopsy. There were inverse correlations between Dev and both FVC and TLC, but a direct correlation between Vb and transfer factor. 99mTc-DTPA clearance changed concordantly with clinical status and radiographic and respiratory function changes during the first year. If glucose utilization (MRglc) remained in the normal range between the initial and first yearly assessment, the patient improved or remained stable during the second year as shown by clinical status and radiographic and respiratory function measurements. If it rose or remained high, the patient's condition deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1977

Pulmonary mechanics in fibrosing alveolitis: the effects of lung shrinkage.

Pulmonary and airway mechanics were studied in 8 patients with severe fibrosing alveolitis. In this disease, the number of functioning alveoli is probably considerably decreased, but static compliance was low even when related to the decreased lung volume. Lung recoil pressures toward full inflation were high but were not increased at and below functional residual capacity. Airway function was broadly normal for lung recoil pressure but supernormal for absolute lung volume. Analysis of model pressure-volume and maximal flow-volume curves showed that (1) these features could be produced simply by replacement of some units by indistensible fibrous tissue and retention of normal function of the surviving alveoli, respiratory muscles, chest wall, and airways; (2) increased lung tissue volume may prevent an increase in lung recoil pressures in the lower part of the vital capacity; and (3) the decreased lung volume could result in a decrease in upstream conductance without structural change in the airways. Measurement of lung compliance, even when corrected for the decreased lung volumes, may not distinguish between loss of units (lung "shrinkage") and abnormal distensibility of the functioning alveoli, but the latter is likely if maximal expiratory flow is excessive in relation to the lung volume expressed as per cent vital capacity.

Adult↗
PubMed1981

Cryptogenic fibrosing alveolitis. Relationships of pulmonary physiology and bronchoalveolar lavage to response to treatment and prognosis.

A minority of patients with cryptogenic fibrosing alveolitis (idiopathic pulmonary fibrosis) respond to treatment with corticosteroids. The purpose of this study was to identify factors other than histologic features that relate to responsiveness and prognosis. An analysis of 120 patients on whom data were prospectively collected is reported. The relationships between pulmonary function measurements, differential cell counts on bronchoalveolar lavage fluid, physiologic response to treatment, and survival are discussed. Patients responding to treatment with corticosteroids or immunosuppressive drugs had more severe initial impairment of the FVC (p less than 0.0001) and a more recent onset of disease (p less than 0.001). Lavage cell counts showed that increased proportions of lymphocytes were associated with responsiveness to corticosteroids and good prognosis (p less than 0.001), whereas increased eosinophils or increased neutrophils without increased lymphocytes were associated with failure to respond (p less than 0.025), and increased eosinophils were associated with a greater likelihood or progressive deterioration (p less than 0.05). Life table comparisons of survival in different groups showed improved survival in patients responding to treatment (p less than 0.05). Among nonresponders, those with more severe impairment of the FVC had shorter survival (p less than 0.05). We concluded that physiologic and bronchoalveolar lavage data allow predictions of responsiveness to treatment and prognosis that are of practical value to clinicians.

Adult↗
PubMed1984

Definition and clinical relevance of antibodies to nuclear ribonucleoprotein and other nuclear antigens in patients with cryptogenic fibrosing alveolitis.

Antinuclear antibodies (ANA) were studied in 122 patients with cryptogenic fibrosing alveolitis (CFA) and compared with age- and sex-matched control subjects. Fluorescent ANA were detected in 32% of the patients and showed a correlation with the presence of a systemic connective tissue disease; ANA were present in 6% of the control subjects, 21% of the patients with CFA alone, and 46% of those with CFA and an associated connective tissue disease. Antibodies to the defined nuclear antigens: deoxyribonucleic acid (DNA), nuclear ribonucleoprotein (nRNP), the Sm antigen, and Sjögren's syndrome A and B antigens (SS-A and SS-B) were examined to establish whether their presence was diagnostic of the associated diseases. Antibodies to DNA and Sm antigens identified 3 patients with CFA and systemic lupus erythematosus. The frequency of antibodies to SS-A and SS-B did not differ from that in control subjects. Antibodies to nRNP, detected in 15 (12%) of the patients (at a high titer in 5), were associated with females, the presence of Raynaud's phenomenon, and rheumatoid factor in the serum. However, despite the detection of these antibodies, none of these patients met fully the proposed criteria for the diagnosis of mixed connective tissue disease.

Adult↗
PubMed1987

The value of serial bronchoalveolar lavages in assessing the clinical progress of patients with cryptogenic fibrosing alveolitis.

This study tested the hypothesis that changes in bronchoalveolar lavage (BAL) inflammatory cell profiles reflect the clinical progress of patients with cryptogenic fibrosing alveolitis (CFA) when followed for substantial periods of time with or without any form of treatment. Two or more bronchoalveolar lavages (mean, 3; maximum, 5) were performed on each of 32 patients who were followed for periods as long as 7 yr (mean, 2.5 yr, median, 4 yr). The majority were studied before and during treatments with prednisolone alone or with prednisolone and cyclophosphamide. A total of 90 lavages were performed, and the changes in BAL inflammatory cell percentage counts were compared with defined categories of clinical progress. At initial lavage, 97% of the patients had an increased percentage of at least 1 BAL cell type. On follow-up, 12 patients showed definite and sustained clinical improvement, and their serial lavage cell counts tended to return towards normal. Falls in neutrophils were significant in patients responding to prednisolone, whereas falls in eosinophils were significant in those responding to cyclophosphamide. By contrast, in patients who failed to improve, neutrophil and eosinophil counts tended to remain elevated. However, several nonresponders appeared to have clinically stable disease, demonstrating that persisting granulocytes are not necessarily paralleled by clinical deterioration. Consecutive BAL cell counts in the pair of samples before and after introduction of prednisolone showed no overall change in any lavage cell type to suggest that the drug has a general effect independent of clinical progress. A similar comparison for cyclophosphamide showed falls in eosinophil percentage counts, but these were mainly responders.(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchi↗
PubMed2002

Histopathologic subsets of fibrosing alveolitis in patients with systemic sclerosis and their relationship to outcome.

Fibrosing alveolitis associated with systemic sclerosis (FASSc) has a better prognosis than idiopathic pulmonary fibrosis. In view of recent reports that idiopathic nonspecific interstitial pneumonia (NSIP) has a better prognosis than idiopathic usual interstitial pneumonia (UIP), we classified histologic appearances of surgical lung biopsies performed in 80 patients with FASSc. NSIP (n = 62, 77.5%), subcategorized as cellular NSIP (n = 15) and fibrotic NSIP (n = 47) was much more prevalent than UIP (n = 6), end-stage lung disease (ESL, n = 6), or other patterns (n = 6). There were 25 deaths (NSIP 16/62, 26%; UIP/ESL 6/12, 50%). Five-year survival differed little between NSIP (91%) and UIP/ESL (82%); mortality was associated with lower initial carbon monoxide diffusing capacity (DL(CO)) and FVC levels (p = 0.004 and p = 0.007, respectively). Survival and serial FVC and DL(CO) trends did not differ between cellular and fibrotic NSIP. Increased mortality in NSIP was associated with lower initial DL(CO) levels (p = 0.04), higher BAL eosinophil levels (p = 0.03), and deterioration in DL(CO) levels during the next 3 years (p < 0.005). We conclude that NSIP is the histopathologic pattern in most patients with FASSc. However, outcome is linked more strongly to disease severity at presentation and serial DL(CO) trends than to histopathologic findings.

Adult↗
PubMed1999

The involvement of Fas-Fas ligand pathway in fibrosing lung diseases.

Pulmonary fibrosis begins with alveolitis, which progresses to destruction of lung tissue and excess collagen deposition. This process could be the result of DNA damage and a form of apoptosis. Therefore, we hypothesized that Fas ligand (FasL), which induces apoptosis in cells expressing Fas antigen (Fas), is associated with pulmonary fibrosis. We examined frozen lung tissues from seven patients with idiopathic pulmonary fibrosis (IPF), and bronchoalveolar lavage fluid (BALF) cells from 19 patients with IPF and from 17 patients with interstitial pneumonia associated with collagen vascular diseases (CVD-IP). We used five frozen lungs with normal lung parenchyma and BALF cells from 10 patients with solitary pulmonary nodule as controls. Reverse transcription-polymerase chain reaction (RT-PCR) showed that FasL messenger RNA (mRNA) was expressed in BALF cells from all patients with IPF and from 15 of 16 patients with CVD-IP. FasL mRNA was not detected in BALF cells except in one of 10 controls. RT in situ PCR detected FasL mRNA in inflammatory cells in BALF from patients with IPF. Immunohistochemistry detected FasL protein in infiltrating lymphocytes and granulocytes in all of seven frozen lung tissues of IPF, but in none of five control lung tissues. Additionally, the expression of Fas appeared to be upregulated in bronchiolar and alveolar epithelial cells in IPF compared with normal lung parenchyma by immunohistochemistry. We conclude that Fas and FasL were upregulated in fibrosing lung diseases and may associate with DNA damage or apoptosis of bronchiolar and alveolar epithelial cells in this disorder.

Adult↗
PubMed1980

A comparative double-blind study of tiaprofenic acid and aspirin in the treatment of muscular rheumatism, fibrositis, sprains and soft tissue injuries in general practice.

Analgesic and anti-inflammatory properties of tiaprofenic acid 200 mg t.d.s. were compared with those of aspirin 600 mg t.d.s. in 100 patients in general practice suffering from muscular rheumatic pain, fibrositis, sprains and soft tissue injuries. Tiaprofenic acid was shown to be better than aspirin in relieving pain by clinical assessment although both drugs were equally effective according to patients daily assessment. It was not possible to demonstrate any anti-inflammatory action by reduction of swelling, but this was only present in 20% of patients initially. Side-effects, none serious, were similar in both groups.

Adult↗
PubMed1986

Dysthymic disorder and rheumatic pain modulation disorder (fibrositis syndrome): a comparison of symptoms and sleep physiology.

It has been suggested that "fibrositis" or rheumatic pain modulation disorder (RPMD) is a variant of depressive illness. Both disorders are associated with abnormalities in sleep physiology. Since the clinical features of RPMD do not meet all the criteria for a major depressive disorder, the symptoms and sleep physiology in subjects with dysthmic disorder (DSM III criteria) (N = 6), and RMPD (N = 6) were compared, in order to determine the similarity between the two groups. The sleep physiology in dysthymic disorder was first examined over three consecutive nights since a systematic evaluation of the sleep physiology in this group of disorders has not yet been reported. All dysthymic patients showed episodic bursts of high-amplitude (75-150 microvolts) theta (3-5 Hz) bursts in stage 2 sleep, and REM onset latency was abbreviated only on night 2. The theta bursts have not been previously reported, and may be an early marker of disorganization of non-REM sleep in the dysthymic subjects. The comparison of the two groups revealed that RPMD subjects reported more pre- and post-sleep pain (p less than 0.01), lighter sleep (p less than 0.01), and more physical ailments during sleep (p less than 0.01), and had more alpha (7-11.5 Hz) in non-REM sleep (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Venous and arterial changes in pulmonary veno-occlusive disease, mitral stenosis and fibrosing mediastinitis.

The pathogenesis of pulmonary veno-occlusive disease (PVOD) is not known. The diagnosis of PVOD frequently relies on its histological changes since it is often difficult to distinguish clinically from primary pulmonary hypertension. This study carried out a systematic analysis of the pulmonary venous and arterial remodelling that occurs in PVOD (n=5) and compared these changes to two other diseases affecting the pulmonary veins, mitral stenosis (MS; n=6) and fibrosing mediastinitis (FM; n=2), using established morphometric techniques. In PVOD, pronounced intimal and adventitial thickening were noted in veins of all sizes and arterialization of veins >50 microm external diameter was found. Similar changes were evident in the arterial wall, but intimal thickening was less severe than in the veins and medial thickening was more pronounced in arteries <300 microm external diameter. Eccentric intimal fibrosis of the veins was also noted for the first time in PVOD, although this feature occurred less frequently (approximately one third) than in MS. Less pronounced structural remodelling was also encountered in the veins in cases of MS and FM. The severity of the venous changes in PVOD may aid its diagnosis and lend insight into its pathogenesis. However, the similarity of the vascular changes in each form of venous hypertension also suggests that pathology alone may not always differentiate between these disease states. The similarity of the vascular changes in the three forms of venous hypertension suggests that, as in pulmonary artery hypertension, pressure, per se, is one of the triggers to vascular remodelling.

Adult↗
PubMed2002

Intracellular glutathione and bronchoalveolar cells in fibrosing alveolitis: effects of N-acetylcysteine.

Extracellular glutathione deficiency and exaggerated oxidative stress may contribute to the pathogenesis of fibrosing alveolitis (FA). High-dose N-acetylcysteine (NAC) supplementation partially reverses extracellular glutathione depletion and oxidative damage, but effects on intracellular glutathione are unknown. Intracellular total glutathione (GSHt) and activation of bronchoalveolar lavage cells (BAC) obtained from 18 FA patients (9 males, aged 52+/-2 yrs), before and after 12 weeks of oral NAC (600 mg t.i.d.), were assessed. Eight healthy nonsmokers (2 males, aged 36+/-6 yrs) served as a control group. Intracellular GSHt was decreased in FA (1.57+/-0.20 nmol 1x10(6) BAC(-1) versus 2.78+/-0.43 nmol x 10(6) BAC(-1)). After NAC treatment, the intracellular GSHt content increased (1.57+/-0.20 versus 1.87+/-0.19 nmol x 1 x 10(6) BAC(-1)). The spontaneous oxidative activity of BAC decreased after NAC treatment (2.7+/-0.8 versus 1.0+/-0.2 nmol x 1 x 10(6) BAC(-1) x h(-1)). Interleukin-8 concentration (82.1+/-31.5 versus 80.0+/-22.6 pg x mL bronchoalveolar fluid (BALF), nonsignificant (NS)) and myeloperoxidase activity (1.93+/-0.64 versus 1.55+/-0.47 mU x mL(-1) BALF, NS) did not change significantly, but were found to be inversely correlated to intracellular GSHt. In conclusion, high-dose N-acetylcysteine supplementation increases intracellular glutathione levels slightly. This increase is associated with a mild reduction of oxidative activity but not with a reduction of bronchoalveolar cell activation in these patients.

Acetylcysteine↗
PubMed2005

Genetics of fibrosing lung diseases.

Genetic studies in familial lung fibrosis have demonstrated an association with surfactant protein C genes: two mutations have been found resulting in protein misfolding and causing type-II epithelial cell injury. Remarkably, different histological patterns were observed in the affected subjects, suggesting the influence of modifier genes and/or environmental factors. Surfactant protein C gene variations have not, however, been associated with sporadic cases, i.e. idiopathic pulmonary fibrosis (IPF). Susceptibility to IPF probably involves a combination of polymorphisms related to epithelial cell injury and abnormal wound healing. To date, the genetic associations with IPF that have been reported in different cohorts include the genes encoding tumour necrosis factor (TNF; -308 adenine), interleukin-1 receptor antagonist (+2018 thymidine) and association with severity and progression (interleukin-6/TNF receptor II and transforming growth factor-beta1 (TGFB1; +869 cytosine)), but none of these associations have been replicated by others. Unlike in IPF, immunological inflammation seems to be more prominent in the pathogenesis of scleroderma lung fibrosis, being an autoimmune disease with specific autoantibodies, such as antitopoisomerase antibodies, in patients with diffuse lung disease, and anticentromere antibodies, in patients with pulmonary vascular disease. Antitopoisomerase antibody positivity is associated with the carriage of human leukocyte antigen DRB1*11 and DPB1*1301 alleles, suggesting the recognition of a specific amino-acid motif. Extended haplotype analysis also supports the conclusion that TNF may be the primary association with anticentromere positivity. Intriguingly, associations with TGFB1 and genes involved in extracellular matrix homeostasis have been reported in this disease. In conclusion, significant steps forward have been taken in the understanding of the genetic contribution to fibrosing lung diseases, but major challenges lay ahead. It is the present authors' opinion that only a combined approach studying large numbers of familial and sporadic cases, all clinically well phenotyped, using multiple distinct cohorts, and genotyped according to relevant gene ontologies will be successful. It will be necessary to be particularly vigilant with regard to phenotype; the absence of very strong reproducible associations may be because of the rigidity of phenotype definition, coupled with the possibility that idiopathic pulmonary fibrosis may still be a heterogeneous group of diseases, despite the more rigid definition set out by the European Respiratory Society/American Thoracic Society statement.

Hermanski-Pudlak Syndrome↗
PubMed1994

Mechanisms of increased epithelial lung clearance of DTPA in diffuse fibrosing alveolitis.

The aim of this study was to elucidate possible mechanisms of increased epithelial lung clearance in diffuse fibrosing alveolitis (DFA). We investigated the relationships between epithelial lung clearance as assessed by the clearance of aerosolized 99mTc-diethylene-triamine-penta-acetic acid (RC-DTPA), luminal alveolitis as assessed by bronchoalveolar lavage, and pulmonary function, in 30 nonsmokers with DFA. In 14 of these patients, RC-DTPA and lung function were determined before and during therapy with prednisolone (0.5 mg.kg-1 daily). RC-DTPA was higher in patients with DFA (4.45 +/- 2.50%.min-1) than in normal subjects (1.18 +/- 0.31%.min-1). RC-DTPA did not correlate with the number of alveolar neutrophils, but correlated positively with the number of alveolar lymphocytes, and negatively with vital capacity (VC). RC-DTPA decreased from 6.1 +/- 2.8 to 3.8 +/- 1.9%.min-1 with prednisolone. RC-DTPA before prednisolone correlated positively with the prednisolone-associated improvement in VC. We conclude that in patient with DFA, RC-DTPA is increased, and decreases but does not return to normal with corticosteroid therapy. Our data suggest that in DFA the increase in RC-DTPA could be related to the recoil-induced stretch of the respiratory epithelium and to alveolar lymphocytic inflammation.

Aerosols↗
PubMed2001

Autoantibodies in cryptogenic fibrosing alveolitis.

The pathogenesis of cryptogenic fibrosing alveolitis (CFA) involves injury, an immune/inflammatory response and fibrosis. The cause of the injury is unknown, but the identification of serum autoantibodies makes an autoimmune aetiology attractive. The core study on which this commentary is based used novel cloning and serum screening technologies in order to identify new public and private autoantibodies in sera from 12 patients with CFA. Largely negative conclusions were drawn from that study. However, we suggest that the prevalence of autoantibodies may have been underestimated, that the study was timely and that this approach is worth pursuing further.

Autoantibodies↗
PubMed2001

Private specificities can dominate the humoral response to self-antigens in patients with cryptogenic fibrosing alveolitis.

BACKGROUND: The pathogenetic mechanisms that underlie the interstitial lung disease cryptogenic fibrosing alveolitis (CFA) may involve an immunological reaction to unidentified antigens in the lung, resulting in tissue damage. METHOD: In order to identify the range of target autoantigens, we used expression cloning, employing serum from an index patient as the probe against an expressed cDNA library that was derived from a tumour cell line. We screened over 5 x 105 recombinants and obtained sequence information on three antigens that had provoked strong responses with immunoglobulin heavy chain class switching, presumably as a consequence of T-cell recognition. RESULTS: All of the antigens were identifiable by comparison with sequence data from the US National Center for Biotechnology Information. Alanyl tRNA synthetase (ATS) was picked on six occasions; five of these incidences reflected independent recombination events, indicating that the library was not biased. Antibodies to ATS (anti-PL-12) represent the most common reactivity that defines the antisynthetase syndrome, which is typically expressed as polymyositis, dermatomyositis and interstitial lung disease (ILD). The index patient never showed symptoms other than those associated with alveolitis, even though sera obtained from him over a period of 2 years contained antibodies with the same specificity. Autoantibodies to ATS were never detected in serial bleeds from 11 other patients with CFA, and neither did we detect antibodies to the other two antigens identified from the serum of the index patient. CONCLUSION: The humoral response in patients with CFA can be dominated by autoantibodies with private specificities. This suggests that the antibodies are epiphenomenal and are a secondary feature of tissue damage induced by some other mechanism.

Antibody Diversity↗
PubMed2001

Tumour necrosis factor-alpha production in fibrosing alveolitis is macrophage subset specific.

BACKGROUND: Previous studies have revealed that tumour necrosis factor (TNF)-alpha is upregulated in fibrosing alveolitis (FA) in humans. The aim of this study was to compare the TNF-alpha secretory profile of alveolar macrophages (AMs) and peripheral blood monocytes (Mos) of patients with cryptogenic FA and systemic sclerosis (SSc), a rheumatological disorder in which lung fibrosis can occur. In particular, we wished to assess whether TNF-alpha levels differ between SSc patients with FA (FASSc) and a nonfibrotic group. METHODS: The reverse haemolytic plaque assay was used to evaluate the secretion of cytokine at a single cell level while immunostaining allowed subtyping of AMs and Mos. RESULTS: This study demonstrated a difference in total TNF-alpha levels produced by AMs when the levels in subjects with FA (cryptogenic FA and FASSc) were compared to levels in either SSc patients without FA (P = 0.0002) or normal healthy controls (P < 0.001). In addition, AMs from patients with FASSc secreted more TNF-alpha than those of patients with no FA (P = 0.003). In contrast, there were no significant differences in Mo TNF-alpha secretion between the groups. A positive correlation was found between total TNF-alpha level and number of neutrophils obtained by bronchoalveolar lavage from patients with FA (r = 0.49, P < 0.04). Finally, it was demonstrated that there was significant heterogeneity of TNF-alpha secretion and that a numerically significant subset of mononuclear phagocytes, RFD7, was responsible for more than 80% of TNF-alpha production. CONCLUSION: By demonstrating the primary cell source of TNF-alpha in FASSc, more accurately targeted, possibly localized, anti-TNF strategies might be employed with success in the future.

Animals↗
PubMed2000

Rat alveolar and interstitial macrophages in the fibrosing stage following quartz exposure.

Exposure to quartz induces pulmonary inflammation and development of fibrosis. In order to study the fibrosing process, we investigated morphology, function and phenotype of alveolar (AMs) and interstitial (IMs) macrophages at an early stage of fibrosis in rats. Rats were exposed by intratracheal instillations of 10 mg quartz (n=8) or saline (n=8) and studied 3 months later. AMs were obtained by bronchoalveolar lavage and IMs by mechanical fragmentation, followed by enzymatic digestion of lung tissue. Histology revealed subacute silicosis, with early focal fibrosis and alveolar lipoproteinosis. AM quartz exposure increased phagocytic activity and expression of major histocompatibility complex (MHC) Ia antigens, the latter being associated with cellular antigen presenting capacity. IM had an even more pronounced expression of MHC than AM after quartz exposure. Both macrophage fractions had a higher expression of OX-42 (complement receptor 3, CR3) than controls, but the increase in the IM fraction might be explained by the remaining AM in the IM fraction. Exposed AM adhered less to extracellular matrix components (vitronectin and fibronectin) than controls. In contrast, the adhesion of IM to vitronectin increased after exposure. Besides increased adhesion, the effects on IM were scarce. Our results therefore do not support the hypothesis that IM has a key role in the process of inflammation, including fibrosis.

Animals↗
PubMed1994

Relief of superior vena cava syndrome due to fibrosing mediastinitis using the Palmaz stent.

Relief of superior vena cava (SVC) syndrome due to non-neoplastic mediastinal disease presents a formidable challenge. Long-term patency of surgically created bypass grafts has been poor, and the morbidity associated with these procedures is substantial. We report a case of SVC syndrome, caused by fibrosing mediastinitis, treated with Palmaz balloon expandable intravascular stents. Intravascular stents are a promising alternative for relief of non-neoplastic SVC obstruction.

Adult↗