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A case of idiopathic pulmonary fibrosis, presenting as a single segmental perfusion defect without a corresponding ventilatory abnormality in a patient suspected of having a pulmonary embolus is reported. This has not been reported previously in the literature.
A report is presented of an 85-yr-old woman who developed severe pulmonary fibrosis while receiving tocainide for treatment of ventricular arrhythmias. Severe bilateral interstitial fibrosis was documented in this patient by open lung biopsy and at autopsy. Review of the literature revealed other cases with an association between the use of tocainide and the development of pulmonary complications such as pulmonary fibrosis and interstitial pneumonitis, and suggested that clinical improvement occurs when the correct diagnosis is made early and tocainide therapy is stopped immediately. Because tocainide is currently being widely used for the treatment of ventricular arrhythmias, the pulmonary status of patients receiving tocainide should be monitored closely. Hopefully, awareness of this potential complication of tocainide therapy will minimize the number of cases of serious pulmonary toxicity.
Herein we report a case of pulmonary fibrosis secondary to chronic administration of nitrofurantoin following radical surgery for a bladder tumor and urinary intestinal diversion. The patient developed pulmonary superinfection and acute respiratory failure. She initially responded to treatment, but relapsed after two weeks. She died from the underlying disease.
Orally administered malotilate was studied as a protective anti-fibrotic agent with respect to experimentally induced pulmonary fibrosis in rats. Intraperitoneally-injected carbon tetrachloride (CCI4) significantly increased the lung weight to body weight ratio, lung total protein and total hydroxyproline content, while the relative protein content of the lungs decreased. CCI4) induction caused diffuse alveolar damage and inflammatory changes mimicking usual interstitial pneumonia with interstitial fibrosis. The morphological findings suggest a primary toxic effect on the lungs. Treatment with malotilate completely normalized the lung weight to body weight ratio, lung total and relative protein content and total hydroxyproline content. Morphologically, malotilate seemed to prevent the exudative inflammatory changes and interstitial fibrosis, but not the primary toxic effect of CCI4 on the capillary endothelium or the alveolar epithelium, the result of which was diffuse alveolar damage. It is concluded that malotilate may be a useful drug for the prevention of pulmonary fibrosis.
OBJECTIVE: To investigate the effect of murine interferon-gamma (IFN-gamma) transgene expression on bleomycin-induced pulmonary fibrosis in mice. METHODS: 6 - 8 week aged pathogen-free male ICR mice were treated with bleomycin (3 mg/kg weight in 70 micro l) by intranasal instillation on day 0 in the model group. Adenoviral vector with murine IFN-gamma cDNA (AdCMVmIFN-gamma) 5 x 10(8) plague forming unit (pfu) was administrated via nastril instillation 48 h before bleomycin treatment in the preventive therapeutic group, but 72 h after bleomycin treatment in the therapeutic group. Mice treated with a same volume of normal saline (NS) and a same dosage of sham recombinant adenoviruses (AdCMVNull) served as controls. The animals were weighted on day 0, 7, 14, and sacrificed on day 14. Bronchial alveolar lavage fluid (BALF) and lungs were recovered. The right lung was stained with either hematoxylin-eosin or masson. The left lung was weighted, and its content of hydroxyproline (HYP) was measured by HCl acid hydrosis method. The IFN-gamma concentration in BALF was determined with enzyme-linked immunosorbent assay. RESULTS: The concentrations of IFN-gamma in BALF from the AdCMVmIFN-gamma treated groups were remarkably increased, (21,250 +/- 6,497) pg/ml and (21,000 +/- 5,451) pg/ml in the IFN-gamma transgenetic preventive therapeutic group and the therapeutic group respectively. IFN-gamma was undetectable in BALF from other groups. Mice in the two groups treated with AdCMVmIFN-gamma had statistically significant weight loss (P < 0.05), higher HYP content (P < 0.05), and tended to have more severe alveolitis and pulmonary fibrosis (P = 0.07) as compared with those in other groups. CONCLUSIONS: (1) mIFN-gamma could be overexpressed in airway and alveolar epithelium by locally administrated AdCMVmIFN-gamma. (2) Early mIFN-gamma transgene expression via adenoviral vector in this bleomycin model aggravated alveolitis and fibrosis to some degree.
Between November 1983 and August 1989, we performed single-lung transplantation for end-stage pulmonary fibrosis in 20 patients. Nine patients (45 percent) who survived for more than one year form the basis of this report. Before surgery, the nine survivors had severe restrictive lung disease, with a mean (+/- SD) vital capacity (VC) of 43 +/- 9 percent, a forced expiratory volume in one second (FEV1) of 50 +/- 9 percent, and a single-breath diffusing capacity (DLCO) of 36 +/- 9 percent of predicted values. One year after transplantation, the patients' VC had reached 69 +/- 10 percent, FEV1 79 +/- 15 percent, and DLCO 62 +/- 16 percent of predicted values. Relative perfusion to the transplanted lung rose from 63 +/- 14 percent (three days after surgery) to 77 +/- 7 percent within three months and stayed constant or increased slightly thereafter. Before surgery, despite supplemental oxygen at flow rates varying from 1 to 9 liters per minute, none of the patients could exercise beyond stage 1/2 (2.7 km [1.7 miles] per hour, 5 percent grade) on a modified Bruce treadmill-exercise protocol. All eight patients tested one year or more after transplantation achieved at least stage 1 (2.7 km [1.7 miles] per hour, 10 percent grade), and usually a higher stage, without supplemental oxygen. Arterial oxygen tension returned to normal values in most patients (87 +/- 13 mm Hg), and supplemental oxygen, which all patients required before surgery, was no longer needed by any patient after transplantation. We conclude that in carefully selected patients with end-stage pulmonary fibrosis, single-lung transplantation is an effective treatment.
Dimethyl sulfoxide (DMSO), a putative anti-inflammatory agent and free radical scavenger, was shown to protect against acute bleomycin-induced pulmonary fibrosis in the rat (Pepin and Langner, Biochem. Pharmacol., 34 (1985) 2386). We examined the effect of DMSO on bleomycin-induced pulmonary toxicity in Swiss outbred mice and Sprague-Dawley rats, and on butylated hydroxytoluene (BHT)-induced pulmonary toxicity in Swiss outbred mice. Bleomycin (BL)-induced mortality in mice (20% at 0.1 units BL) and rats (50% at 1.5 units BL) was increased to 100% by daily DMSO (5 g/kg 50% in saline). Similar DMSO treatment after lower doses of bleomycin (1 unit BL in rats and 0.075 or 0.050 units in mice) increased lung hydroxyproline content in the rat but had no effect in the mouse. Lung hydroxyproline content in mice 14 days after 400 mg/kg BHT in corn oil was also slightly increased by daily DMSO at 5 g/kg, but not at 1 or 2 g/kg. Daily DMSO (5 g/kg) did not alter cellular proliferation [( 14C]thymidine incorporation into pulmonary DNA) in the lung at 2 or 5 days after BHT. Thus, we found that DMSO potentiated the lethality of bleomycin, and potentiated or had no effect on bleomycin or BHT-induced pulmonary fibrosis in the rat and mouse.
In order to assess the role of collagens I and IV during the angiogenic process associated with bleomycin-induced pulmonary fibrosis in rat, in situ hybridization and immunocytochemical studies were carried out. An increased expression of collagen IV was observed before an enhanced expression of collagen I after intratracheal instillation of bleomycin. Deposits of both collagen types were detected on the 21st day after treatment with bleomycin, surrounding the new blood vessels formed during the fibrotic process. At this time, the presence of new lymphatic vessels was associated uniquely with deposition of collagen I. These observations lead us to conclude that, at least during pulmonary fibrosis, lymphangiogenesis takes place after blood angiogenesis.
5 patients suffering from progressive scleroderma with interstitial pulmonary fibrosis have been treated since 1971 with D-penicillamine (Artamin) as basic therapeutic agent. All patients showed a significant tendency towards normalization of the pathological findings in regard to functional capacity of the lungs and scintigraphic and radiological assessment. These results, in our opinion, justify the recommendation of a new indication for D-penicillamine therapy, namely in cases of progressive scleroderma with interstitial pulmonary fibrosis.
We describe the case of a patient with psoriasis, peripheral and axial arthropathy, and upper lobe fibrosis. This association of findings has not, to the best of our knowledge, been described in the past. Pulmonary fibrosis is not found to be more common in people with psoriasis than would be expected in a control Veterans Administration population and, while this association may be coincidental, pulmonary fibrosis in psoriatic spondylitis should be searched for in other patients.
We have reported that tranilast, an anti-allergic drug that inhibits chemical mediator release from mast cells, suppresses bleomycin (BLM)-induced pulmonary fibrosis in mice through mechanisms other than inhibiting chemical mediator release from mast cells. The purpose of this paper is to examine the effect of tranilast on alveolar macrophage (AM) activation and on the development of fibrosis in ICR mice instilled with BLM intratracheally. Twenty eight days after the BLM instillation (0.01 mg/mouse), AM often migrated into alveolar spaces surrounding the fibrotic areas. Flow cytometry analysis for the size and density of AM (MAC-1 positive cells) suggested that AM were activated not only in the earlier acute inflammatory phase, but also in the later chronic phase. The p.o. administration of tranilast suppressed an increase of AM activity to produce reactive oxygen species in BLM-instilled mice, and it inhibited the subsequent development of pulmonary fibrosis. In vitro treatment with tranilast suppressed the reactive oxygen species production from murine peritoneal macrophages. However, several different anti-oxidants failed to inhibit the development of fibrosis. These results suggest that the activation of AM plays an important role in the development of fibrosis, and it is likely that tranilast suppresses fibrosis by inhibiting AM activation but not by scavenging reactive oxygen species.
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HLA antigens were identified in 64 patients with radiographic asbestosis and 37 matched controls with equivalent asbestos exposure but no radiographic pulmonary fibrosis. A high prevalence of HLA-B18, B27 and Cw2 was found in the controls. This result might indicate that the possessors of these HLA antigens are thus protected from the development of diffuse pulmonary fibrosis from asbestos exposure. Signs of susceptibility were not demonstrated. The radiographic severity and progression of asbestosis were not associated with any of the HLA antigens tested.
BACKGROUND: Neutrophils are thought to play an important role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). Human neutrophils contain antimicrobial and cytotoxic peptides in the azurophil granules which belong to a family of mammalian neutrophil peptides named alpha-defensins. A study was undertaken to investigate the role of alpha-defensins in the pathogenesis of IPF. METHODS: The concentrations of alpha-defensins (human neutrophil peptides (HNPs) 1, 2, and 3) in plasma and bronchoalveolar lavage (BAL) fluid of 30 patients with IPF and 15 healthy subjects were measured by radioimmunoassay. RESULTS: The concentrations of alpha-defensins in plasma, but not in BAL fluid, were significantly higher in IPF patients than in controls. BAL fluid concentrations of interleukin (IL)-8 in patients with IPF, which were significantly higher than in controls, correlated with those of alpha-defensins. An inverse relationship was seen between plasma alpha-defensin levels and the arterial oxygen tension (PaO(2)) and pulmonary function (vital capacity (%VC), forced expiratory volume in 1 second (FEV(1)), and carbon monoxide transfer factor (%TLCO)) in patients with IPF. Plasma levels of alpha-defensins also correlated with the clinical course in IPF patients with an acute exacerbation. Immunohistochemically, positive staining was observed inside and outside neutrophils in the alveolar septa, especially in dense fibrotic areas. CONCLUSION: These findings suggest that alpha-defensins play an important role in the pathogenesis of IPF, and that the plasma alpha-defensin level may be a useful marker of disease severity and activity.
Although fibrosing alveolitis is a rare complication of dermatomyositis, early detection and treatment are important in preventing pulmonary fibrosis. Anti-Jo-1 antibody, an antibody to the cellular enzyme histidyl-t-RNA synthetase, has been found to correlate closely with the subset of dermatomyositis/polymyositis associated with fibrosing alveolitis. This association is well known to rheumatologists but has received little attention in the dermatologic literature. We wish to alert dermatologists to the importance of the association of anti-Jo-1 antibody in patients with dermatomyositis and present a patient with anti-Jo-1 antibody who had Raynaud's phenomenon and mild arthritis in association with dermatomyositis and pulmonary fibrosis. We suggest screening patients with polymyositis/dermatomyositis for this antibody, to detect the population at high risk of developing pulmonary complications.