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PubMed1996

Correlation between pulmonary fibrosis and the lung pressure-volume curve.

The severity of pulmonary fibrosis is the main prognostic factor for survival of patients with interstitial lung diseases (ILD). Unfortunately, lung biopsy, which is the best method to assess fibrosis quantitatively, is done only once during the evolution of the disease. In this study we analyzed the relationship between the degree of fibrosis and the exponential constant k, derived from the lung pressure-volume curve (LPVC) in 33 patients with chronic ILD, 19 with pigeon breeder's disease (PBD), and 14 with idiopathic pulmonary fibrosis (IPF). Pulmonary function tests, including the LPVC, were obtained before biopsy. A semiquantitative histologic assessment of the severity of fibrosis was performed on lung tissues. All patients showed a decrease of total lung capacity, residual volume, compliance, and Pao2. The mean value of the constant k was 0.08 +/- 0.06. When expressed as a percent of normal values, 25 patients exhibited values of k lower than 70% of predicted; of the remaining 8 patients whose values were above 70% of predicted, 7 had PBD and only one IPF. On morphologic analysis, 19 patients displayed more than 50% fibrosis. No significant correlations were found between the extent of the lesion or severity of lung fibrosis and the conventional pulmonary function tests. By contrast, a moderate but significant correlation was found between k and the severity of lung fibrosis (r = -0.38, p < 0.05). These findings show that the shape of the LPVC, represented by the constant k, predicts the degree of lung fibrosis and could be useful in the clinical assessment and follow-up of patients with ILD.

Adolescent↗

PubMed1997

[Evaluation of treatment with cyclosporine in three patients with pulmonary fibrosis].

There are few reports on the use of cyclosporine in idiopathic pulmonary fibrosis, in experimental animals or humans. We report three patients with advanced pulmonary fibrosis in whom steroid therapy failed and that received cyclosporine in a dose of 3 to 5 mg/kg for three to five months. One patient developed systemic hypertension that subsided reducing the dose of cyclosporine. No positive changes in dyspnea were obtained and pulmonary function tests deteriorated during the treatment period. We conclude that cyclosporine treatment had no clinical benefit in these patients with pulmonary fibrosis.

Aged↗

PubMedDate not supplied

Mice with focal pulmonary fibrosis caused by monocrotaline are insensitive to urethane induction of lung tumorigenesis.

To establish the characteristics of an optimized pulmonary fibrosis model, male ICR mice were given 4 weekly sc injections of 150 or 0 mg/kg monocrotaline (MCT) and maintained without further treatment for 33 wk (Experiment 1). The final mortality in the MCT group was 64%. Epithelial cells with large bizarre nuclei and an increased incidence of alveolar/bronchiolar hyperplasias were typically observed. In areas of pulmonary fibrosis, the PCNA labeling index (LI) in the alveolar/airway epithelium was significantly elevated. DNA content analysis demonstrated a larger range (4-8C) for the ploidy pattern of alveolar epithelium with large bizarre nuclei than in the normal epithelium (2C). In Experiment 2, the relationship between pulmonary fibrosis development and lung tumorigenesis was investigated. Mice were given 4 weekly sc injections of 150 and 0 mg/kg MCT, followed by a single i.p. injection of 1,000 or 500 mg/kg urethane (UR) on week 7, then maintained without further treatment for an additional 15 wk. UR following MCT-induced inflammatory changes, fibrosis, and epithelia with large bizarre nuclei but no tumorous lesions, in spite of the fact that treatment with UR alone caused a high incidence of pulmonary tumors. Hyperplasias were seen in all groups, but the multiplicity in the combined groups tended to be decreased by the MCT pretreatment. The present study demonstrated that this new protocol is more suitable than previous one for the experimental production of pulmonary fibrosis. Furthermore, the induction of lung tumors by UR was completely depressed in mice with MCT-induced pulmonary fibrosis, suggesting that alveolar epithelial cells are resistant to this lung carcinogen under these conditions.

Animals↗

PubMed2003

Epidermal growth factor receptor tyrosine kinase inhibition augments a murine model of pulmonary fibrosis.

The inappropriate regeneration of sequentially injured epithelium is an important process leading to pulmonary fibrosis. Previous studies have shown that the epithelial expression of epidermal growth factor receptor (EGFR) is increased in fibrotic lung tissue, compared with normal lung tissue, suggesting that EGFR-mediated signaling is involved in epithelial regeneration in fibrotic lung diseases. We examined the effect of EGFR inhibition using ZD1839, a selective EGFR tyrosine kinase inhibitor (TKI), on bleomycin-induced pulmonary fibrosis in mice. ICR mice were administered a single intratracheal injection of bleomycin (5 units/kg) on day 1. ZD1839 (200 mg/kg) or vehicle alone were administered p.o. 1 h before this injection and on days 1-5 each week for 3 weeks. Lung tissue was harvested on day 21. Lung histology and collagen analysis performed on day 21 showed more severe fibrosis in the mice receiving both bleomycin and the EGFR-TKI than in the mice receiving bleomycin and the vehicle. An immunohistochemistry analysis showed that phosphorylated EGFR and proliferation cell nuclear antigen were highly expressed by the regenerated epithelial cells in the mice treated with bleomycin and the vehicle. In contrast, the expression of these antigens was attenuated in the mice treated with bleomycin and the EGFR-TKI. In vitro studies also demonstrated that the addition of ZD1839 at a concentration of < or =1 microM suppressed the proliferation of type II-like epithelial cells (A549) but not that of lung fibroblasts (IMR90). These results suggest that the inhibition of EGFR phosphorylation augments bleomycin-induced pulmonary fibrosis by reducing regenerative epithelial proliferation. Our data suggest that EGFR-TKIs should be used with caution in cancer patients with pulmonary fibrosis.

Animals↗

PubMed1995

Increased interleukin-1 receptor antagonist in idiopathic pulmonary fibrosis. A compartmental analysis.

Idiopathic pulmonary fibrosis (IPF) is a poorly understood interstitial disease that usually proves refractory to therapy and results in irreversible tissue scarring and pulmonary dysfunction. Previous investigations have suggested a number of possible mediators of inflammation and fibrosis that typify IPF. We report increases in lung interleukin-1 receptor antagonist protein (IRAP) content in patients with IPF, as compared with normal control subjects. Importantly, this increase in IRAP was not accompanied by concomitant increases in interleukin-1 beta (IL-1 beta), resulting in a local environment that may be profibrotic. Tissue homogenates and bronchoalveolar lavage fluid from patients with IPF both demonstrate elevated IRAP content compared with that in normal subjects. Immunohistochemical staining and in situ hybridization localize IRAP to hyperplastic type II pneumocytes, macrophages, and local stromal cells. Finally, in vitro studies utilizing fibroblasts isolated from patients with IPF demonstrated no difference in constitutive IRAP production compared with that in normal subjects, but they revealed an exaggerated response to stimulation with transforming growth factor-beta (TGF-beta). These findings suggest that the fibrotic tissue changes of IPF and possibly other chronic interstitial lung diseases may result in part from the local effects of IRAP, and they also demonstrate that pulmonary nonimmune cells may influence local tissue changes through the elaboration of IRAP.

Bronchoalveolar Lavage Fluid↗

PubMed2003

Idiopathic pulmonary fibrosis: a composite physiologic index derived from disease extent observed by computed tomography.

In idiopathic pulmonary fibrosis, the quantitation of disease severity using pulmonary function tests is often confounded by emphysema. We have identified the composite physiologic index (CPI) most closely reflecting the morphologic extent of pulmonary fibrosis. Consecutive patients with a clinical/computed tomography (CT) diagnosis of idiopathic pulmonary fibrosis (n = 212) were divided into group I (n = 106) and group II (n = 106). The CPI was derived in group I (by fitting pulmonary function tests against disease extent on CT) and was tested in Group II. The formula for the CPI was as follows: extent of disease on CT = 91.0 - (0.65 x percent predicted diffusing capacity for carbon monoxide [DLCO]) - (0.53 x percent predicted FVC) + (0.34 x percent predicted FEV1). In group II, the CPI correlated more strongly with disease extent on CT (r2 = 0.51) than the individual pulmonary function test (DLCO the highest value, r2 = 0.38). A subanalysis demonstrated that the better fit of the CPI was ascribable to a correction of the confounding effects of emphysema. Mortality was predicted more accurately by the CPI than by a pulmonary function test in all clinical subgroups, including a separate cohort of 36 patients with histologically proven usual interstitial pneumonia (CPI, p < 0.0005; FVC, p = 0.002; PO2, p = 0.002). In conclusion, a new CPI, derived against CT and validated using split sample testing, is a more accurate prognostic determinant in usual interstitial pneumonia than an individual pulmonary function test.

Aged↗

PubMed1993

Colchicine in the treatment of pulmonary fibrosis.

There is no standard or known optimal treatment for idiopathic pulmonary fibrosis. Corticosteroids have been used with widely variable benefit. Colchicine has been reported to suppress fibroblast growth factors and to inhibit collagen deposition. A potential role has been proposed for colchicine in the treatment of fibrotic pulmonary diseases. We retrospectively assessed the outcome of 23 patients with idiopathic pulmonary fibrosis in whom colchicine was used as empiric treatment. Eighteen patients had received prior corticosteroid therapy. By clinical and pulmonary function criteria, five patients (22 percent) improved following colchicine, nine (39 percent) remained stable, and nine (39 percent) worsened. The average duration of follow-up was 22 months. Despite limitations of this retrospective analysis, colchicine may be of benefit in pulmonary fibrosis and should be considered for further clinical trials.

Adult↗

PubMed2005

Familial idiopathic pulmonary fibrosis: clinical features and outcome.

STUDY OBJECTIVES: Familial idiopathic pulmonary fibrosis (FIPF) has been defined as idiopathic pulmonary fibrosis (IPF) occurring in two or more members of a family. The clinical course of FIPF has not been fully defined. Accordingly, the current study was undertaken to establish clinical, radiologic, and histologic features, and survival in a consecutive series of patients with FIPF. DESIGN: Retrospective analysis of clinical, radiologic, and pathologic data from a consecutive series of patients with FIPF who were seen at Mayo Medical Center. Survival in patients with FIPF was contrasted to that of previously characterized patients with nonfamilial IPF who were evaluated at our institution. SETTING: Tertiary referral medical center. PATIENTS: We screened 47 patients and family members with FIPF from 15 families who were identified between the years 1992 and 2002. We further analyzed the subgroup of FIPF patients that was composed of 27 patients from 15 families in whom the complete clinical course was monitored at our institution. MEASUREMENTS: All patients exhibited clinical features that were compatible with IPF and either compatible high-resolution CT (HRCT) scan findings or histologic evidence of usual interstitial pneumonia. Clinical data, including symptoms, physical findings, HRCT scan findings, lung function test results, biopsy results, and survival were abstracted from the clinical records. RESULTS: Compared to patients with nonfamilial IPF, patients with FIPF did not demonstrate any notable differences in clinical, radiologic, or pathologic features. We observed that the total number of affected members in a family with FIPF was a significant risk factor for earlier mortality (p = 0.0157; hazard ratio, 1.434). Overall, however, patients with FIPF had a statistically similar outcome to those patients with nonfamilial IPF. CONCLUSIONS: Although uncommon, FIPF represents a distinct syndrome, which has clinical features and patient survival rates that are similar to those of nonfamilial IPF.

Adult↗

PubMed2004

Induction of CDK inhibitor p21 gene as a new therapeutic strategy against pulmonary fibrosis.

Alveolar epithelial cells are known to be present at the primary site of lung damage in pulmonary fibrosis. Apoptosis has been implicated as being involved in epithelial cell damage and pulmonary fibrosis. Because the cyclin-dependent kinase inhibitor p21 induces G1 arrest and DNA repair and because it also prevents apoptosis in some cells, we hypothesized that p21 gene transfer may attenuate bleomycin-induced pulmonary fibrosis in mice, the pathogenesis of which likely involves epithelial cell apoptosis. Human p21 protein was expressed in mouse alveolar epithelial cells at 1-7 days in vitro and was detected predominantly in lung epithelial cells at 1-7 days in vivo after adenoviral transfer of the human p21 gene. Inflammatory cell infiltration and fibrosis had already begun at 7 days in this model. Adenoviral transfer of the human p21 gene at 7 days after intratracheal instillation of bleomycin led to a decrease in the number of apoptotic cells, lung inflammation, and fibrosis at 14 days. Therefore, the forced expression of p21 exerted both anti-apoptotic and anti-fibrotic effects, which would facilitate the ultimate goal of treatment for pulmonary fibrosis.

Adenoviridae↗

PubMed1996

Pulmonary fibrosis deaths in the United States, 1979-1991. An analysis of multiple-cause mortality data.

We sought to describe pulmonary fibrosis mortality in the United States from 1979 through 1991 by analyzing death certificate reports compiled by the National Center for Health Statistics. Of the 26,866,600 people who died during the study period, 107,292 had a diagnosis of pulmonary fibrosis listed on their death certificates. Among men, age-adjusted mortality rates increased from 48.6 per 1,000,000 in 1979 to 50.9 per 1,000,000 in 1991 and, among women, these rates increased from 21.4 per 1,000,000 in 1979 to 27.2 per 1,000,000 in 1991. Among both men and women rates were higher in older age strata than in younger age strata. Age-adjusted mortality rates were consistently higher among whites and people of races than blacks. The frequency with which pulmonary fibrosis was listed as the underlying cause of death increased from 40% in 1979 to 56% in 1991. Age-adjusted mortality rates varied by state, with lowest rates in the Midwest and Northeast, and the highest rates in the West and Southeast. We conclude that the age-adjusted rate of pulmonary fibrosis among decedents in the United States increased, and pulmonary fibrosis was listed as the underlying cause of death with increasing frequency, over the study period. We cannot determine whether the differences we detected between regions, sexes, and races are related to characteristics of the disease or problems in death certification and coding.

Adolescent↗

PubMed1977

Frequency of HLA antigen in asbestos workers with and without pulmonary fibrosis.

HLA antigens were determined in 37 patients with asbestosis and 37 matched controls with equivalent asbestos exposure but no pulmonary fibrosis. All had worked in the same textile factory. No significant differences in the prevalence of antigens were found between the two groups or between either group and controls who had not been exposed to asbestos. When the data were combined with findings from other pilot studies the previously suggested association between asbestosis and HLA-B27 was not confirmed. Subjects who were positive for HLA-B12 tended also to have advanced radiographic fibrosis. Asbestos workers without pulmonary fibrosis had an unexpectedly high frequency of HLA-BW5, which might indicate that this antigen protects against the development of pulmonary fibrosis.

Asbestosis↗

PubMedDate not supplied

[Fatal pulmonary fibrosis caused by gold therapy?].

The case of a 33-year-old female patient with rheumatoid arthritis who developed a severe pulmonary fibrosis during chrysotherapy of 3.5 months' duration is reported. The course of the fibrosis was progressive and led to respiratory insufficiency and death. The microscopic picture revealed a honeycomb lung with perialveolar proliferation of connective tissue and mononuclear cell infiltration. The clinical and temporal circumstances gave evidence that this pulmonary fibrosis is possibly to be interpreted as a gold-induced lung disease, though a causal connection could not be established with absolute security. However, gold-induced pulmonary fibrosis is usually completely reversible and has no fatal outcome: this would be the first report of a lethal outcome of a gold-induced pulmonary fibrosis. The clinical data of 39 further cases of gold-induced pulmonary fibrosis published elsewhere are presented.

Adult↗

PubMed1986

Inhibition of bleomycin-induced pulmonary fibrosis by nordihydroguaiaretic acid. The role of alveolar macrophage activation and mediator production.

The role of alveolar macrophage activation and release of mediators remains unclear. In this study, this role is examined with respect to the effects of relatively selective inhibitors of arachidonate metabolism on the pathogenesis of pulmonary fibrosis. CBA/J mice were administered bleomycin (0.037 units) endotracheally to induce pulmonary fibrosis. Daily intraperitoneal injections of a lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA) inhibited pulmonary fibrosis in a dose-dependent manner (15-25 mg/kg body weight), as assessed by both lung collagen synthesis and total lung hydroxyproline content. The less specific inhibitor BW755c was also effective at a dose of 25 mg/kg. In contrast, the cyclooxygenase inhibitor, ibuprofen (15 mg/kg), was completely ineffective. Correlated with this antifibrogenic activity of NDGA was the inhibition of several other parameters of bleomycin-induced pulmonary fibrosis. Bleomycin treatment caused a greater than threefold increase in the percentage of alveolar macrophages expressing Ia antigen (from 7.7% +/- 1.07% to 29.9% +/- 4.16% of total recoverable alveolar macrophages). NDGA, but not ibuprofen, inhibited this increase in a dose-dependent manner. Associated with this indication of macrophage stimulation was an increase in spontaneous macrophage production of fibroblast growth factor (MDGF) activity as a result of bleomycin instillation. This increase was also inhibited by NDGA treatment. In contrast, bleomycin treatment caused a reduction in alveolar macrophage interleukin-1 (IL-1) production, and NDGA treatment did not alter this reduction, which suggests that MDGF is separate from IL-1 in this case, and that MDGF played a more dominant role, at least in this model of pulmonary fibrosis. This antifibrogenic activity of NDGA was accomplished without any reduction in spontaneous macrophage prostaglandin (PG)E2 production, which suggests the selectivity (versus cyclooxygenase pathway) of NDGA inhibition and the relative lack of importance of macrophage-derived PGE2 in modulating fibrogenesis in this model. The results of this study have thus demonstrated the importance of alveolar macrophage stimulation and increased production of MDGF in the pathogenesis of bleomycin-induced pulmonary fibrosis. The data also suggest that both macrophage parameters are subject to regulation by arachidonate metabolites.

Animals↗

PubMed1989

[Fibrin deposition and fibrinolysis in the pathogenesis of pulmonary fibrosis].

Fibrin deposition is prominent in the course of several forms of pulmonary fibrosis. To elucidate the role of fibrin deposition and fibrinolysis in the process of pulmonary fibrosis, we studied bleomycin-induced fibrosis and the effect of urokinase on it. Beagle dogs were injected intramuscularly 20 times with bleomycin in doses of 2 and 6 mg/kg body weight every other day. Intravenous urokinase treatment was subsequently performed with 3,000 units daily for 40 days and 9,000 units twice daily for 70 days. Histopathologic examination of the lungs of dogs receiving bleomycin alone revealed fibrosis. The lungs of bleomycin-treated dogs which received urokinase had less severe fibrosis and this was confirmed by morphometry with planimetry and the point counting method. Urokinase treatment also diminished the increase of hydroxyproline content of the lung of bleomycin-treated dogs. Decrease of lung tissue fibrinolytic activity assayed by fibrin plate method in bleomycin-treated dogs was also prevented by urokinase. Intravenous urokinase, 24,000 units per day in divided doses, was administered daily in cancer patients with bleomycin treatment. Incidence of pulmonary fibrosis was decreased by urokinase. These data indicate that fibrin deposition and fibrinolysis may have an important influence on the fibrotic process in the lung.

Animals↗

PubMed2006

[Effect of hydrogen sulfide on Bleomycin-induced pulmonary fibrosis in rats].

OBJECTIVE: To explore the change of endogenous hydrogen sulfide and the effect of exogenously applied H(2)S on Bleomycin-induced pulmonary fibrosis in rats. METHODS: (1) Forty-eight male Wistar rats were randomly divided into control group, fibrosis group, fibrosis+NaHS-low group (1.4 micromol/kg, bid intraperitoneally) and fibrosis+NaHS-high group (7.0 micromol/kg, bid intraperitoneally). Pulmonary fibrosis was induced by intratracheal instillation of bleomycin. The control group and pulmonary fibrosis group were injected with the same volume of normal saline. Pulmonary pathology changes were observed, the plasma H(2)S concentration,the activity of CSE in lung tissue and the contents of MDA, hydroxyproline were detected on the 7th and 28th days respectively after bleomycin administration. CSE mRNA was also measured using quantitative RT-PCR. (2) Isolated lung tissues were exposed to Fe(2+)/H(2)O(2) without or with different concentrations of NaHS (10(-5), 5 x 10(-5), 10(-4), 10(-3) mmol/L) at 37 degree Celsius for 10 minutes, and the MDA content was assayed by biochemical method. RESULTS: (1) Compared with rats in control group, the concentration of plasma H(2)S and the activity of CSE in lung tissues in fibrosis group decreased on day 7 (all P<0.01); On the 28th day, the level of plasma H(2)S increased clearly (P<0.01) and the activity of CSE was ascendant without significant difference compared with that of control group. Relative CSE mRNA amounts in lung tissues increased 34%, 144%, respectively (all P<0.01) in rats of fibrosis group compared with those of control group. The contents of MDA and hydroxyproline increased significantly in fibrosis group compared with those of control group on days 7, 28 (all P<0.01). In NaHS-low group and NaHS-high group, the contents of MDA and hydroxyproline decreased markedly (all P<0.01). (2) The contents of MDA in incubation of lung tissues at different concentrations of NaHS were all decreased as compared with those in incubation with Fe(2+)/H(2)O(2) alone (all P<0.01). When NaHS was at 10(-4) mol/L, the MDA content reversed to the lowest value, which had the highest value at 10(-3) mol/L of NaHS. CONCLUSION: Endogenous CSE/H(2)S pathway was involved in the pathogenesis of rat pulmonary fibrosis. Exogenously applied H(2)S could attenuate the process of pulmonary fibrosis possibly because of reducing oxidative stress.

Animals↗

PubMed1986

Familial idiopathic pulmonary fibrosis. Evidence of lung inflammation in unaffected family members.

We evaluated 17 clinically unaffected members of three families with an autosomal dominant form of idiopathic pulmonary fibrosis for evidence of alveolar inflammation. Each person in the study was examined by gallium-67 scanning for a general estimate of pulmonary inflammation, and by bronchoalveolar lavage for characterization of the types of recovered cells and their state of activation. Eight of the 17 subjects had evidence of alveolar inflammation on the lavage studies. Supporting data included increased numbers of neutrophils and activated macrophages that released one or more neutrophil chemoattractants, and growth factors for lung fibroblasts--findings similar to those observed in patients with overt idiopathic pulmonary fibrosis. Four of these eight also had a positive gallium scan; in all the other clinically unaffected subjects the scan was normal. During a follow-up of two to four years in seven of the eight subjects who had evidence of inflammation, no clinical evidence of pulmonary fibrosis has appeared. These results indicate that alveolar inflammation occurs in approximately half the clinically unaffected family members at risk of inheriting autosomal dominant idiopathic pulmonary fibrosis. Whether these persons with evidence of pulmonary inflammation but no fibrosis will proceed to have clinically evident pulmonary fibrosis is not yet known.

Adult↗

PubMed1984

Paraquat-induced pulmonary fibrosis. Role of the alveolitis in modulating the development of fibrosis.

Paraquat, a widely used herbicide, can cause severe and often fatal pulmonary fibrosis in humans and in laboratory animals. Although paraquat is known to be directly cytotoxic to lung parenchymal cells, the mechanism by which this leads to pulmonary fibrosis is not completely understood. In a model of paraquat-induced pulmonary fibrosis using the cynomolgus monkey, the administration of paraquat (10 mg/kg/wk subcutaneously for 2 consecutive wk) was followed by an alveolitis comprised of neutrophils and macrophages in the exposed animals as evaluated by lung morphologic examination and bronchoalveolar lavage. The lungs of the exposed animals showed typical interstitial fibrosis within 4 to 8 wk. At 1 to 2 wk after paraquat exposure, bronchoalveolar lavage cells harvested from the paraquat-exposed animals were spontaneously releasing a chemotactic factor for neutrophils, thus providing a possible mechanism for the recruitment of neutrophils to the alveolar structures. Lavage fluid from paraquat-exposed animals contained increased amounts of the fibroblast chemoattractant fibronectin (paraquat, 3.1 +/- 0.3 ng/micrograms albumin; control, 1.6 +/- 0.7 ng/micrograms albumin; p less than 0.05), and alveolar macrophages from these animals showed increased fibronectin production suggesting that local production accounted for part of the increased amounts of this glycoprotein (paraquat, 6.1 +/- 2.5 ng/10(6) cell/h; control, 1.4 +/- 0.5 ng/10(6) cell/h; p less than 0.05). In addition, alveolar macrophages from the exposed animals were spontaneously releasing a growth factor for fibroblasts, and normal alveolar macrophages exposed to paraquat in vitro were induced to release this growth factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Interstitial pneumonitis, pulmonary fibrosis, and chronic graft-versus-host disease.

Pneumonopathies in association with graft-versus-host disease (GVHD) are known, but the evolution of biopsy-proven interstitial pneumonitis (IP) to pulmonary fibrosis as a major pulmonary manifestation in an individual patient with chronic GVHD has not been previously reported. We present a patient with chronic GVHD who developed IP and then pulmonary fibrosis. We suggest that IP with evolution to pulmonary fibrosis was a major pulmonary manifestation of chronic GVHD in this patient.

Adolescent↗