A case of interstitial pneumonia induced by an ACE inhibitor (temocapril hydrochloride)]

A 51-year-old woman who had been treated for years for rheumatoid arthritis presented with a persistent dry cough and shortness of breath three weeks after administration of the ACE inhibitor temocapril hydrochloride against essential hypertension. Chest radiography and computed tomography showed diffuse reticular shadows and ground-grass opacities in both lung fields. Bronchoalveolar lavage fluid analysis showed an increase of lymphocytes and CD8+ T cells (93.3% of lymphocytes), and a decrease of the CD4/8 ratio of the T cell subset (0.04). Histopathological analysis of trans-bronchial lung biopsy specimens showed infiltration of lymphocytes into the alveolar septa and exudation of alveolar macrophages, signs characteristic of interstitial pneumonia. A drug lymphocyte stimulation test was positive for temocapril, but negative for other drugs. On the basis of these findings, we diagnosed temocapril hydrochloride-induced interstitial pneumonia.     

Cost-minimization analysis of intravenous adenosine and dipyridamole in thallous chloride TI 201 SPECT myocardial perfusion imaging

This paper deals with two patients with acetaminophen-induced pneumonitis. A 64-year-old woman suffered from mastitis while being treated by corticosteroid therapy for phemphigoid. She was administered antibiotics and acetaminophen. However, her fever continued and she subsequently developed dyspnea and interstitial pneumonia. The other patient, a 70-year-old woman, was treated with corticosteroid for lower motor neuron disease. Anti-GM1-IgM antibodies were positive in her serum. She developed wet cough and mild fever. During treatment with antibiotics and acetaminophen, her illness was complicated by dyspnea and interstital pneumonia. As a result of histological findings of transbronchial lung biopsy specimens showing interstitial infiltration of mononuclear cells, as well as clinical courses in which cessation of acetaminophen directly lead to the improvement of interstitial pneumonia, both patients were diagnosed to have acetaminophen-induced pneumonitis. The peumonitis responded well to steroid therapy. In vitro culture of peripheral lymphocytes showed stimulated proliferation by acetaminophen in both patients. These findings suggest that allergic mechanism was involved in the pathogenesis of the pneumonitis. Underlying immunological disorders may have enhanced the occurrence. Although acetaminophen is one of the most popular drugs because of a very low incidence of side effects, this drug should be applied carefully, especially with patients who have such immunological disorders.     

A case of interstitial pneumonia of polymyositis-dermatomyositis with various pathological findings in open lung biopsy

A 60-year-old woman was admitted to our hospital with a two month history of dry cough and dyspnea on exertion. A chest roentgenogram revealed diffuse interstitial shadows with a reduction of lower lung volume. Laboratory examinations revealed an increase in CPK and aldolase. There was decreased proximal muscle power, and the findings of a biopsy of the right deltoid were compatible with polymyositis. Myositic symptoms were stable, but the respiratory symptoms worsened, and an open lung biopsy was performed for diagnosis and to determine the best treatment. The histological findings of biopsy materials demonstrated active interstitial pneumonia complicated by cellular interstitial pneumonia, bronchiolitis obliterans organizing pneumonia, usual interstitial pneumonia and lymphoid hyperplasia. The patient responded well to adrenocorticosteroid and immunosuppressive therapy, and is now attending as an out patient. It is well known that PM-DM can be associated with interstitial pneumonia, and this complication is an important prognostic factor clinically. The pathological patterns of interstitial pneumonia in PM-DM may be divided into usual interstitial pneumonia and bronchiolitis obliterans organizing pneumonia. Furthermore, it is well documented that these patterns are concurrent with the response to adrenocorticosteroid and prognostic factors. However, our case of PM-DM, in which various patterns such as rheumatoid arthritis (RA) were pathologically revealed, cannot be considered as having uniform pathological pattern. We consider that pulmonary pathological patterns of PM-DM are very varied, as with RA. It is a very important to evaluate the nature of these patterns and the subsequent clinical course in PM-DM with interstitial pneumonia.     

A case of lymphocytic interstitial pneumonia

A 56-year-old female was admitted on November 1995 to our hospital because of the abnormal shadow on her chest X-ray. Although the chest X ray film revealed diffuse reticulonodular shadows in the bilateral lung fields and right hilar lymphadenopathy, she had not any complaints. Furthermore, mediastinal lymphadenopathy and polyclonal hypergammaglobulinemia were noted. For a further examination, transcutaneous thoracoscopic lung biopsy was performed on August 1996. The lung specimens showed a interstitial infiltration of small lymphocytes exclusively around bronchioles. And the diagnosis of lymphocytic interstitial pneumonia (LIP) was made. She had been suffered from bronchial asthma for 27 years. This is the first report of LIP accompanied with bronchial asthma. Its relationship between LIP and bronchial asthma remains unclear. In the 2 years of follow-up, she remained asymptomatic with unchanged chest radiogram. And her pulmonary function was preserved for the 2 years. But lymphocytic interstitial pneumonia may induce malignant lymphoproliferative disease potentially, we should carefully follow up.     

Bronchiolitis obliterans with organizing pneumonia in a patient treated with amiodarone]

Bronchiolitis obliterans organizing pneumonia (BOOP) is a well-defined clinicopathological entity. The aetiology of BOOP is generally unknown, although it has been associated with specific diseases or various pharmaceutical drugs. The amiodarone is one of them. We report a patient with BOOP secondary to amiodarone therapy, who presented with cough, fever and sputum production, dyspnoea and night sweats lasting for two months. A chest radiograph showed bilateral patchy and interstitial infiltrates. Lymphocyte phenotyping of bronchoalveolar lavage fluid showed decreased ratio of CD4+:CD8+ lymphocytes. Transbronchial lung biopsy established the diagnosis of BOOP. After stopping amiodarone therapy, symptoms disappeared and the chest radiograph remained normal within two months.     

Structural and functional consequences of alveolar cell recognition by CD8(+) T lymphocytes in experimental lung disease

CD8(+) T cells infiltrate the lung in many clinical conditions, particularly in interstitial lung disease. The role(s) that CD8(+) T cells might be playing in the pathogenesis of inflammatory lung disease is unclear at present, as is the direct contribution of CD8(+) T cell effector activities to lung injury. This report describes a transgenic model used to evaluate the impact, on respiratory structure and function, of CD8(+) T lymphocyte recognition of a target antigen expressed endogenously in alveolar epithelial cells. We found that adoptive transfer of cloned CD8(+) cytotoxic T lymphocytes (CTLs) specific for an alveolar neo-antigen (influenza hemagglutinin) leads to progressive lethal injury in transgenic mice, which dramatically affects lung structure and function. Transgenic recipients of CD8(+) CTLs exhibited tachypnea and progressive weight loss, becoming moribund over a period of several days. Concomitantly, the animals developed a progressive interstitial pneumonitis characterized initially by lymphocytic infiltration of alveolar walls and spaces, followed by an exuberant mononuclear cell infiltration that correlated with restrictive pulmonary mechanics and a progressive diffusion impairment. These results indicate that antigen-specific CD8(+) T cell recognition of an alveolar epithelial "autoantigen" is, in and of itself, sufficient to trigger an inflammatory cascade that results in the histological and physiological manifestations of interstitial pneumonia.     

Interstitial pneumonia treated with intermittent cyclophosphamide pulse therapy

A 52-year-old woman was admitted to the hospital because of polyarthralgia and dry coughing. A chest X-ray film showed bilateral diffuse reticulo-nodular shadows. A specimen obtained by transbronchial lung biopsy revealed alveolar septal thickening and infiltration by mononuclear cells. Interstitial pneumonia associated with rheumatoid arthritis was diagnosed. Interstitial pneumonia relapsed soon after the first pulse of corticosteroid therapy. Cyclophosphamide pulse therapy was given in addition to a second pulse of corticosteroid therapy; 700 mg of cyclophosphamide (500 mg/m2) was administered intravenously every month and the dose of steroids was gradually reduced. Cyclophosphamide pulse therapy was repeated three times and the dose of oral corticosteroids was reduced from 60 mg to 35 mg. There was no bone marrow suppression or hemorrhagic cystitis after the cyclophosphamide pulses. Eventually, corticosteroid therapy was stopped with no clinical deterioration. This case suggests that intermittent cyclophosphamide pulse therapy can be effective for treatment of interstitial pneumonia unresponsive to corticosteroids.     

Effect of haemoglobin concentration on brain oxygenation in focal stroke: a mathematical modelling study

A 56-year-old woman was admitted to the hospital because of dry coughing and shortness of breath on exertion. In addition, dry eyes and cornea guttata suggested Sj?gren's syndrome. Chest radiography revealed linear, reticular shadows throughout the lung fields, and enlargement of hilar and mediastinal lymph nodes. A specimen was obtained by transbronchial lung biopsy but the findings were not condusive; open-lung biopsy was done. The histopathological findings suggested lymphocytic meterstitial pneumonia. Results of genetic analysis and of immuno-histochemical examination conformed that the proliferating lymphocytes were polyclonal. Corticosteroids and immunosuppressive drugs have been used to treat lymphocytic interstitial pneumonia, and they were effective in this case.     

Implant-supported prostheses after maxillary cancer resection: preliminary report

Interstitial pneumonia and aseptic neutrophilic infiltration in the lung are rare pulmonary manifestations of myelodysplastic syndrome (MDS). We report a patient with progressive interstitial pneumonia associated with MDS. Histological examination of the lung revealed infiltration of atypical haematopoietic cells associated with MDS and diffuse alveolitis with honeycombing. Neutrophils obtained from the patient showed superoxide hyperproduction after stimulation with phagocytosis and phorbol myristate acetate, which might be attributed to the pathogenesis of interstitial pneumonia.     

Neutralization of interferon-gamma exacerbates pneumocystis-driven interstitial pneumonitis after bone marrow transplantation in mice

The role of IFNgamma in the development of infection-driven interstitial pneumonitis in a model of murine graft-versus-host disease was investigated. Mice were given either syngeneic or allogeneic bone marrow transplants along with lung Pneumocystis carinii infections and were treated with either control mAb or anti-IFNgamma mAb. At day 21 after transplant, lung weights were elevated nearly twofold in all groups. By day 41, mice in all groups had cleared the P. carinii but only the mice given allogeneic transplants and anti-IFNgamma had increased lung weights. Increased lung weights in the anti-IFNgamma-treated mice corresponded to alveolar infiltration of eosinophils, neutrophils, and multinucleated giant cells and exacerbated interstitial pneumonitis compared with mice treated with control antibody. Intracellular staining indicated that there were 3- to 10-fold more CD4+ cells producing IFNgamma than those producing IL-4 in the lung lavages of mice given either syngeneic or allogeneic transplant. Treatment of transplanted mice with anti-IFNgamma resulted in a significant decrease in IFN-gamma-producing CD4+ and CD8+ cells in the lung lavages but no change in the number of IL-4-producing CD4+ cells. These data indicate that IFNgamma is critical for controlling the development of P. carinii-driven interstitial pneumonia after either syngeneic or allogeneic bone marrow transplant in mice.     

A rapidly progressive case of interstitial pneumonia

We treated a 51-year-old woman who had rapidly progressive respiratory distress with an interstitial shadow on chest roentgenogram. Pathologically, open lung biopsy specimens showed an acutely changed lesion such as interstitial inflammatory thickening, polypoid intraluminal organizing exudates, and also honeycombing which was not recognized on chest computed tomogram. These findings were considered unconformable to acute interstitial pneumonia (AIP), bronchiolitis obliterans organizing pneumonia (BOOP), and also usual interstitial pneumonia, although the clinical diagnosis was AIP or BOOP. We diagnosed a rapidly progressive interstitial pneumonia showing an acute lung injury pattern like AIP and BOOP. She showed significant recovery with corticosteroid and cyclophosphamide.     

An unusual case of cardiac insufficiency

A 70 year old patient with a past history of a left ventricular cardiomyopathy with concentric hypertrophy presented with an exacerbation of cardiac failure; radiology revealed bilateral lung infiltrations, predominantly on the right and a restrictive ventilatory disorder. The broncho-alveolar lavage revealed a lymphocytosis with CD4 prominence. Microbiological examination was negative. With a worsening radiological picture despite increased anti-failure treatment a video-assisted surgical biopsy was performed. The histological examination revealed diffuse interstitial pulmonary amyloidosis. This observation underlined the value of looking for this rare cause of cardiac failure and pulmonary infiltration in a situation where the pulmonary images did not improve on diuretics.     

A case report of pneumonia due to Chlamydia trachomatis with pleural effusion

A 64-year-old male consulted our hospital with a 6-day history of malaise, body temperature to 38 degrees C, anorexia, and light headedness. The chest radiograph showed consolidation in the left lower lung area. Chest CT and ultrasonography revealed left pleural fluid. The pleural fluid was exudative (yellowish in color, protein 3.0 g/dl, Rivalta reaction positive, adenosine deaminase 19.4 U/L), and had a total cell count of 4.7 x 10(6)/ml with 45% lymphocytes, 40% histiocytes, and 15% polymorphonuclear leukocytes. He had kept a budgerigar, but we could not isolate Chlamydia from the pleural fluid or the pet bird. Transbronchial lung biopsy from left S10 revealed an increase of mononuclear leukocytes within the interstitial spaces, and the alveolar spaces contained polymorphonuclear leukocytes, fibrin, and organized alveolar exudate. Bronchoalveolar lavage cellular constituents were 50% lymphocytes, 27% neutrophils, and 23% macrophages. Serologic studies demonstrated C. trachomatis specific IgM antibody titers at 1:20 in a serum sample and at 1:10 in pleural fluid. We report a case of community-acquired pneumonia caused by C. trachomatis diagnosed by serologic studies.     

Ganglionitis in paraneoplastic subacute sensory neuronopathy: a morphologic study

A 69-year-old woman presented with subacute sensory neuropathy and autonomic dysfunction of 9 months' duration, associated with high serum titers of anti-Hu antibodies. A small cell carcinoma of the lung was diagnosed by biopsy. She died after cardiorespiratory arrest. At autopsy, spinal and autonomic ganglia showed subacute inflammation with diffuse endoneurial T-cell, B-cell, and plasma cell infiltration. The cytoplasm and nuclei of some ganglion neurons displayed IgG immunocytochemical positivity. CD8+ T cells were tightly attached to, and indented the cell surface of, IgG-positive and IgG-negative neurons. This observation suggests that both cytotoxic T-cell-mediated attack against neurons and humoral mechanisms play a role in paraneoplastic subacute sensory neuronopathy.     

Respiratory symptoms, lung function tests, airway responsiveness, and bronchoalveolar lymphocyte subsets in B-chronic lymphocytic leukemia

A respiratory questionnaire was completed and spirometry, tests for lung volumes, diffusion capacity for CO, and methacholine bronchial challenge were performed in 24 outpatients with B-chronic lymphocytic leukemia (B-CLL), aged 44-79, presenting in different stages of their disease. In 10 patients, bronchoalveolar lavage (BAL) fluid was also obtained. Ten of twenty-four patients had symptoms consistent with chronic bronchitis, unrelated both to smoking history and to the clinical stage. Abnormal values (< 2 SD) were found in 4 patients for total lung capacity (TLC), in 9 for vital capacity (VC), 8 for forced expiratory volume in 1 sec (FEV1), 11 for MEF50, 15 for MEF25 and in 7 for diffusing capacity for carbon monoxide. Seven of nineteen patients had PD20FEV1 at less than 1,600 micrograms of methacholine chloride. There was a significantly negative correlation between white blood cell count and VC (r = 0.41, P < 0.05). A positive correlation was found between PD20FEV1 and FEV1/VC (r = 0.61, P < 0.01). The mean and SEM for BAL cells/ml was 463 (71.8) x 10(3). No leukemic cells but a marked increase in T lymphocytes (32.5 +/- 7.8%) were found in BAL fluid. There were significantly negative correlations between the number of BAL CD3+ T lymphocytes and PD20FEV1 (r = 0.61, P < 0.05), and between the number of BAL CD8+ T lymphocytes and PD20FEV1 (r = 0.84, P < 0.01). In conclusion, patients with B-CLL have a high prevalence of respiratory symptoms, small airway dysfunction and CD8 "alveolitis" related to airway responsiveness; despite the well-known lung interstitial lymphocyte infiltration in B-CLL, leukemic cells are not found in BAL fluid.     

HMG-CoA reductase inhibitor and risk of stroke

A 75-year-old-man who had been occupationally exposed to asbestos over several decades was admitted complaining of dry cough and mild exertional dyspnea. Chest X-ray films revealed the presence of bilateral infiltrates. An open biopsy showed the lung pathology to be desquamative interstitial pneumonitis (DIP), and detected a calcified plaque of the left parietal pleura at cost-phrenic sulcus, which on microscopic inspection demonstrated thin needle-like structures suggestive of asbestos particles. A hormonal examination showed decreased levels of tri-iodothyronine and tetraiodothyronine and an increased level of thyroid stimulating hormone. Additionally, a positive microsome test indicated autoimmune hypothyroidism. A serological study was positive for anti-nuclear antibody and direct Coombs, and showed heightened levels of IgG. The patient was placed on oral prednisolone therapy; one month later, his symptoms had subsided, and his lung function and chest x-ray findings had improved significantly. In addition, the abnormal values for autoimmune and thyroid function eventually returned to normal ranges. These findings suggest that DIP and humoral immune dysfunction were caused by asbestos exposure, and responded well to steroid treatment.     

An Analytical Formula for the Energy of the Bound Long-Range 0(-)g((1)3Pig) State of Cs2

In an asymptomatic 4 yr old child with radiographic evidence of parenchymal lung disease, bronchoalveolar lavage (BAL) yielded the diagnosis of chronic lipid pneumonia caused by chronic aspiration of mineral oil given as a laxative. BAL analysis showed a marked reduction in the total number of alveolar macrophages; almost 70% of these cells contained intracytoplasmic lipid vacuoles. It also disclosed lymphocytic (cytotoxic/suppressor) alveolitis. A high percentage of lymphocytes expressed antigen markers of activation (human leucocyte antigen (HLA)-DR), CD54 and CD25). BAL analysis 18 months after mineral oil intake revealed that lymphocytes bearing antigen markers of activation had markedly decreased whereas alveolar macrophages (normal and lipid-laden) had increased. A subsequent whole lung BAL was considered unnecessarily invasive in this otherwise healthy child.     

Prospective study of the value of transbronchial lung biopsy after lung transplantation

Transbronchial lung biopsy (TBB) has become the gold standard for the diagnosis of acute rejection and cytomegalovirus (CMV) pneumonia in lung transplant recipients. The aim of this study was to assess the value of regular surveillance TBB in stable asymptomatic patients and to establish the role of TBB as a follow-up procedure 1 month after a previous pathological biopsy result. We prospectively evaluated 76 TBBs performed in 17 lung transplant recipients. A definite pathological results was found in 14 of 15 TBBs performed for clinical indications: CMV pneumonia (5), acute rejection grade > or = A2 according to the criteria of the International Society for Heart and Lung Transplantation (ISHLT) (4), bronchiolitis obliterans (3), and desquamative interstitial pneumonitis (2). Fifteen of 45 surveillance TBBs performed in asymptomatic patients revealed significant abnormalities. Ten episodes of acute rejection ISHLT grade > or = A2 and three episodes of CMV pneumonia detected by TBB had direct therapeutic consequences. Nine of 16 follow-up TBBs performed 1 month after a pathological biopsy result again showed relevant pathological findings. With the exception of one severe haemorrhage, no life-threatening complications occurred. Our results suggest that transbronchial lung biopsies performed on a regular basis after lung transplantation are important for the detection of asymptomatic and/or persistent acute rejection or injection. In the long-term, this strategy might be the most effective tool in reducing the incidence of bronchiolitis obliterans, which is still the main obstacle for further improvement of long-term survival after lung transplantation.     

Spontaneous remission of desquamative interstitial pneumonia

We report a case of spontaneous remission of desquamative interstitial pneumonia (DIP) in a 50-year-old male. The histological diagnosis of DIP was based on open lung biopsy. A chest X-ray revealed reticulo-nodular shadows in the bilateral lung fields, and the patient had mild dyspnea on exertion. Without treatment, these shadows decreased gradually and disappeared after several months. The patient recovered completely within one year, and recurrence of the disease has not been observed for 4 years. Recently, DIP has rarely been described, and the spontaneous remission of DIP has not been reported since Carrington et al in 1978 (1).     

Dermatomyositis complicated by sarcoidosis

We encountered a patient with dermatomyositis complicated by sarcoidosis. A 57-year-old woman was admitted to our hospital because of fever dry cough, and myalgias. There were reticular shadows on her chest X-ray film. Although the typical skin rash and myositis suggested the diagnosis of dermatomyositis biopsy specimens from a salivary gland, muscle, and lung revealed noncaseating granulomas as well. Uveitis was also noted. These findings suggested the coexistence of sarcoidosis with dermatomyositis. Examination of the lung-biopsy specimens showed interstitial pneumonia compatible with dermatomyositis, except for the granuloma. The typical rash of dermatomyositis and pathological findings of the lung specimen were inconsistent with sarcoidosis. Therefore we concluded that this patient had both dermatomyositis and sarcoidosis. This case sheds new light on the importance of pathological examinations.