Incidence of comprehensive hospitalization due to infection, cardiovascular disease, fractures, and malignancies in patients with rheumatoid arthritis.

To comprehensively analyze the overall incidence of hospitalization for comorbidities in patients with rheumatoid arthritis (RA). We prospectively analyzed overall hospitalizations for comorbidities using the Institute of Rheumatology, Rheumatoid Arthritis (IORRA) cohort. The incidence of hospitalized comorbidity was calculated. Risk factors for the most frequent hospitalized comorbidities were determined by multivariate logistic regression analysis. Among 5519 RA patients contributing 5336.5 person-years of observation, 435 incidences of hospitalized comorbidity [8.15/100 person-years; 95% confidence interval (CI) 7.40-8.95] were confirmed. The most frequent cause of hospitalized comorbidity was infection (1.52/100 person-years), primarily respiratory system infection (0.77/100 person-years), followed by malignancy (1.03/100 person-years), extra-articular manifestations (0.78/100 person-years), bone fracture (0.77/100 person-years), and acute coronary syndrome (0.22/100 person-years). Death occurred in 0.34/100 person-years (95% CI 0.20-0.53), and in 94.4% of cases the cause of death was the same as that of admission. The risk factors for the most frequent cause of hospitalization, hospitalized infection, were age [odds ratio (OR) 1.03; 95% CI 1.00-1.05], serum albumin level (OR 0.30; 95% CI 0.13-0.69), and corticosteroid use (prednisone > 5 mg/day; OR 3.66; 95% CI 1.81-7.35), but not methotrexate or biological agent use. The present study determined the overall burden of hospitalized comorbidities in patients with RA. These comprehensive data on hospitalized comorbidities may provide a basis for future improvements in the treatment of RA.

Benign clear cell "sugar" tumor of the lung in a patient with Birt-Hogg-Dubé syndrome: a case report.

BACKGROUND: Birt-Hogg-Dubé (BHD) syndrome is a rare inherited autosomal genodermatosis and caused by germline mutation of the folliculin (FLCN) gene, a tumor suppressor gene of which protein product is involved in mechanistic target of rapamycin (mTOR) signaling pathway regulating cell growth and metabolism. Clinical manifestations in BHD syndrome is characterized by fibrofolliculomas of the skin, pulmonary cysts with or without spontaneous pneumothorax, and renal neoplasms. There has been no pulmonary neoplasm reported in BHD syndrome, although the condition is due to deleterious sequence variants in a tumor suppressor gene. Here we report, for the first time to our knowledge, a patient with BHD syndrome who was complicated with a clear cell "sugar" tumor (CCST) of the lung, a benign tumor belonging to perivascular epithelioid cell tumors (PEComas) with frequent causative relation to tuberous sclerosis complex 1 (TSC1) or 2 (TSC2) gene. CASE PRESENTATION: In a 38-year-old Asian woman, two well-circumscribed nodules in the left lung and multiple thin-walled, irregularly shaped cysts on the basal and medial area of the lungs were disclosed by chest roentgenogram and computer-assisted tomography (CT) during a preoperative survey for a bilateral faucial tonsillectomy. Analysis of the resected tumor showed large polygonal cells with clear cytoplasm proliferating in a solid pattern. Immunohistochemistry revealed that these tumor cells were positive for microphthalmia-transcription factor, S100, and CD1a but negative for HMB45, indicating that the tumor was a CCST. Genetic testing indicated that the patient had a germline mutation on exon 12 of the FLCN gene, i.e., insertion of 7 nucleotides (CCACCCT) (c.1347_1353dupCCACCCT). Direct sequencing of the FLCN exon 12 using genomic DNA obtained from her microdissected CCST cells clearly revealed loss of the wild-type FLCN sequence, which confirmed complete functional loss of the FLCN gene. On the other hand, no loss of heterozygosity around TCS1- or TSC2-associated genetic region was demonstrated. CONCLUSION: To our knowledge, this is the first report of CCST of the lung in a patient with BHDS, indicating that CCST should be added to the spectrum of pulmonary manifestations of BHDS.

Pneumocystis jirovecii pneumonia in non-HIV-infected patients in the era of novel immunosuppressive therapies.

In human immunodeficiency virus (HIV)-infected patients, Pneumocystis jirovecii pneumonia (PCP) is a well-known opportunistic infection, and its management has been established. However, PCP is an emerging threat to immunocompromised patients without HIV infection, such as those receiving novel immunosuppressive therapeutics for malignancy, organ transplantation, or connective tissue diseases. Clinical manifestations of PCP are quite different between patients with and without HIV-infections. In patients without HIV infection, PCP rapidly progresses, is difficult to diagnose correctly, and causes severe respiratory failure with a poor prognosis. High-resolution computed tomography findings are different between PCP patients with HIV infection and those without. These differences in clinical and radiologic features are the result of severe or dysregulated inflammatory responses that are evoked by a relatively small number of Pneumocystis organisms in patients without HIV infection. In recent years, the usefulness of PCR and serum ß-D-glucan assay for rapid and noninvasive diagnosis of PCP has been revealed. Although corticosteroid adjunctive to anti-Pneumocystis agents has been shown to be beneficial in some populations, the optimal dose and duration remain to be determined. Recent investigations revealed that Pneumocystis colonization is prevalent, and that asymptomatic carriers are at riskfor developing PCP and can serve as the reservoir for the spread of Pneumocystis by person-to-person transmission. These findings suggest the need for chemoprophylaxis in immunocompromised patients without HIV infection, although its indication and duration are still controversial. Because a variety of novel immunosuppressive therapeutics have been emerging in medical practice, further innovations in the diagnosis and treatment of PCP are needed.

Acute- or subacute-onset lung complications in treating patients with rheumatoid arthritis.

Rheumatoid arthritis (RA) is a common systemic disease that manifests as inflammatory arthritis of multiple joints and produces a wide variety of intrathoracic lesions, including pleural diseases, diffuse interstitial pneumonia, rheumatoid nodules, and airway disease. Patients treated for RA can have associated lung disease that commonly manifests as diffuse interstitial pneumonia, drug-induced lung injury, and infection. The purpose of this pictorial review is to illustrate the radiographic and clinical features of lung complications of acute or subacute onset in patients treated for RA and to show the computed tomography features of these complications.

Clinical characteristics and risk factors for Pneumocystis jirovecii pneumonia in patients with rheumatoid arthritis receiving adalimumab: a retrospective review and case-control study of 17 patients.

OBJECTIVES: To investigate the clinical characteristics and risk factors of Pneumocystis jirovecii pneumonia (PCP) in rheumatoid arthritis (RA) patients treated with adalimumab. METHODS: We conducted a multicenter, retrospective, case-control study to compare RA patients treated with adalimumab with and without PCP. Data from 17 RA patients who were diagnosed with PCP and from 89 RA patients who did not develop PCP during adalimumab treatment were collected. RESULTS: For the PCP patients, the median age was 68 years old, with a median RA disease duration of eight years. The median length of time from the first adalimumab injection to the development of PCP was 12 weeks. At the onset of PCP, the median dosages of prednisolone and methotrexate were 5.0 mg/day and 8.0 mg/week, respectively. The patients with PCP were significantly older (p < 0.05) and had more structural changes (p < 0.05) than the patients without PCP. Computed tomography of the chest revealed ground-glass opacity without interlobular septal boundaries in the majority of the patients with PCP. Three PCP patients died. CONCLUSIONS: PCP may occur early in the course of adalimumab therapy in patients with RA. Careful monitoring, early diagnosis, and proper management are mandatory to secure a good prognosis for these patients.

Extended survival observed in adoptive activated T lymphocyte immunotherapy for advanced lung cancer: results of a multicenter historical cohort study.

PURPOSE: To clarify the long-term effect of immunotherapy, the effect of adoptive activated T lymphocyte immunotherapy on advanced lung cancer was evaluated in terms of survival time. In addition, the performance status of cancer patients under immunotherapy was examined. EXPERIMENTAL DESIGN: Over 5 × 10(9) alpha-beta T lymphocytes cultured ex vivo with an immobilized anti-CD3 antibody and interleukin-2 were injected intravenously into patients, once every 2 weeks for 3 months or longer. Follow-up of these patients was carried out using clinical records and by telephone interview questionnaire. Patients undergoing immunotherapy in immunotherapy clinics and those undergoing other anticancer therapies without immunotherapy in seven hospitals in Tokyo were enrolled in this study. Data were analyzed by a third-party statistician. Performance status was studied on another series of various cancer patients who underwent immunotherapy. RESULTS: The overall median survival time of the patients with the best supportive care, which was obtained using Kaplan-Meier's model, was 5.6 months, and those with immunotherapy alone, chemotherapy alone, and immuno-chemotherapy were 12.5, 15.7, and 20.8 months, respectively. Using Cox' proportional hazard model, we examined the possible factors on survival time by univariate analysis. Then, the patients were stratified by gender and histological type for multivariate analysis. Significantly low hazard ratios were observed for immunotherapy and radiotherapy in males with squamous cancer; for chemotherapy and radiotherapy in male with adenocarcinoma; and for immunotherapy in females with adenocarcinoma. Addition of immunotherapy to chemotherapy resulted in a statistically significant decrease in hazard ratio in females with adenocarcinoma. Studies on the performance status (PS), determined according to the European Cooperative Oncology Group criteria, revealed a continuous high level of PS under immunotherapy until around 2 months before death, in contrast to the gradual increase of tumor marker level. CONCLUSIONS: The effectiveness of immunotherapy on advanced lung cancer is limited but may extend life span under certain conditions. Immunotherapy itself provided no clinical benefit by itself as compared with chemotherapy, but a significant additive effect of immunotherapy on chemotherapy was observed in females with adenocarcinoma. Moreover, immunotherapy can maintain good quality of life of the patients until near the time of death.

Pneumocystis jirovecii pneumonia in non-HIV-infected patients in the era of novel immunosuppressive therapies.

In human immunodeficiency virus (HIV)-infected patients, Pneumocystis jirovecii pneumonia (PCP) is a well-known opportunistic infection, and its management has been established. However, PCP is an emerging threat to immunocompromised patients without HIV infection, such as those receiving novel immunosuppressive therapeutics for malignancy, organ transplantation, or connective tissue diseases. Clinical manifestations of PCP are quite different between patients with and without HIV infections. In patients without HIV infection, PCP rapidly progresses, is difficult to diagnose correctly, and causes severe respiratory failure with a poor prognosis. High-resolution computed tomography findings are different between PCP patients with HIV infection and those without. These differences in clinical and radiologic features are the result of severe or dysregulated inflammatory responses that are evoked by a relatively small number of Pneumocystis organisms in patients without HIV infection. In recent years, the usefulness of PCR and serum ß-D-glucan assay for rapid and noninvasive diagnosis of PCP has been revealed. Although corticosteroid adjunctive to anti-Pneumocystis agents has been shown to be beneficial in some populations, the optimal dose and duration remain to be determined. Recent investigations revealed that Pneumocystis colonization is prevalent, and that asymptomatic carriers are at risk for developing PCP and can serve as the reservoir for the spread of Pneumocystis by person-to-person transmission. These findings suggest the need for chemoprophylaxis in immunocompromised patients without HIV infection, although its indication and duration are still controversial. Because a variety of novel immunosuppressive therapeutics have been emerging in medical practice, further innovations in the diagnosis and treatment of PCP are needed.

Radiological features and therapeutic responses of pulmonary nontuberculous mycobacterial disease in rheumatoid arthritis patients receiving biological agents: a retrospective multicenter study in Japan.

OBJECTIVE: This study was performed to evaluate the radiological features of and therapeutic responses to pulmonary disease caused by nontuberculous mycobacteria (NTM) in the setting of biological therapy for rheumatoid arthritis (RA). METHODS: We conducted a retrospective chart review of 13 patients from multiple centers who had developed pulmonary NTM disease during biological therapy for RA, including infliximab, etanercept, adalimumab, and tocilizumab. RESULTS: Most cases were asymptomatic or resulted in only common-cold-like symptoms. Abnormalities in computed tomography (CT) imaging were protean and frequently overlapped. The most predominant pattern was nodular/bronchiectatic disease (six cases), followed by alveolar infiltrate (three cases), cavitary disease (two cases), and pulmonary nodules (two cases). In most cases, pulmonary NTM disease had spread from a preexisting lesion; in particular, bronchial/bronchiolar abnormalities. In three cases, one or more nodular lesions with or without calcification were a focus of disease. Following the discontinuation of biological agents, most patients responded to anti-NTM therapy. Two patients showed no exacerbation in the absence of any anti-NTM therapy. In one patient, restarting tocilizumab therapy while continuing to receive adequate anti-NTM therapy produced a favorable outcome. In two other patients with a previous history of pulmonary NTM disease, introducing biological therapy led to recurrence, but anti-NTM therapy was effective in these patients. CONCLUSION: CT abnormalities of pulmonary NTM disease in RA patients receiving biological therapy were variable, but were not unique to this clinical setting. NTM disease can spread from preexisting structural abnormalities, even if they are minute. Contrary to our expectations, the therapeutic outcomes of pulmonary NTM disease were favorable in these patients.

[A case of pulmonary Mycobacterium lentiflavum infection diagnosed by microbiological analysis].

In 1998, a 51-year-old woman was diagnosed with Mycobacterium avium infection on the basis of chest radiographic findings, positive smear test results, and positive results of polymerase chain reaction (PCR) specific for Mycobacterium avium DNA in bronchial lavage fluid. Antimycobacterial therapy was administered for 11 months, and the chest radiographic findings improved. In 2001, re-treatment was performed because radiographic findings indicated exacerbation of disease and poor response. After 2005, the patient remained both smear and culture positive for mycobacterium. However, the precise species could not be identified using PCR and DNA-DNA hybridization, and her left lung lesions gradually worsened. The culture isolate was subjected to DNA analysis with PCR amplification and sequence analysis; this ultimately revealed the presence of Mycobacterium lentiflavum. Combination antimicrobial therapy was administered for 10 months. The patient's symptoms were alleviated, and the radiographic appearance remained stable.

Incidence, Characteristics, Clinical Course, and Risk Factors of Ulcerative Colitis-related Lung Diseases.

BACKGROUND: Ulcerative colitis (UC) is a chronic GI inflammatory disorder involving various extraintestinal organs, including the lungs. Although UC-related lung diseases (UC-LDs) have been widely recognized, much remains unclear. RESEARCH QUESTION: What are the incidence, characteristics, clinical course, and risk factors of UC-LD? STUDY DESIGN AND METHODS: This study retrospectively identified and classified UC-LDs by reviewing the medical records of consecutive patients with UC. The incidence, characteristics, and clinical course of each UC-LD type were investigated, and the clinical characteristics of patients with and without each UC-LD type were compared. RESULTS: Among 563 patients with UC, 28 (5.0%) developed UC-LD during a mean follow-up period of 77 months. A majority of them displayed airway disease (AD) (n = 13 [2.3%]) or organizing pneumonia (OP) (n = 10 [1.8%]); there were six cases of interstitial pneumonias other than OP (IP) (0.8%) and one of pleuritis (0.2%). All 13 patients with AD responded favorably to inhaled or systemic corticosteroids, although five experienced frequent exacerbations. Older age and a history of colectomy were identified as the risk factors for developing AD. Nine of the 10 cases of OP were possibly due to drug-induced pathogenesis. Only one case showed recurrence, and all cases of OP exhibited a favorable clinical course with discontinuation of the suspicious drug and/or initiation of corticosteroid. The clinical course of IP depended on the existence of fibrosis, and IP with fibrosis was associated with gradual deterioration. Older age was associated with the development of IP. INTERPRETATION: A nonnegligible number of patients with UC may develop UC-LD. AD, OP, and IP without fibrosis show good prognosis following steroid therapy along with the specific management for each UC-LD type, whereas IP with fibrosis shows gradual deterioration with poor prognosis. Our results provide cues to establish better management of UC-LDs.

[Clinical and radiological features of tuberculous pneumonia in patients with emphysema].

PURPOSE: To elucidate the clinical and radiological features of tuberculous pneumonia in patients with pulmonary emphysema. MATERIAL AND METHOD: Three emphysematous cases diagnosed with tuberculous pneumonia are clinically and radiologically reviewed. RESULT: Case 1 was a 62-year-old male with an infiltrate in the right upper lobe. A CT scan showed diffuse emphysema and a nonsegmental infiltrate without typical signs of bronchogenic spread. Sputum was negative for acid-fast bacilli. The infiltrate showed a nonsegmental spread unresponsive to antibiotics. Mycobacterium tuberculosis grew from a needle biopsy specimen five weeks after admission. The infiltrate disappeared with antituberculous treatment. Case 2 was an 82-year-old male, who presented with seven weeks of low-grade fever followed by high fever and lobar pneumonia in the right upper lobe. Sputum was positive for acid-fast bacilli on smear and tuberculosis PCR, leading to a diagnosis of tuberculous pneumonia. Case 3 was a 57-year-old male who had a history of dry cough lasting for one month. CT findings included a diffuse emphysematous change and a left upper lobe infiltrate, indistinguishable from bacterial pneumonia. His bronchoalveolar lavage was positive for tuberculosis PCR, which led to a diagnosis of tuberculous pneumonia. CONCLUSION: Tuberculous pneumonia in emphysematous patients can be nonsegmental, lacks bronchogenic spread, is indistinguishable from bacterial pneumonia, and clinically shows a poor inflammatory reaction, which is distinct from classical "caseous pneumonia.

[Various aspects of acinar lesions--the key finding of pulmonary tuberculosis on HRCT].

Acinar lesions, a pathologist's naming for granulomatous lesions formed in the peripheral air space, that is, in the bronchiole or its adjacent alveolar space, is very characteristic and pathognomonic for tuberculosis on HRCT imaging. As a radiological term, it is equal to centrilobular nodule or branching shadow, or tree-in-bud appearance in the recent trend. It is universally seen in most of tuberculosis cases, irrespective of its stage or extensity. Although thus common, its appearance is not always uniform. Firstly they are not well defined in some cases. Exudative tendency in pathological process may explain for this appearance. Secondarily they are not always arranged in an orderly manner or in other words centrilobular manner on CT, but often in a random fashion. Pathologically this phenomenon can be explained by the randomness of formation site of granulomas or by scarring in spontaneous healing process of the disease. Finally, although rare, an extreme pattern, in which acinar lesions are diffusely disseminated in both lung fields without other type of lesions, is well known as Oka's Classification of Pulmonary Tuberculosis Type IIB. This rare type of tuberculosis could be formed through indolent dissemination of bacilli via the airway or from the hematogenous dissemination. It should also be noted that in tuberculous pneumonia, especially when it develops in emphysematous lung, acinar lesions is not seen, making differential diagnosis difficult.

Hemophagocytic Syndrome-Associated Variant of Methotrexate-Associated Intravascular Large B-Cell Lymphoma in a Rheumatoid Arthritis Patient.

A 59-year-old man was treated for rheumatoid arthritis (RA) for 12 years with methotrexate (MTX) and prednisolone. After MTX-associated interstitial pneumonia developed, he was treated with cyclophosphamide and prednisolone for 7 months. Arthritis worsened, and tacrolimus was added to the treatment regimen. One month later, he had fever, loss of appetite, and dyspnea on exertion. Blood tests showed pancytopenia with large, atypical lymphocytes. Computed tomography showed mild splenomegaly. Bone marrow examination demonstrated CD20-positive, EBER-positive atypical lymphocytes, and hemophagocytosis. Random skin biopsy led to the diagnosis of intravascular large B-cell lymphoma (IVLBCL). The final diagnosis was a hemophagocytic syndrome-associated variant of IVLBCL. Complete remission was achieved after seven courses of R-CHOP. However, within a month, he complained of dizziness. Magnetic resonance imaging revealed focal infarctions in the cerebellum and around the left lateral ventricle. Central nervous system relapse was suspected. Although salvage chemotherapy (CHASER), whole brain irradiation, and intrathecal injection of cytarabine and prednisolone were temporarily effective, he died. Autopsy revealed infiltration of lymphoma cells in the brain and adrenal glands. To the best of our knowledge, this is the sixth case of IVLBCL and the first case of the hemophagocytic syndrome-associated variant of IVLBCL in RA patients in the literature.

[Pathogenesis of chronic disseminated acinar pulmonary tuberculosis: Oka's classification of pulmonary tuberculosis type IIB--a discussion through an analysis of two typical cases].

PURPOSE: To elucidate the pathogenesis of chronic disseminated acinar pulmonary tuberculosis (Oka's classification type IIB). SUBJECTS AND METHODS: The subjects are two cases of chronic disseminated acinar pulmonary tuberculosis. The pathogenesis were discussed through an analysis of their radiologic findings on admission and in the past. RESULTS: Case 1 is a 36 year-old woman whose complaint was slight fever and cervical lymphadenopathy for past four months. Disseminated granular shadows were observed in both lung fields on the chest X-ray on admission. The CT examination indicated that each granule was composed of circumscribed lesion within terminal or respiratory bronchiole, so called acinar lesion. It is compatible with pulmonary tuberculosis type IIB according to Oka's classification. The bronchial lavage yielded Mycobacterium tuberculosis. When compared the chest X-ray with that at 4 months before, it is suggested that the granular lesions were first spread hematogeneously and each granule thereafter ruptured into the airway. Case 2 is a 90 year-old man with slight fever and weight loss. The chest X-ray showed diffuse granular shadows. The CT examination indicated that the lung shadows were composed of disseminated acinar lesions. The diagnosis of tuberculosis was established by a bronchoscopic examination. Comparison of the chest X-ray findings between those at 3 years 9 months before and 8 months before suggests the bronchogenic development of the disease. CONCLUSION: Through an analysis of these two cases, two kinds of pathogenesis were suggested in chronic disseminated acinar pulmonary tuberculosis; namely, one is hematogeneous route and the other is in bronchogenic route.

[A case of recurrent Helicobacter cinaedi-associated bacteremia in a small cell lung cancer patient during chemotherapy].

A 46-year-old man was admitted to our hospital, because of cough and exertional dyspnea. We diagnosed small cell lung cancer, clinically staged as T2N3M0, limited disease. Radiation therapy was performed at first to relieve the severe stenosis of the proximal airway, followed by anti-cancer chemotherapy. Fever developed on the fifth day of chemotherapy, and he was successfully treated with intravenous antibiotics. A blood culture yielded Helicobacter cinaedi on the seventh day of incubation. H. cinaedi bacteremia occurred again during the second course of chemotherapy. The same bacteria were also found in his intestinal contents, with no gastrointestinal symptoms. We assume that the bacteria found in the blood was derived from his own intestinal contents. When bacteremia occurs in lung cancer patients during chemotherapy, an uncommon strain such as H. cinaedi is a possible causative agent.

[Two cases of respiratory infection complicating treatment with infliximab].

Infliximab, an anti-TNF-alpha agent, is highly effective against rheumatoid arthritis and Crohn's disease. However, respiratory infection can occur as a complication. We report two cases complicated by respiratory infection following administration of infliximab. The first case, a 67-year-old woman with rheumatoid arthritis, developed pneumocystis pneumonia after three courses of infliximab therapy. The second case, a 31-year-old man with Crohn's disease, developed pulmonary tuberculosis after four courses of infliximab therapy. Respiratory complications associated with anti-TNF therapy include infectious diseases such as pneumocystis pneumonia, tuberculosis, and bacterial pneumonia. They often lead a fulminant course, and early diagnosis is essential. The final report of a survey of the initial 5000 cases with rheumatoid arthritis treated with infliximab in Japan was released in April 2006; pulmonary infectious complications included 22 cases of pneumocystis pneumonia, 14 cases of tuberculosis, and 108 cases of bacterial pneumonia. The growing use of anti-TNF therapy might lead to increasing pulmonary complications. Accumulation of similar cases is expected to elucidate the mechanism of the complications and methods for effective prophylaxis.

[A case of salazosulfapyridine-induced pneumonitis presenting with multiple pulmonary nodules and lymphadenopathy].

We report a rare case of drug-induced pneumonitis, probably caused by salazosulfapyridine, showing a radiographic pattern of multiple pulmonary nodules and lymphadenopathy. An 18-year-old woman was admitted to our hospital because of fever, skin rash, dry cough and dyspnea on exertion. She had been given salazosulfapyridine for two weeks to treat Crohn's disease. A chest radiograph and computed tomographic scan showed multiple nodular shadows in both lung fields, mediastinal lymphadenopathy, and bilateral pleural effusions. Cessation of salazosulfapyridine followed by corticosteroid therapy led to an immediate symptomatic improvement. The drug-induced lymphocyte stimulation test for salazosulfapyridine was negative. The same symptoms reappeared with rechallenge of SASP, however, which led to diagnosis as salazosulfapyridine-induced pneumonitis. This is apparently the first case report of salazosulfapyridine-induced pneumonitis with a radiographic pattern of multiple pulmonary nodules; accumulation of similar case reports are needed to confirm the association.

Noncardiogenic pulmonary edema in low-dose oral methotrexate therapy.

In the past two decades, low-dose methotrexate (MTX) has been widely used in the treatment of rheumatoid arthritis (RA). As adverse effects, various types of pulmonary toxicity have been reported with this therapy. We report a case of MTX-induced noncardiogenic pulmonary edema in a 35-year-old woman. MTX used in high dose for anti-cancer therapy is known to cause non-cardiogenic pulmonary edema. However, there are no previous reports of noncardiogenic pulmonary edema caused by low-dose MTX therapy. This report suggests that patients receiving oral weekly, low-dose MTX may be at risk for the development of noncardiogenic pulmonary edema.

[A case of bronchial ulcer due to infection by Mycobacterium abscessus].

We present a rare case of tracheobronchitis caused by Mycobacterium abscessus. The patient was a 79-year-old man with a previous history of tuberculosis. For smear examinations, he repeatedly expectorated many acid-fast bacilli. Bronchoscopic examination revealed the presence of ulceration on the lower end of the trachea and extending to the right main bronchus. Mycobacterial cultures were used to grow Mycobacterium abscessus. Following an antimicrobial regimen of clarithromycin, amikacin, and cefoxitin, the patient exhibited marked improvement. After initial multidrug therapy, the patient was placed on clarithromycin for 10 months. No relapse has occurred to date.