Sarcoidosis with Pancreatic Mass, Endobronchial Nodules, and Miliary Opacities in the Lung.

Sarcoidosis affects multiple organs and rarely has unusual manifestations. A 78-year-old woman was referred to our hospital for coughing symptoms. A chest computed tomography (CT) scan revealed bilateral diffuse miliary patterns and right pleural effusion. Bronchoscopy showed multiple nodules in the carina and the bronchus intermedius. A CT scan of her abdomen revealed hypovascular lesions involving the pancreatic head and body. A transbronchial lung biopsy, bronchial mucosal biopsy, and endoscopic ultrasound-guided fine-needle aspiration of the pancreatic mass demonstrated non-caseating granulomas. We diagnosed the patient with sarcoidosis. She received no treatment for sarcoidosis and has been followed up for one year, during which no pulmonary disease progression had been observed and the pancreatic masses partially regressed.

[Outcome of pulmonary Mycobacterium avium complex (MAC) disease treated with clarithromycin (CAM)-containing regimens].

We retrospectively investigated the efficacy of regimens including clarithromycin (CAM) in 129 patients with Mycobacterium avium complex (MAC) pulmonary disease and their outcomes. None of the patients suffered from acquired immunodeficiency syndrome. All were observed for over 12 months. We studied the factors that may affect sputum conversion and fatal outcomes by logistic regression analysis. The results indicated that the presence of either cavitation or bronchiectasis was significantly correlated with persistent MAC-positive culture results in sputum (Odds ratio, 4.71, 95%; CL, 1.21-18.5; P<0.05). Regimens including antituberculous drugs and CAM were administered to 118 patients, 11 of whom received CAM alone because of the adverse events of antituberculous agents. There was no difference in sputum conversion or mortality between the two groups, suggesting that the pattern of drug combination should be further investigated.

[A case of subacute idiopathic interstitial pneumonia resistant to steroids, successfully treated with cyclophosphamide].

A 47-year-old woman was admitted to our hospital because of dry cough, fever, and subacute, progressive dyspnea. Chest radiography and computed tomography showed ground glass opacities in the lower lung fields. We suspected pneumonia caused by atypical pathogens and administered antibiotics, but they had no effect at all. Histopathologic findings from a transbronchial lung biopsy (TBLB) included intensive infiltration of mononuclear cells and edema on the alveolar wall with no evidence of fibrosis, fibroblasts, hyaline membrane, or granuloma. On the basis of these findings, we suspected interstitial pneumonia, but a surgical lung biopsy was not possible because the patient would not give her consent. After TBLB, corticosteroid was administered repetitively, but dyspnea was deteriorating as the ground glass opacities became more widespread, and tractional bronchiectasis appeared throughout the lung fields. Therefore, we decided to administer cyclophosphamide (CPA). This was very effective: all of her symptoms improved and the ground glass opacities and tractional bronchiectasis disappeared. Though we tapered and then discontinued corticosteroids a few months after CPA, there was no recurrence whatever. No signs suggesting the association of collagen vascular diseases were detected. The effectiveness of CPA in interstitial pneumonia associated with collagen vascular disease is occasionally reported, but the effect on idiopathic interstitial pneumonia, especially in acute and subacute progressive cases, is rarely reported. We think this is an interesting case to consider the availability of CPA in idiopathic interstitial pneumonia with subacute progression.

Elevated complement C3a in plasma from patients with severe acute asthma.

BACKGROUND: Complement component C3a, an anaphylatoxin, provokes acute inflammatory responses, including smooth muscle contraction, mucus hypersecretion, increase in vascular permeability, and recruitment of inflammatory cells. Thus C3a may be related to airway inflammation and bronchoconstriction in acute asthma exacerbation. OBJECTIVE: We sought to determine whether plasma C3a is elevated in patients presenting for emergency treatment of acute asthma exacerbations and to correlate C3a concentrations with response to therapy. METHODS: Plasma C3a and serum eosinophil cationic protein were measured in 52 patients with acute asthma with peak expiratory flow of < or =50% the predicted value. Control subjects were 42 patients with stable chronic asthma. Patients with severe acute asthma were classified into 2 groups (admitted and discharged), according to how effective inhaled bronchodilators and systemic corticosteroids were in the first 2 hours of treatment. RESULTS: Concentrations of C3a in plasma from subjects in the admitted group (median, 256 ng/mL; range, 94 to 454) were significantly higher than those in the discharged group (197 ng/mL; 72 to 300) or those in patients with stable chronic asthma (166 ng/mL; 89 to 254; P <.0001). Elevated plasma C3a concentrations in admitted asthmatic patients decreased significantly by 7 days after admission (P =.0005). No significant difference was evident in serum eosinophil cationic protein concentration between the admitted group (33.1 microg/L; 6.3 to 143) and the discharged group (32.7 microg/L; 14.6 to 160; P =.99). CONCLUSIONS: Concentrations of C3a, which can induce airway inflammation and bronchoconstriction, were associated with differences in response to emergency treatment of severe asthma exacerbation.

Efficacy of a consensus protocol therapy in adults with acute, severe asthma.

BACKGROUND: International guidelines recommend multiple doses of inhaled beta2-agonists and anticholinergics plus early administration of systemic corticosteroids for acute, severe asthma. This study examined the efficacy of this protocol in adults and analyzed those factors associated with unresponsiveness to the protocol therapy. OBJECTIVE: Ninety-three consecutive patients 18 to 55 years old presenting for treatment of acute asthma with a peak expiratory flow rate (PEFR) < or = 50% of the predicted value were analyzed. METHODS: All subjects received 400 microg of salbutamol every 20 minutes for three doses and 400 microg of oxitropium bromide with each of the three salbutamol doses by means of a metered-dose inhaler with a spacer device, plus intravenously 8 mg betamethasone. PEFR was measured at baseline and at 20, 40, 60, and 120 minutes. RESULTS: Sixty-nine percent of subjects improved sufficiently to be discharged. In 31% of subjects, the protocol therapy failed. There were no significant differences in age, sex, smoking status, or beta-agonist use within 6 hours between the two groups. Logistic regression analysis demonstrated that a PEFR < 35% of the predicted value at presentation (odds ratio [OR]; 16.3, 95% confidence interval [CI] 4.5 to 59.9), viral respiratory tract infection symptoms > or = 2 days (OR, 4.8, 95% CI 1.3 to 17.1), and asthma hospitalization in the past year (OR, 4.6, 95% CI 1.1 to 19.9) were significantly associated with unresponsiveness to the protocol. CONCLUSIONS: Unresponsiveness to protocol therapy occurs in nearly one-third of individuals presenting with acute, severe asthma. Our findings underscore the need to explore more effective strategies for improving lung function and reducing hospital admission rates.