[Efficacy of three-dimensional computed tomography for evaluating airway tract involvement in patients with relapsing polychondritis].

The airway tract involvement is known to be one of the most important prognostic factors in patients with relapsing polychondritis (RP). Sequential evaluations of airway tract involvements are necessary, however, the insertion of flexible bronchoscope into the affected airway tract may exacerbate their airway tract stenosis. Three-dimensional computed tomography (3D-CT) showed stenosis of the trachea and bilateral main bronchi in 2 patients with RP. 3D-CT is an effective non-invasive method for evaluating airway tract involvement in RP.

Matrix metalloproteinase-1 polymorphism of promoter region in sarcoidosis and tuberculosis patients.

BACKGROUND AND AIM OF THE WORK: Matrix metalloproteinases (MMPs) are associated with several diseases. MMP-1 is one of the interstitial collagenases and the most highly expressed. Recent studies have found that a single nucleotide polymorphism located in the promoter region of the MMP-1 gene affects transcriptional activity. This polymorphism, 1G/2G, has been reported to associate with several malignant tumors and lung diseases. In this study, we investigated whether this polymorphism is associated with sarcoidosis or tuberculosis. METHODS: Polymerase chain reaction-restriction fragment length polymorphism was used to determine the MMP-1 genotypes of 103 sarcoidosis patients, 105 tuberculosis patients and 106 healthy control subjects. RESULTS: We found no differences in genotype distributions and allele frequency between sarcoidosis or tuberculosis patients and healthy control subjects. In sarcoidosis patients with ocular involvement, a significant increase in 1G/1G or 1G/2G genotype was observed compared with patients without (p = 0.009, odds ratio (OR) = 3.22, 95% confidence interval (CI): 1.34-7.71). In sarcoidosis patients with three or more organs involved, 1G/1G type tended to increase compared with patients without (p = 0.035, OR = 5.17, 95% CI: 1.12-23.9). In tuberculosis patients with cavity formation, an increasing trend of 1G/1G type was observed compared with patients without (p = 0.064, OR = 7.69, 95% CI: 0.89-66.3). CONCLUSIONS: Although MMP-1 polymorphism was not associated with onset risk of sarcoidosis and tuberculosis, the clinical characteristics of both diseases were affected by this polymorphism.

[A case of sarcoidosis with rheumatic features (Löfgren's syndrome)].

Rheumatoid arthritis was diagnosed in a 30-year-old woman with erythema nodosum and arthritic symptoms since 1994, and she was treated with anti-rheumatic agents. Mediastinal and bilateral hilar lymphadenopathy and abnormal pulmonary shadows were detected in 1996, and she was admitted to our hospital in 1997. We also recognized the elevation of ACE and lysozyme, and found granulomas in a transbronchial lung biopsy and an arthrosis synovia biopsy. From these findings, sarcoidosis was diagnosed. Sarcoidosis demonstrating erythema nodosum, arthritis, and bilateral hilar lymphadenopathy is called Löfgren's syndrome. In Caucasians, Löfgren's syndrome is frequently encountered, but it is rare in Japanese. Our case had coexisting arthrosis symptoms, and satisfied the diagnosis criteria of rheumatic arthritis. Therefore, the differential diagnosis was important. We emphasize that it is necessary to consider Löfgren's syndrome when diagnosing patients with rheumatic features, even in Japan.

p185(HER-2/neu) and p21(CIP1/WAF1) expression in primary tumors and lymph node metastases in non-small cell lung cancer.

p185(HER-2/neu), a tyrosine kinase receptor, is one of the target molecules for cancer therapy, and its expression may reduce the sensitivity of tumor cells to anti-cancer drugs. p21(CIP1/WAF1) is a cyclin-dependent kinase inhibitor, and its expression may also be involved in chemoresistance. Non-small cell lung cancer (NSCLC) is a potentially systemic disease, and systemic therapies play an important role in its treatment. However, there have been no studies comparing the expression of these molecules between primary and metastatic tumors. We investigated the expression of p185(HER-2/neu) and p21(CIP1/WAF1) in 57 paired samples of primary NSCLC tumors and corresponding lymph node metastases by immunohistochemistry. Expression of each of p185(HER-2/neu) and p21(CIP1/WAF1) was highly correlated between primary tumors and lymph node metastases, and similar correlations were also obtained when adenocarcinoma and squamous cell carcinoma cases were analyzed individually. However we failed to detect any correlation between p185(HER-2/neu) and p21(CIP1/WAF1) expression. Our results suggested that expression of both p185(HER-2/neu) and p21(CIP1/WAF1) is concordant between primary and metastatic tumors.

[Successful use of immunosuppressive agents for the treatment of progressive rheumatoid interstitial lung disease: a case report].

Interstitial pneumonia (IP) is sometimes a fatal complication of rheumatoid arthritis (RA). We describe a patient with progressive rheumatoid interstitial pneumonia, who responded to intravenous intermittent cyclophosphamide (IV-CY) and cyclosporine (CsA). A 62-year-old man with rheumatoid arthritis was admitted to this hospital because of dyspnea. Examinations on admission revealed that he had active RA with vasculitis and IP Initially, he responded to high-dose corticosteroid therapy. A lung biopsy performed after initial corticosteroid therapy revealed diffuse interstitial pneumonia with marked infiltrations of macrophages into the air spaces. On corticosteroid therapy with prednisolone 30 mg/day, the IP became exacerbated and was refractory to the current high-dose steroid treatment. He responded to intravenous cyclophosphamide, but his IP remained unstable. After CsA treatment was started, a clinical remission was obtained. In this case, CsA was the most effective agent tried. Clinical and pathological considerations led us to speculate that activated alveolar macrophages played a crucial role in the pathogenesis of steroid-resistant IP in this patient, and that the clinical remission induced by CsA may have been due to its inhibitory effect on alveolar macrophages.