[Subtotal Esophagectomy for Mediastinal Lymph Node Oligo-Recurrence of ALK-Positive Lung Adenocarcinoma - A Case Report].

The patient was a 54-year-old woman with anaplastic lymphoma kinase-positive stage III B lung cancer. She received 4 courses of carboplatin(CBDCA)plus paclitaxel(PTX)plus bevacizumab(Bev)chemotherapy and crizotinib. Chemotherapy reduced the size of the primary site and mediastinal lymphadenopathy; however, the right supraclavicular and subcarinal lymph nodes were enlarged again during crizotinib treatment. Because it was an oligo-recurrence, we performed radiotherapy for these lymph nodes and changed systemic chemotherapy to alectinib. After 16 months, the patient exhibited esophageal stenosis due to subcarinal lymphadenopathy. We performed a subtotal esophagectomy, which improved the quality of life, and she was continued on an oral treatment of alectinib. Therefore, we suggest that an invasive surgical treatment is useful for oligo-recurrence cases.

[Advanced lung cancer with recurrence of liver and tracheal metastases responsive to multimodality therapy - a case report].

We report a case of advanced lung cancer with recurrence of liver and tracheal metastases that were responsive to multimodality therapy. The patient was a 77-year-old man who suffered from advanced lung cancer with chronic obstructive pulmonary disease (COPD) and alcohol-induced liver cirrhosis. The primary lung cancer was surgically resected. Eight months after resection of the primary lung cancer, a solitary liver tumor appeared and hepatic resection was performed. Histological findings showed that both the primary lung tumor and the solitary liver tumor were squamous cell carcinoma (SCC). Subsequently, he developed a recurrence in his trachea 8 months after hepatic resection. Radiotherapy, endobronchial argon plasma coagulation (APC), and systemic chemotherapy were administered. The tracheal tumor remained stable without any liver metastasis for 25 months.

Polymorphisms of CYP2D6 gene and gefitinib-induced hepatotoxicity.

INTRODUCTION: Gefitinib induces severe hepatotoxicity in approximately a quarter of Japanese patients with epidermal growth factor receptor (EGFR) mutation-positive non-small-cell lung cancer (NSCLC). Gefitinib is metabolized by cytochrome P450 (CYP) enzymes--including CYP3A4/5, CYP1A1, and CYP2D6--in the liver. We hypothesized that polymorphisms of the CYP2D6 gene may account for gefitinib-induced hepatotoxicity. PATIENTS AND METHODS: Polymorphisms of the CYP2D6 gene were analyzed in 55 patients with NSCLC who experienced grade ≥ 2 transaminase elevation from gefitinib. The distribution of the CYP2D6 genotype was compared with that of the healthy Japanese population. The correlations between the nonfunctional allele *5 or the reduced-function allele *10 and hepatotoxicity-related clinical factors were also examined. RESULTS: The distribution of the CYP2D6 genotype in the study participants was not different from that of the general Japanese population, reported previously. Existence of allele *5 or *10 did not correlate with clinical factors such as onset of hepatotoxicity within 2 months, grade ≥ 3 serum transaminase elevation, and tolerability to dose reduction or rechallenge of gefitinib. However, in 7 patients taking CYP3A4-inhibitory drugs, rechallenge of gefitinib again caused hepatotoxicity in 4 patients with allele *5 or *10 but not in 3 patients with normal alleles (P = .029). Moreover, switching to erlotinib did not cause hepatotoxicity in any of 17 patients with allele *5 or *10 but did in 3 of 8 patients without these alleles (P = .024). CONCLUSION: Reduced function of CYP2D6 may partly account for gefitinib-induced hepatotoxicity when CYP3A4 is inhibited. Erlotinib could be safely used in patients with decreased CYP2D6 activity even after they experienced gefitinib-induced hepatotoxicity.

Anaphylaxis due to intravenous levofloxacin with tolerance to garenoxacin.

Fluoroquinolones are widely used in the management of infectious diseases, and are generally safe and well tolerated. However, immediate hypersensitivity reactions, including anaphylactic reactions, have been reported. We present here a case of anaphylactic shock in a 26-year-old man following intravenous levofloxacin administration. Skin tests confirmed an immediate hypersensitivity reaction to levofloxacin. Subsequent oral challenge tests for garenoxacin, which showed negative skin test results, confirmed that garenoxacin was well tolerated. This is the first report of tolerance to full-dose garenoxacin in a patient who developed an immediate hypersensitivity reaction to levofloxacin.

[A case of relapsing polychondritis monitored by repeated measurements of flow-volume curve].

A 57-year-old man was admitted to our hospital with hoarseness, productive cough, and dyspnea. Chest CT revealed a thickening of the tracheal wall, and the flow-volume curve showed a constrictive upper airway flow pattern. Bronchoscopy revealed disappearance of cartilaginous rings and tracheal stenosis. Biopsy of the cricoid cartilage showed findings compatible with relapsing polychondritis and a diagnosis of relapsing polychondritis was made in accordance with Damiani's criteria. The flow-volume curve and symptoms were immediately improved by methylprednisolone pulse therapy, but on reduction of oral prednisorone, recurrence was identified by flow-volume curve and bronchoscopy. Administration of dapson and cyclophosphamide in addition to oral prednisolone after intravenous methylprednisolone and flow-volume curve resulted in improvement. In this case, monitoring of flow-volume curve was useful for the evaluation of airway complication in relapsing polychondritis.