The prompt and correct recognition of MG following treatment with immune checkpoint inhibitors in patients with cancer is important.

No abstract

Gefitinib, a selective epidermal growth factor receptor tyrosine kinase inhibitor, is an effective treatment for patients with non-small cell lung cancer (NSCLC). Some investigators have recently reported several patients complicated by acute lung injury after the initiation of gefitinib administration. In this report, we investigated the efficacy and adverse events during treatment with gefitinib. The subjects of this study were all of the 110 patients with NSCLC who were treated in our hospital and its eight branch hospitals. Patients received gefitinib at a dose of 250 mg once daily. The response rate was 30%. The frequently reported adverse events were skin disorders, gastrointestinal disturbances, liver dysfunction and acute lung injury. Five of the 12 patients who were considered to have suffered acute lung injury died of progressive respiratory failure. Of the nine patients who had pulmonary fibrosis before use of gefitinib, five developed acute lung injury during the treatment. Sera from three of the 12 patients were evaluated and all three showed increases of surfactant protein (SP)-A, SP-D and KL-6. We conclude that gefitinib was clinically useful. However, several patients suffered acute lung injury which could have been caused by gefitinib. A detection system including SP-A, SP-D and KL-6 as prime candidates as markers should be established as promptly as possible. Clinicians should be aware that treatment of NSCLC with gefitinib involves the risk of acute lung injury and therefore careful consideration should be given before deciding whether or not gefitinib is indicated for treatment. Further study is necessary to elucidate the mechanism of acute lung injury by gefitinib.

The aim of this study is to evaluate the patient positioning uncertainty in noncoplanar stereotactic radiosurgery or stereotactic radiotherapy (SRS/SRT) for intracranial lesions with the frameless 6D ExacTrac system. In all, 28 patients treated with SRS/SRT of 70 treatment plans at our institution were evaluated in this study. Two X‐ray images with the frameless 6D ExacTrac system were first acquired to correct (XC) and verify (XV) the patient position at a couch angle of 0º. Subsequently, the XC and XV images were also acquired at each planned couch angle for using noncoplanar beams to detect position errors caused by rotating a couch. The translational XC and XV shift values at each couch angle were calculated for each plan. The percentages of the translational XC shift values within 1.0 mm for each planned couch angle for using noncoplanar beams were 77.86%, 72.26%, and 98.47% for the lateral, longitudinal, and vertical directions, respectively. Those within 2.0 mm were 98.22%, 97.96%, and 99.75% for the lateral, longitudinal, and vertical directions, respectively. The maximum absolute values of the translational XC shifts among all planned couch angles for using noncoplanar beams were 2.69, 2.45, and 2.17 mm for the lateral, longitudinal, and vertical directions, respectively. The overall absolute values of the translational XV shifts were less than 1.0 mm for all directions except for one case in the longitudinal direction. The patient position errors were detected after couch rotation for using noncoplanar beams, and they exceeded a planning target volume (PTV) margin of 1.0–2.0 mm used commonly in SRS/SRT treatment. These errors need to be corrected at each planned couch angle, or the PTV margin should be enlarged.

Clara cell 10-kD protein (CC10) exhibits potent antiinflammatory properties. G38A polymorphism was found in the CC10 gene. We investigated the genetic influence of the allele on the development of sarcoidosis using case control analysis in a Japanese population (265 sarcoidosis cases and 258 control subjects). The A allele frequency in sarcoidosis cases (45.1%) was significantly higher than healthy control subjects (34.9%, p = 0.0002). According to outcomes, we divided 223 patients with follow-up periods of 3 years or more into two subgroups (55 progressive and 168 regressive disease). The A allele frequency in patients with progressive disease was significantly higher than control subjects (odds ratio = 4.55; 95% confidence interval, 2.97-6.97; p < 0.0001), whereas that of regressive disease was not. The A/A genotypes had significantly lower bronchoalveolar lavage fluid CC10 levels than the G/G (nonsmokers, p = 0.0054, and smokers, p = 0.0045) and G/A genotypes (nonsmokers, p = 0.0022, and smokers, p = 0.0402). The reporter gene assay showed significantly lower reporter activities in the presence of interferon-gamma for the 38A construct than the 38G construct (p = 0.0177). The G38A polymorphism in the CC10 gene may influence protein expression and be associated with the development of progressive sarcoidosis.