Factors related to fixedness after transbronchial fiducial marker placement for image-guided proton therapy: A retrospective study.

BACKGROUND: The usefulness of transbronchially inserted gold fiducial markers has been reported in radiation therapy and proton therapy for mobile lesions, such as lung tumors. However, there is occasional dropout of inserted markers. This retrospective study investigated the factors related to dropout of markers inserted for image-guided proton therapy (IGPT). METHODS: Between June 2013 and October 2021, 535 markers were inserted in 171 patients with lung tumors. We investigated whether marker dropout was affected by the location of marker insertion, distance between the marker and the chest wall (DMC), and difference in forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC). Marker dropout from the time of planning computed tomography (CT) to follow-up CT was also evaluated. RESULTS: Of the 535 inserted markers, 417 were confirmed on planning CT and 356 on follow-up CT after IGPT. Multivariate analysis revealed that marker insertion into the upper lobe and FEV1/FVC ≥70% were factors associated with total marker dropout. Marker dropout between planning CT and follow-up CT was associated with DMC, FEV1/FVC ≥70%, and planning CT performed within 4 days of marker insertion. CONCLUSIONS: Marker dropout can be minimized by inserting markers more peripherally, by considering the planned insertion location, and FEV1/FVC. Additionally, planning CT should be scheduled at least 5 days after marker insertion.

Lambert-Eaton Myasthenic Syndrome Caused by Atezolizumab in a Patient with Small-cell Lung Cancer.

We herein report a 74-year-old man who developed Lambert-Eaton myasthenic syndrome (LEMS) during atezolizumab treatment for extensive-stage small-cell lung cancer. He was started on maintenance immunotherapy with atezolizumab every three weeks after four cycles of atezolizumab plus carboplatin plus etoposide combination therapy. After 13 cycles of maintenance atezolizumab therapy, he complained of muscular weakness and fatigue. Findings from a nerve conduction study and positive findings for anti-P/Q-type voltage-gated calcium channel antibody resulted in a diagnosis of LEMS. This was a rare case of LEMS as a neurological immune-related adverse event induced by atezolizumab therapy.

Streptococcal Toxic Shock Syndrome Induced by Group A Streptococcus with the emm28 Genotype That Developed after a Uterine Cancer Test.

A 69-year-old woman without pre-existing disease visited our hospital due to general malaise, diarrhea, and arthralgia 3 days after a uterine cancer test. We diagnosed her with sepsis of unknown focus and started treatment immediately, but she died 20 hours after the first visit due to multi-organ failure and septic shock. Later, group A streptococcus was detected from the blood culture, and streptococcal toxic shock syndrome (STSS) was diagnosed. The strain had the emm28 genotype and a mutation in csrR with increased NADase activity. These virulence factors were considered to be related to STSS development in this patient.

Concurrent Chemo-Proton Therapy Using Adaptive Planning for Unresectable Stage 3 Non-Small Cell Lung Cancer: A Phase 2 Study.

PURPOSE: This study prospectively evaluated the efficacy and safety of concurrent chemo-proton therapy (CCPT) using adaptive planning for unresectable stage III non-small cell lung cancer (NSCLC). METHODS AND MATERIALS: The primary endpoint was overall survival (OS). Secondary endpoints were local control rate (LCR), progression-free survival (PFS), incidence of grade 3 or higher adverse events, and changes in quality of life (QOL). Patients received cisplatin (60 mg/m2) on day 1 and S-1 (∼40 mg/m2 twice daily) on days 1 to 14, q4w, for up to 4 cycles, plus concurrent proton therapy at a total dose of 70 GyRBE for the primary lesion and 66 GyRBE for lymph node metastasis with 2 GyRBE per day. Proton therapy was performed using respiratory-gated and image guided techniques, and adaptive plans were implemented. RESULTS: Forty-seven patients were enrolled between August 2013 and August 2018. Four cycles of cisplatin plus S-1 were completed in 34 patients. The mean number of cycles was 4 (range, 1-4). The median follow-up of all and surviving patients was 37 (range, 4-84) and 52 months (range, 26-84), respectively. The mean number of replanning sessions was 2.5 (range, 1-4). The 2- and 5-year OS, LCR, and PFS were 77% (95% confidence interval 64%-89%) and 59% (43%-76%), 84% (73%-95%) and 61% (44%-78%), and 43% (28%-57%) and 37% (22%-51%), respectively. The median OS was not reached. No grade 3 or higher radiation pneumonitis was observed. There was no significant deterioration in the QOL scores after 24 months except for alopecia. CONCLUSIONS: CCPT with adaptive planning was well tolerated and yielded remarkable OS for unresectable stage III NSCLC.

Disseminated Mycobacterium avium Infection Complicated with Chylous Ascites in a Patient with Neutralizing Autoantibodies to Interferon-γ.

A 68-year-old man visited our hospital due to anorexia, weight loss and a fever. We diagnosed the patient with disseminated Mycobacterium avium complex (MAC) and confirmed the presence of interferon (IFN)-γ neutralizing autoantibodies (IFN-γAb). His lesions improved following antibiotic therapy, but chylous ascites (CA) developed seven months after treatment. CA was able to be controlled by subcutaneous octreotide and diet therapy. IFN-γAb is recognized as having a critical role in the pathogenesis of disseminated MAC disease, but its clinical features are not fully understood. CA may be a complication that develops during the treatment of disseminated MAC infection.

Pulmonary Mycobacterium abscessus Subspecies abscessus Disease That Showed a Discrepancy Between the Genotype and Phenotype of Clarithromycin Resistance.

Mycobacterium abscessus subspecies abscessus is major subspecies in the M. abscessus complex and is usually refractory to standard antibiotherapy. Genetic tracing of erm (41) T28 is a mechanism for monitoring macrolide resistance. We treated a patient with a pulmonary infection caused by M. abscessus subsp. abscessus with the erm (41) T28 polymorphism, which was susceptible to clarithromycin, and his clinical treatment course was good. The identification of the M. abscessus complex genotype is important, but clinical confirmation of clarithromycin susceptibility is also needed to plan individual treatment strategies.