Caudal epidural anesthesia during intracavitary brachytherapy for cervical cancer.

It has been suggested that pain control during intracavitary brachytherapy for cervical cancer is insufficient in most hospitals in Japan. Our hospital began using caudal epidural anesthesia during high-dose-rate (HDR) intracavitary brachytherapy in 2011. The purpose of the present study was to retrospectively investigate the effects of caudal epidural anesthesia during HDR intracavitary brachytherapy for cervical cancer patients. Caudal epidural anesthesia for 34 cervical cancer patients was performed during HDR intracavitary brachytherapy between October 2011 and August 2013. We used the patients' self-reported Numeric Rating Scale (NRS) score at the first session of HDR intracavitary brachytherapy as a subjective evaluation of pain. We compared NRS scores of the patients with anesthesia with those of 30 patients who underwent HDR intracavitary brachytherapy without sacral epidural anesthesia at our hospital between May 2010 and August 2011. Caudal epidural anesthesia succeeded in 33 patients (97%), and the NRS score was recorded in 30 patients. The mean NRS score of the anesthesia group was 5.17 ± 2.97, significantly lower than that of the control group's 6.80 ± 2.59 (P = 0.035). The caudal epidural block resulted in no side-effects. Caudal epidural anesthesia is an effective and safe anesthesia option during HDR intracavitary brachytherapy for cervical cancer.

Successful hyperbaric oxygen therapy for laryngeal radionecrosis after chemoradiotherapy for mesopharyngeal cancer: case report and literature review.

Laryngeal radionecrosis is one of the most troublesome late complications of radiotherapy, because it is frequently resistant to treatment and laryngectomy is required in the worst case. Here, we report a case of laryngeal radionecrosis, successfully treated by use of hyperbaric oxygen (HBO) therapy, in which laryngectomy was avoided. A 67-year-old male received radical chemoradiotherapy (CRT) for mesopharyngeal cancer, which included radiotherapy with a total dose of 71.4 Gy/38 Fr and chemotherapy with CDDP + S-1. He developed dyspnea and throat pain 9 months after completion of CRT. Laryngoscopy revealed vocal cord impairment because of severe laryngeal edema. He was diagnosed as having laryngeal radionecrosis and initially received conservative therapy combined with antibiotics, steroids, and prostaglandins. Because his dyspnea was persistent despite this treatment, HBO therapy was administered 20 times, and resulted in complete remission of the dyspnea. HBO therapy, therefore, is regarded as an effective conservative therapeutic option for laryngeal radionecrosis.

Glucose-6-phosphate dehydrogenase is a regulator of vascular smooth muscle contraction.

Glucose-6-phosphate dehydrogenase (G6PD) is the rate-limiting enzyme in the pentose phosphate pathway and a major source of nicotinamide adenine dinucleotide phosphate reduced (NADPH), which regulates numerous enzymatic (including glutathione reductase and NADPH oxidase that, respectively, generates reduced glutathione and reactive oxygen species) reactions involved in various cellular actions, yet its physiological function is seldom investigated. We, however, recently showed that inhibiting G6PD causes precontracted coronary artery (CA) to relax in an endothelium-derived relaxing factor- and second messenger-independent manner. Here we assessed the role of G6PD in regulating CA contractility. Treating bovine CAs for 20 min with potassium chloride (KCl; 30 mM), amphotericin B (50 µM), or U46619 (100 nM) significantly (p < 0.05) increased both G6PD activity and glucose flux through the pentose phosphate pathway. The effect was Ca(2+) independent, and there was a corresponding increase in protein kinase C (PKC) activity. Activation of G6PD by KCl was blocked by the PKCδ inhibitor rottlerin (10 µM) or by knocking down PKCδ expression using siRNA. Phorbol 12, 13-dibutyrate (10 µM), a PKC activator, significantly increased G6PD phosphorylation and activity, whereas single (S210A, T266A) and double (S210A/T266A) mutations at sites flanking the G6PD active site significantly inhibited phosphorylation, shifted the isoelectric point, and reduced enzyme activity. Knocking down G6PD decreased NADPH and reactive oxygen species generation, and reduced KCl-evoked increases in [Ca(2+)](i) and myosin light chain phosphorylation, thereby reducing CA contractility. Similarly, aortas from G6PD-deficient mice developed less KCl/phorbol 12, 13-dibutyrate-evoked force than those from their wild-type littermates. Conversely, overexpression of G6PD augmented KCl-evoked increases in [Ca(2+)](i), thereby augmenting CA contraction. Our findings demonstrate that G6PD activity and NADPH is increased in activated CA in a PKCδ-dependent manner and that G6PD modulates Ca(2+) entry and CA contractions evoked by membrane depolarization.

Erythema multiforme and Stevens-Johnson syndrome following radiotherapy.

Erythema multiforme (EM) and Stevens-Johnson syndrome (SJS) are thought to be hypersensitivity syndromes with various causes, and radiotherapy might be one of the causes of these syndromes. We herein report two cases of EM/SJS following radiotherapy. The first case was a 63-year-old woman with breast cancer. At the end of postoperative radiotherapy with 60 Gy, severe pruritic erythema appeared in the irradiated area and spread over the whole body. She was diagnosed with EM by a skin biopsy. The second case was a 77-year-old woman with uterine cervical cancer who underwent postoperative radiotherapy. At a dose of 30.6 Gy, pruritic redness appeared in the irradiated area and the precordial region, and it became widespread rapidly with polymorphic transformation. Although without any histological confirmation, SJS was strongly suspected because of her pruritic conjunctivitis. Because both patients were given medicines during irradiation, radiotherapy may not be the only cause of EM/SJS. However, it should be noted that radiotherapy might trigger EM/SJS.

Low pre-radiotherapy prostate-specific antigen level is a significant predictor of treatment success for postoperative radiotherapy in patients with prostate cancer.

BACKGROUND: The optimal role of postoperative radiotherapy for patients with prostate cancer remains undefined. MATERIALS AND METHODS: The medical records of 70 patients (median age: 66 years), who had received radical radiotherapy (RT) between the years 1996 and 2004 after radical prostatectomy (RP), were analyzed. Fifteen patients had received immediate adjuvant RT, while the other 55 patients had received salvage therapy. Hormonal therapy had been performed in 28 patients before RT and continued in two of them concurrently with RT. A median dose of 60 Gy was delivered to the prostate bed. Pelvic node irradiation was performed in all patients. RESULTS: After a median follow-up period of 23 months, 21 patients had experienced biochemical failure. Actuarial 3- and 5-year biochemical relapse-free survival estimates were 67.4%. No patient had local failure, although distant metastases with biochemical failure were found in five patients. On univariate analysis, the following were significant for biochemical failures: seminar vesicle involvement, serum PSA level >1 ng/ml before RT, pathological pelvic node involvement, RT indication (adjuvant vs. salvage) and Gleason score. However, only the serum PSA level before RT was significant on multivariate analysis. CONCLUSION: Postoperative RT with a pre-RT PSA level <0.1 ng/ml seemed to be effective in patients with prostate cancer.