Very Late Recurrence in Breast Cancer: Is Breast Cancer a Chronic Disease?

Although breast cancer treatments have made great strides in recent decades, there are still many recurrences. Late recurrence is one of the characteristics of breast cancer. Here, we present four cases of recurrence more than 10 years after the initial diagnosis. The time from diagnosis to recurrence was 13 to 20 years in our four cases, which were all estrogen receptor (ER)-positive, and one was also human epidermal growth factor receptor 2-positive. Long-term hormone therapy for 10 years is necessary to prevent late recurrence of breast cancer, but we need to know that late recurrence remains common. Risk factors for late recurrence include ER positivity, progesterone receptor positivity, and low Ki67. The most common sites of recurrence are the lungs/pleura and bones, which was also the case in our experience. It is no exaggeration to say that breast cancer is a chronic disease similar to hypertension and diabetes. This is because breast cancer is not completely cured by surgery alone and lasts for a long time, with patients requiring long-term hormone therapy. Moreover, it can recur even after 10 years or more.

Bilevel positive airway pressure therapy in a patient with myotonic dystrophy and postoperative respiratory failure: A case report.

Respiratory failure is a common complication in patients with myotonic dystrophy (MD) and might be a presenting symptom in the perioperative setting. We report the case of a 59-year-old woman with MD who underwent open cholecystectomy and developed postoperative respiratory failure. Without reintubation, the patient was successfully managed with bilevel positive airway pressure (BiPAP) and was discharged uneventfully. BiPAP may be considered as an alternative for postoperative respiratory failure in patients with MD. Careful observation of patients' postoperative condition and an earlier application of BiPAP are instrumental in avoiding retracheal intubation, which may cause further serious problems in patients with MD.

[A Case of Long-Term Survival Following Two-Stage Surgery for Perforated Advanced Gastric Cancer Caused by Chemotherapy].

A 74-year-old man with bloody vomit was diagnosed as having clinical Stage Ⅳ advanced gastric cancer with lymph node metastasis around the abdominal aorta. Initially, for curative surgery, he was administered neoadjuvant chemotherapy. On day 32, in the second course of chemotherapy containing S-1 after 12 courses of chemotherapy containing S-1 and cisplatin, he developed pan-peritonitis owing to the perforation of gastric cancer caused by chemotherapy, and thus, we performed emergency omental implantation and peritoneal drainage. He was discharged from the hospital after 14 days with no trouble. His gastric cancer was judged to be resectable without retaining metastatic lymph nodes based on intraoperative findings and abdominal computed tomography. Therefore, 3 months after the emergency surgery, he underwent total gastrectomy with D1+(+No. 11d)lymphadenectomy. The postoperative course was uneventful. He rejected adjuvant chemotherapy despite our recommendation. Regrettably, intraabdominal dissemination was observed 15 months after total gastrectomy, and he then received chemotherapy again. He has remained alive for 57 months after the first visit to our hospital.

Modulation of glucocorticoid receptor expression, inflammation, and cell apoptosis in septic guinea pig lungs using methylprednisolone.

The use of glucocorticoids for treatment of sepsis has waxed and waned during the past several decades, and recent randomized controlled trials have evoked a reassessment of this therapy. Most glucocorticoid actions are mediated by its specific intracellular receptors (GRs). Thus we initially evaluated whether sepsis and high-dose corticosteroid therapy can regulate guinea pig pulmonary expression of GRs: active receptor, GRalpha, and dominant negative receptor, GRbeta. Sepsis induction by LPS injection (300 mug/kg ip) decreased mRNA and protein levels of GRalpha and increased protein expression of GRbeta in lungs. High-dose methylprednisolone (40 mg/kg ip), administered simultaneously with LPS, markedly potentiated the decrease in GRalpha expression but slightly affected the increase in GRbeta expression. Consequently, this led to a significant reduction in GRalpha nuclear translocation. Nevertheless, methylprednisolone treatment strongly eliminated LPS induction of NF-kappaB activity, as determined by NF-kappaB nuclear translocation and by gel mobility shift assays. Furthermore, the LPS-induced increase in inflammatory cells in bronchoalveolar lavage fluid was blunted by administration of the corticosteroid. On the other hand, immunofluorescent staining for cleaved caspase-3 showed a marked increase in this proapoptotic marker in lung sections, and terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling (TUNEL) represented an enhanced appearance of cell apoptosis in lungs and spleen when methylprednisolone was given together with LPS. Cell apoptosis is now considered to play a role in the pathogenesis of septic syndrome. We thus suggest that the action of glucocorticoids at high doses to accelerate sepsis-induced cell apoptosis may overwhelm their therapeutic advantages in septic shock.