A case of cystitis after administration of nivolumab.

A case of cystitis occurring after administration of nivolumab, an anti-programmed death-1 antibody, which was considered to be an immune-related adverse event, is reported. A 62-year-old man with pulmonary squamous cell carcinoma (T4N0M1a Stage IV) was being treated with nivolumab as fourth-line chemotherapy. He was hospitalized for a fever and diarrhea after 3 courses. Fasting and antibiotic medication reduced the fever and alleviated the diarrhea. He then developed cystitis with no evidence of infection. Cystoscopy showed diffused redness and erosion of the bladder mucosa; urine cytology was negative. Imaging examinations showed no abnormalities. Urinary tract pain and hematuria due to nivolumab were diagnosed by exclusion following a bladder biopsy. Since symptomatic treatment was unsuccessful, steroid pulse therapy was given, which resolved the patient's signs and symptoms. The patient was then switched to maintenance prednisolone and tapered gradually. The 4th course of nivolumab was then resumed with concomitant administration of steroid, and it was possible to continue administration of nivolumab without progression of cystitis.

Adult case of accessory cardiac bronchus presenting with bloody sputum.

We report an adult case of accessory cardiac bronchus (ACB) which extended from the carina to the diaphragm. A 32-year-old woman, with a history of frequent respiratory infections since childhood, recently presented with bloody sputum, and was admitted to our hospital. The ACB was detected as a supernumerary bronchus diverging from tracheal bifurcation. Complete resection of the ACB was performed by video-assisted thoracic surgery via minithoracotomy, approaching from the 5th intercostal space. The bloody sputum was caused by chronic inflammation of the ACB. She has been asymptomatic since surgery.

Monomethoxypolyethylene glycol-modified cardiac myosin treatment blocks the active and passive induction of experimental autoimmune myocarditis.

BACKGROUND: Injecting various protein antigens conjugated to monomethoxypolyethylene glycol (mPEG) results in antigen-specific tolerance to subsequent immunization. In the present study the ability of mPEG-modified cardiac myosin (CM) to block the development of experimental autoimmune myocarditis (EAM) induced by CM immunization or by the transfer of lymphocytes from CM-immunized donors was studied. METHODS AND RESULTS: A/J mice were injected with mPEG-CM before active or passive EAM induction. We examined the suppressive mechanism by the transfer of lymphocytes from mPEG-CM-treated mice into naïve mice. To ascertain the cells responsible for suppressing EAM induction, in vivo or in vitro depletion of CD4(+) or CD8(+) T cells was performed. mPEG-CM administered before active or passive EAM induction markedly suppressed the incidence and severity of EAM and reduced CM-specific antibody responses. When lymphocytes from mPEG-CM treated mice were transferred into naïve mice that were then immunized with CM, the suppressive effect was recapitulated. CONCLUSIONS: mPEG-CM treatment blocked the active and passive induction of EAM.

Immunohistochemical study of endocrine cells in ductal adenocarcinoma of the pancreas.

To clarify whether scattered endocrine cells in pancreatic ductal adenocarcinoma are neoplastic or not, we immunohistochemically studied 29 cases of invasive pancreatic ductal adenocarcinomas, 17 with metastases, for chromogranin A, insulin, glucagon, pancreatic polypeptide, serotonin, gastrin, laminin, and Ki-67. Endocrine cells were found in primary sites in 24 cases (82.3%), where endocrine cells showed at least a visibly close location to adjacent islet cells. Although endocrine cells in neoplastic glands were within the neoplastic basement membrane, endocrine cells were not seen in invasive sites beyond the pancreas where islets were not present. Endocrine cells in neoplastic glands were reactive for two or three of the islet hormones in all cases, and different types of hormonal reactivity was recognized in the same neoplastic gland or the same cluster of neoplastic glands in 22 (91.7%) cases, thus suggesting a close relation with islets. Ki-67 did not stain any endocrine cells in ten of the adenocarcinomas studied. In three (10.3%) cases, endocrine cells were found in the intraductal extensions. They may have pre-existed in non-neoplastic ducts. In 17 cases with metastatic sites, all but one had no endocrine cells in the metastases. Serotonin-positive cells were found in one metastatic lymph node in one case. We concluded that most endocrine cells seen in ductal adenocarcinomas of the pancreas are non-neoplastic and are derived from the surrounding islets. Some neoplastic endocrine cells may exist, though their frequency is low.

Gastric inverted hyperplastic polyp. Report of four cases and relation to gastritis cystica profunda.

Gastric inverted hyperplastic polyp (IHP) is a rare type of gastric polyp, and is characterized by downward growth of the hyperplastic mucosal components into the submucosa. To the best ofour knowledge, 16 gastric IHP cases have been described in the English literature, but the pathogenesis has not been established. We report the clinical and pathological findings of four gastric IHP cases. The lesions were mainly composed of hyperplastic foveolar-type glands with focal cystic dilatation. Pyloric type glands, endocrine cells, acinic cell metaplasia, and smooth muscle bundles were also seen as components of the polyp. Two cases (cases 1 and 4) coexisted with multifocal gastritis cystica profunda (GCP) and gastric adenocarcinoma. Case 4 furthermore exhibited an intermediate form between IHP and GCP. We suggest that IHP may be GCP associated with exaggeratedly hyperplastic and metaplastic changes. In case 4, the coexisting gastric carcinoma was mainly located in the submucosa, whilst the mucosal component was minimal. Five out of twenty reported gastric IHP cases, including our cases, coexisted with gastric adenocarcinoma. These facts would lead us to further investigate the relation between gastric IHP and carcinoma.