Liver Injury Due to Penetration of the Common Iliac Vein by an Extracorporeal Membrane Oxygenation Cannula.

Extracorporeal membrane oxygenation (ECMO) cannulas inserted through the femoral vein can stray into the ascending lumbar vein. No case has been reported in which the cannula has penetrated the common iliac vein and entered the abdominal cavity. A 52-year-old man was brought to the emergency room with ventricular fibrillation, and the cannula inserted from the left femoral vein for extracorporeal cardiopulmonary resuscitation penetrated the common iliac vein, passed between the pancreas and horizontal portion of the duodenum, and entered the abdominal cavity to reach the hepatic left lateral lobe. The cannula was removed, and organ damage was confirmed through laparotomy. When it is necessary to remove a cannula that has penetrated a vessel, surgical removal is preferable to evaluate the damage and prevent complications associated with removal.

Isolated Superior Mesenteric Artery Dissection following Blunt Trauma: A Case Report.

Isolated superior mesenteric artery dissection (ISMAD) is rare, with symptoms ranging from asymptomatic to acute intestinal ischemia. Risk factors for ISMAD include hypertension, atherosclerosis, abnormal elastic fibers, and pregnancy. In the present case, blunt trauma, which has not been previously reported, was suggested as a risk factor. A 46-year-old man was brought to the emergency room after he was found unconscious after a motor vehicle collision. At presentation, he had no abdominal symptoms; however, on the fourth day of admission, he presented with severe abdominal pain and vomiting. A contrast-enhanced computed tomography scan revealed an ISMAD with associated intestinal ischemia and necrosis; hence, emergency surgery was performed. Herein, we report a case of ISMAD caused by blunt abdominal trauma.

Enterolith Causing Afferent Loop Perforation After Distal Gastrectomy.

Afferent loop syndrome is a complication that occurs after the Billroth Ⅱ reconstruction or Roux-en-Y reconstruction and can also be caused by enteroliths. We experienced a case of duodenal perforation due to afferent loop syndrome caused by an enterolith, in which surgical removal of the enterolith and decompression of the duodenum were effective. A 73-year-old female who underwent distal gastrectomy and Roux-en-Y reconstruction for gastric cancer 14 years ago came to the hospital with acute abdominal pain and underwent emergency surgery for afferent loop syndrome and duodenal perforation due to enterolith. The patient underwent removal of the enterolith, drain placement, and placement of a decompression tube in the duodenum. Postoperatively, percutaneous drainage of the intra-abdominal abscess was necessary, but the patient was saved without reoperation. Afferent loop perforation may occur with obstruction due to enteroliths, and the surgical insertion of a tube to decompress the afferent loop is effective.

Preperitoneal herniation after transabdominal preperitoneal patch plasty: a case report.

Hernial repair is a common procedure performed by general surgeons. The use of laparoscopic hernial repair has recently increased; it was introduced in the 1980s, is minimally invasive and has few complications. However, because of this increase, rare complications that were previously unknown have been reported. A 63-year-old man underwent transabdominal preperitoneal patch plasty (TAPP) for a left inguinal hernia. Tension was felt in the peritoneum during peritoneal closure. On the fifth postoperative day, the patient was admitted for small bowel obstruction (SBO) and underwent reoperation; the closed peritoneum was lacerated, causing SBO because of herniation of the preperitoneal space. After the hernia was released, the peritoneum was closed again, and the surgery was completed. SBO after TAPP surgery is a rare complication. Several reports have shown staplers, barbed sutures and tacks causing SBO; this complication can be prevented with appropriate peritoneal closure techniques and treated with early laparoscopic surgery.

Laparoscopic subtotal cholecystectomy for Mirizzi syndrome: A report of a case.

INTRODUCTION: Mirizzi syndrome is a rare complication of gallstone disease. The purpose of this report is to describe the utility of laparoscopic subtotal cholecystectomy for Mirizzi syndrome. PRESENTATION OF CASE: A 53-year-old female presented with dark urine and right upper quadrant pain. Blood tests revealed elevated liver and biliary enzyme levels. Magnetic resonance cholangiopancreatography showed a narrowed common hepatic duct compressed by a large gallstone, consistent with Mirizzi syndrome. Semi-urgent laparoscopic cholecystectomy was planned. At operation, circumferential dissection of the gallbladder neck was difficult. The fundus of the gallbladder was opened and a 2 cm stone extracted. The gallbladder neck was sutured and a drain placed. The postoperative clinical course was uneventful. DISCUSSION: After laparoscopic cholecystectomy in patients with Mirizzi syndrome, complication rates, including bile duct injuries, is high. In patients with Mirizzi syndrome, removal of the responsible stone is the main purpose of treatment. CONCLUSION: Laparoscopic subtotal cholecystectomy is a useful technique for patients with Mirizzi syndrome to avoid bile duct injury.

Metastatic colon cancer derived from a diverticulum incidentally found at herniorrhaphy: a case report.

BACKGROUND: There are few reports of metastases from colon cancer to an inguinal hernia sac, and few reports of colon cancer originating in diverticula. We report a patient with carcinoma of the sigmoid colon arising in two diverticula, who presented with peritoneal seeding to an inguinal hernia sac, and a review of the literature. CASE PRESENTATION: A 55-year-old male underwent open herniorrhaphy for a left inguinal hernia. At operation, a nodule in the inguinal hernia sac was resected and histologic examination revealed adenocarcinoma, which was suspected to be a metastasis from a distant primary lesion. Postoperative evaluation included colonoscopy and positron emission tomography which showed two suspected lesions in sigmoid diverticula. Laparoscopic subtotal colectomy was performed, and pathology revealed adenocarcinoma in two sigmoid diverticula. CONCLUSIONS: If a nodule is found in an inguinal hernia sac, especially in older patients, peritoneal metastases should be considered. Resection of the nodule with histopathologic evaluation is essential. Colon cancer arising in a diverticulum should be considered as a possible site of the primary lesion.

[A case of breast adenocarcinoma changed to squamous cell carcinoma after neoadjuvant chemotherapy].

Squamous cell carcinoma(SCC)of the breast is a rare pathological-type cancer with an unclear origin. It has been suggested that breast SCC may originate from squamous metaplasia of the ductal epithelium. We report a case of SCC of the breast which histological carcinoma type changed after neoadjuvant chemotherapy. A 66-year-old woman visited our hospital for a tumor of the left breast. Mammography indicated breast cancer. On CT scan the tumor was 40mm in diameter, and was located in the upper lateral quadrant of the left breast. Because she requested breast-conserving surgery, core needle biopsy(CNB)was performed. The histological findings showed solid-tubular adenocarcinoma, PgR(-), ER(-), HER2(-), cT2cN1cM0, cStage II B. She received neoadjuvant chemotherapy consisting of 4 courses of CEF(cyclophosphamide, epirubicin, 5-fluorouracil)and 3 courses of paclitaxel. After chemotherapy, she was considered to have progressive disease, and a modified radical mastectomy was performed. The resected tumor was cystic and 60mm in diameter, containing muddy fluid. Histopathological examination showed pure squamous cell carcinoma, PgR(-), ER(-), HER2(-), pT3pN0pM0, pStage II B. The cancer metastasized with the light axillary lymph nodes at the 6th month after the operation, and she underwent chemo-radiation therapy. She died 6 years after the operation from brain metastasis.

[A case of esophageal small cell carcinoma with syndrome of inappropriate antidiuretic hormone secretion].

A 66-year-old man was referred to our hospital with esophageal tumor. He was diagnosed with esophageal small cell carcinoma by endoscopic biopsy. He had a low serum sodium level at admission and was diagnosed syndrome of inappropriate secretion of antidiuretic hormone (SIADH). His CT scan revealed esophageal wall thickness and swelling of thoracic and abdominal lymph nodes. He was classified as Stage IV a (cT3cN4cM0). He received systemic chemotherapy with CDDP and CPT-11. After three courses of chemotherapy, his tumor disappeared on CT scan and endoscopy. He was diagnosed as in complete remission and his SIADH recovered. The patient was then discharged and visited our outpatient clinic. Seven months after diagnosis, a tumor recurrence was indicated by CT scan and endoscopy. He received radiation therapy, and chemotherapy of paclitaxel, followed by CBDCA+VP-16. He is presently alive sixteen months after diagnosis.

[Efficacy of FEC and trastuzumab/docetaxel combination therapy for metastatic breast cancer].

A 56-year-old female visited our department due to bleeding from a mass in her left breast in November 2007. There was a tumor (diameter, 5 cm) accompanied by ulcer formation and fixation to the pectoral muscle, centering on the left breast Carea. CT examination showed multiple lung metastasis and liver metastasis. Core needle biopsy demonstrated scirrhous carcinoma. The tumor was positive for ER and strongly positive for HER2. After 4 courses of FEC100, 10 courses of trastuzumab / docetaxel combination therapy were performed for a total of 30 weeks. After the therapy, the breast tumor decreased in size, and the lung and liver metastatic lesions disappeared, showing a partial response (PR). FDG-PET examination revealed no abnormal accumulation. In February 2009, left mastectomy was performed. Pathological examination revealed Grade 2b and only a slight residue of cancer cells. This patient with advanced breast cancer accompanied by distant metastasis responded to trastuzumab/docetaxel combination therapy.

[A fatal case of meningeal carcinomatosis in a stage IV rectal cancer patient who had long time survival by multi- line chemotherapy].

A 65-year-old man was referred with Stage IV rectal cancer with lung and liver metastasis. He had done low anterior resection. One month after operation, he was administered anti-cancer drugs of FOLFOX4 protocol. Six months after operation, partial response was obtained of abdominal CT scan evaluation. Nine months after operation, FOLFOX4 was stopped by peripheral nerve injuries. FOLFIRI protocol started as second-line chemotherapy. Nineteen months after operation, he was diagnosed left hydro-nephrosis by retro peritoneal lymph-node metastasis. He was treated by urethral stenting, and FOLFOX protocol was re-started. Twenty one months after operation, FOLFOX4 was stopped by drug allergy, and changed to FOLFIRI protocol. Twenty five months after operation, He felt difficulty of walking and dizziness. He was diagnosed meningeal carcinomatosis by brain CT scan. He was administered glycerol and steroid. His neurological symptoms was improved. Although he died of disease progression at twenty six months after operation.

Erythropoietin attenuates cachectic events and decreases production of interleukin-6, a cachexia-inducing cytokine.

In cancer cachexia, erythropoietin often yields beneficial therapeutic effects by improving patient's metabolic and exercise capacity via an increased erythrocyte count. However, erythropoietin also has counter-regulatory effects against pro-inflammatory cytokines, which are postulated to be mediators of cancer cachexia. We investigated the mechanisms by which erythropoietin improves the cachectic condition. In this study, 100 Units/day of erythropoietin were administered intraperitoneally to BALB/c male mice, carrying a subclone of colon 26 adenocarcinoma, beginning on the day after tumor inoculation and continuing until they died. Erythropoietin administration attenuated the decline in body weight, as well as the decline in fat and muscle weights, of tumor-bearing mice, but improved the survival of cachectic mice. Mice receiving erythropoietin had increased erythrocyte and platelet counts, but significantly decreased white blood cell count. In addition, erythropoietin administration significantly decreased interleukin-6 levels, not only in serum but also in the inoculated tumor. These results indicate that the positive therapeutic effects of erythropoietin on cancer cachexia are due, not only to improving metabolic and exercise capacity via an increased erythrocyte count, but also to attenuation of cachectic manifestations by decreased production of the cachexia-inducing cytokine, interleukin-6.

Granulocyte/macrophage colony-stimulating factor and interleukin-4-induced dendritic cells.

BACKGROUND: We investigated whether GM-CSF/IL-4 is the most efficient cytokine combination for differentiating dendritic cells (DC) in terms of its ability to elicit an antitumor immune response. MATERIALS AND METHODS: Two experimental models were examined: C57BL/6 mice bearing MC38 cells and Balb/c mice bearing cachexia-inducible Colon-26 cells. After immunization with DC pulsed with whole tumor cell lysate, tumors were inoculated into the subcutis. RESULTS: C57BL/6 mice immunized with lysate-pulsed DC effectively rejected the MC38 challenge and detectable MC38-specific cytotoxic lymphocytes (CTL) were observed. However, even those groups immunized with lysate-pulsed DC exhibited no protective immunity against Colon-26 challenge in Balb/c mice. Unexpectedly, mice inoculated with lysate-unpulsed DC showed an acceleration of cachectic progression (p=0.031) compared to control mice. CONCLUSION: We speculate that GM-CSF/IL-4-induced DC promotes Th2-dominated immunity in Balb/c mice. Consideration might be given to which combination of cytokines is appropriate for the ex vivo differentiation of DC in tumor immunotherapy.

Incidental adenomas of the human pituitary gland.

Using conventional histological technique, we investigated 44 adenomas (31 men, 13 women) incidentally found in 36 pituitaries (25 men, 11 women) obtained from 1,117 unselected autopsies. The overall incidence of adenomas was 3.2% (men, 3.8%; women, 2.4%) without any significant sex predominance. Size, age distribution, and histological appearances of these adenomas were similar to those previously reported by others. Statistical analysis showed that the adenomas had a predilection for occurrence at the anterior margin of the gland. We further investigated 33 available adenomas with immunohistochemistry using antibodies for various adenohypophyseal hormones, S-100 protein, and glial fibrillary acidic protein, of which 6 contained growth hormone, 3 contained growth hormone and prolactin, 7 contained prolactin, 6 contained follicle-stimulating hormone, 3 contained follicle-stimulating and luteinizing hormones, 2 contained thyroid-stimulating and adrenocorticotrophic hormones (separately), and 6 contained no adenohypophyseal hormones. None of adenomas revealed neoplastic proliferation of folliculostellate cells. To investigate tumor proliferation, nucleolar organizer regions were studied in 9 adenomas using the argyrophil method. The mean number per nucleus was slightly higher than that of corresponding, nontumorous adenohypophysis at a statistically significant level. No adenoma caused symptoms of adenohypophyseal hormone abnormalities.

Immunohistochemical study of crooke's hyaline change.

Crooke's hyaline change of the human pituitary gland appears as an intracytoplasmic accumulation of fine filaments under electron microscopy. This study was attempted to identify the fine filaments by immunohistochemical methods. Twenty-eight postmortem, formalin-fixed or chrome-alum-fixed, paraffin-embedded pituitary glands revealing unequivocal Crooke's hyaline change on hematoxylin and eosin stain were selected for this study. To demonstrate Crooke's cells and fine filaments simultaneously, mirror image sections were sliced and stained with the following monoclonal antibodies using an avidin-biotin-peroxidase complex method: an antibody against synthesized adrenocorticotropic hormone 1-24, human cytokeratins (55-57 kilodalton [kd] and 68 kd), porcine vimentin (57 kd), porcine desmin (53 kd), bovine neurofilaments (70, 160, and 210 kd), human glial fibrilfary acidic protein (GFAP) (56 kd), and chicken actin. Crooke's cells showed a variable intensity of cytoplasmic staining for 55- to 57-kd cytokeratins, from focal to more even and intense staining revealing a characteristic wide brown ring around the nucleus or beneath the cell membrane. The most severely affected cells were totally replaced by dark brown reaction products with no secretory granules detectable in the cytoplasm. However, 68-kd cytokeratin could not be unequivocally demonstrated. Crooke's cells were all negative for vimentin, desmin, neurofilaments, GFAP, and actin. Thus far, it could be concluded that Crooke's hyaline change was composed of intermediate-subunit molecular weight cytokeratins that are normal constituents of the ACTH cell.

Further immunohistochemical study of crooke's hyaline change.

In a previous study, we immunohistochemically investigated Crooke's hyaline change and concluded that it was composed of cytokeratin. The present study was undertaken to further identify the cytokeratin subfamily by immunohistochemistry. Twenty-eight postmortem, routinely processed pituitary glands revealing unequivocal Crooke's hyaline change were selected. To demonstrate Crooke's cellsand cytokeratin subfamilies simultaneously, serial hori zontal sections were sliced. Using an avidin-biotin peroxidase complex method, one was stained with a monoclonal antibody against synthesized adrenocorticotropic hormone (ACTH) 1-24, and the adjacent ones were stained with one of eight test monoclonal antibodies against cytokeratin subfamilies (containing cytokeratins 1, 3, 7, 8, 13, 18, and 19, and one containing 1,5, 10, and 11, respectively). A different antibody for each type of cytokeratin was applied. Crooke's cells showed a variable intensity of cytoplasmic stainingfor antibodiesagainst cytokeratins 8 and 18 (molecular weight 52.5 and 45 kD, respectively), from focal to more even and intense staining, revealing a characteristic wide brown ring around the nucleus or under the plasmalemma. The most severely affected cells were totally replaced by dark brown reaction products with no secretory granules detectable in the cytoplasm. However, Crooke's cells did not react with other test anticytokeratin antibodies. Thus far, it can be concluded that Crooke's hyaline change was composed of low-molecular-weight cytokeratin subfamilies 8 and 18, which are found in pairs in normal ACTH cells.