Background-Glucocorticoid-induced granulocytosis has been attributed to enhanced release of polymorphonuclear leukocytes (PMNs) from bone marrow, delayed apoptosis, and reduced egress of PMNs into tissues. This study was designed to determine the relative contributions of PMNs released from the bone marrow and those entering the circulation from the marginated pool to the granulocytosis produced by a single dose of dexamethasone (2.0 mg/kg) in rabbits. Methods and Results-PMN transit through the mitotic and postmitotic pools of the bone marrow and rate of release of PMNs into the circulation were measured by use of the thymidine analogue 5Ј-bromo-2Ј-deoxyuridine (BrdU) to pulse-label PMNs in the bone marrow. The shift of PMNs from the marginated to the circulating pool was measured with BrdU-labeled PMNs transferred from donor rabbits to recipients before dexamethasone was delivered. The data show that dexamethasone increased bone marrow release of PMNs and shortened their transit time through the postmitotic pool (PϽ0.001) but not the mitotic pool of the bone marrow (PϾ0.05). Dexamethasone slowed the clearance of BrdU-labeled PMNs from the circulation (PϽ0.05) and lengthened their disappearance (half-life) from the circulation compared with control (half-life, 4.95 versus 9.45 hours). At 6 hours after dexamethasone, bone marrow release contributed Ϸ10%, mobilization from the marginated pool Ϸ61%, and a lengthened half-life in the circulation Ϸ29% to the glucocorticoid-induced granulocytosis. Conclusions-We conclude that a single dose of dexamethasone causes a granulocytosis primarily by a shift of PMNs from the marginated to the circulating pool, with a minor contribution from marrow release. (Circulation. 1998;98:2307-2313.)

Introduction The optimal surgical management strategy for isolated para‐aortic lymph node (PALN) metastases from colorectal cancer (CRC) remains unclear. However, the complication rates for open approaches remain high. In this study, the outcomes of laparoscopic para‐aortic lymphadenectomy in patients with clinically suspected PALN metastasis were evaluated. Methods Between April 2013 and April 2018, we performed laparoscopic primary resection and para‐aortic lymphadenectomy in 11 patients with advanced colorectal cancer and clinically suspected PALN metastasis. This study was a single‐center, retrospective, case series analysis, and the surgical outcomes were reviewed. Results There were no cases of perioperative mortality, and conversion to open surgery was necessary in only one patient (9%) because of invasion into a rib. One patient (9%) required a blood transfusion. Postoperative complications occurred in three patients, and the morbidity rate was 27% (3/11). Pathologically, PALN metastasis was confirmed in five patients (45%), all of whom received postoperative chemotherapy. The median survival time for all patients was 25 months, and one patient died of recurrence at 25 months after the initial surgery. Two other patients were alive with recurrence after 47 and 36 months, and two patients were alive without recurrence after 17 and 2 months. Conclusion Laparoscopic para‐aortic lymphadenectomy for advanced colorectal cancer with clinically suspected PALN is technically feasible and may be beneficial in selected patients. It is necessary to investigate the feasibility of this procedure in a future case series, and information regarding true oncologic outcome will require long‐term follow‐up.

When active bone marrow release is induced by inflammatory stimuli, it is associated with an increase in L-selectin expression on circulating polymorphonuclear leukocyte (PMN). This contrasts sharply with glucocorticoid-induced granulocytosis that is associated with decreased L-selectin expression on PMN. The present study was designed to determine if the reduced L-selectin expression observed after glucocorticoid treatment is the result of suppression of L-selectin synthesis in the bone marrow. New Zealand white rabbits treated with dexamethasone (2.0 mg/kg, a single dose intravenously) were shown to have decreased L-selectin expression on circulating PMN 12 to 24 hours after treatment (P < .01) with a return to baseline levels by 48 hours. When dexamethasone was administered 48 hours after the bone marrow PMN were pulse labeled with the thymidine analogue, 5′-bromo-2′-deoxyuridine (BrdU), L-selectin expression on BrdU-labeled PMN released from the bone marrow was decreased (P< .01). Dexamethasone decreased L-selectin expression on segmented PMN in the bone marrow (P < .05) but not on PMN already in the circulation. We conclude that glucocorticoids decrease L-selectin expression on circulating PMN by downregulating L-selectin expression in the maturation pool of bone marrow and speculate that this is an important glucocorticoid effect that influences the recruitment of PMN into inflammatory sites.

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We report a case of spontaneous rupture of a giant cavernous hemangioma of the liver arising from the caudate lobe, with extrahepatic growth, in a 67-year-old man. At emergency laparotomy, partial resection of the caudate lobe was performed and the hemangioma was found to measure 13 x 12 x 8cm. The patient had a 10-year history of severe asthma requiring steroid therapy. To investigate the risk factors for spontaneous rupture of hepatic hemangioma, we compared the characteristics of patients with ruptured and non-ruptured lesions showing extrahepatic growth reported in the Japanese literature. Lesions with a diameter ->4cm located on the surface of the liver or showing extrahepatic growth appear to have a high risk of spontaneous rupture if the patient receives steroid therapy for a coexisting disorder. Even in patients who have not received steroid therapy, hemangiomas ->7-8cm in diameter located in the left lobe with extrahepatic growth may also have a high risk of rupture. The treatment of hepatic hemangioma should be decided on the basis of the size and the location, and on the requirement for steroid therapy.

Background: Conventional lymphangiography cannot detect leakage sites of hepatic lymphatic vessels. Percutaneous transhepatic lymphangiography can be used to visualize leakage sites, and once the leakage site has been confirmed, effective sclerotherapy can be performed. Case presentation: A rare case of intractable hepatic lymphorrhea due to injury of the hepatoduodenal ligament following pancreaticoduodenectomy is reported. Drainage of massive ascites from the drainage tube continued after surgery. Percutaneous transhepatic lymphangiography visualized the intrahepatic lymphatic vessels and the leakage site at the hepatic hilum. An 8-Fr drainage catheter was inserted adjacent to the leakage point under fluoroscopic computed tomography guidance. Repeated sclerotherapy using intraperitoneal administration of OK-432 (picibanil) through the catheter was performed, which exposed the leakage site, and control of the ascites was finally achieved. Conclusions: To the best of our knowledge, this is the first successful case of detection of a leakage site using intrahepatic lymphangiography, followed by sclerotherapy using OK-432.

CD117 (c-kit proto-oncogene protein product) is expressed in most gastrointestinal stromal tumors (GISTs) and plays a crucial role in the pathogenesis and treatment of this disease. However, the clinicopathological and immunohistochemical features of CD117-positive mesenchymal tumors without connection to the gastrointestinal tract, known as extragastrointestinal stromal tumors (EGISTs), are not well documented because these tumors are rare. We describe the clinicopathological and immunohistochemical features of two cases of EGIST and compare them with those of GIST. Of the 1855 abdominal or esophageal tumors resected during the past 10 years at our hospital, 23 were GISTs and 2 were EGISTs. The clinicopathological or immunohistochemical characteristics do not seem to differ remarkably between EGISTs and GISTs. Although rare, CD117 positivity should be tested in abdominal mesenchymal tumors that have no connection to the gastrointestinal tract. The clinicopathological features of CD117-positive abdominal mesenchymal tumors may not depend on whether the tumor is connected to the gastrointestinal tract.

When active bone marrow release is induced by inflammatory stimuli, it is associated with an increase in L-selectin expression on circulating polymorphonuclear leukocyte (PMN). This contrasts sharply with glucocorticoid-induced granulocytosis that is associated with decreased L-selectin expression on PMN. The present study was designed to determine if the reduced L-selectin expression observed after glucocorticoid treatment is the result of suppression of L-selectin synthesis in the bone marrow. New Zealand white rabbits treated with dexamethasone (2.0 mg/kg, a single dose intravenously) were shown to have decreased L-selectin expression on circulating PMN 12 to 24 hours after treatment (P &lt; .01) with a return to baseline levels by 48 hours. When dexamethasone was administered 48 hours after the bone marrow PMN were pulse labeled with the thymidine analogue, 5′-bromo-2′-deoxyuridine (BrdU), L-selectin expression on BrdU-labeled PMN released from the bone marrow was decreased (P&lt; .01). Dexamethasone decreased L-selectin expression on segmented PMN in the bone marrow (P &lt; .05) but not on PMN already in the circulation. We conclude that glucocorticoids decrease L-selectin expression on circulating PMN by downregulating L-selectin expression in the maturation pool of bone marrow and speculate that this is an important glucocorticoid effect that influences the recruitment of PMN into inflammatory sites.