Calcification of the aortic valve leads to stenosis or regurgitation or both. To clarify the mechanism of heart valve calcification, comparative studies using histological and ultrastructural examinations were performed of calcified aortic valves. These valves were obtained at valve replacement surgery from 11 patients with rheumatic aortic valvular disease (RAVD), 10 patients with degenerative aortic valve disease (DAVD), and 10 patients with congenitally bicuspid aortic valves (CBAV). For electron microscopic study, 5 cases were selected from each group. In RAVD, histological examination revealed calcification in a degenerated amorphous area at the center of fibrous thickened regions and in laminar fibrous thickened areas near the valve surface. In DAVD, calcification was observed mainly in the fibrosa near the valve ring. In CBAV, basic pathological changes were similar to those in DAVD; however, additional severe calcification of the raphe was observed, if the raphe was present. Ultrastructural examinations showed deposition of electron-dense materials in two patterns in all three groups; one pattern was observed in the interfibrillar spaces of collagen fibrils, and the other pattern was widespread macular deposition unrelated to the preexisting structure. In RAVD, microfibril-like fibrillar structures were found in the areas of deposition of electron-dense materials. These findings suggest that newly formed connective tissue degraded and became necrotic because of nutritional deprivation, especially in the thickened central area, causing calcium deposition. In DAVD and CBAV, numerous lipid vacuoles were found in the electron-dense deposition areas similar to lipid deposition in aortic atherosclerosis. Localized calcium deposition in the fibrosa suggests that the stress of valvular motion and pressure load induces sclerotic changes with the degeneration of collagen fibers, providing a core for calcification. In CBAV, the raphe was the main location of calcification, wherein spiraled collagen fibrils were observed. Increasing the hemodynamic load with abnormal structure might influence calcification. The ultrastructural pattern of calcification of the valve is common; however, additional findings suggest that the cause and mechanism are different in each type of heart valve disease.

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Background: The incidence of placenta previa has been increasing. It is of a great importance to determine the clinical risk factors for peripartum blood transfusion in women with placenta previa in an effort to anticipate cases of severe hemorrhage.
Methods: A total of 129 consecutive cases of placenta previa (64 cases of complete placenta previa and 65 cases of marginal placenta previa), including 43 cases requiring blood transfusion, were retrospectively analyzed. Maternal and neonatal clinical data were examined with univariate and multivariate logistic regression analyses for potential risk factors for peripartum blood transfusion.
Results: The independent risk factors for blood transfusion were maternal age greater than 34 years (adjusted odds ratio [OR]=3.7; 95% confidence interval [CI]=1.5-7.5, p<0.05), history of having undergone dilatation and curettage more than once (adjusted OR=4.8; 95% CI=1.1-26.2, p<0.05), and complete placenta previa (adjusted OR=2.6, 95% CI=1.2-5.9, p<0.05). Body mass index, gravidity, parity, previous cesarean section, antepartum hemorrhage, use of tocolytic agents, gestational age at delivery, preoperative anemia, emergent surgery, birth weight, and Apgar score were not associated with the incidence of blood transfusion.
Conclusion: Risk factors for blood transfusion in women with placenta previa are advanced maternal age, repeat dilatation and curettage, and complete placenta previa. Women with placenta previa who are at risk for blood transfusion should be carefully managed with sufficient preparation for blood transfusion.

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Background: Refractory hepatic encephalopathy (HE) frequently develops in patients with cirrhosis and portal-systemic shunt. Recently, patients with refractory HE associated with portal-systemic shunt have been treated with interventional radiology. We describe a promising new treatment for portal-systemic shunt, ligation of the patent paraumbilical vein (PUV) after partial splenic embolization, in patients with refractory HE.
Patients: Four patients with cirrhosis (3 women and 1 man; mean age, 56 years) and refractory HE due to a patent PUV were studied. Patency of the PUV had recurred in 1 patient after primary occlusion by interventional radiological procedures. The Child-Pugh class was B in 2 patients and C in 2. Before the present treatment, all patients had been hospitalized at least 3 times because of recurrent HE.
Surgical Procedure: Partial splenic embolization was performed in all patients to decrease portal venous pressure before surgery. Surgical ligation of the patent PUV was performed under epidural anesthesia. The patent PUV was carefully skeletonized and doubly ligated. Esophageal varices were evaluated with upper gastrointestinal endoscopy before and after surgery.
Result: The mean follow-up duration was 15.8 months. After ligation, there were no clinically significant complications. Esophageal varices were unchanged. The serum ammonia level was higher before surgery (162.3 ± 56.4 μg/dL, mean ± SD) than after surgery (41.8 ± 20.2 μg/dL; p=0.0299). No patient had symptoms of HE.
Conclusion: Ligation of the patent PUV is an effective treatment for patients with refractory HE.

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Although most patients with colonic diverticula have no symptoms, perforation or bleeding can be troublesome. Recently, we treated an elderly patient with a diverticular perforation of the sigmoid colon who required a loop colostomy and later resection of the diseased colon. Between the operations, the colostomy resembled a sea slug with horns, which represented eversions of the diverticula. This interesting phenomenon suggests that diverticula may be everted as pseudopolyps and ligated endoscopically. Therefore, the procedure was tested on a Landrace pig, of which the large bowel wall was pulled with an endoscope at 9 different sites using forceps (n=6) or suction (n=3) and ligated. Four days later, reexamination revealed total necrosis at 8 sites and ulceration at 1. The animal was well. The bowel removed 2 weeks later showed mucosal fold convergences without perforations.
Our procedure can be used for prophylactic or therapeutic treatment of patients with colonic diverticula.

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A 43-year-old woman presented with a persistent high fever of 39°C and edematous erythema accompanied by pustules on the face, trunk and extremities. Conjunctivitis and nodules were also observed in the right eye. On the basis of the clinical symptoms and histopathological findings. Sweet's syndrome was diagnosed. Eruptions quickly progressed to extensive necrosis and ulcers, mimicking clinical features of pyoderma gangrenosum. A bone marrow biopsy indicated myelodysplastic syndrome. Oral administration of 50 mg/day of prednisolone induced epithelialization of ulcers, with remaining scarring and pigmentation. Six months later, myelodysplastic syndrome had progressed to acute myelogenous leukemia.

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Intussusception in adults represents only 5% of all cases and is usually caused by a small bowel lesion acting as the apex of the intussusception. We report an unusual case of intussusception in man caused by a lipomatous lesion located in the ileum acting as the lead point. After repeated admissions to our hospital for ileus, the possibility of intussusception was finally raised by a computed tomographic scan of the abdomen. The patient underwent primary resection of the intussuscepted intestine, which resulted in a long-lasting resolution of the symptoms. The resected specimen contained a round tumor measuring 27 × 27 × 40 mm which was diagnosed histopathologically as an intestinal lipoma. This case highlights the uncommon causation of adult intussusception by an intestinal lipoma.

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The carcinosarcoma of the esophagus is a rare malignant neoplasm consisting of both carcinomatous and sarcomatous components. A case of so-called carcinosarcoma of the esophagus is described herein. A 69-year-old man presented with dysphagia and was admitted to our hospital. Imaging studies revealed a localized ulcerative tumor in the middle intrathoracic esophagus without any invasion or metastasis. The patient was initially thought to have squamous cell carcinoma and underwent subtotal esophagectomy with lymphadenectomy. Final diagnosis of the tumor was so-called carcinosarcoma of the esophagus. The patient had an uneventful postoperative course and showed no evidence of recurrence or metastasis in the 4-year postoperative period.

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We report a case of acute pulmonary thromboembolism after gastrectomy. A 67-year-old woman was found to have gastric cancer and a giant lipoma in the ascending colon. We performed distal gastrectomy and enucleation of the ascending colon lipoma. On postoperative day 9, an acute pulmonary thromboembolism developed, and thrombolytic therapy was urgently performed. The 2004 Japanese guidelines for preventing pulmonary thromboembolism/deep vein thrombosis are discussed in relation to the present case.

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An inflammatory fibroid polyp (IFP) is a rare benign lesion, originating in the submucosa of the gastrointestinal tract. It is histopathologically characterized by distinctively arranged fibrous connective tissue and blood vessels with inflammatory cell infiltration. It typically arises in the stomach and small intestine but also arises infrequently in the colon. This report describes a case of IFP of the cecum. A 63-year-old woman presented with persistent bloody stool for more than 1 month. Colonoscopy revealed a polypoid lesion, measuring 2.5 cm in diameter and 4 cm in length, with a thick pedicle in the cecum. Histopathological examination of the biopsy specimen showed hyperplastic changes of the mucosa. The lesion was diagnosed to be a submucosal tumor. We concluded that endoscopic mucosal resection would be difficult because the polyp showed signs of infiltration into the submucosa. Furthermore, the possibility of malignancy could not be ruled out. Laparoscopy-assisted ileocecal resection with lymphnode dissection was performed after the patient's informed consent was obtained. The lesion was finally diagnosed to be IFP on the basis of histopathological examination of the resected specimen. Immunohistochemical staining of the spindle-shaped cells, which were present around the small vessels in the stroma of the tumor, showed that the tissue expressed vimentin but not α-smooth muscle actin, desmin, S-100, c-kit or CD 34. IFP is difficult to diagnose without the recognition of its clinical and pathological characteristics. It is also important to determinate the depth of the lesion before selecting the therapeutic method.

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We present a case report of a posttransplant patient who had hepatotoxicity due to both tacrolimus and cyclosporine and cholestatic jaundice due to tacrolimus. The patient did not show sustained improvement in enzyme and bilirubin abnormalities after an initial change from tacrolimus to cyclosporine or with a change back to tacrolimus, but he ultimately showed improvement when the blood concentration of tacrolimus was lowered. A 56-year-old man with subacute fulminant hepatitis induced by acarbose was admitted to our hospital for living donor liver transplantation. The liver graft consisted of the left lobe from his ABO-identical son. The early posttransplant course was uneventful. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin improved initially, but the ALT and AST levels later increased. A liver biopsy suggested a presumptive diagnosis of drug reaction. All drugs were discontinued, the immunosuppressive agent was changed from tacrolimus to cyclosporine. After initial improvement, the ALT and AST levels increased again. Assuming a reaction to cyclosporine, we decreased the concentration of cyclosporine in the blood. The enzyme levels improved temporarily but again began to rise. We changed the immunosuppressive agent to tacrolimus, which resulted in improvements in the ALT and AST levels; however, the total bilirubin level increased. We interpreted this increase as tacrolimus-induced cholestasis; in response, we decreased the blood concentration of tacrolimus to between 3 and 5 ng/dL and added 1,000 mg of mycophenolate mofetil to the drug regimen. The patient recovered without further complications. Repeated liver biopsies throughout the hospital course suggested that the mild mononuclear cell infiltration observed in a few triads had not been caused by acute rejection but had possibly been drug-induced.

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