Isolated Pulmonary Cryptococcosis Confused with Lung Tumor 5 Years After Kidney Transplantation: A Case Report.

BACKGROUND: In transplant recipients, due to the use of immunosuppressive therapy, it is occasionally difficult to distinguish between an infection and malignancy, especially in the case of a lung lesion. Here, we report a case of isolated pulmonary cryptococcosis after kidney transplantation that was difficult to distinguish from a lung tumor. CASE REPORT: A 52-year-old man underwent a kidney transplant from his mother when he was 44 years old. Immunosuppression was maintained with tacrolimus, methylprednisolone, and mycophenolate mofetil. His post-transplant course was uneventful and serum creatinine levels were maintained. Five years post-transplantation, a non-contrast computed tomography (CT) examination revealed a nodule measuring 3 mm in diameter in the middle lobe of the right lung. The nodule gradually increased to 12 mm in 2 years. Positron emission tomography/CT examination showed a maximum standardized uptake value of 0.5 for the nodule. Biochemical examination revealed no elevation in total leucocyte count and C-reactive protein levels. However, tumor markers were elevated: serum carcinoembryonic antigen, 5.9 ng/mL; pro-gastrin-releasing peptide, 84.6 pg/mL. Furthermore, the serum cryptococcus antigen was negative. Therefore, thoracoscopic partial lung resection was performed. Pathologically, a number of spherical fungi from the necrotic substance of the tumor were confirmed positive by periodic acid-Schiff and Grocott-Gomori staining. The patient was therefore diagnosed with pulmonary cryptococcosis. Two years later, the patient is alive and has shown no evidence of recurrence. CONCLUSIONS: In lung nodules after kidney transplantation, even if serum cryptococcus antigen is not identified, it is necessary to keep in mind the possibility of pulmonary cryptococcosis.

Changes in the levels of endogenous coenzyme Q homologs, alpha-tocopherol, and glutathione in rat liver after hepatic ischemia and reperfusion, and the effect of pretreatment with coenzyme Q10.

The present study was undertaken to determine whether hepatic ischemia and the subsequent reflow of blood had any effect on the levels of endogenous coenzyme Q homologs, alpha-tocopherol, and glutathione, and whether coenzyme Q10 (6 mg/kg of body weight) altered these levels. Ischemia of the rat liver for 90 min resulted in decreases of 19.1 and 19.6% of endogenous alpha-tocopherol and total glutathione (GSH + GSSG) without significant changes in the levels of endogenous total coenzyme Q homologs (oxidized and reduced). Restoration of the blood flow resulted in marked decreases in endogenous coenzyme Q homologs, alpha-tocopherol, and total glutathione in the control group. In coenzyme Q10-treated animals, however, there were no changes in the levels of endogenous total coenzyme Q9, alpha-tocopherol, or total glutathione as well as in the level of the enhanced total coenzyme Q10 during the reperfusion period. On the other hand, decreases in alpha-tocopherol and total glutathione during the period of ischemia remained unchanged. These results are compatible with the assumption that cellular damage caused by hepatic ischemia can be explained by free radical reaction processes during ischemia and especially, reperfusion and suggest that exogenous coenzyme Q10 functions as an antioxidant with endogenous coenzyme Q homologs, alpha-tocopherol, and glutathione in lipid peroxidation during reperfusion.

Adenine nucleotide metabolism during hepatic ischemia and subsequent blood reflow periods and its relation to organ viability.

In an experimental model system for liver transplantation, the ability of the rat liver to synthesize ATP and to maintain adequate energy charge and total adenine nucleotides during restoration of hepatic blood flow following warm ischemia was found to determine tissue viability and survival of the animal. A portafemoral shunt prepared to relieve portal congestion enhanced the rate and extent of ATP resynthesis by the reflow following hepatic ischemia and this was accompanied by an increase in the survival rate of the rat.

Role of conversion of xanthine dehydrogenase to oxidase in ischemic rat liver cell injury.

This study was undertaken to determine whether hepatic ischemia and the subsequent reflow of blood have any effect on the conversion of xanthine dehydrogenase to xanthine oxidase (XO). Ischemia of the liver for 90 or 120 minutes did not permit survival of the animals. XO represented 15% of the total xanthine dehydrogenase plus XO activity in the control liver. XO activity remained unchanged even after 90 minutes of hepatic ischemia, although a marked increase in lipid peroxide in the liver tissue was observed during the reperfusion. When hepatic ischemia was prolonged for 6 hours (animals were dead), XO activity rose to 35% of the total activity. Incubation of the liver at 37 degrees C resulted in a definite change in XO activity dependent on the length of incubation period. Although no significant changes occurred in XO activity during the first 2 hours of incubation, a marked XO conversion was observed between 2 and 4 hours, and a maximal conversion was achieved after 6 hours of incubation. These results suggest that XO newly generated during ischemia has a very limited role in oxygen free radical production after resuming perfusion.

Role of free radicals in ischemic rat liver cell injury: prevention of damage by alpha-tocopherol administration.

The present study was undertaken to determine whether alpha-tocopherol pretreatment could modify cellular free radical metabolism during hepatic ischemia and subsequent reperfusion and prolong the viability of the liver. Although ischemia of the liver for 90 minutes did not permit survival of the animals, alpha-tocopherol administration (10 mg/kg of body weight) for 3 days increased the survival rate to 45.5%. The period of ischemia was accompanied by decreases in the hepatic adenosine triphosphate (ATP) level, endogenous alpha-tocopherol, and total glutathione (reduced and oxidized) without any significant increase in endogenous coenzyme Q (CoQ) homologs (CoQ9 and CoQ10) and lipid peroxide formation. The subsequent restoration of blood flow resulted in a low recovery of ATP and marked decreases in endogenous alpha-tocopherol, total glutathione, and CoQ homologs and, on the contrary, a marked increase in lipid peroxide levels. In alpha-tocopherol-treated animals, however, resynthesis of ATP was accelerated even after 90 minutes of ischemia, and there were no changes in the levels of total glutathione or CoQ homologs or in the level of the enhanced alpha-tocopherol during the reperfusion period. The pretreatment also completely suppressed the elevation of lipid peroxide levels. These results are compatible with the assumption that cellular damage caused by hepatic ischemia can be explained by free radical reaction processes during ischemia and especially reperfusion and suggest that administration of a free radical scavenger and antioxidant, alpha-tocopherol, is effective in ischemic liver cell injury.

Effect of the 21-aminosteroid on nuclear factor-kappa B activation of Kupffer cells in endotoxin shock.

BACKGROUND: The 21-aminosteroid (U-74389G) is a nonglucocorticoid steroid that was synthesized to inhibit lipid peroxidation without the glucocorticoid activity. We recently demonstrated that the 21-aminosteroid administered to endotoxin shock mice reduces liver injury and improves the survival rate of mice through inhibition of nuclear factor-kappa B activation in the liver. The study was undertaken to determine whether the 21-aminosteroid could suppress pro-inflammatory gene up-regulation through inhibition of nuclear factor-kappa B activation in Kupffer cells. METHODS: Kupffer cells were isolated from rats by collagenase perfusion followed by pronase digestion. After a lipopolysaccharide addition, each assay was performed for tumor necrosis factor-alpha, interleukin-6, tumor necrosis factor-alpha messenger RNA, nuclear factor-kappa B, and I kappa B proteins. RESULTS: After the lipopolysaccharide addition, Kupffer cells released both tumor necrosis factor-alpha and interleukin-6. The 21-aminosteroid treatment suppressed the release of tumor necrosis factor-alpha in a dose-dependent manner. The 21-aminosteroid also inhibited the increase of tumor necrosis factor-alpha messenger RNA expression and nuclear factor-kappa B activation in Kupffer cells 1 hour and 30 minutes, respectively, after lipopolysaccharide addition. Furthermore, the 21-aminosteroid treatment suppressed the degradation of I kappa B proteins in lipopolysaccharide-stimulated Kupffer cells. CONCLUSIONS: These results suggest that the 21-aminosteroid inhibits release of the tumor necrosis factor-alpha and interleukin-6 from lipopolysaccharide-stimulated Kupffer cells by inhibiting nuclear factor-kappa B activation. This is accomplished by inhibiting I kappa B degradation in endotoxin shock and this may prove useful for the treatment of endotoxin shock.

Preservation of ischemic rat liver mitochondrial functions and liver viability with CoQ10.

The present study was undertaken to determine whether CoQ10 administration to rats can protect hepatic mitochondrial functions, improve energy metabolism during hepatic ischemia and subsequent reperfusion, and prolong the viability of the organ. Although ischemia of the liver for 90 minutes did not permit survival of the animals, CoQ10 administration (6 mg/kg of body weight) increased the survival rate to 60%. The period of ischemia was accompanied by decreases in hepatic adenosine triphosphate (ATP) level and respiratory control index without significant increases in mitochondrial calcium content and lipid peroxide formation. The subsequent restoration of blood flow resulted in a low recovery of ATP level, recovery of respiratory control and ADP:O ratio to levels significantly lower than normal, and on the contrary, marked increases in mitochondrial calcium and lipid peroxide levels. However, in CoQ10-treated animals mitochondrial functions were all completely reversible, and resynthesis of ATP was accelerated even after 90 minutes of ischemia. The pretreatment also completely suppressed the elevation of mitochondrial calcium and lipid peroxide levels. These results suggest that preservation with CoQ10 of cellular damages caused by hepatic ischemia is probably due to protection of cellular and subcellular membranes from lipid peroxidation, so that mitochondrial functions are restored and cellular calcium homeostasis is maintained.

Successful treatment by simultaneous hepatic venoplasty and cavoplasty for Budd-Chiari syndrome with obstruction of retrohepatic inferior vena cava.

BACKGROUND: Various surgical procedures for treating chronic Budd-Chiari syndrome have been established, but none are adequate because of the variation in underlying pathologic vascular changes. METHODS: This article presents a 32-year-old patient with a 5 cm long segment of obstruction of the retrohepatic inferior vena cava involving the main hepatic veins with severe portal hypertension. RESULTS: After five unsuccessful attempts at percutaneous transluminal angioplasty, simultaneous hepatic venoplasty was conducted with the saphenous vein patch and retrohepatic inferior venacavoplasty by the expanded polytetrafluoroethylene patch with a 3 cm long cuff interposition for suprahepatic reconstruction of the inferior vena cava. Hypothermic preserved liver perfusion after vascular isolation and femoroportoaxillary venovenous bypass with a centrifugal blood pump throughout the anhepatic stage ensured safe operation on the liver and maintained hemodynamics. Early postoperative anticoagulant is recommended. CONCLUSIONS: An uneventful postoperative course and a 10-month follow-up showing excellent condition indicated this one-stage simultaneous patch hepatic venoplasty and cavoplasty to be adequate for appropriate correction very of complex obstructive vascular lesions in Budd-Chiari syndrome.

Ischemic damage prevention by coenzyme Q10 treatment of the donor before orthotopic liver transplantation: biochemical and histologic findings.

This study was undertaken to determine whether pretreatment of the donor rat with coenzyme Q10 (CoQ10) would protect against hepatic ischemia induced for 30 minutes at normothermic body temperature. Fresh liver transplants were used as controls (minus warm ischemia of 30 minutes) and gave a 1-week survival rate of 84.6%. CoQ10 was administered intravenously (10 mg/kg body weight) to the donor rat 1 hour before induction of warm ischemia (group A). In another group (B), the same dose was given intravenously not only to the donor rat but also to the recipient rat 1 hour before grafting. None of the placebo group survived more than 2 days. The 1-week survival rates of the groups pretreated with CoQ10 were 45.5% for group A and 50% for group B. There was no significant difference between groups A and B. A statistically significant difference was demonstrated between the placebo group and both CoQ10-treated groups (p less than 0.05). It was therefore assumed that CoQ10, accumulated in the donor liver, was a primary factor in improving survival. Serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), serum alkaline phosphatase (SALP), total bilirubin, and total protein were measured by means of light and electron microscopic examination of the liver 6 months after transplantation. Long-term-surviving rats with transplanted, ischemically damaged liver that was pretreated with CoQ10 showed a decrease in the activity of SGOT and SGPT and an increase in levels of total protein to the normal range (as well as to those levels exhibited by fresh-liver-transplanted rats) with practically no change in levels of SALP, total bilirubin, or in histologic findings. These results indicate that donor pretreatment with CoQ10 is useful for increasing survival after warm ischemic damage of rat liver grafts.

Effect of lazaroid U-74389G and methylprednisolone on endotoxin-induced shock in mice.

BACKGROUND: Lazaroids are nonglucocorticoid analogs of methylprednisolone with multiple actions. We investigated whether lazaroid U-74389G could attenuate endotoxin-induced liver injury. We hypothesized that U-74389G treatment may protect against hepatic injury by suppressing proinflammatory gene up-regulation through inhibition of activation of nuclear factor kappa B (NF-kappa B). We also compared the efficacy of U-74389G with methylprednisolone in endotoxin-induced liver injury. METHODS: Lipopolysaccharide (Escherichia coli, 30 mg/kg given intraperitoneally) was administered to male ICR mice, and U-74389G (3 mg/kg intraperitoneally) or methylprednisolone (30 mg/kg intravenously) was administered simultaneously. Phosphate-buffered saline solution (0.15 mL intravenously) was administered to mice that served as a control group. RESULTS: U-74389G and methylprednisolone treatment significantly increased survival rates 48 hours after lipopolysaccharide injection and protected against lipopolysaccharide-induced liver injury in vivo, as indicated by the decreased hepatic lipid peroxidation, tumor necrosis factor-alpha, and inducible nitric oxide synthase messenger RNA formation, hepatic enzyme release, and neutrophil infiltration in the liver. U-74389G and methylprednisolone also showed inhibitory effects on NF-kappa B activation in the liver. CONCLUSIONS: These findings suggest that U-74389G can suppress proinflammatory gene up-regulation through inhibition of NF-kappa B activation and that it is a promising new antioxidant drug for the treatment of endotoxin shock.

Protective effect of monoclonal antibodies to adhesion molecules on rat liver ischemia-reperfusion injury.

BACKGROUND: The source of reactive oxygen species in the liver remains to be elucidated. The present study was undertaken to determine whether polymorphonuclear neutrophils (PMNs) can contribute to hepatic ischemia-reperfusion injury, and pretreatment with monoclonal antibodies (mAbs) to intercellular adhesion molecule-1 (ICAM-1), lymphocyte function associated antigen-1 (LFA-1), and CD 18 could improve energy metabolism and prolong the viability of the organ. METHODS: Male Wistar rats were used. Rat liver ischemia was induced by clamping blood vessels supplying median and left lateral hepatic lobes. Monoclonal antibodies to ICAM-1, LFA-1, or CD18 were injected intravenously 5 minutes before inducing ischemia. To determine the effect of mAbs on the survival rate, total hepatic ischemia was induced by clamping the hepatic artery, portal vein, and bile duct after making a portafemoral shunt. RESULTS: Although ischemia of the liver for 90 minutes did not permit survival of the animals, pretreatment with mAbs to ICAM-1 plus LFA-1 increased the survival rate to 57%. Pretreatment with mAb to ICAM-1 failed to increase the survival rate. The number of PMNs in the liver increased continually up to 24 hours after reperfusion after 90 minutes of ischemia, and the expression of ICAM-1 was enhanced 4 hours after reperfusion. This is accompanied by a low recovery of hepatic adenosine triphosphate and, on the contrary, a marked increase in lipid-peroxide in the reperfused liver. Pretreatment with mAbs suppressed the infiltration of PMNs and the elevation of lipid peroxide and enhanced the recovery of hepatic adenosine triphosphate 6, 12, or 24 hours after reperfusion. Pretreatment with mAbs also prevented the rise in serum alanine aminotransferase level after reperfusion. CONCLUSIONS: These results suggest that PMNs contribute to ischemia-reperfusion injury in the liver 4 hours and more after reperfusion, and pretreatment with mAbs to adhesion molecules is useful for the prevention of ischemic liver cell injury.

Percutaneous microwave coagulation therapy for primary or recurrent hepatocellular carcinoma: long-term results.

BACKGROUND/AIMS: To clarify the indication of percutaneous microwave coagulation therapy for hepatocellular carcinoma. METHODOLOGY: Thirty-three hepatocellular carcinoma patients who underwent percutaneous microwave coagulation therapy were enrolled in this study, including 18 primary and 15 recurrent hepatocellular carcinoma patients. We examined the local recurrence rates and the long-term results after the treatment. RESULTS: The overall survival rates of the primary group at 1, 2, 3, 4 and 5 years were 94.4%, 77.8%, 77.8%, 77.8% and 48.6%, respectively, whereas those of the recurrent group were 100%, 85.7%, 66.7% and 50.0% at 1, 2, 3 and 4 years, respectively. Local recurrence after percutaneous microwave coagulation therapy was found in about 50% of patients in both groups. Seventeen of the 27 patients (63.0%) with a moderately or poorly differentiated hepatocellular carcinoma tumor had local recurrence, while none of the 6 patients with a well-differentiated hepatocellular carcinoma tumor did (P = 0.005). CONCLUSIONS: Irrespective of primary or recurrent hepatocellular carcinoma, the indication of percutaneous microwave coagulation therapy as an alternative to hepatic resection should be limited to cases of a well-differentiated hepatocellular carcinoma tumor smaller than 2 cm in diameter.

Studies of postoperative transarterial infusion chemotherapy for liver metastasis of colorectal carcinoma after hepatectomy.

BACKGROUND/AIMS: The aim of this study was to evaluate the efficacy of postoperative transarterial infusion chemotherapy (PTIC) for the prevention of metastatic liver cancer recurrence after hepatectomy following curative surgery for colorectal carcinoma. METHODOLOGY: Thirty-eight patients who underwent curative hepatectomy for metastatic liver cancer from colorectal carcinoma were studied. Ten out of the 38 patients received PTIC (experimental group) and 28 patients did not receive chemotherapy (control group). PTIC was performed with an intrahepatic indwelling catheter, which was set-up for 3 weeks and repeated 3 times in two monthly intervals. RESULTS: In the control group, no significant differences were observed in the survival between patients with a single hepatic nodule and those with multiple hepatic nodules. Between patients with hepatic tumors of more than 3 cm in diameter and those with tumors less than 3 cm, and between patients with tumors located at H1 and H2, no significant differences were seen, either. However, the 5-year survival rate of the patients with metachronous liver metastases was 90% which was significantly better than for those patients with synchronous liver tumors (p < 0.05). The 100% of 3- and 100% of 4-year survival rates of the experimental group were significantly better than the 60% and 47% respectively of the control group (p < 0.05). The non-recurrence rate in the remnant liver was also significantly better in the experimental group than that in the control group (p < 0.01). The adverse effect of this protocol was negligible. CONCLUSION: We conclude that PTIC improved the survival and non-recurrence rate in the remnant liver of the patients with liver metastases from colorectal cancer after hepatectomy, and was considered to be safe and an important protective factor for the prevention of recurrence of liver metastases after hepatectomy.

Study of portal arterialization with auxiliary liver in rats.

The effect of portal arterialization was examined in 20 heterotopic auxiliary rat livers. Portal blood was supplied from recipient iliac artery (0.58 mm in diameter) connected to the donor portal vein using the cuff technique. Portal hypertension caused by arterial blood pressure resulted in the immediate operative death by bleeding in four of the rats (20%) from the spontaneous rupture of the graft capsule. Severe graft congestion was noticed at autopsy 3-14 days after transplantation in 13 rats. Massive portal and sinusoidal congestion and focal hemorrhagic necrosis were confirmed by pathological examination. The results of our study demonstrate that the portal arterialization used in the auxiliary rat liver transplantation would not be applicable unless the optimal hemodynamic condition is warranted.

Surgical treatment for renal hyperparathyroidism--report of 23 cases.

The present study describes surgical resection in 23 patients under maintenance hemodialysis with hyperparathyroidism. Twenty-three patients under maintenance hemodialysis had subtotal parathyroidectomy (s-PTx, n = 12) or parathyroid gland transplantation combined with total parathyroidectomy (Tx, n = 11) performed from January 1979 to January 1991. Their ages ranged from 8 to 63 years. The PTH levels were elevated in all patients preoperatively from 2.5 to 120 times over the upper limit of normal. After s-PTx, PTH levels sharply declined in all but one patient. Clinical symptoms improved in 11 cases with PTH decrease. After Tx, an abrupt decline in PTH was observed after surgery in 10 patients. One patient was reoperated because of persistent hyperparathyroidism. Another patient showed a PTH increase 13 months after surgery. The transplanted parathyroid gland was subtotally resected. Five months after reoperation, the condition recurred and the patient underwent total resection of the transplanted parathyroid gland and its re-autografting into the forearm. In the patients with renal hyperparathyroidism, s-PTx or Tx improved clinical symptoms; this indicates the high reliability of both procedures in treating the disease. A long-term follow-up study must be conducted to check the possible postoperative recurrence of hyperparathyroidism from residual and/or autograft parathyroid gland.

Granular cell tumor of the breast: report of a case.

A case of granular cell tumor of the breast in a 43-year-old woman is described. The patient presented with a painless mass in the upper-outer quadrant of her right breast. Mammography showed a spiculated tumor and ultrasonography demonstrated a hypoechoic mass with an irregular border. Magnetic resonance (MR) mammography revealed a homogeneous enhanced mass in T1-weighted images using Gd-DTPA and a ringed high-intensity area around the mass in T2-weighted images. Fine-needle aspiration cytology failed to show any malignant cells. A partial resection of the breast was performed and histological examination revealed a granular cell tumor. Granular cell tumors are generally always benign, but they may be misdiagnosed as malignant tumors because of their mammographic and ultrasonographic findings. MR mammography did not reveal a typical breast cancer in either T1- or T2-weighted images in the present case. This case illustrates the need for care in preoperative examinations in order to avoid overdiagnosis of breast cancer.

Effect of the angiotensin-converting enzyme inhibitor enalapril on post-transplant erythrocytosis.

Post-transplant erythrocytosis (PTE) is increasingly recognized as a complication of kidney transplantation. In this study we report the effect of the angiotesin-converting enzyme (ACE) inhibitor enalapril on hematocrit (Ht) and erythropoietin in four patients with PTE. Four renal allograft recipients with Ht greater than 51% were studied. Treatment was initiated with enalapril administered orally at a dose of 2.5 mg/day. All the patients had an increase of hemoglobin (Hb) (17.7 +/- 0.64 g/dl), Ht (54.5 +/- 1.29%) and red blood cell count (RBC) (584 +/- 19.2 x 10(4)/microliter). All patients responded to enalapril in 8 weeks with a significant decrease of Hb, Ht, and RBC. In one patient, the downward trend was more rapid and sustained, and treatment had to be discontinued to prevent the development of anemia. Serum erythropoietin showed normal in all four patients and remained unchanged during the study, even after discontinuation of enalapril treatment. Serum creatinine remained relatively stable throughout the study. These results suggest that PTE may not be dependent upon circulating erythropoietin and that enalapril treatment may be an effective treatment of PTE without renal dysfunction.

Tumor localization studies and surgical treatment in patients with insulinoma.

In the present study, we retrospectively reviewed thirteen consecutive patients with insulinomas including 2 reoperations at our department for insulinomas, from the viewpoint of preoperative localization studies, surgery and long term follow-up. The results of the preoperative localization studies proved to be percutaneous transhepatic portal venous sampling (PTPVS) 6/7, angiography 8/15, ultrasonography (US) 6/11, endoscopic ultrasonography (EUS) 4/4, computed tomography (CT) 3/10, and magnetic resonance imaging (MRI) 2/2. The tumor was visualized by intraoperative ultrasonography (IUS) in 6 of 6 patients (100%). Six patients underwent enucleation, 6 patients underwent distal pancreatectomy, 2 patients underwent subtotal (80%) distal pancreatectomy, and one patient a pylorus preserving pancreaticoduodenectomy (PPPD). Two patients, one of whom belonged to the MEN-I group, underwent reoperations because they had multiple adenomas. The development of iatrogenic diabetes occurred in the case of 3 patients. These results suggest that the use of selected preoperative localization studies (PTPVS and probably EUS) may be very helpful for detecting insulinoma, and that IUS is an essential part of the operative exploration for insulinoma. Our data may further indicate the need for an aggressive surgical procedure in the case of multiple adenoma or insulinoma in MEN-I.

A case of abdominal aortic aneurysm associated with systemic lupus erythematosus.

A case of abdominal aortic aneurysm associated with systemic lupus erythematosus (SLE) is reported. A 45-year-old woman with a 18-year history of SLE was admitted with severe lumbago radiating to the bilateral inguinal region. CT and DSA showed a dumbbell shaped true aneurysm of the abdominal aorta. An aorto-biiliac Y shaped graft replacements was performed. SLE is rarely associated with aneurysm of the great arteries. We could find only 4 reports of abdominal aneurysm associated with SLE. Common features were the young age of the patient, the long term of the systemic disease, and administration of corticosteroid therapy for a relatively long period of time. We speculate that atherosclerosis, hypertension, and corticosteroid may all work in concert, possibly together with aortic wall involvement or vasculitic damage, to produce the rare abdominal aneurysm in SLE.

Factors affecting postoperative prognosis in the solitary-nodule type of hepatocellular carcinoma: experience of 132 cases in our institute.

A retrospective analysis of clinical and pathological factors was performed on 132 surgical cases with solitary-nodule type HCC in our hospital. The overall cancer-free survival rates after 1, 3 and 5 years were 82.2%, 42.3% and 26.5%, respectively. With univariate analysis, the significant prognostic factors for survival were tumor size, cancer cell infiltration of the fibrous capsule of the tumor (fc-inf), invasion into portal vein (vp), and intrahepatic metastasis (im), while significant prognostic factors for non-recurrence were tumor size, fc-inf, vp, im, Edmondson-Steiner's classification and perioperative blood transfusion. With multivariate analysis for recurrence, significant factors were vp, clinical stage (CS), and perioperative blood transfusion. Therefore, prognostic factors for long-term survival in surgical cases of HCC are thought to be good hepatic function, absence of portal invasion, and avoidance of perioperative blood transfusion if possible.