[Chemotherapy-naïve advanced malignant fibrohistiocytoma presenting IVC syndrome case report].

The case was a 77-year-old male with swelling of his right leg. Physical examination revealed an ill-defined mass at RLQ. Computed tomography (CT) and 3 dimensional CT showed an 8-cm tumor on the IVC, partially replacing iliac vessels and invading the psoas muscle. A diagnosis of malignant fibrohistiocytoma was made by pathological examination of biopsied specimens at exploratory laparotomy. Five courses of combination chemotherapy of ifosfamide (IFM) and doxorubicin (DXR) resulted in PR. Edema of the lower leg and hydronephrosis were both alleviated. Another 5 courses of chemotherapy with epirubicin and IFM were added. PR lasted 2 years, though the patient succumbed to the disease in 2 years and 8 months.

[A case of small cell carcinoma of the esophagus with SIADH].

The patient was a 63-year-old male admitted for further evaluation of the bleeding esophageal tumor. Endoscopic biopsy revealed small cell carcinoma. CT scan of the abdomen demonstrated nodular enlargement at the celiac axis. Under diagnosis of small cell carcinoma of the esophagus at Stage IVa, neoadjuvant chemotherapy with FP (5-FU+CDDP) was given. Immediately after fluid load, levels of serum sodium decreased to 117 mEq/L and persisted during chemotherapy treatment despite aggressive corrections. Response and shrinkage of the distant nodal metastases were confirmed, and an esophagectomy was conducted. Pathological examination with IHC demonstrated positive staining for CD56, NSE and synaptophysin but negative for ADH. Lymph node and liver metastases recurred. Progression of the disease again triggered hyponatremia.

Gas chromatography-mass spectrometry of cis-9,10-epoxyoctadecanoic acid (cis-EODA). I. Direct evidence for cis-EODA formation from oleic acid oxidation by liver microsomes and isolated hepatocytes.

Oleic acid, cis-9-octadecenoic acid, is the major fatty acid in mammals. Its oxide, cis-9,10-epoxyoctadecanoic acid (cis-EODA), has been identified in blood and urine of humans, its origin is, however, still unknown. Lipid peroxidation and enzyme-catalyzed epoxidation of oleic acid are two possible sources. In the present article, we investigated by HPLC and GC-MS whether cis-EODA is formed enzymatically from oleic acid by the cytochrome P450 (CYP) system. Oleic acid, cis-EODA and its hydratation product threo-9,10-dihydroxyoctadecanoic acid (threo-DiHODA) were quantitated by HPLC as their p-bromophenacyl esters. For structure elucidation by GC-MS, the pentafluorobenzyl (PFB) esters of these compounds were isolated by HPLC and converted to their trimethylsilyl ether derivatives. Liver microsomes of rats, rabbits and humans oxidized oleic acid into cis-EODA. This is the first direct evidence for the enzymatic formation of cis-EODA from oleic acid. The epoxidation of oleic acid was found to depend on CYP, NADPH+H(+), and O(2). cis-EODA was measurable in incubates of liver microsomes for up to 30 min of incubation. Maximum cis-EODA concentrations were reached after 5-7 min of incubation and found to depend upon oleic acid concentration. Isolated rat hepatocytes hydratated cis-EODA into threo-DiHODA which was further converted to unknown metabolites. However, from incubation of oleic acid with these cells we could not detect threo-DiHODA or cis-EODA. Our study suggests that circulating and excretory cis-EODA may originate, at least in part, from CYP-catalyzed epoxidation of oleic acid. GC-MS of intact cis-EODA as its PFB ester in the negative-ion chemical ionization mode should be useful in investigating the physiological role of cis-EODA in man.

Allogeneic hepatocyte transplantation: Contribution of Fas-Fas ligand interaction to allogeneic hepatocyte rejection.

Hepatocyte transplantation is a potential therapeutic modality for overcoming the shortage of liver donors, and the clinical application of allogeneic hepatocyte transplantation has been considered. However, there are two major problems with allogeneic hepatocyte transplantation: protection of transplanted hepatocytes from rejection and stimulation of the rapid proliferation of surviving cells. Without immunosuppression, allogeneic hepatocytes are rapidly rejected within a few days after transplantation, even though it is relatively easy to induce immunotolerance after allogeneic whole liver transplantation. Accordingly, different rejection mechanisms seem to operate after allogeneic hepatocyte transplantation and whole liver transplantation. To overcome the rejection of transplanted hepatocytes, induction of donor-specific unresponsiveness to graft without compromising the host immune system would be ideal. We previously reported that the Fas-Fas ligand system plays a critical role in the CD28-independent pathway of hepatocyte rejection. Therefore, blockade of rejection using CTLA4 immunoglobulin (CTLA4Ig) or anti-CD80/86 monoclonal antibodies and anti-FasL monoclonal antibody may prolong the survival of transplanted allogeneic hepatocytes. Furthermore, administration of hepatocyte growth factor (HGF) can promote the proliferation of allogeneic hepatocytes and this may lead to the development of a functioning liver substitute.