[A Case of Recurrent Hyperammonemic Encephalopathy during Adjuvant Chemotherapy(Modified FOLFOX6)for Colorectal Cancer].

A 60-year-old woman was administered mFOLFOX6 therapy as postoperative adjuvant chemotherapy for fStage III a ascending colon cancer. The patient developed a disorder of consciousness(Japan Coma Scale[JCS]III-200)immediately after the completion of the therapy. Blood ammonia levels were high at 319 mg/dL, and a diagnosis of disturbance of consciousness due to hyperammonemia was made. The patient's state of consciousness improved on the following day as blood ammonia levels decreased due to treatment with branched chain amino acid(BCAA)formulation and oxygen. Two months later, mFOLFOX6 therapy was again administered with strengthening measures for side effects to nausea and vomiting and reducing 5-FU, but the patient again developed a disorder of consciousness(JCS III-200). The 5-FU administration rate was considered as a potential cause of hyperammonemia. Hyperammonemia induced by 5-FU is relatively rare, with a reported incidence of 5-9%; however, caution is required with high dosage regimens of 5-FU that are currently recommended for colorectal cancer therapy because hyperammonemia is an important side effect.

Total parenteral nutrition treatment efficacy in adolescent eating disorders.

BACKGROUND: Management of adolescent patients with severe eating disorders who refuse treatment for weight loss is complicated. Nutritional rehabilitation is most important during the growth period; thus, strong support in the form of total parenteral nutrition (TPN) as soon as possible is necessary in severe cases. No studies involving detailed, long-term follow up have evaluated biochemical markers and gonadotropin in patients undergoing TPN treatment. METHODS: Twenty-five adolescent female patients admitted to hospital received TPN immediately, and biochemical marker and gonadotropin levels were measured and analyzed. If subsequent weight gain was observed, TPN treatment was gradually reduced and stopped. RESULTS: No patients dropped out of the study. A significant increase in weight was observed during hospitalization (average, 8.0 kg). Under this treatment, serum total bilirubin was significantly decreased at 3 months, total cholesterol was significantly decreased at 2 months, and alkaline phosphatase (ALP) was significantly increased at 3 and 6 months. Follicle-stimulating hormone response significantly preceded both luteinizing hormone response and appetite recovery. After this treatment, nine of the 25 patients were readmitted for recurrence of appetite loss. Two patients required additional TPN treatment, but seven immediately recovered their appetite after hospitalization without TPN treatment. Bodyweight gain per day was significantly lower and ALP on admission was significantly higher in patients with than without recurrence. CONCLUSIONS: Most patients had a remarkable recovery of appetite without refusal behaviors and without evidence of malnutrition after admission. Nutrition maintenance with TPN support is particularly important during the growth period.

[Case report of a liver metastasis from rectal cancer achieving complete response (CR) by a combination of intra-hepatic arterial infusion of irinotecan (CPT-11) with degradable starch microspheres (DSM) and weekly high-dose intra-hepatic arterial chemotherapy with 5-FU].

A 67-year-old woman, who was diagnosed with rectal cancer and liver metastasis, underwent a low anterior resection of the rectum in May 2004. Two months later, the level of tumor markers increased and a CT scan revealed a 45 x 35 mm liver metastasis in the S(8) segment. She was referred to our hospital for treatment of the liver tumor. Intra-hepatic arterial infusion of irinotecan (CPT-11) and mitomycin C (MMC) with degradable starch microspheres (DSM) was given in July 2004. Following this, a 34-week course of weekly high-dose intra-hepatic arterial 5-FU infusion (5-FU 1,000 mg/m(2)) was performed. In April 2005, the size of the liver metastasis decreased, and the level of serum tumor marker normalized. A CT and echo scan revealed a calcified tumor, and therefore all chemotherapy was stopped. She was followed in the outpatient clinic, with no evidence of recurrence for 12 months. This case suggests that the use of intra-hepatic arterial infusion of CPT-11 and MMC with DSM is useful for the treatment of liver metastases in colorectal cancer.

The leaf extract of Ginkgo Biloba L. suppresses oxidized LDL-stimulated fibronectin production through an antioxidant action in rat mesangial cells.

1 The leaf extract of Ginkgo Biloba L. exhibits a variety of pharmacological effects through an antioxidant action. We examined the effects of the leaf extract (Ginkgolon-24) on the production of fibronectin induced by oxidized low-density lipoprotein (oxLDL) in rat mesangial cells. 2 Stimulation with oxLDL accelerated the production of fibronectin with the preceding generation of reactive oxygen species (ROS). Pretreatment with Ginkgolon-24 inhibited the oxLDL-induced fibronectin production as well as ROS generation. 3 oxLDL also elicited the activation of SP-1, nuclear factor-kappaB, and cAMP response element-binding protein, which are transcription factors involved in the fibronectin production. Among these activated transcription factors, Ginkgolon-24 inhibited the activation of SP-1 only. 4 Furthermore, 7-ketocholesterol, an oxidized lipid in oxLDL particles, induced the production of fibronectin and the activation of SP-1, which were also suppressed by Ginkgolon-24. 5 These results suggest that the leaf extract of Ginkgo Biloba L. inhibits the oxLDL-induced production of fibronectin probably through inhibitory effects on ROS generation and SP-1 activation in rat mesangial cells.

Differences in the extent of primary ischemic damage between middle cerebral artery coagulation and intraluminal occlusion models.

The authors studied the differences between heat-shock/stress protein 70 (hsp70) gene expression and protein synthesis in the unilateral middle cerebral artery (MCA) microsurgical direct occlusion (Tamura's) model and the unilateral intraluminal occlusion model. In Tamura's model, expression of hsp70 mRNA and HSP70 protein and decreased protein synthesis were detected in the ischemic areas, including the ipsilateral cortex and caudate. These phenomena, however, were not observed in the areas outside the MCA territory, including the ipsilateral thalamus, hippocampus, and substantia nigra. These results were consistent among the experimental rats. In the intraluminal occlusion model, however, induction of both hsp70 mRNA and HSP70 protein and impairment of protein synthesis were noted in the areas outside the MCA territory, including the ipsilateral thalamus, hypothalamus, hippocampus, and substantia nigra, as well as in the MCA territory, including the ipsilateral cortex and caudate. These results were not consistent among the experimental rats. These different results might be due to widespread damage resulting from internal carotid artery (ICA) occlusion in the intraluminal occlusion model. Accordingly, the authors suggest that this model be called an ICA occlusion model, rather than a pure MCA occlusion model.