Two cases of pseudoglaucoma were presented in this paper, which had been caused by lues and arteriosclerosis. We discussed the pathogenesis of pseudoglaucoma and reviewed the literature. Besides compression of the optic nerve and chiasm, ischemic optic neuropathy due to arteriosclerosis, lues, methanol intoxication, recurrent blood loss. and so forth, may produce optic nerve excavation and visual field defect without increase of IOP. We had much difficulty in explaining Rheese's view of our case, in which the optic canal was irregulary narrowed. We are of the opinion that narrowing of the optic canal may suggest secondary pathologic change due to chronic luetic optochiasmatic arachnoiditis.
Arachnoid ; Arachnoiditis ; Arteriosclerosis ; Methanol ; Optic Nerve ; Optic Neuropathy, Ischemic ; Visual Fields

The blood sugar control has been a significant problem after transplantation. Cyclosporine is partly responsible for post-transplantation diabetes mellitus (PTDM), but steroid has been well known to have diabetogenic effect and mainly responsible for glucose intolerance after transplantation. Deflazacort, a new steroid, has been introduced as a substitute of conventional steroid to prevent glucose intolerance after transplantation. We performed prospective study of deflazacort conversion from conventional steroid in kidney transplant patients with pre-transplantation diabetes mellitus(pre-Tx DM) or PTDM. A total of 82 kidney transplant patients was included for this study. Forty two patients were converted to deflazacort as a conversion group and 40 patients were remained on conventional steroid as a control group. In conversion group, the patients were converted from steroid to deflazacort with ratio of 5:6 in dosage. Nine patients developed severe anorexia with nausea/vomiting and three patients among them went back on steroid within 3 months after conversion(conversion failure 7.1%). After minimal 6 months of follow-up, there was neither episodes of graft dysfunction nor rejection. There was a significant improvement of glucose control in conversion group. In 12 patients(30.8%), more than 50% dose reduction of insulin or oral hypoglycemics requirement was possible. In control group, however, only 2 patients showed greater than 50% of insulin or oral hypoglycemics dose reduction. We could find that deflazacort conversion had a significant impact on blood sugar control in PTDM patients(11/26) but not in pre-Tx DM patients(1/13). In conclusion, conversion to deflazacort in PTDM patients with stable graft function was safe and blood sugar control was readily possible without an increment of risks of rejection and infection. We propose to use deflazacort as a substitute for prednisone in PTDM patients with stable graft function.
Anorexia ; Blood Glucose ; Cyclosporine ; Diabetes Mellitus ; Follow-Up Studies ; Glucose ; Glucose Intolerance ; Humans ; Hypoglycemic Agents ; Insulin ; Kidney* ; Prednisone* ; Prospective Studies ; Transplants

An association between drug treatment for viral infections and severe cutaneous adverse reactions has been noted. We investigated six patients diagnosed with Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) after being prescribed acetaminophen for suspected viral illnesses. Multiplex analysis was performed to measure cytokine levels in sera before and after treatment. IL-2Rα levels significantly decreased during the convalescence phase. Although acetaminophen is relatively safe, the drug can trigger SJS/TEN in patients with suspected viral infections. T-cells and monocytes may be key components of the link between viral infection and acetaminophen-induced SJS/TEN.
Acetaminophen* ; Convalescence ; Humans ; Monocytes ; Stevens-Johnson Syndrome* ; T-Lymphocytes

PURPOSE: Excess proliferation of mesenchymal cells such as vascular smooth muscle cells and glomerular mesangial cells, cause transplant vascular sclerosis and glomerulosclerosis, which are typical pathological lesions of chronic allograft dysfunction. Mycophenoic acid (MPA) and rapamycin (RPM) were recently reported to have strong anti-proliferative potentials toward vascular smooth muscle cells. However, the potential effects of these drugs, either alone or in combination, on glomerular mesangial cells, remain to be reported. METHODS: Primary cultured mesangial cells, from Sprague-Dawley rats, were isolated, and stimulated with 10ng/ml of PDGF. The test drugs MPA and RPM were administered at various concentrations, either alone or in combination, 15 minutes before the addition of the PDGF. The cell proliferation was assessed by [3H]-thymidine incorporation. RESULTS: The PDGF effectively stimulated the proliferation of the mesangial cells. The MPA inhibited the proliferation in a dose-dependent manner. In comparison to the stimulated control, the MPA (above 500 nM) showed a significant inhibitory effect. The IC50 of the MPA, against PDGF-stimulated mesangial cell proliferation, was between 500 nM and 1microM. The RPM, at 10 nM, showed a significant inhibitory effect. In a linear regression analysis, the RPM was supposed to suppress the mesangial proliferation in a dose-dependent manner (P<0.05). The pattern of inhibition for the MPA and RPM combination was very similar to that of either the MPA or the RPM alone. Both the MPA and RPM were shown to independently suppress the mesangial proliferation from a multiple regression analysis (R2=0.415, P<0.001). CONCLUSION: We demonstrated that MPA and RPM significantly inhibited the proliferation of glomerular mesangial cells, and that these effects were well maintained when used in combination. Our data indicate that both MPA and RPM have unique potentials in preventing the development of transplant mesangial proliferation in renal transplant recipients.
Allografts ; Animals ; Cell Proliferation ; Inhibitory Concentration 50 ; Linear Models ; Mesangial Cells* ; Muscle, Smooth, Vascular ; Mycophenolic Acid* ; Rats* ; Rats, Sprague-Dawley ; Sclerosis ; Sirolimus* ; Transplantation

BACKGROUND/AIMS: This study examined the efficacy and safety of oxaliplatin-5-fluorouracil-leucovorin (FOLFOX-4) combination chemotherapy as first-line treatment in patients with advanced gastric cancer. METHODS: This retrospective study enrolled 35 patients diagnosed with pathologically proven surgically unresectable gastric cancer who received FOLFOX-4 combination chemotherapy between August 2006 and February 2009, using medical records. The administered dose of oxaliplatin was 85 mg/m2 for 2 hrs and leucovorin 200 mg/m2 for 2 hrs on day 1, 5-fluorouracil 400 mg/m2 as a bolus and 5-fluorouracil 600 mg/m2 for 22 hrs on days 1 and 2, every 2 weeks. The response was assessed every three cycles. Toxicity was evaluated for every course of chemotherapy according to the NCI toxicity criteria ver. 2.0. RESULTS: The median patient age was 61 (range 27-77) years. The median overall survival was 8.50 (6.23-10.90) months and the median time to progression was 4.50 (0.38-9.75) months. With FOLFOX-4, there was no complete remission and 19 partial responses, for a response rate of 54.3%. Over 298 cycles, anemia worse than NCI toxicity grade 3 occurred in 1.3%, leukopenia in 1.6%, neutropenia in 9%, and thrombocytopenia in 3.2%. Grade 1-2 neuropathy occurred in 14.7% of the cycles. Neutropenic fever occurred in two cycles and the regimen was changed because of side effects in one cycle. CONCLUSIONS: FOLFOX-4 has a very high response rate with mild toxicity in patients with advanced gastric cancer as a first-line treatment.
Anemia ; Drug Therapy, Combination ; Fever ; Fluorouracil ; Humans ; Leucovorin ; Leukopenia ; Medical Records ; Neutropenia ; Organoplatinum Compounds ; Retrospective Studies ; Stomach Neoplasms ; Thrombocytopenia

BACKGROUND/AIMS: Previous studies have reported that the frequency of re-diagnosing as carcinoma after endoscopic resection of gastric adenoma ranges between 6% and 47%. Therefore, specific endoscopic findings have been used to predict re-diagnosing as carcinoma after endoscopic resection of gastric adenoma at our center. We evaluated whether there is a use for these indicators for predicting carcinoma as a final diagnosis in forceps biopsy-proven adenomas. MATERIALS AND METHODS: We investigated 378 tissue samples from 308 patients. Classification of specimens as adenoma and carcinoma was based on postresection specimen. Endoscopic findings were reviewed for tumor location, size, gross appearance, surface nodularity, central concavity, surface color, and presence of ulcers. These variables were analyzed and compared between the adenoma group (275 cases) and the carcinoma group (103 cases), assigned based on post-resection diagnosis. RESULTS: The mean patient age was 61, and 227 of the patients were male. The mean lesion diameter was 14.9+/-8.1 mm in the adenoma group and 17.9+/-9.3 mm in the carcinoma group. A lesion size of 15 mm or greater, depressed appearance, surface nodularity, central concavity, and presence of high-grade dysplasia were all independently associated with re-diagnosing as carcinoma after endoscopic resection. CONCLUSIONS: Lesion size of 15 mm or greater, depressed-type appearance, central concavity, and nodular surface are feasible predictors of carcinoma as a final diagnosis in forceps biopsy-proven adenomas. Physicians need to recommend immediate endoscopic resection for forceps biopsy-proven adenomas with these four independent features so as not to miss the optimal window for treatment.
Adenoma ; Humans ; Male ; Stomach ; Surgical Instruments ; Ulcer

BACKGROUND/AIMS: Previous studies have reported that the frequency of re-diagnosing as carcinoma after endoscopic resection of gastric adenoma ranges between 6% and 47%. Therefore, specific endoscopic findings have been used to predict re-diagnosing as carcinoma after endoscopic resection of gastric adenoma at our center. We evaluated whether there is a use for these indicators for predicting carcinoma as a final diagnosis in forceps biopsy-proven adenomas. MATERIALS AND METHODS: We investigated 378 tissue samples from 308 patients. Classification of specimens as adenoma and carcinoma was based on postresection specimen. Endoscopic findings were reviewed for tumor location, size, gross appearance, surface nodularity, central concavity, surface color, and presence of ulcers. These variables were analyzed and compared between the adenoma group (275 cases) and the carcinoma group (103 cases), assigned based on post-resection diagnosis. RESULTS: The mean patient age was 61, and 227 of the patients were male. The mean lesion diameter was 14.9+/-8.1 mm in the adenoma group and 17.9+/-9.3 mm in the carcinoma group. A lesion size of 15 mm or greater, depressed appearance, surface nodularity, central concavity, and presence of high-grade dysplasia were all independently associated with re-diagnosing as carcinoma after endoscopic resection. CONCLUSIONS: Lesion size of 15 mm or greater, depressed-type appearance, central concavity, and nodular surface are feasible predictors of carcinoma as a final diagnosis in forceps biopsy-proven adenomas. Physicians need to recommend immediate endoscopic resection for forceps biopsy-proven adenomas with these four independent features so as not to miss the optimal window for treatment.
Adenoma ; Humans ; Male ; Stomach ; Surgical Instruments ; Ulcer

PURPOSE: Vascular smooth muscle cell (VSMC) proliferation and extra-cellular matrix (ECM) protein accumulation play important roles in transplant vascular sclerosis and re- stenosis after balloon vascular injury. Mycophenolic acid (MPA), rapamycin (RPM), and carvedilol (CA) were proven to inhibit the proliferation of VSMC. Fibronectin is a multifunctional ECM protein and induces tissue fibrosis. Since mitogen-activated protein kinases (MAPK) are upstream signaling molecules of VSMC proliferation and fibronectin production, this study examined the effects of MPA, RPM, and CA on the fibronectin secretion and MAPK activation in rat VSMC stimulated by platelet derived growth factor (PDGF). METHODS: VSMC was isolated from the aorta of male Sprague-Dawley rat, weighing 200-250 g and cultured with EMEM containing 10% fetal bovine serum and insulin/transferrin supplement. Near confluent VSMC were incubated with serum-free media for 48 hours to arrest and synchronize the cell growth. Test drugs were administered 15 minutes before the addition of PDGF 10 ng/mL. Cell proliferation, fibronectin secretion, and MAPK activation in VSMCs were measured by Western blot analysis. RESULTS: PDGF induced cell proliferation, fibronectin secretion, and extracellular- regulatary protein kinase 1/2 (ERK 1/2) and p38 MAPK activation by 1.7-, 1.5-, 3.3-, 3.9-fold, respectively, compared to control. MPA (>1 microM), CA (>100 nM), PD98059 (>30 microM), and p38 MAPK inhibitor (>10 nM) effectively inhibited PDGF-induced proliferation and fibronectin secretion. RPM, up to 100 nM, effectively inhibited cell proliferation, but did not inhibit fibronectin secretion. MPA and CA, but not RPM, inhibited PDGF-induced ERK 1/2 and p38 MAPK activation. CONCLUSION: The present study demonstrates that MPA and CA inhibit both cell proliferation and fibronectin secretion in rat VSMC stimulated by PDGF. Inhibition of both ERK 1/2 and p38 molecules are significantly associated with these events. Even though, it has a significant anti-proliferative effect on the rat VSMC, RPM neither affected the phosphorylation of ERK 1/2 and p38 nor secretion of fibronectin. These data suggest that ERK 1/2- and p38 MAPK-independent, more proximal pathway may exist for PDGF-induced proliferation of rat VSMC.
Animals ; Aorta ; Blotting, Western ; Cell Proliferation ; Constriction, Pathologic ; Culture Media, Serum-Free ; Fibronectins* ; Fibrosis ; Humans ; Male ; Mitogen-Activated Protein Kinases ; Muscle, Smooth, Vascular* ; Mycophenolic Acid* ; Myocytes, Smooth Muscle ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Phosphotransferases* ; Platelet-Derived Growth Factor ; Protein Kinases ; Rats* ; Rats, Sprague-Dawley ; Sclerosis ; Sirolimus* ; Vascular System Injuries

PURPOSE: Vascular smooth muscle cells (VSMCs) migration and proliferation play important roles in transplant vascular sclerosis and restenosis after balloon vascular injury. The anti-proliferative and anti- migratory effects of carvedilol (CA), a unique alpha- and beta-blocking anti-hypertensive drug, on the VSMCs were confirmed previously. Since reactive oxygen species (ROS) and mitogen-activated protein kinases (MAPK) family play important roles in proliferation of VSMCs, the present study examined the effects of CA on intracellular ROS generation, activation of ERK1/2 and p38 MAPK, and proliferation of VSMCs cultured under platelet derived growth factor (PDGF). METHODS: Human VSMCs obtained from ATCC were cultured with RPMI-1640 containing 10% fetal bovine serum. Near confluent VSMCs were incubated with serum-free media for 48 hours to arrest and synchronize the cell growth. CA was administered 1 hour before the addition of PDGF. 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein (DCF)-sensitive intracellular ROS was detected by FACS. Activations of ERK1/2 and p38 MAPK were measured by Western blot analysis. Proliferation of VSMCs was assessed by [3H]-thymidine incorporation. RESULTS: PDGF at 10 ng/ml, which induced human VSMCs proliferation, rapidly increased intracellular ROS by 1.6-fold (P<0.01), ERK1/2 activation by 2.1-fold (P<0.01), and p38 MAPK activation by 1.9-fold (P<0.01), respectively, as compared to the control. CA 1 and 10muM effectively inhibited PDGF-induced human VSMCs proliferation. CA also effectively inhibited PDGF-induced intracellular ROS generation as well as ERK1/2 and P38 MAPK activation. CONCLUSION: The present study suggests that CA inhibits PDGF-induced human VSMCs proliferation, possibly by inhibiting intracellular ROS generation and activation of ERK1/2 and p38 MAPK.
Blotting, Western ; Cell Proliferation* ; Culture Media, Serum-Free ; Humans* ; Mitogen-Activated Protein Kinases ; Muscle, Smooth, Vascular* ; Myocytes, Smooth Muscle ; p38 Mitogen-Activated Protein Kinases ; Platelet-Derived Growth Factor ; Reactive Oxygen Species ; Sclerosis ; Signal Transduction* ; Vascular System Injuries

PURPOSE: Vascular smooth muscle cells (VSMCs) migration and proliferation play important roles in chronic allograft rejection. Mycophenolic acid (MPA) inhibits the proliferation of VSMCs, glomerular mesangial cells and fibroblasts as well as lymphocytes. Since reactive oxygen species (ROS) and mitogen-activated protein kinase (MAPK) play important roles in the proliferation of VSMCs, the present study examined the effects of MPA on intracellular ROS generation, activation of ERK and p38 MAPK, and the proliferation of VSMCs cultured under platelet derived growth factor (PDGF). METHODS: Human VSMCs obtained from ATCC were cultured with RPMI-1640 containing 10% fetal bovine serum. Near confluent VSMCs were incubated with serum-free media for 48 hours to arrest and synchronize the cell growth. MPA was administered 1 hour before the addition of PDGF. 5-(and-6)- chloromethyl-2',7'-dichlorodihydrofluorescein (DCF)-sensitive intracellular ROS was detected by FACS. Activations of ERK1/ERK2 and p38 MAPK were measured by Western blot analysis. Proliferation of VSMC was assessed by [(3)]. RESULTS: PDGF administered at 10 ng/ml, which induced human VSMCs proliferation, rapidly increased intracellular ROS by 1.6-fold (P<0.05), ERK1/ERK2 activation by 2.1-fold, (P<0.05) and p38 MAPK activation by 1.9-fold (P<0.05), respectively, as compared to the control. MPA 1 and 10nM effectively inhibited PDGF-induced human VSMCs proliferation. MPA also effectively inhibited PDGF-induced intracellular ROS generation as well as ERK1/ERK2 and p38 MAPK activation. CONCLUSION: The present study suggests that MPA inhibits PDGF-induced human VSMCs proliferation, possibly by inhibiting intracellular ROS generation and the phosphorylation of ERK1/ERK2 and p38 MAPK. H]-thymidine incorporation.
Allografts ; Blotting, Western ; Cell Proliferation* ; Culture Media, Serum-Free ; Fibroblasts ; Humans* ; Lymphocytes ; Mesangial Cells ; Muscle, Smooth, Vascular* ; Mycophenolic Acid* ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Platelet-Derived Growth Factor ; Protein Kinases ; Reactive Oxygen Species ; Signal Transduction*