Leiomyoblastoma is uncommon and has been known as a neoplasm of smooth muscle origin. However, with recent pragress in immunohistochemical staining techniques, many clinicopathological discrepancies have been pointed out about the origin of leiomyoblastoma. We present here a case of gastric leiomyoblastoma did not expressed desmin and neuron specific enolase, and was thought to be of unknown derivation.
Desmin ; Leiomyoma, Epithelioid* ; Muscle, Smooth ; Phosphopyruvate Hydratase

Leiomyoblastoma is uncommon and has been known as a neoplasm of smooth muscle origin. However, with recent pragress in immunohistochemical staining techniques, many clinicopathological discrepancies have been pointed out about the origin of leiomyoblastoma. We present here a case of gastric leiomyoblastoma did not expressed desmin and neuron specific enolase, and was thought to be of unknown derivation.
Desmin ; Leiomyoma, Epithelioid* ; Muscle, Smooth ; Phosphopyruvate Hydratase

A case of peripheral neuroblastoma of a 33-year-old male, which was located on the left buttock, is presented. Histologcally, this tumor demonstrated smaliound cell infiltrations which were arranged in a characteristic rosette pattern and the tumor cells were positively stained with neuron specific enolase. We review the clinical, histopathological ultrastructural and immunohisto chemical characteristics of this rare tumor, as well as the differential diagnosis with other small round cell tumors.
Adult ; Buttocks ; Diagnosis, Differential ; Humans ; Male ; Neuroblastoma* ; Phosphopyruvate Hydratase

Since granular cell tumor was first described by Abrikossoff in 1926, it has been known as a rare disease. The histogenesis of this tumor is still controversial, but the origin is thought to be from a Schwann cell. About one third of the tumors occur in the tongue, and uncommonly in the perianal region. We report a case of granular cell tumor that developed in the perianal region. The tumor grew slowly for 5 years and was removed by a local excision. This tumor showed positive staining with neuron-specific enolase (NSE).
Granular Cell Tumor* ; Phosphopyruvate Hydratase ; Rare Diseases ; Tongue

Primary small cell neuroendocrine carcinoma in stomach is known to be very rare and only the twelve cases have been reported in the English literature. This tumor appears to be analogous to small cell carcinoma and carcinoid tumors of the lung, and is characterized by a very aggressive clinical course. Recently, we have experienced a 68-year-old man with primary small cell neuroendocrine carcinoma in the stomach, which had liver metastasis and peritoneal seeding. A positive Grimelius stain was present and immunohistochemical studies revealed positivity for neuron-specific enolase in the tumor. For its rarity, we report this case with review of literatures.
Aged ; Carcinoid Tumor ; Carcinoma, Neuroendocrine* ; Carcinoma, Small Cell ; Humans ; Liver ; Lung ; Neoplasm Metastasis ; Phosphopyruvate Hydratase ; Stomach*

PURPOSE: To determine the role of zinc in febrile convulsion and to evaluate whether febrile convulsion causes neuronal damage, serum and cerebrospinal fluid(CSF), zinc and CSF neuron-specific enolase(NSE) levels were measured in patients with febrile convulsion, epilepsy and aseptic meningitis. METHODS: Three groups were formed as follows: group I:53 children with febrile convulsion; group II:34 children with epilepsy; and group III, 40 children with aseptic meningitis. Serum and CSF zinc and CSF NSE levels were measured in each groups. RESULTS: The serum zinc levels of groups I, II and III had a mean of 74.71+/-18.26 microgram/dL, 104.35+/-31.43 microgram/dL and 87.03+/-24.47 microgram/dL, respectively, and the values of group I were significantly lower than those of the other two groups. The CSF zinc levels of groups I, II and III were found to have a mean 27.72+/-17.93 microgram/dL, 44.73+/-26.72 microgram/dL and 54.44+/-28.43 microgram/dL, respectively. In group I, the CSF zinc levels were significantly lower than those of other two groups. The CSF NSE levels of groups I, II and III had a mean of 11.61+/-2.96 ng/mL, 16.51+/-5.46 ng/mL and 14.60+/-3.02 ng/mL respectively and the values of group I were significantly lower than those of others. CONCLUSION: We confirmed that low zinc levels in serum and CSF are participants in the pathogenesis of febrile convulsion, but we could not find out the evidence of neurologic damage in patients with febrile convulsion using NSE levels in CSF.
Child ; Epilepsy ; Humans ; Meningitis, Aseptic ; Neurons ; Phosphopyruvate Hydratase* ; Seizures, Febrile* ; Zinc*

PURPOSE: Neuron-specific enolase(NSE) has been established as a reliable marker of neuronal damage in various neurologic disorders. The aim of this study was to evaluate whether febrile seizure cause brain damage, based on the serum and cerebrospinal fluid (CSF) levels of NSE. METHODS: Twenty-one pateints were enrolled. The maximal seizure duration was 90 mins. Blood and CSF samples for the measurement of NSE were obtained immediately after the seizure. NSE was measured using an immunoradiometric assay(IRMA). RESULTS: The CSF NSE level of the febrile seizure group was 11.7+/-2.04 ng/mL and that of the control group was 11.3+/-5.7 ng/mL. The serum NSE level of the febrile seizure group was higher than the serum NSE level of the control group, but there was no significant correlation. The serum NSE level of the febrile seizure group was 19.0+/-7.5 ng/mL and that of the control group was 12.8+/-5.1 ng/mL. The serum NSE level of the febrile seizure group was significantly higher than the serum NSE level of the control group. The CSF/serum ratio of NSE in the febrile seizure group was 0.7+/-0.3 and that of the control group was 1.0+/-0.5. The CSF/serum ratio of NSE in the febrile seizure group was lower than the CSF/serum ratio of NSE in the control group and there was a significant correlation. There was no significant correlation between seizure duration, serum NSE, CSF NSE, and the ratio of the CSF to the serum level of NSE. CONCLUSION: Children with febrile seizure are at relatively low risk for neuronal damage following seizures.
Brain ; Cerebrospinal Fluid* ; Child* ; Humans ; Nervous System Diseases ; Neurons ; Phosphopyruvate Hydratase* ; Seizures ; Seizures, Febrile*

PURPOSE: Neuron-specific enolase(NSE) has been established as a reliable marker of neuronal damage in various neurologic disorders. The aim of this study was to evaluate whether febrile seizure cause brain damage, based on the serum and cerebrospinal fluid (CSF) levels of NSE. METHODS: Twenty-one pateints were enrolled. The maximal seizure duration was 90 mins. Blood and CSF samples for the measurement of NSE were obtained immediately after the seizure. NSE was measured using an immunoradiometric assay(IRMA). RESULTS: The CSF NSE level of the febrile seizure group was 11.7+/-2.04 ng/mL and that of the control group was 11.3+/-5.7 ng/mL. The serum NSE level of the febrile seizure group was higher than the serum NSE level of the control group, but there was no significant correlation. The serum NSE level of the febrile seizure group was 19.0+/-7.5 ng/mL and that of the control group was 12.8+/-5.1 ng/mL. The serum NSE level of the febrile seizure group was significantly higher than the serum NSE level of the control group. The CSF/serum ratio of NSE in the febrile seizure group was 0.7+/-0.3 and that of the control group was 1.0+/-0.5. The CSF/serum ratio of NSE in the febrile seizure group was lower than the CSF/serum ratio of NSE in the control group and there was a significant correlation. There was no significant correlation between seizure duration, serum NSE, CSF NSE, and the ratio of the CSF to the serum level of NSE. CONCLUSION: Children with febrile seizure are at relatively low risk for neuronal damage following seizures.
Brain ; Cerebrospinal Fluid* ; Child* ; Humans ; Nervous System Diseases ; Neurons ; Phosphopyruvate Hydratase* ; Seizures ; Seizures, Febrile*

BACKGROUND: Neuron-specific enolase (NSE) is a useful indicator of neuronal injury in acute cerebral infarction. We investigated the changes in serial serum NSE levels in patients with acute cerebral infarction. METHODS: We measured serial serum NSE levels at 24, 48, 72, and 96 hours, and 2 weeks after the onset of cerebral infarction in 30 patients (15 territorial and 15 lacunar infarctions). We also measured the NSE levels in age-matched controls (n=15) who had no evidence of acute stroke or other neurological disorders. The NSE level was measured using a radioimmunoassay. RESULTS: The initial serum NSE level was significantly higher in the cerebral infarction group than in the control group (6.6+/-2 vs 4.7+/-1.6 ng/mL [mean+/-SD], p=0.006). This difference was also observed between the territorial and lacunar infarction groups until 72 hours after the cerebral infarction. The serum NSE level peaked at 72 hours after the infarction in both lacunar and territorial infarction groups. The correlation between the NSE level and the score on the NIH Stroke Scale was strongest at 48 hours after the cerebral infarction (r=0.469). CONCLUSIONS: Serum NSE level can be a good indicator for distinguishing lacunar from territorial infarction during the acute stage of cerebral infarction.
Cerebral Infarction ; Humans ; Infarction ; Nervous System Diseases ; Neurons ; Phosphopyruvate Hydratase ; Stroke ; Stroke, Lacunar

PURPOSE: We studied the plasma neuron-specific enolase (NSE) and glutamic acid levels as a marker of the severity of acute ischemic stroke (AIS). METHODS: We enrolled 93 patients who visited to the emergency department from April to September, 2005. The AIS patients included those who visited the emergency department within 24 hours due to ischemic stroke symptoms. The AIS patients was subclassified according to large-vessel, small-vessel, cardioembolic, or unclassified infarction. RESULTS: The plasma NSE and glutamic acid level were 15.1+/-7.9 ng/ml and 204.5+/-86.5 nM/ml, respectively, in the AIS patients. Plasma NSE and Glutamic acid in the was higher than reference range (NSE 0-12 ng/ml, Glutamic acid 0-130 nM/ml). According to the type of infarction, no differences were observed in the plasma NSE and glutamic acid levels. CONCLUSION: In cases of AIS, NSE and glutamic acid have no statistical usefulness in classifying the type of infarction. However, the value of plasma NSE and glutamic acid levels have statistical usefulness in deciding on the existence or nonexistence of an AIS.
Cerebral Infarction ; Emergency Service, Hospital ; Glutamic Acid* ; Humans ; Infarction ; Phosphopyruvate Hydratase* ; Plasma* ; Reference Values ; Stroke*