A 38-year-old man, with recurrent oral ulcers for 10 years, was admitted because of recent aggravation of odynophagia and sore throat. About 4 years earlier, he had been performed abdominal surgery for intestinal perforation. Gastrofiberscopic examination showed small round ulcers at hypiopharynx and 6cm sized longitudinal linear ulcer at mid esophagus. Biopsy specimens at mid-esophagus showed chronic inflammation. Besides oral ulcer, he had perianal ulcers and skin rashes. He was managed with steroid, colchicine and sulfasalazine under the diagnosis of esophageal involvement in Behcet's disease. After 3 months from discharge, esophagogram and gastrofiberscopic examination showed some improved appearance, but symptoms recurred for steroid tapering. He has been followed in much improved status for 8 months after discharge.
Adult ; Biopsy ; Colchicine ; Diagnosis ; Esophagus ; Exanthema ; Humans ; Inflammation ; Intestinal Perforation ; Oral Ulcer ; Pharyngitis ; Sulfasalazine ; Ulcer*

Epstein's syndrome is a rare disease whish is characterized by the association of thrombocytopenia, macrothrombocytopathia, nephritis and deafness. We experienced a case of Epstein's syndrome in a 12 years old male patient who was presented with a life long history of bleeding, usually as epistaxis, bilateral sensorineural deafness and hematuria with proteinuria starting in late childhood. Hematologic studies showed thrombocytopenia with giant platelets and anemia. A bone marrow aspirate revealed the megakaryocytes to be adequate in number and many giant size platelets. Platelet do not respond to addition of A and epinephrine; collagen and ristocetin induced agglutination response is decreased. It is difficult to be certain the association of thrombocytopenia with giant platelets, nephritis and deafness constitutes a new hereditary disease with a distinct pathogenesis or if it is an expansion of the well recognized Alport's syndrome of hereditary nephritis deafness. We report a case of Epstein's syndrome syndrome with brief review of related literatures.
Agglutination ; Anemia ; Blood Platelets ; Bone Marrow ; Child ; Collagen ; Deafness ; Epinephrine ; Epistaxis ; Genetic Diseases, Inborn ; Hematuria ; Hemorrhage ; Humans ; Male ; Megakaryocytes ; Nephritis ; Nephritis, Hereditary ; Proteinuria ; Rare Diseases ; Ristocetin ; Thrombocytopenia

Segmental non-familial colonic polyposis was first reported by Chiang et al. in 1992. It is characterized by segmental distributlion of colonic polyposis usually confined to the descending colon, absence of family history of polyposis, large bowel malignancy, inflammatory bowel disease, or other pre-malignant colonic conditions. We experienced a nineteen-year-old male, who suffered from 2 years watery diarrhea about five to ten times a day, intermittent hematochezia, and weight loss of 12 kg in a year. He had no family history of colonic polyps, colon cancer, or inflammatory bowel disease. Colon study showed variable sized multiple colonic polyps on the rectum and sigmoid colon. Colonoscopy showed that 0.5 to 1.5 cm sized multiple polyps were scattered from the 6cm site to the 30cm site above the anal verge and the intervening mucosa between polyps was edematous. Colonoscopic biopsy revealed hyperplastic, adenomatous, and mixed hyperplastic and adenomatous polyps, After partial colectomy, we discovered 169 polyps from the resected specimen. After operation, diarrhea and abdominal pain had disappeared. We experienced a case of segmental non-familial polyposis and report it with review of the literatures related to it.
Abdominal Pain ; Adenomatous Polyps ; Biopsy ; Colectomy ; Colon* ; Colon, Descending ; Colon, Sigmoid ; Colonic Neoplasms ; Colonic Polyps ; Colonoscopy ; Diarrhea ; Gastrointestinal Hemorrhage ; Humans ; Inflammatory Bowel Diseases ; Male ; Mucous Membrane ; Polyps ; Rectum ; Weight Loss

BACKGROUND: There are many evidences that inflammation is an important determinant of the development of atherosclerosis and one of the systemic markers of inflammation, C-reactive protein(CRP), is associated with extent of coronary artery disease and risk of coronary events. We assessed the time response of CRP response after coronary angioplasty and it's influence on the clinical restenosis in angina patients. MATERIALS AND METHODS: Patients included 36 angina patients undergoing single vessel angioplasty. Levels of CRP were measured before and 12, 24, 48, and 72 hours after angioplasty. Clinical restenosis was assessed at 6 months after procedure. RESULTS: Baseline CRP level was 0.30+/-0.01 mg/dL in stable and 0.46+/-0.28 mg/dL in unstable angina patients(p<0.05). After angioplasty, CRP level was increased with peak at 24 hour and persisted to 72 hours after angioplasty. At 24 hour after angioplasty, the magnitude of CRP change was 0.32+/-0.31 mg/dL in stable and 0.79+/-0.73 mg/dL in unstable angina patient(p<0.05). The change of CRP level was not associated with troponin-T after angioplasty. In unstable angina patients, clinical restenosis was developed in 8% of patients with low baseline CRP levels and in 50% of those with high baseline CRP levels more than 0.6 mg/dL(p<0.05). CONCLUSION: In unstable angina patients, inflammatory response is more increased than stable angina patients, and increased inflammatory response effects on the restenosis after coronary angioplasty.
Angina, Stable ; Angina, Unstable ; Angioplasty* ; Atherosclerosis ; C-Reactive Protein* ; Coronary Artery Disease ; Humans ; Inflammation ; Troponin T

No abstract available.
Paranasal Sinuses*

No abstract available.
Liver Transplantation* ; Liver*

PURPOSE: The purpose of this article is to evaluate the result of treatment of unstable intertrochanteric fractures by lateralization of distal fragment and antero-medial cortex contact of the distal shaft piece. MATERIALS AND METHODS: We conducted an analysis of 20 cases of unstable intertrochanteric fractures treated using a gamma-3 nail from August 2011 to August 2012 and followed up for more than one year. Using postoperative and last follow-up radiographs, we measured NSA, TAD, Cleveland index, sliding length of the lag screw, and union time. Adequacy of reduction was assessed by a modification in the criteria of Baumgaertner and classified as good, acceptable, or poor. RESULTS: The mean NSA was 140degrees postoperative and 135degrees at last follow-up. The mean TAD was 11.3 mm. The position of the lag screw was in center-center in 12 cases, center-inferior in eight cases. The mean distance of lag screw sliding was 5.5 mm at last follow-up. The mean union time was 3.7 months. The state of reduction postoperatively was good in 15 cases, and acceptable in five cases. There was no failure of reduction, lag screw cut-out, or other complications at last follow-up. CONCLUSION: The reduction method for lateralization of distal fragment and antero-medial cortex contact of the distal shaft piece in an unstable intertrochanteric fracture is very useful for prevention of collapse of the fracture site, lag screw cut-out, and mechanical failure.
Follow-Up Studies ; Hip Fractures* ; Methods

No abstract available.
Classification* ; von Willebrand Diseases* ; von Willebrand Factor*

BACKGROUND/AIMS: Genetic variations of ethanol-metabolizing enzymes can affect alcohol drinking behavior. The aims of this study were to investigate and compare the distributions of these genetic polymorphisms between a healthy control group and a heavy drinker group which included an alcoholic liver cirrhosis group. METHODS: Genotypes of ADH2, ALDH2, CYP2E1, and catalase were identified by polymerase chain reaction and restriction fragment length polymorphism. Genomic DNA was extracted from peripheral leukocytes in 42 healthy controls, 12 heavy drinkers, and 30 alcoholic liver cirrhosis patients. RESULTS: 1) The genotype frequencies of ALDH2 (1*1), ADH2 (1*1), CYP2E1 (c1c1), and catalase1 (TT) were 69%, 55%, 38%, and 12%, respectively in healthy Korean males. 2) There was a significant difference in the distribution of the genetic polymorphism of ALDH2 between the control group and heavy drinker group (12 heavy drinkers and 30 alcoholic liver cirrhosis patients). The genotype frequency of ALDH2 mutant, ALDH2 (1*2) and ALDH2 (2*2) in the heavy drinker group (12%) was significantly lower than that in the control group (30%). 3) We didn't find anyone with ALDH2 homozygote mutant (DD) in the heavy drinker group. 4) There was no significant difference in the distribution of genetic polymorphisms in ADH2, CYP2E1 and catalase1 between the two groups. CONCLUSIONS: These results suggest that the absence of ALDH2 mutant genotype is strongly related to heavy drinking behavior. We can not prove, however, any evidence that the polymorphisms of other ethanol-metabolizing enzymes are associated with the determination of alcohol-drinking behavior.
Adult ; Alcohol Dehydrogenase/*genetics ; Alcohol Drinking ; Alcoholism/enzymology/*genetics ; Aldehyde Dehydrogenase/*genetics ; Cytochrome P-450 CYP2E1/*genetics ; Ethanol/metabolism ; Humans ; Liver Cirrhosis, Alcoholic/enzymology/*genetics ; Male ; Middle Aged ; *Polymorphism, Genetic