Henoch-Schonlein purpura or Anaphylactiod purpura is rare syndrome in adults characterized by a symmetrical, non traumatic, nonthrombocytopenic, painless purpuric rash, arthritis, nephritis, gastrointestinal manifestation. G-I tract involvement is characterized by abdominal pain, G-I bleeding. Although the small bowel is more frequently involved, cases of esophageal, gastroduodenal and colorectal localization have been rarely reported. Recently, we have experienced a case of Henoch-schonlein purpura with renal, skin, extensive gastrointestinal involvement in a 53 year-old male patient who complained of pain, purpura, generalized abdominal pain, dyspnea. The endoscopic findings of duodenum and colon in a patient with Henoch-Schonlein purpura are presented.
Abdominal Pain ; Adult ; Arthritis ; Colon ; Colon, Sigmoid ; Duodenum ; Dyspnea ; Exanthema ; Hemorrhage ; Humans ; Male ; Middle Aged ; Nephritis ; Purpura* ; Purpura, Schoenlein-Henoch ; Skin

Henoch-Schonlein purpura or Anaphylactiod purpura is rare syndrome in adults characterized by a symmetrical, non traumatic, nonthrombocytopenic, painless purpuric rash, arthritis, nephritis, gastrointestinal manifestation. G-I tract involvement is characterized by abdominal pain, G-I bleeding. Although the small bowel is more frequently involved, cases of esophageal, gastroduodenal and colorectal localization have been rarely reported. Recently, we have experienced a case of Henoch-schonlein purpura with renal, skin, extensive gastrointestinal involvement in a 53 year-old male patient who complained of pain, purpura, generalized abdominal pain, dyspnea. The endoscopic findings of duodenum and colon in a patient with Henoch-Schonlein purpura are presented.
Abdominal Pain ; Adult ; Arthritis ; Colon ; Colon, Sigmoid ; Duodenum ; Dyspnea ; Exanthema ; Hemorrhage ; Humans ; Male ; Middle Aged ; Nephritis ; Purpura* ; Purpura, Schoenlein-Henoch ; Skin

BACKGROUND: Recently, the mechanism involved in nitric oxide (NO)-mediated motor neuron death is under extensive investigation. The role of Cu/Zn superoxide dismutase (SOD) mutation, which is found in about 2% of all ALS patients, has been implicated in selective motor neuron death and it is said to play an important role in NO-mediated motor neuron death. Estrogen is reported to have neuroprotective effect in various neurological diseases. However, neuroprotective effect on estradiol on spinal motor neuron exposed to NO has rarely been studied. METHODS: Motor neuron-neuroblastoma hybrid cell expressing wild-type or mutant (G93A or A4V) SOD gene was treated with 200 micro M Snitrosoglutathione. After 24 hours, cell viability was measured by MTT assay. To see the neuroprotective effect of estradiol, pretreatment with 5 nM or 50 nM 17 beta-estradiols was done 24 hours before S-nitrosoglutathione treatment. RESULTS: S-nitrosoglutathione showed significant neurotoxic effect in all three cell lines. Percentage of cell death was significantly different in each cell line. Both 5 nM and 50 nM estradiols showed neuroprotective effect in G93A cell line. In wild-type cell line, 50 nM estradiol showed neuroprotective effect, but 5 nM estradiol did not. In A4V cell line, estradiol did not showed neuroprotective effect. CONCLUSIONS: This study showed that NO-mediated motor neuron death could be influenced by presence or absence of mutation and type of mutation in SOD gene. Neuroprotective effect of estradiol is also influenced by SOD gene mutation. This study implies that estrogen might be beneficial to some ALS patients.
Cell Death ; Cell Line ; Cell Survival ; Estradiol ; Estrogens* ; Humans ; Hybrid Cells ; Motor Neurons* ; Neuroprotective Agents* ; Nitric Oxide ; S-Nitrosoglutathione ; Superoxide Dismutase* ; Superoxides*

Both the inherited and acquired forms of vitamin E deficiency are implicated in chronic progressive neurological deficit. The clinical features include ataxia and prominent proprioceptive loss with depressed or absent tendon reflexes. We report a 63-year-old man with vitamin E deficiency syndrome caused by chronic fat malabsorption following exten-sive intestinal resection. Although replacement therapy prevented further deterioration, symptomatic improvement was not observed for two years. Early diagnosis and appropriate treatment is crucial.
Ataxia ; Early Diagnosis ; Humans ; Middle Aged ; Reflex, Stretch ; Vitamin E Deficiency* ; Vitamin E* ; Vitamins*

The spinal accessory nerve is well known to be injured by surgical procedures in the posterior cervical triangle. The trapezius muscle innervated by the spinal accessory nerve is a major scapular stabilizer, so the paralysis of this muscle results in shoulder droop, limited range of motion, and displacement of scapula as well as shoulder pain. Spinal accessory neuropathy from a local surgical procedure may begin immediately. We experienced three spinal accessory neuropathy cases with delayed onset after local surgical procedures.
Accessory Nerve ; Paralysis ; Range of Motion, Articular ; Scapula ; Shoulder ; Shoulder Pain ; Superficial Back Muscles ; Surgical Procedures, Operative*

Cerebral venous thrombosis (CVT) is a multifactorial disease characterized by various clinical manifestations and predisposing factors. The association of CVT with hyperthyroidism has been suggested and the high plasma level of factor VIII in hyperthyroidism has been hypothesized to increase the risk of recurrent thromboembolism. We report a 30-year-old man who presented with headache. He was diagnosed with CVT and concomitant hyperthyroidism with increased factor VIII.
Adult ; Causality ; Factor VIII* ; Headache ; Humans ; Hyperthyroidism* ; Plasma ; Thromboembolism ; Venous Thrombosis*

BACKGROUND: Mutations in Cu, Zn-superoxide dismutase (SOD1) cause about 20% of familial amyotrophic lateral sclerosis (FALS) cases. The mechanism of late-onset disease manifestation despite the innate mutation has no clear explanation. The relationship between homocysteine (HC) and amyotrophic lateral sclerosis (ALS) has not been investigated fully, in spite of the similarity in their pathogenesis. METHODS: We investigated the effect of HC on the motor neuronal cell-line (VSC4.1) transfected with SOD1 of either wild-type or mutant forms (G93A and A4V) using various methods including the MTT assay for the cytotoxic assay, the immunocytochemical staining using anti-SOD1 for the aggregation of SOD1, the western blotting using anti-nitrotyrosine and anti-DNPH for the oxidative protein damage, and the measurement of the intracellular Ca2+ concentration using Fura2-AM. RESULTS: In the MTT assay, the HC induced significant cytotoxicity in the mutants, as compared with wild-type. This HC-induced cytotoxicity was inhibited by the trolox and the bathocuproinedisulfonate (BC). HC increased the carbonylation and nitrosylation of the mutant proteins. HC also increased significant SOD1-aggregation in mutants. This HC-induced SOD1-aggregation in mutants was inhibited by trolox, N-nitro-L-arginine methyl ester, BC, and z-VAD-FMK. HC did not change the intracellular concentration of Ca2+ in the mutants compared with the wild-type. CONCLUSIONS: The authors showed that the vulnerability of the SOD1 mutant motor neuronal cells to HC involves the copper-mediated oxygen radical toxicity, and that HC may be a lifelong precipitating factor in some forms of FALS, suggesting a possible treatment modality with vitamin supplements.
Amyotrophic Lateral Sclerosis ; Blotting, Western ; Homocysteine* ; Motor Neurons* ; Mutant Proteins ; Oxygen ; Precipitating Factors ; Vitamins

Hydrogen peroxide has been used for various medical purposes and also recommended in the disinfection process for endoscopes. However, hydrogen peroxide as a cause of chemical colitis or disinfectant colitis has been infrequently reported. The endoscopic findings of hydrogen peroxide induced colitis revealed pseudomembranous-like enteritis such as white plaques, erythema, foamy liquid, patchy, granularity, and ulcerations, resulting from effervescence caused by the release of oxygen from the breakdown of hydrogen peroxide. A 36 year-old single male, who had 30 ml of 3% hydrogen peroxide inserted into his anus the day before due to sexual reasons, was hospitalized as a result of suffering from hematochezia, tenesmus, and lower abdominal pain. Colonoscopy revealed discrete or confluent white plaques adherent to the colonic mucosa, severe erythema on the surrounding mucosa, patchy granularity, and scattered ulcerations up to 28 cm from the anal verge. Pathologic finding revealed inflammatory cells infiltration, variable sized vacuoles, vascular congestion, hemorrhage, fibrin deposition and ulcerations with regenerating epithelium in the lamina propria, consistent with acute mucosal injury caused by hydrogen peroxide. A case of hydrogen peroxide induced colitis is herein reported.
Abdominal Pain ; Adult ; Anal Canal ; Colitis* ; Colon ; Colonoscopy ; Disinfection ; Endoscopes ; Enteritis ; Epithelium ; Erythema ; Estrogens, Conjugated (USP) ; Fibrin ; Gastrointestinal Hemorrhage ; Hemorrhage ; Humans ; Hydrogen Peroxide* ; Hydrogen* ; Male ; Mucous Membrane ; Oxygen ; Ulcer ; Vacuoles

The term enterolith refers to concretions formed within the gastrointestinal tract. Enteroliths are thought to result from stasis and are usually found proximal to an area of stricture or within diverticulum. Meckel's diverticulum occurs in 1% to 3% of the population at autopsy and is the most common congenital anomaly of the gastrointestinal tract. Common complications of Meckel's diverticulum include hemorrhage, infection, inflammation, and intussusception. However, enterolith formation in a Meckel's diverticulum, which referred to as Meckel's enterolith, is rare. A 58-year-old female who experienced constipation and low abdominal pain for 20 years, was admitted due to severe low abdominal pain for 3 days. A 3 2 cm sized, lozenge-shaped radiopaque stone with peripheral dense calcification and radiolucent center, located between two areas of stricture in the distal ileum, was observed in abdominal radiograph, abdominal sonogram, small bowel study, and CT scan. Pathologic findings after surgery reveal an enterolith in Meckel's diverticulum without ectopic gastric mucosa. The case of Meckel's enterolith is herein reported.
Abdominal Pain ; Autopsy ; Constipation ; Constriction, Pathologic ; Diverticulum ; Female ; Gastric Mucosa ; Gastrointestinal Tract ; Hemorrhage ; Humans ; Ileum ; Inflammation ; Intussusception ; Meckel Diverticulum ; Middle Aged ; Tomography, X-Ray Computed

Gastric angiodysplasia may be responsible for up to 2% to 6% of upper gastrointestinal bleeding. Moreover, gastric angiodysplasia may be particularly difficult to treat and is usually associated with a high rebleeding rate. Bleeding due to gastric angiodypsplasia is usually treated by various endoscopic approaches, including argon and Nd:YAG laser photocoagulation, monopolar or biopolar electrocoagulation, heater probe, or injection. Associated complications of these methods, however, such as perforation, acute bleeding during the procedure, or delayed massive hemorrhage have been reported. Recently a few reports have been suggested that endoscopic ligation therapy is a safe, effective treatment for gastric angiodysplasia. A 70-year-old man, who had undergone subtotal gastrectomy for perforation of a duodenal ulcer for 20 years, was admitted due to melena and dizziness persisting for 1 week. A gastroscopy revealed a single angiodysplasia with active bleeding just above the anastomotic site of the remnant stomach. Endoscopic ligation therapy was performed successfully and the bleeding stopped immediately after endoscopic ligation. Since then, no recurrence of bleeding has been reported to date.
Aged ; Angiodysplasia* ; Argon ; Dizziness ; Duodenal Ulcer ; Electrocoagulation ; Gastrectomy ; Gastric Stump ; Gastrointestinal Hemorrhage ; Gastroscopy ; Hemorrhage ; Humans ; Ligation* ; Light Coagulation ; Melena ; Recurrence