Aspergillosis ; drug therapy ; etiology ; pathology ; Aspergillus flavus ; isolation & purification ; Dermatomycoses ; drug therapy ; etiology ; pathology ; Female ; Humans ; Middle Aged ; Skin Ulcer ; etiology

Henoch-Schonlein purpura (H-S purpura) is a systemic small-vessel vasculitis involving skin, joint, gastrointestinal tract, and kidney. It is characterized by the classic tetrad of abdominal pain, arthralgia, typical rash, and renal involvement. All of these clinical findings can occur in any order and at any time over several days to weeks. Gastrointestinal manifestations such as abdominal pain, melena, or hematochezia occur in 45-85% and preceed skin lesions upto 40% in H-S purpura. However, endoscopically proven gastrointestinal lesion is rare because majority of involved sites are small intestine. We report a case of Henoch-Schonlein purpura with terminal ileal ulcer, healed after treatment with high dose steroid, proven by colonoscopy.
Adult ; Anti-Inflammatory Agents/*therapeutic use ; Colonoscopy ; Humans ; Ileal Diseases/*drug therapy/etiology/pathology ; Leg/pathology ; Male ; Prednisolone/*therapeutic use ; Purpura, Schoenlein-Henoch/complications/*diagnosis/drug therapy ; Ulcer/*drug therapy/etiology/pathology

An 8-year-old girl who had experienced intermittent cough and fever over a 3 year period, was admitted after experiencing a recurrence for one month. One year ago the patient experienced a recurrent oral mucosal ulcer. Physical examination showed vitiligo in the skin of the upper right back. Routine blood tests and immune function tests performed in other hospitals had shown normal results. Multiple lung CT scans showed pulmonary infection. The patient had recurrent fever and cough and persistent presence of some lesions after anti-infective therapy. The antitubercular therapy was ineffective. Routine blood tests after admission showed agranulocytosis. Gene detection was performed and she was diagnosed with dyskeratosis congenita caused by homozygous mutation in RTEL1. Patients with dyskeratosis congenita with RTEL1 gene mutation tend to develop pulmonary complications. Since RTEL1 gene sequence is highly variable with many mutation sites and patterns and can be inherited via autosomal dominant or recessive inheritance, this disease often has various clinical manifestations, which may lead to missed diagnosis or misdiagnosis. For children with unexplained recurrent pulmonary infection, examinations of the oral cavity, skin, and nails and toes should be taken and routine blood tests should be performed to exclude dyskeratosis congenita. There are no specific therapies for dyskeratosis congenita at present, and when bone marrow failure and pulmonary failure occur, hematopoietic stem cell transplantation and lung transplantation are the only therapies. Androgen and its derivatives are effective in some patients. Drugs targeting the telomere may be promising for patients with dyskeratosis congenita.
Child ; Dyskeratosis Congenita ; complications ; therapy ; Female ; Humans ; Mouth Diseases ; etiology ; Mouth Mucosa ; pathology ; Recurrence ; Respiratory Tract Infections ; etiology ; Telomere ; drug effects ; Ulcer ; etiology

Administration, Oral ; Adolescent ; Female ; Histiocytosis, Langerhans-Cell ; complications ; drug therapy ; pathology ; Humans ; Lymph Nodes ; pathology ; Prednisone ; administration & dosage ; therapeutic use ; Retrospective Studies ; Skin Ulcer ; drug therapy ; etiology ; pathology ; Thalidomide ; administration & dosage ; therapeutic use ; Treatment Outcome

Acute esophageal necrosis (AEN) is a very rare disorder typically presenting as a diffuse black esophageal mucosa on upper endoscopy. For this reason, AEN is often considered to be synonymous with 'black esophagus'. The pathogenesis of entity is still unknown. We report a case of AEN with duodenal ulcer causing partial gastric outlet obstruction. A 53-year-old man presented with hematemesis after repeated vomiting. The upper gastrointestinal endoscopy revealed circumferential black coloration on middle 315 to lower esophageal mucosa that stopped abruptly at the gastroesophageal junction. Pyloric ring deformity and active duodenal ulceration with extensive edema was observed. After conservative management with NPO and intravenous proton pump inhibitor, he showed clinical and endoscopic improvement. He resumed an oral diet on day 7 and was discharged. In our case the main pathogenesis of disease could be accounted for massive esophageal reflux due to transient gastric outlet obstruction by duodenal ulcer and following local ischemic injury.
Acute Disease ; Duodenal Ulcer/drug therapy/etiology ; Endoscopy, Gastrointestinal ; Esophageal Diseases/complications/*diagnosis/drug therapy ; Esophagus/*pathology ; Gastric Outlet Obstruction/*complications/pathology ; Humans ; Ischemia/pathology ; Male ; Middle Aged ; Necrosis ; Proton Pump Inhibitors/therapeutic use ; Tomography, X-Ray Computed

Pyoderma gangrenosum (PG) is a rare, noninfectious neutrophilic dermatosis. Clinically, it begins with sterile pustules that rapidly progress into painful ulcers of variable depth and size with undermined violaceous borders. The diagnosis of PG is based on the history of an underlying disease, a typical clinical presentation, histopathology, and exclusion of other diseases. The peak incidence occurs between the ages of 20 to 50 years with women being more often affected than men. There have been very few reports of pyoderma gangrenosum with oral mucosal involvement. Oral lesions in previously reported cases have included ulcers of varying sizes from a few mm to several cm and have been reported to have been found on the tongue, soft and hard palate, buccal mucosa, and gingiva. Some of these oral lesions have been associated with ulcerative colitis, inflammatory bowel disease, and polycythemia rubra vera. A few cases were reported with biopsy findings, the histological picture being nonspecific, showing ulceration, and necrosis with inflammatory cell infiltrate. A peculiar case of pyoderma gangrenosum with an oral lesion is presented here, and the differential diagnosis is discussed.
Adult ; Anti-Infective Agents ; therapeutic use ; Chlorhexidine ; therapeutic use ; Dapsone ; therapeutic use ; Drug Therapy, Combination ; Female ; Glucocorticoids ; therapeutic use ; Humans ; Metronidazole ; therapeutic use ; Oral Ulcer ; drug therapy ; etiology ; pathology ; Prednisolone ; therapeutic use ; Pyoderma Gangrenosum ; complications ; Tooth Mobility ; etiology

Administration, Topical ; Humans ; Immunosuppressive Agents ; administration & dosage ; adverse effects ; therapeutic use ; Lichen Planus, Oral ; complications ; drug therapy ; pathology ; Oral Ulcer ; drug therapy ; etiology ; Tacrolimus ; administration & dosage ; adverse effects ; therapeutic use ; Treatment Outcome

Helicobacter pylori can cause variety of upper gastrointestinal disorders such as peptic ulcer, mucosa associated lymphoid tissue (MALT)-lymphoma, and gastric cancer. The prevalence of H. pylori infection has significantly decreased in Korea since 1998 owing to active eradication of H. pylori. Along with its decrease, the prevalence of peptic ulcer has also decreased. However, the mean age of gastric ulcer increased and this is considered to be due to increase in NSAID prescription. Gastric cancer is one of the leading causes of cancer deaths in Korea and Japan, and IARC/WHO has classified H. pylori as class one carcinogen of gastric cancer. Despite the decreasing prevalence of H. pylori infection, the total number of gastric cancer in Korea has continuously increased from 2006 to 2011. Nevertheless, the 5 year survival rate of gastric cancer patients significantly increased from 42.8% in 1993 to 67% in 2010. This increase in survival rate seems to be mainly due to early detection of gastric cancer and endoscopic mucosal dissection treatment. Based on these findings, the prevalence of peptic ulcer is expected to decrease even more with H. pylori eradication therapy and NSAID will become the main cause of peptic ulcer. Although the prevalence of gastric cancer has not changed along with decreased the prevalence of H. pylori, gastric cancer is expected to decrease in the long run with the help of eradication therapy and endoscopic treatment of precancerous lesions.
Anti-Bacterial Agents/therapeutic use ; Anti-Inflammatory Agents, Non-Steroidal/adverse effects ; Gastrointestinal Diseases/complications/*epidemiology ; Helicobacter Infections/complications/drug therapy/epidemiology ; Humans ; Lymphoma, B-Cell, Marginal Zone/epidemiology ; Peptic Ulcer/epidemiology/etiology ; Prevalence ; Stomach Neoplasms/etiology/mortality/pathology

Endoscopic mucosal resection (EMR) is widely accepted as a standard treatment for early gastric cancer or gastric adenoma. However, EMR inevitably results in the formation of large iatrogenic ulcer at the resected area. Although the characteristics of EMR-induced ulceration are not fully understood, this type of ulcer is thought to heal faster and to recur less often than non-iatrogenic gastric ulcer. Current available evidences have suggested that EMR-induced ulcers heal within 2-3 months. Herein, we report two cases of non-healing persistent gastric ulcers after EMR. One is a case of gastric carcinoma which developed at the same site of previous EMR site for the low grade dysplasia. The other is a case in which persistent EMR-induced ulcer was healed in the long run after Helicobacter pylori eradication therapy.
Aged ; Endoscopy, Gastrointestinal ; Gastric Mucosa/pathology/*surgery ; Helicobacter Infections/complications/drug therapy ; Helicobacter pylori ; Humans ; Iatrogenic Disease ; Male ; Middle Aged ; Stomach Neoplasms/complications/diagnosis/*surgery ; Stomach Ulcer/diagnosis/*etiology/pathology

Severe congenital neutropenia is a rare hematological disease characterized by a selective decrease in circulating neutrophils, maturation arrest of granulocytic precursors at the promyelocyte stage, and recurrence of infections. A 2-month-old male infant (patient A) and a 14-month-old female child (patient B) were referred to our hospital due to severe neutropenia. Sequencing analysis of ELA2 and HAX1 genes was performed. Two single nucleotide polymorphisms of HAX1 gene were found. They were 5,104T-->G point mutation of exon 1 and 5,474A-->G point mutation of intron 1 in HAX1 gene. The mutation of ELA2 gene was not found. The patient A showed a good response to granulocyte colony-stimulating factor (G-CSF) treatment and the absolute neutrophil count recovered to 1,195/microliter. But the patient B showed a partial response to G-CSF treatment and experienced several episodes of herpetic gingivostomatitis, oral ulcer, acute pharyngotonsillitis and otitis media during follow-up.
Adaptor Proteins, Signal Transducing/genetics ; Bone Marrow/pathology ; Female ; Granulocyte Colony Stimulating Factor, Recombinant/adverse effects/therapeutic use ; Humans ; Infant ; Male ; Neutropenia/congenital/drug therapy/*genetics ; Neutrophils/cytology/pathology ; Oral Ulcer/etiology ; Otitis Media/etiology ; Polymorphism, Single Nucleotide ; Serine Endopeptidases/genetics ; Stomatitis, Herpetic/etiology