To investigate the effects of prostaglandin E1(PGX1) in prevention of proliferative scar formation, we cultured fibroblasts of normal skin (NS), hypertrophic scar (HS) and keloid (KL) tissues obtained from patients. We have compared type I collagenase production of cultured fibroblasts from normal skin, hypertrophic scar, and keloid tissues under various concentrations of PGE1. Our results demonstrate that type I collagenase production was significantly increased after addition of PGE1 in HS and KL, but not NS. Type I collagenase production of HS and KL fibroblasts were increased similarly in 10M and 10M of PGE1 and maximally increased in the concentration of 10M. This promotive effects of PGE1 on the production of type I collagenase was larger in KL than in HS. These results also suggest that PGE1 may play the promotive effects on type I collagenase production in dose-dependent manner. PGE1 may have a role in the prevention of hypertrophic scar and keloid by enhancing the production of type I collagenase of HS and KL fibroblasts. The promotive effects of PGE1 on type I collagenase production was variable depending on its concentration, and its effects was maximum in certain optimal condition. The maximally effective concentration of PGE1 in the prevention of proliferative scar formation should be searched in further investigations for clinical use.
Alprostadil ; Cicatrix ; Cicatrix, Hypertrophic* ; Collagenases* ; Fibroblasts* ; Humans ; Keloid* ; RNA, Messenger* ; Skin

Eradication of Helicobacter pylori has contributed to the treatment of peptic ulcers and mucosa-associated lymphoid tissue lymphoma. Moreover, it has possibly decreased the prevalence of gastric cancer. However, eradication therapy is associated with various adverse effects, of which diarrhea is the most common. The incidence of diarrhea after eradication treatment varies from 8% to 48%. In particular, the incidence is higher in patients who receive first-line standard triple therapy compared with those who receive second-line therapy. Both antibiotics and proton pump inhibitors, components of eradication therapy, have short-term and long-term impacts on gut microbiota. The alterations of gut microbiota may not recover until 1 year after eradication therapy. Most cases of diarrhea that occur after eradication therapy are antibiotic-associated diarrhea caused by the destruction of the normal gut microbiota. In some cases, Clostridioides difficile-associated diarrhea occurs after eradication therapy. If bloody diarrhea occurs after eradication therapy and the Clostridioides difficile toxin is not detected, antibiotic-associated hemorrhagic colitis associated with Klebsiella oxytoca infection should be suspected. It is crucial to explain the possibility of diarrhea before initiating eradication therapy to increase compliance. Furthermore, probiotics may be administered to reduce diarrhea. If severe diarrhea or symptoms other than the usual antibiotic-associated diarrhea occur during or after eradication therapy, antibiotics should be discontinued. In addition, appropriate tests to determine the cause of diarrhea should be performed. This review summarizes the alteration of the gut microbiota, the causes of diarrhea after Helicobacter pylori eradication therapy, and its management.

Eradication of Helicobacter pylori has contributed to the treatment of peptic ulcers and mucosa-associated lymphoid tissue lymphoma. Moreover, it has possibly decreased the prevalence of gastric cancer. However, eradication therapy is associated with various adverse effects, of which diarrhea is the most common. The incidence of diarrhea after eradication treatment varies from 8% to 48%. In particular, the incidence is higher in patients who receive first-line standard triple therapy compared with those who receive second-line therapy. Both antibiotics and proton pump inhibitors, components of eradication therapy, have short-term and long-term impacts on gut microbiota. The alterations of gut microbiota may not recover until 1 year after eradication therapy. Most cases of diarrhea that occur after eradication therapy are antibiotic-associated diarrhea caused by the destruction of the normal gut microbiota. In some cases, Clostridioides difficile-associated diarrhea occurs after eradication therapy. If bloody diarrhea occurs after eradication therapy and the Clostridioides difficile toxin is not detected, antibiotic-associated hemorrhagic colitis associated with Klebsiella oxytoca infection should be suspected. It is crucial to explain the possibility of diarrhea before initiating eradication therapy to increase compliance. Furthermore, probiotics may be administered to reduce diarrhea. If severe diarrhea or symptoms other than the usual antibiotic-associated diarrhea occur during or after eradication therapy, antibiotics should be discontinued. In addition, appropriate tests to determine the cause of diarrhea should be performed. This review summarizes the alteration of the gut microbiota, the causes of diarrhea after Helicobacter pylori eradication therapy, and its management.

The use of 5-ASA, immunomodulators, biologics, and small molecule drugs are the main treatment for inflammatory bowel disease (IBD), however, fecal microbiota transplantation (FMT) is also drawing attention as a treatment to improve intestinal dysbiosis by transplantaing normal human stool into patients with IBD. FMT demonstrates relatively good effects in inducing clinical remission in IBD, but unlike Clostridium difficile infection, multiple FMT can enhance the clinical effect. There are no reports of the long-term effectiveness and safety of FMT conducted in IBD yet, therefore, well-designed, prospective studies will be needed. Gut microbiota can affect inflammatory response, intestinal barrier function, and host metabolism, so microbe-based therapies are likely to be a new treatment option for IBD. The deeper the understanding of microbe products or effectors, the more likely it is to provide personalized therapy in IBD.

The treatment of portal vein thrombosis (PVT) in patients with liver cirrhosis (LC) has been controversial, and it is generally caseand institution-dependent. The occurrence of acute or extensive PVT is critical and requires urgent treatment because it is usually accompanied by symptoms, particularly when total occlusion occurs, causing acute decompensation of liver disease. Even in severe cases, drug selection and treatment duration are determined based on each institution’s experience. Therefore, consistent guidelines for the treatment of patients with LC with PVT are required. Recently, a patient with acute occlusive PVT with LC who showed signs of acute decompensation was treated by administering low molecular weight heparin as anticoagulant therapy. After anticoagulant treatment, the portal vein was almost completely recanalized, and the deteriorated liver function improved. In addition, the patient recovered well and showed no recurrence of PVT for more than a year. Thus, the most recent knowledge regarding the treatment of nonmalignant PVT in LC was reviewed along with a case report.

The use of 5-ASA, immunomodulators, biologics, and small molecule drugs are the main treatment for inflammatory bowel disease (IBD), however, fecal microbiota transplantation (FMT) is also drawing attention as a treatment to improve intestinal dysbiosis by transplantaing normal human stool into patients with IBD. FMT demonstrates relatively good effects in inducing clinical remission in IBD, but unlike Clostridium difficile infection, multiple FMT can enhance the clinical effect. There are no reports of the long-term effectiveness and safety of FMT conducted in IBD yet, therefore, well-designed, prospective studies will be needed. Gut microbiota can affect inflammatory response, intestinal barrier function, and host metabolism, so microbe-based therapies are likely to be a new treatment option for IBD. The deeper the understanding of microbe products or effectors, the more likely it is to provide personalized therapy in IBD.

The treatment of portal vein thrombosis (PVT) in patients with liver cirrhosis (LC) has been controversial, and it is generally caseand institution-dependent. The occurrence of acute or extensive PVT is critical and requires urgent treatment because it is usually accompanied by symptoms, particularly when total occlusion occurs, causing acute decompensation of liver disease. Even in severe cases, drug selection and treatment duration are determined based on each institution’s experience. Therefore, consistent guidelines for the treatment of patients with LC with PVT are required. Recently, a patient with acute occlusive PVT with LC who showed signs of acute decompensation was treated by administering low molecular weight heparin as anticoagulant therapy. After anticoagulant treatment, the portal vein was almost completely recanalized, and the deteriorated liver function improved. In addition, the patient recovered well and showed no recurrence of PVT for more than a year. Thus, the most recent knowledge regarding the treatment of nonmalignant PVT in LC was reviewed along with a case report.

Drainage of pancreatic abscesses is required for effective control of sepsis. Endoscopic ultrasound (EUS)-guided endoscopic drainage is less invasive than surgery and prevents local complications related to percutaneous drainage. Endoscopic drainage with stent placement in the uncinate process of the pancreas is a technically difficult procedure. We report a case of pancreatic abscess treated by repeated EUS-guided aspiration and intravenous antibiotics without an indwelling drainage catheter or surgical intervention.
Abscess* ; Anti-Bacterial Agents ; Catheters ; Drainage ; Endoscopic Ultrasound-Guided Fine Needle Aspiration ; Pancreas ; Sepsis ; Stents ; Ultrasonography

Metastatic tumors to the heart are far more frequent than primary tumors of the heart. Cardiac metastasis may be detected up to 30 percent of patients with fatal lung cancers. Metastatic cancer to the heart is difficult to suspect. Where cardiac metastasis is diagnosed ante-mortem, signs and symptoms of the primary cancer are usually the presenting features and the presence of cardiac involvement is often incidentally detected. We experienced a case of 35-year-old woman with metastatic lung cancer invading the left atrium via pulmonary vein, which was not proved pathologically. She presented with hemoptysis and chest pain. Transthoracic echocardiography demonstrated massive cardiac infiltration with tumor and decreased cardiac wall motion, correlating with the chest CT findings, which were also remarkable for the presence of intracardiac mass and direct invasion to adherent pericardium, pulmonary vein and left atrium. We suggest that careful examination of 2D echocardiography can be noninvasive and valuable tool for diagnosis of metastatic cancer to the heart.
Adult ; Carcinoma, Large Cell* ; Chest Pain ; Diagnosis ; Echocardiography ; Female ; Heart ; Heart Atria* ; Hemoptysis ; Humans ; Lung Neoplasms ; Lung* ; Neoplasm Metastasis* ; Pericardium ; Pulmonary Veins ; Tomography, X-Ray Computed