Dendritic Cell Dysfunction in Patients with End-stage Renal Disease

End-stage renal disease (ESRD) with immune disorder involves complex interactions between the innate and adaptive immune responses. ESRD is associated with various alterations in immune function such as a reduction in polymorphonuclear leukocyte bactericidal activity, a suppression of lymphocyte proliferative response to stimuli, and a malfunction of cell-mediated immunity at the molecular level. ESRD also increases patients' propensity for infections and malignancies as well as causing a diminished response to vaccination. Several factors influence the immunodeficiency in patients with ESRD, including uremic toxins, malnutrition, chronic inflammation, and the therapeutic dialysis modality. The alteration of T-cell function in ESRD has been considered to be a major factor underlying the impaired adaptive cellular immunity in these patients. However, cumulative evidence has suggested that the immune defect in ESRD can be caused by an Ag-presenting dendritic cell (DC) dysfunction in addition to a T-cell defect. It has been reported that ESRD has a deleterious effect on DCs both in terms of their number and function, although the precise mechanism by which DC function becomes altered in these patients is unclear. In this review, we discuss the effects of ESRD on the number and function of DCs and propose a possible molecular mechanism for DC dysfunction. We also address therapeutic approaches to improve immune function by optimally activating DCs in patients with ESRD.

Recurrent Acute Pulmonary Embolism Associated With Protein S Deficiency

Pulmonary embolism is a common clinical problem in patients with immobilization, cancer, indwelling central venous catheter and surgery. However, although rare, it may occur in patients with inherited thrombophilia. Protein S deficiency is known to increase the risk of venous thrombosis and pulmonary embolism. There are many reports of venous thrombosis with protein S deficiency, but there are few reports of arterial thrombosis, especially recurrent acute pulmonary embolism. Here, we report a case of recurrent pulmonary embolism associated with type II protein S deficiency.

A Case of Systemic Inflammatory Response Syndrome Secondary to an Acute Polyarticular Gout

Gout occurs as a response to monosodium urate crystal, that is present in joints, bones and soft tissue. The classic symptoms of gouty arthritis are recurrent attacks of acute, markedly painful monoarticular or oligoarticular inflammation; but polyarthritis and chronic arthritis can also occur. Differential diagnosis from infectious arthritis is important. A definitive diagnosis requires the direct identification of urate crystals in the joint, and the exclusion of infection. We report the case of systemic inflammatory response syndrome (SIRS), developed from acute polyarticular gout. SIRS is characterized by loss of local control of inflammation, or an overly activated response resulting in an exaggerated systemic response. The SIRS was presumably due to systemic effects of a localized inflammatory response to urate crystals.

Surgical Removal of Endovascular Stent after Migration to the Right Ventricle Following Right Subclavian Vein Deployment for Treatment of Central Venous Stenosis

Central venous stenosis or occlusion occurs in 11-50% of hemodialysis patients with prior subclavian vein cannulation and ipsilateral fistula or shunt. Most patients are asymptomatic but some require treatment to reduce the risk of thrombosis and improve inadequate hemodialysis pressure. In these cases, endovascular intervention, including ballooning and stenting, is a feasible strategy for selected patents. We report an unusual case of a 40-year-old man on hemodialysis that underwent endovascular stenting to treat right subclavian vein stenosis and experienced stent migration to the right ventricle, requiring surgical removal.

Delayed Pleural Effusion after Right Subclavian Vein Catheterization: A Case Report / 대한구급학회지

Central venous catheterization is commonly used for supplying large amounts of fluids, total parenteral nutrition and for monitoring central venous pressure. Numerous complications exist with the technique, including pneumothorax, arterial puncture with vessel injury, catheter embolus, mediastinal hematoma, hydrothorax, and the thrombus of the vein. We reported an uncommon case of pleural effusion, due to catheter tip migration and penetration, which occurred 4 days after central venous catheterization.

Gastric Mucosal Injury after Ingestion of a Hot Liquid Diet via Gastric Feeding Tube / 대한소화기내시경학회지

When a patient complains of gastrointestinal symptoms such as nausea, vomiting, and upper abdominal pain after ingestion of a substance such as a corrosive agent and certain drugs which can cause mucosal injury to the esophagus and stomach, we always keep in mind gastrointestinal injury and should perform an endoscopic procedure promptly and use the appropriate treatment. It is well known that common corrosive agents which can cause gastrointestinal injury are acidic and alkaline chemicals, and the common causative drug for gastrointestinal injury is NSAID. However, it is not well known that consuming hot food and drinks can cause gastrointestinal injury also. Up to now, there have only been a few case reports of esophageal mucosal injury due to the consumption of hot food and drinks. Gastric mucosal injury after ingesting hot food and drinks is rare and has not been reported often. So here, we report a case of gastric mucosal injury after ingesting a hot liquid diet via gastric feeding tube.