Valproic acid induced aplastic crisis and Stevens-Johnson syndrome in a single pediatric patient.

Valproic acid (VPA) is a commonly used antiepileptic drug (AED). Aplastic crisis is defined as acute arrest of hematopoiesis. Stevens-Johnson syndrome (SJS) is a fatal cutaneous adverse drug reaction. We herein report a rare case of aplastic crisis and SJS in a single pediatric patient that were probably caused by VPA. A 2-year-old girl was involved in a car accident. She was diagnosed with skull fractures, cerebral contusions, pulmonary contusions, and fractures of the left iliac bone by computed tomography. VPA was administered as prophylaxis for post-traumatic epilepsy. From day 13, she developed repeated high fevers, and multiple antibiotics were ineffective; she was then transferred to our pediatric intensive care unit. After transfer, she developed liver function impairment, decreased peripheral blood cell counts, and skin damage. After withdrawal of the VPA and administration of prednisone, intravenous immunoglobulin, local skin care, and nutritional support, her body temperature normalized and her hematopoietic function and skin lesions successively resolved. She was transferred out of the pediatric intensive care unit on day 56 and discharged on day 70. At the 6-month follow-up, a blood examination was normal, and repeat computed tomography revealed multiple softening foci of the bilateral brain and less subdural effusion than before. To our knowledge, no report to date has described aplastic crisis and SJS in a single patient. The purpose of this paper is to increase clinicians' knowledge in the treatment of adverse drug reactions (ADRs) and emphasize the importance of standardized application and strict monitoring of VPA in patients with post-traumatic brain trauma.

Immune Tolerance Therapy: A New Method for Treatment of Traumatic Brain Injury.

OBJECTIVE: Due to the special anatomical structure and pathophysiological mechanism of the central nervous system (CNS), there is a big difference between the repair of brain injury and other systems of the body. More and more evidence shows that targetedly reducing the autoimmune response of brain tissue without affecting the immune function in other parts of the body will be the best optimized treatment for brain injury. DATA SOURCES: This review was based on data in articles published in PubMed up to June 5, 2017, with the following keywords: "immune tolerance", "traumatic brain injury", and "central nervous system". STUDY SELECTION: Original articles and critical reviews on immune tolerance and brain damage were selected for this review. References of the retrieved articles were also screened to search for potentially relevant papers. RESULTS: The CNS is isolated from the immune system through the blood-brain barrier. After brain injury, brain antigens are released into the systemic circulation to induce damaging immune responses. Immune tolerance can effectively reduce the brain edema and neurological inflammatory response after brain injury, which is beneficial to the recovery of neurological function. The clinical application prospect and theoretical research value of the treatment of immune tolerance on traumatic brain injury (TBI) is worth attention. CONCLUSIONS: The establishment of immune tolerance mechanism has a high clinical value in the treatment of TBI. It opens up new opportunities for the treatment of brain damage.

Case-Control Study of Injury Intervention for Preschool Children in Henggang, Shenzhen.

AIM: To explore effective interventions for child accidental injury prevention and to reduce the incidence of injury. METHODS: Cluster random sampling method was adopted, and children in 19 kindergartens in Henggang, Shenzhen and their parents were selected as the objects of study. Nineteen kindergartens were randomly divided into intervention group and control group to carry out the injury intervention case-control study. RESULTS: Through a series of interventions, there were certain effects. After the end of the project, the injury incidence rates of the intervention group and the control group were 4.91%, 10.64%, and the difference was significant; the average costs of treatment for injuries of the intervention group and the control group were 168.4 Yuan and 206.8 Yuan, and the difference was statistically significant; compared with before the implementation of the project, the rate of various types of injuries after the end of the project declined, in which, the rate of mechanical injury, pet bites, accidental falls, burns, and traffic accidents decreased significantly. The differences were significant. CONCLUSIONS: Injury interventions can effectively prevent and control the occurrence of injury.

Cell fusion contributes to the rescue of apoptotic cardiomyocytes by bone marrow cells.

Cardiomyocyte apoptosis is an important contributor to the progressive cardiac dysfunction that culminates in congestive heart failure. Bone marrow cells (BMCs) restore cardiac function following ischaemia, and transplanted BMCs have been reported to fuse with cells of diverse tissues. We previously demonstrated that the myogenic conversion of bone marrow stromal cells increased nearly twofold when the cells were co-cultured with apoptotic (TNF-α treated) cardiomyocytes. We therefore hypothesized that cell fusion may be a major mechanism by which BMCs rescue cardiomyocytes from apoptosis. We induced cellular apoptosis in neonatal rat cardiomyocytes by treatment with hydrogen peroxide (H(2)O(2)). The TUNEL assay demonstrated an increase in apoptosis from 4.5 ± 1.3% in non-treated cells to 19.0 ± 4.4% (P < 0.05) in treated cells. We subsequently co-cultured the apoptotic cardiomyocytes with BMCs and assessed cell fusion using flow cytometry. Fusion was rare in the non-treated control cardiomyocytes (0.3%), whereas H(2)O(2) treatment led to significantly higher fusion rates than the control group (P < 0.05), with the highest rate of 7.9 ± 0.3% occurring at 25 µM H(2)O(2). We found an inverse correlation between cell fusion and completion of cardiomyocyte apoptosis (R(2) = 0.9863). An in vivo mouse model provided evidence of cell fusion in the infarcted myocardium following the injection of BMCs. The percentage of cells undergoing fusion was significantly higher in mice injected with BMCs following infarction (8.8 ± 1.3%) compared to mice that did not undergo infarction (4.6 ± 0.6%, P < 0.05). Enhancing cell fusion may be one method to preserve cardiomyocytes following myocardial infarction, and this new approach may provide a novel target for cardiac regenerative therapies.

One-layer pancreaticojejunostomy for prevention of pancreatic fistulae.

BACKGROUND: Anastomotic leakage at the pancreaticojejunostomy remains a common and dreaded complication after pancreaticoduodenectomy. This study was to introduce a method for lowering the mortality, morbidity, and other postoperative complications after pancreaticoduodenectomy. METHODS: From January 1991 to December 2001, twenty-six patients were treated using one-layer pancreaticojejunostomy. The mean age of these patients was 52.3 years. Some of these patients were complicated by hypoproteinemia, anemia and jaundice. All patients were subjected to pancreaticoduodenectomy, reconstruction of the digestive tract by Child's method, and one-layer or Braun's anastomosis after pancreaticojejunostomy, choledochojejunostomy, and gastrojejunostomy. RESULT: No death and pancreatic fistula were observed after operation. CONCLUSION: One-layer pancreaticojejunostomy is simple and safe.