Subject(s)
Anemia, Iron-Deficiency/etiology , Gastritis/etiology , Helicobacter Infections/complications , Helicobacter pylori/isolation & purification , Purpura, Thrombocytopenic/etiology , Adolescent , Amoxicillin/therapeutic use , Anemia, Iron-Deficiency/drug therapy , Breath Tests , Clarithromycin/therapeutic use , Female , Gastritis/drug therapy , Gastritis/microbiology , Helicobacter Infections/diagnosis , Helicobacter Infections/drug therapy , Humans , Immunoglobulins, Intravenous/therapeutic use , Iron/therapeutic use , Lansoprazole/therapeutic use , Purpura, Thrombocytopenic/drug therapy , Remission InductionABSTRACT
Acquired haemophilia A (AHA) is a life-threatening haemorrhagic disorder that occurs with various underlying conditions such as autoimmune disease, drug reactions, lymphoproliferative diseases, solid tumours and pregnancy/postpartum status. However, in half of all reported cases, the underlying disease is unknown. Most AHA cases develop in adults; paediatric/adolescent cases are extremely rare. The main clinical symptom is bleeding into the skin, muscles, soft tissues and/or mucous membranes. Here, we report the case of an otherwise healthy 12-year-old girl who presented with prolonged bleeding postexodontia. After being diagnosed with AHA, she was successfully treated with recombinant activated factor VII infusion and oral prednisolone. To avoid such unanticipated bleeding when performing dental extraction, preoperative haemostatic screening tests are recommended.
Subject(s)
Exsanguination/drug therapy , Hemophilia A/drug therapy , Tooth Extraction/adverse effects , Child , Exsanguination/blood , Exsanguination/etiology , Exsanguination/pathology , Factor VIIa/therapeutic use , Female , Hemophilia A/blood , Hemophilia A/etiology , Hemophilia A/pathology , Hemostatics/therapeutic use , Humans , Prednisolone/therapeutic use , Recombinant Proteins/therapeutic use , Treatment OutcomeABSTRACT
To examine the effects of hyperglycemia on a transient ischemia in the neonatal brain, neuropathological and biochemical evaluations were performed. In 10-day-old rats, brain ischemia was induced by permanent occlusion of the right external and internal carotid and subclavian arteries and the clamping of the left external and internal carotid arteries for 2h. The peritoneal injection of a 50% glucose solution (0.10 ml/15 g weight) 5 min before the induction of brain ischemia increased the plasma glucose concentration to 20-25 mmol/l during ischemia. It preserved brain tissue glucose levels at 1h of ischemia in the glucose-treated group, while tissue glucose was exhausted in the saline-injected group. Tissue lactate concentrations increased slightly at the end of the ischemic insult (6.7 mmol/kg) in the saline-injected group and remarkably (18.7 mmol/kg) in the glucose-treated group. Two distinct forms of ischemic neuronal change were found in this study: ischemic cell change and reactive neuronal change. A quantitative neuropathological assessment indicated that hyperglycemia significantly reduced the volume of ischemic cell change in the neocortex from 85% to 33%, but not that of reactive neuronal change (from 5.5% to 2.4%). These results indicated that hyperglycemia attenuated ischemic cell change, but not reactive neuronal change, in the neonatal rat brain and suggested that it reduced ischemic cell change probably because of reserved brain glucose.
