A 21-year-old female with a history of bulimia nervosa came to the emergency room due to severe abdominal pain after excessive eating five hours previously. On arrival at the emergency room, extreme abdominal distension was detected and the patient's legs changed color. Computed tomography suggested severe gastric dilatation, so abdominal compartment syndrome was suspected and an emergent laparotomy was supposed to be conducted. Though anesthesia was induced without event, abrupt hemodynamic collapse developed just after the operation started. In spite of active resuscitation for 29 min, the patient did not recover and expired. As the incidence of eating disorders is increasing, anesthesiologists should keep in mind the possibility of abdominal compartment syndrome in patients with a recent history of binge eating, and prepare optimal anesthetic and resuscitation remedies against sudden deteriorations of a patient's condition.
Abdominal Pain ; Anesthesia ; Bulimia ; Bulimia Nervosa ; Eating ; Feeding and Eating Disorders* ; Emergency Service, Hospital ; Fatal Outcome* ; Female ; Gastric Dilatation* ; Hemodynamics ; Humans ; Incidence ; Intra-Abdominal Hypertension ; Laparotomy ; Leg ; Resuscitation ; Young Adult

BACKGROUND: TNF-alpha is related to the generation of lung fibrosis in patients with UIP. The precise mechanism leading to lung fibrosis by TNF-alpha is unknown. However, the activation of a transcription factor like AP-1(down stream of c-jun N-terminal kinase, JNK) by TNF-alpha may be related to the induction of fibrogenic cytokines like PDGF or IGF-I. Furthermore, JNK was reported to be activated in the radiation-in-duced lung fibrosis model. This study examined JNK activity in patients with UIP. METHODS: The expression of phosphorous JNK(p-JNK), macrophage/moncoyte specific markers, CD68, and cytokeratin was evaluated by immunohistochemical (IHC) staining of lung tissues from patients with UIP and lung cancer. An in vitro kinase assay was performed with alveolar macrophages obtained by a bronchollung cancer. An in vitro kinase assay was performed with alvolar macrophages obrtained by a bronchol avleolar lavage from patients with UIP and healthy persons as the control. RESULTS: The IHC stain showed that p-JNK is expressed in the almost all of the alveolar macrophages and smooth muscle cells in patients with UIP. In case of the normal areas of the lung from patients with lung cancer, the alveolar macrophages showed little p-JNK expression. Interestingly, increased JNK activity was not found in the in vitro kinase assay of the alveolar macrophages obtained from both patients with UIP and healthy persons as the control. Furthermore, 10 ng/ml of TNF-alpha failed to increase the JNK activity of the alveolar macrophages in both patients with UIP and healthy people. CONCLUSION: The JNK was activated constitutionally in patients with UIP. However, the role of JNK in the pathogenesis of lung fibrosis needs to be clarified.
Constitution and Bylaws ; Cytokines ; Fibrosis ; Humans ; Insulin-Like Growth Factor I ; JNK Mitogen-Activated Protein Kinases* ; Keratins ; Lung ; Lung Neoplasms ; Macrophages ; Macrophages, Alveolar ; Myocytes, Smooth Muscle ; Phosphotransferases ; Rivers ; Therapeutic Irrigation ; Transcription Factors ; Tumor Necrosis Factor-alpha