Acute Appendicitis after Liver Transplantation: A Case Report and Review of the Literature.

Acute appendicitis is one of the most common etiologies for acute abdomen. However, fewer than 30 cases of acute appendicitis after liver transplantation have so far been reported in the literature. Previous case studies have concluded that acute appendicitis after liver transplantation may present differently than in non-immunosuppressed patients and thus may lead to more complications. Herein, we describe the fourth case of laparoscopic appendectomy in a 40-year-old female presenting with an acute abdomen, 10 years after orthotopic liver transplantation for autoimmune hepatitis. Additionally, we review the literature, and emphasize the importance for laparoscopic, rather than open appendectomy after liver transplantation. Overall, despite the small number of reported cases of appendicitis after orthotopic liver transplantation, we found the incidence and clinical presentation are similar to patients without liver transplantation. The etiologies for appendicitis in patients after liver transplantation may be different than in those not chronically immunosuppressed, with significantly less lymphoid hyperplasia and increased fecalith and cytomegaloviral infections. Preliminary results showed that laparoscopic appendectomy after liver transplantation results in decreased hospital stays and fewer complications.

Efficacy of continuation ECT and antidepressant drugs compared to long-term antidepressants alone in depressed patients.

OBJECTIVE: The purpose of this study was to evaluate the efficacy of continuation ECT in depression. METHOD: The authors used retrospective chart review to identify 29 patients who received continuation ECT plus long-term antidepressant treatment after a positive response to acute treatment with ECT for a depressive episode (continuation ECT group). A retrospective case-controlled approach was used to ascertain a matching group of 29 patients who received long-term antidepressant treatment alone after responding positively to acute ECT (antidepressant-alone group). All 58 patients (46 with unipolar depression, 12 with bipolar disorder) had been chronically depressed before receiving acute ECT. Data from medical records were analyzed by using survival analysis and proportional hazards regression to determine outcome and risk factors. RESULTS: The mean duration of the follow-up period for all patients was 3.9 years (5.4 years for the continuation ECT patients and 2.4 years for the antidepressant-alone patients). Outcome was significantly better in the continuation ECT group. The cumulative probability of surviving without relapse or recurrence at 2 years was 93% for continuation ECT patients and 52% for antidepressant-alone patients. At 5 years, survival declined to 73% for continuation ECT patients, but fell to 18% for antidepressant-alone patients. Mean survival times were 6.9 years for the continuation ECT patients and 2.7 years for the antidepressant-alone patients. CONCLUSIONS: The findings provide strong support for the efficacy of continuation ECT plus long-term antidepressant treatment in preventing relapse and recurrence in chronically depressed patients who have responded to acute treatment with ECT.

Interleukin-1 pretreatment prevents interleukin-1-induced lung leak in rats.

We found that rats pretreated with interleukin-1 (IL-1) intraperitoneally did not develop the acute oxidative, neutrophil-dependent lung leak that occurs after administration of IL-1 intratracheally (IL-1-induced tolerance). IL-1-pretreated rats also had increased lung catalase and glucose-6-phosphate dehydrogenase (G6PDH) activity and increased plasma catalase activity compared with sham-pretreated rats. In contrast to reducing lung leak, IL-1 pretreatment did not reduce the numbers of neutrophils that are increased in lung lavages of rats given IL-1 intratracheally. IL-1-induced tolerance to IL-1-mediated lung leak and the associated increases in lung catalase, lung G6PDH, and serum catalase activities were all prevented by treating rats with the IL-1-receptor antagonist or with N-acetyl-L-cysteine, an agent that increases intracellular glutathione levels. Our results indicate that IL-1 pretreatment confers tolerance to IL-1-mediated lung leak without decreasing IL-1-induced increases in lung neutrophils. The possible protective actions of IL-1 should be considered in experiments and clinical trials where IL-1 activity is reduced pharmacologically.