Background: A hydatid cyst is still a serious health problem in endemic areas. Invasion of the spleen is rare in hydatid disease. In the medical literature, reports about isolated splenic hydatidoses are quite rare. Also there is not a consensus about the way of treatment. Methods: Between 1978 and 2000, in our clinic approximately 900 patients were operated on for an abdominal hydatidosis; 850 of these patients were treated for a hepatic hydatidosis and 14 patients for an isolated splenic hydatidosis. Six (42.8%) of the latter patients were male and 8 (57.1%) were female. The mean age of the patients was 47.14 ± 4.9 (range 17–72) years. Ten patients (71.4%) presented with a painful mass in the left upper quadrant of the abdomen, and the other 4 patients (28.5%) were asymptomatic and were diagnosed incidentally. Results: All of the patients underwent elective splenectomy. There was no mortality, but complications occurred in 4 (28.5%) patients. The period of hospitalization ranged from 7 to 17 days with a mean of 9.8 days. 1 patient died from an acute myocardial infarction during the 2nd postoperative year, and 1 patient died as a consequence of a traffic accident during the 5th postoperative year. Nine patients, after follow-up periods of between 2 and 14 years, are living free from disease. No recurrence occurred in any of them. In the remaining 3 patients, long-term follow-up could not be maintained. Conclusions: A hydatid cyst must be included in the differential diagnosis of cystic lesions of the spleen. A splenic hydatid cyst should be treated surgically due to the high risk of a rupture, and the ideal procedure in adulthood is standard splenectomy.

Patients with large pancreas body-tail tumors and high CA 19-9 level are at greater risk for latent distant organ metastasis or PM, and should undergo staging laparoscopy routinely for accurate diagnosis (UMIN000023125).

Pediatric PTLD is often associated with primary EBV infection and immunosuppression. The aim was to retrospectively review the spectrum of histologically documented PTLD for two time intervals differentiated by changes in use of molecular EBV monitoring. Eleven of 146 patients (7.5%) in 2001-2005 (Era A) and 10 of 92 (10.9%) in 1993-1997 (Era B) were diagnosed with PTLD. The median age at liver transplantation (0.8 and 0.9 yr, respectively) and the median duration between liver transplant and diagnosis of PTLD (0.6 and 0.7 yr, respectively) were similar in both eras. However, patients in Era A presented with significantly less advanced histological disease compared to patients in Era B (p=0.03). Specifically, nine patients (82%) in Era A had Pl hyperplasia/polymorphic PTLD, whereas in Era B, six had advanced histological disease (five monomorphic and one unclassified). Three transplant recipients in Era B died secondary to PTLD, whereas there were no PTLD-related deaths in Era A (p=0.03). Heightened awareness of risk for PTLD, alterations in baseline immunosuppression regimens, implementation of molecular EBV monitoring, pre-emptive reduction in immunosuppression and improved therapeutic options may have all contributed to a milder PTLD phenotype and improved clinical outcomes.

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