The aim of this study was to review the literature regarding the rupture of hydatid cysts into the abdominal cavity after trauma. We present both a new case of hydatid cyst rupture that occurred after blunt abdominal trauma and a literature review of studies published in the English language about hydatid cyst rupture after trauma; studies were accessed from PubMed, Google Scholar, EBSCO, EMBASE, and MEDLINE databases. We identified 22 articles published between 2000 and 2011 about hydatid cyst rupture after trauma. Of these, 5 articles were excluded because of insufficient data, duplication, or absence of intra-abdominal dissemination. The other 17 studies included 68 patients (38 males and 30 females) aged 8 to 76 years who had a ruptured hydatid cyst detected after trauma. The most common trauma included traffic accidents and falls. Despite optimal surgical and antihelmintic therapy, 7 patients developed recurrence. Complications included biliary fistula in 5 patients, incisional hernia in 2 patients, and gastrocutaneous fistula in 1 patient. Death occurred from intraoperative anaphylactic shock in 1 patient and gastrointestinal bleeding and pulmonary failure in 1 patient. Rupture of a hydatid cyst into the peritoneal cavity is rare and challenging for the surgeon. This condition is included in the differential diagnosis of the acute abdomen in endemic areas, especially in young patients.

CATS is a safe procedure and may decrease the risk of tumor recurrence in HCC patients.

The rupture of hydatid cysts into the peritoneal cavity should be included in the differential diagnosis of acute abdominal pain in endemic areas. Perforation in a young patient may be the first presentation of hydatid cyst. Multiple hydatid cysts may be a predisposing factor for perforation. Location of the cyst on segment VI of the liver may be a predisposing factor as well. Emergency surgery is the main treatment for intraperitoneal rupture of hydatid cysts and medical treatment should be given postoperatively.

No abstract

Adiponectin, an adipocyte-secreted hormone, is an important negative regulator in the immune system and hematopoiesis. In this study, we investigated the association of adiponectin levels with chronic lymphocytic leukemia (CLL) and myeloproliferative diseases (MPDs). We measured adiponectin levels in 19 patients with CLL and 30 patients with MPD (chronic myelogenous leukemia, 15; polycythemia vera, 9; myelofibrosis, 4; essential thrombocythemia, 2). The data were (chronic myelogenous leukemia, 15; polycythemia vera, 9; myelofibrosis, 4; essential thrombocythemia, 2). The data were compared with results from a control group of healthy volunteers who were matched according to age, sex, and body mass index. The adiponectin levels in patients with CLL were lower than in the controls (4.71 +/- 1.33 microg/mL versus 16.61 +/- 3.91 microg/mL; P <.001). They were also significantly lower in patients with MPD than in the controls (8.95 +/- 1.33 microg/mL versus 16.16 +/- 4.77 microg/mL; P <.001). In addition, we compared the adiponectin levels of MPD patients who were treated with interferon (IFN) to the levels of patients who were not treated with IFN. Adipnectin levels were significantly higher in IFN-treated patients (11.03 +/- 1.39 microg/mL versus 6.87 +/- 1.79 microg/mL; P <.001). These results suggest that lymphopoiesis and myelopoiesis negatively influence adiponectin levels. Adiponectin may be related to inflammatory cytokine release. IFN therapy appears to have a positive influence on adiponectin secretion by suppressing inflammatory cytokines. Future studies are needed to prove causality and to provide insight about this hormone's mechanism of action and its potential role regarding the etiology and progression of CLL and MPD.