This study is aimed at contributing to defining a correct therapeutic management of pancreatic pseudocysts (PPCs): indications for treatment, operative timing and technical approach.
A retrospective ...analysis of 28 patients affected by PPC, 22 males (78.5%) and 6 females (21.5%), with a mean age of 52 years (range 17-76) has been performed. The diagnosis was realised by clinical assessment and US (ultrasonography) or CT (computerized tomography) scanning. The treatment consisted in surgical drainage (internal or external) or percutaneous drainage with US guidance: the cystojejunostomy with a Roux-en-Y loop was the first choice technique.
Twenty-two patients (78.5%) under-went a surgical procedure: 19 cystojejunostomies with a Roux-en-Y loop and 3 external drainages. The mean interval between acute pancreatic event and elective surgery was 9 weeks (range 5-21). Perioperative morbidity and mortality was respectively 22.7% (5/22) and 13.6% (3/22). In 4 cases a percutaneous drainage with US-guidance, without morbidity and mortality was performed, but 2 patients required a successive surgical operation for lack of resolution of the PPC. The last 2 patients of this series recovered spontaneously.
Currently the cystojejunostomy with a Roux-en-Y loop remains the first choice technique for an elective and definitive treatment of PPCs: other techniques (endoscopic internal drainage, surgical or percutaneous external drainage) should be limited to complicated PPCs or to high surgical risk patients. A waiting period of 4-6 weeks following the acute pancreatic event is considered the minimal time necessary before the elective treatment.
The relationship between cancer onset and the immune response became a subject of great interest in the early 1900s, and led Ehrlich 1 to establish what came to be known as the theory of ...immunological surveillance. This theory is based on three principles: (1) cancer cells are antigenic, (2) these cells can be destroyed by the immune response of the organism (by a mechanism similar to that observed in transplanted tissue or organ rejection), and (3) immune depression is related to a higher incidence of neoplastic disease 2. The theory is based on the concept that the immune system is able to recognize cancer cells as non-self and consequently to destroy them. Furthermore, this response involves both branches of the immune system. However, this defensive system is not as perfect as it may seem at first sight, because more often than not a certain number of cancer cells do avoid surveillance and subsequent destruction by immune-competent cells and thus continue to proliferate, until they give rise to the various forms of malignancies. The mechanisms by which cancer cells elude immunological surveillance may be explained by some intrinsic characteristics of these cells and/or the patient’s condition, including an immune deficiency.
5'-N-ethylcarboxamideadenosine (NECA) greater than 2-chloroadenosine greater than adenosine greater than (-)-N6-(R-phenyl-isopropyl)-adenosine (-)-R-PIA greater than ...(+)-N6-(S-phenyl-isopropyl)-adenosine (+)-S-PIA inhibited in vitro human platelet aggregation in a dose-dependent fashion. 6-nitrobenzylthioinosine and dipyridamole, which inhibit adenosine uptake, and erythro-9-(2-hydroxy-3-nonyl)-adenine, which blocks adenosine metabolism, did not impair the inhibition induced by NECA and adenosine. 8-phenyltheophylline and theophylline, two competitive antagonists of adenosine receptors, blocked the inhibition of platelet aggregation caused by NECA and adenosine. NECA greater than 2-chloroadenosine greater than adenosine greater than (-)-R-PIA greater than (+)-S-PIA increased platelet cyclic adenosine monophosphate (cAMP) levels in a dose-dependent fashion. A significant linear correlation (r = 0.70, p less than 0.001) was found between the increase of platelet cAMP and the inhibition of platelet aggregation induced by adenosine and its analogs. 8-phenyltheophylline, which is a competitive antagonist of adenosine in platelets, also blocked the cAMP accumulation caused by NECA. These data suggest that NECA and other adenosine analogs activate a specific cell surface adenylate cyclase-linked adenosine receptor whose properties are similar to those of an adenosine A2/Ra receptor.
