Genetic Basis of Acquired Immunodeficiency Syndrome-Related Lymphomagenesis

The molecular pathogenesis of systemic acquired immunodeficiency syndrome(AIDS)-related non-Hodgkin's lymphomas (AIDS-NHL) is a complexprocess involving both host factors and the accumulation ofgenetic lesions within the tumor clone. On the basis of thepattern of molecular lesions involved in these tumors, severaldistinct pathogenetic pathways can be presently identified inAIDS-related lymphomagenesis. These pathways selectively associatewith the different clinicopathologic variants of AIDS-NHL. AIDS-relatedBurkitt's lymphoma is characterized by activation of c-MYC inall cases, disruption of p53 in 60% of the cases, and infectionby Epstein-Barr virus (EBV) in 30% of the cases. AIDS-relateddiffuse large-cell lymphoma harbor frequent EBV infection (80%) and,in 20% of the cases, BCL-6 rearrangements. Finally, the pathogenesisof AIDS-related body cavity-based lymphoma involves infectionby human herpesvirus-8 in all cases and frequently also theco-infection by EBV.     

Correlation between CD11b/CD18 and increase of aggregability of granulocytes in coronary artery disease

Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial injury. Rabbit-derived antiseram-dependent reduction of circulating PMNs in the dog or using monoclonal antibody anti-CD11b/CD 18 of PMNs resulted in smaller myocardial infarcts. Experience in humans shows the modification of PMN function in angina and during myocardial ischemia. In our studies, patients affected by coronary artery disease presented an increase in granulocyte aggregability in coronary sinus and showed a related higher expression of CD11b/CD18 in coronary sinus with respect to aorta leukocytes. The potential role of this modification of PMNs was analyzed.     

Retroperitoneal abscesses — rare causes and atypical manifestations: Report of two cases

Retroperitoneal space abscesses are a life-threatening illness which is difficult to diagnose and treat because of both their rarity and insidious clinical manifestations. The insidious development of this illness is a challenge for all medical and surgical subspecialists. The discovery of the real source of the infection is very important but not always possible, and knowledge of the anatomy and borders of the retroperitoneal space is helpful in understanding all such atypical cases and for establishing a definitive treatment. Two cases are reported that are both characterized by rare causes, uncommon development, and atypical manifestation. The normally undefined inferior borders of some parts of the retroperitoneal space or previous retroperitoneal surgery could have been the cause of the abnormal and misleading development of the abscesses. Chronically infected organs can be the true origin of this abscess, and their discovery in a nonemergency situation is mandatory for complete surgical treatment. These cases show that knowledge of the anatomy of the retroperitoneal space is important to establish the suspicion of an abscess, to understand its manifestations, which are sometimes caused by a rare pathophysiology, and to initiate appropriate treatment.     

Intracardiac migration of nitinol TrapEase vena cava filter and paradoxical embolism.

The nitinol TrapEase inferior vena cava filter is a new device for pulmonary embolism prophylaxis. No cases of filter migration or filter-related complications with this type of device have so far been described. We report a case of intracardiac migration of this filter in a patient with a patent foramen ovale, resulting in severe cardiogenic shock, cerebral and right arm paradoxical embolism. Surgical treatment, results, causes of these complications are discussed.     

Granulocyte Dysplasia and Dysfunction, and CD11/CD18 Defects in Myelodysplastic Syndromes

In myelodysplastic syndromes (MDS), dysplastic changes in neutrophils are a common feature reflecting the total degree of bone marrow dysplasia. Furthermore, granulocyte function is abnormal, so that a high risk of life-threatening infections has been documented. In this review we shall focus on the defects of both granulocytes and their CD1Ib/CD 18 glycoprotein complex, which regulate granulocyte adherence, locomotion, diapedesis and migration into inflammatory sites, in patients suffering from primary MDS.

The defective surface membrane glycoprotein expression of myelodysplastic phagocytes is not only a useful diagnostic tool, but also a powerful prognostic one, since MDS patients with such defects present both an increased susceptibility to infections and a decreased survival. Moreover, the administration of colony-stimulating factors is known to be able to elicit long-lasting improvement in neutrophil count, CD1Ib/CD 18 expression and function, marrow myeloid maturation, and possibly to decrease bacterial infections in MDS patients.     

Participation of tumour necrosis factor and nitric oxide in the mediation of vascular dysfunction in splanchnic artery occlusion shock

1 Splanchnic artery occlusion (SAO) shock is characterized by irreversible circulatory failure. Tumour necrosis factor (TNF-α) may affect the L-arginine/nitric oxide (NO) pathway, thus contributing to the cardiovascular derangements of circulatory shock.2 We investigated the contribution of both TNF-α and the L-arginine/nitric oxide pathway to the vascular dysfunction of SAO shock. Anaesthetized rats, subjected to total occlusion of the superior mesenteric artery and the coeliac trunk for 45 min developed a severe shock state (SAO shock) resulting in a fatal outcome within 75-90 min after the release of occlusion. Sham operated animals were used as controls. SAO shocked rats had also a marked hypotension and enhanced macrophage and serum levels of TNF-α. Furthermore, aortic rings from shocked rats showed a marked hyporeactivity to phenylephrine (PE 1 nM—10 μM) and reduced responsiveness to acetylcholine (ACh 10 nM—10 μM). Endotheliumdenuded aortic rings had also a marked hyporeactivity to phenylephrine, which was restored to control values by in vitro administration of N^G nitro-L-arginine-methyl ester (L-NAME 10 μM).3 In vivo administration of cloricromene (2 mg kg^-1, i.v.), an inhibitor of TNF-α biosynthesis, increased survival, enhanced mean arterial blood pressure and reduced macrophage and serum levels of TNF-α. Furthermore, aortic rings from shocked rats treated with cloricromene exhibited a greater contractile response to phenylephrine and improved responsiveness to ACh when compared to aortic rings from vehicle-treated SAO shocked rats.4 Our results suggest that TNF-α alters both endothelial and muscular L-arginine/nitric oxide pathways which in turn produce vascular dysfunction in SAO shock.     

Two distinct intracranial tumors of different cell types in a single patient. Case report and review of the literature

We report the case of a patient with two distinct brain tumors. A meningioma was resected surgically. Nine months later a glioblastoma appeared in the same region, but at a different site. This was not treated, because the patient died. The clinical significance and etiology of these tumors are considered.