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Phlebology is not a specialty for its own in Italy. Phlebological patients are treated by vascular and general surgeons, dermatologists, phlebologists, angiologists, internists and even general practitioners. Even tough guidelines present a series of recommendations based on evidence-based medicine, guidelines may also be a tool to unify the diagnostic and therapeutic approach in a vast medical field like phlebology. Since vascular surgeons and phlebologists are particularly involved in phlebology-related pathologies the scientific societies of the Italian Society of Phlebology (SIF) and the Italian Society for Vascular and Endovascular Surgery (SICVE) decided to cooperate for the preparation of phlebo-lymphological guidelines. These guidelines comprehend also an important chapter dealing with the lymphology of the lower extremities; phlebological active physicians are often faced with lymphatic pathologies and a good differential diagnosis can be sometimes very helpful. Sclerotherapy and Surgery as the major therapeutical alternatives are extensively analyzed, but also the compression therapy, the medical and physical therapy are presented under the critical view of evidence based analyses. Separate chapters deal with the treatment alternatives for superficial and deep venous thromboses and the recommendations for the treatment of venous ulcers. The current scientific evidences were confronted with the experiences of Italian specialists and the particular practice and reality in Italy. They represent therefore the actual valid positions and recommendations in Italy which shall be updated regularly.

Aim: The prevalence of venous thromboembolic disease (VTED) is between 0.05% and 0.1% whereas its incidence is approximately 0.1%. Out of 100 patients with deep vein thrombosis (DVT), 5 will develop clinically serious pulmonary embolism (PE), one of which will be fatal. It is well known from the literature that surgical interventions carried out without antithrombotic prophylaxis have a 30% incidence of DVT, which can be halved with adequate prophylaxis. The aim of this study is to evaluate the immediate, middle- and long-term complications of caval filters by identifying any of the problems connected with or independent of the presence of the filter, also in relation to international literature data., Methods: In view of the evolution of VTED surgical prevention methods, we have analyzed our case record composed of 821 patients (October 1984-October 2002), treated with different surgical solutions for VTED, with indications for the placement of 634 caval filters., Results: The 30-day follow-up of all the 634 filters placed (100%) shows no mortality from the procedure and any of its immediate complications. The middle-term follow-up (from 1 month to 5 years) of 361 filters (57%) shows 0.55% mortality from PE while the long-term follow-up (5-16 years) of 105 filters (17%) shows a percentage decrease in all complications and no mortality from PE. The results also show a progressive annual decrease in the number of filters placed., Conclusions: The lower incidence of complications, compared to that reported in the literature, can be attributed to both improved operator dexterity in the placement of the filter and correct management of the complications. The lower number of filters used can be explained by improved therapeutic possibilities with new low molecular weight heparins (LMWH) and by current diagnostic as well as instrumental and biochemical monitoring methodologies.

Pancreatic ductal carcinoma still is an aggressive disease with a fatal prognosis due to late diagnosis and resistance to pharmacological and surgical treatments. Molecular investigations of pancreatic cancer are complicated by the restricted accessibility of the organ for biopsies. However, recent studies have indicated that pancreatic cancer is a multi-stage process resulting from the accumulation of genetic changes in the somatic DNA of normal cells. These molecular alterations, including overexpression of receptor-ligand systems, oncogene activation and loss of tumour suppressor genes, leads to a profound disturbance in cell cycle regulation and continuous growth. The molecular findings are now integrated in a pancreatic tumour progression model, with genetically and morphological defined precursor lesions. However, it remains unclear whether the initial target cells of this cancer develop from ductal or acinar cells. This review will present recent emerging questions on the biology of pancreatic cancer with particular emphasis on the cell origin and tumour microenvironment.

Esophageal motility abnormalities are usually diagnosed when esophageal manometry is performed in patients with unexplained non-cardiac chest pain, non obstructive dysphagia or as a part of the preoperative evaluation for surgery of gastroesophageal reflux. Classification of these abnormalities has been a subject of controversy. These esophageal contraction abnormalities can be separated manometrically from the motor pattern seen in normal subjects, however, their clinical relevance is still unclear and debated. Many patients demonstrate motility abnormalities in the manometry laboratories, but may lack correlation with their presenting symptoms. Medical treatment can decrease symptoms particularly chest pain or acid reflux but there is no significant changes in the manometric patterns. Such motor abnormalities may not reflect a true disease state, but they could be markers of other abnormalities and they can modify the initial manometric findings in time.

Programmed cell death, also known as apoptosis, is a normal physiologic process which occurs during embryonic development as well as in maintenance of tissue homeostasis. Increasing evidence suggests that alterations in cell death contribute to the pathogenesis of a number of human diseases, including cancer, viral infections, autoimmune diseases and acquired immunodeficiency syndrome (AIDS). The extraordinary research activity of the past few years has resulted in the characterization of the principal proteins involved in the apoptosis machinery. An area of particular interest has been the induction of apoptosis by two death receptor/ligand pairs, Fas/Fas Ligand and DR4-DR5/TRAIL. The identification of these molecules with the recruited signaling pathways could clarify their physiopathological implications, having a significant impact upon potential therapeutic interventions in diseases associated with cell survival alterations.

Background: Pancreatic adenocarcinomas are among the most aggressive types of cancer with an extremely poor diagnosis. Since this type of cancer is not well amenable to chemo- and radiotherapy or immunotherapy, surgical resection remains the only feasible treatment to date. Transforming Growth Factor (TGF)-beta and Interleukin (IL)-10 are potent immunomodulators that have been shown to suppress several aspects of the immune response. Vascular Endothelial Growth Factor (VEGF) is a powerful angiogenic factor, recently thought to be involved in neoangiogenesis and metastasis spreading. Therefore the three cytokines may contribute, by different pathways, to immune escape and growth of tumor. This study was conducted to determine the possible significance of TGF-beta1, IL-10 and VEGF as markers for monitoring the clinical course of pancreatic adenocarcinoma patients., Methods: Cytokine serum levels were measured in 30 pancreatic cancer patients and in 30 age and sex-matched healthy subjects., Results: In comparison to serum concentrations in controls, TGF-beta1, IL-10 and VEGF levels were significantly elevated in all patients. Where the patients were divided by groups on the basis of the clinical stage of the disease, no differences were observed in TGF-beta1 levels among the groups. On the contrary, IL-10 and VEGF were more represented in stage IV patients than in stage II and III patients. In addition, the 14 patients who underwent surgical resection had postoperative cytokine serum levels markedly lower than those observed at diagnosis., Conclusions: Overall, the results suggest the importance of these markers in predicting the biological activity of the disease and suggest new targets for future rational therapies.

There is increasing evidence to support the concept that growth and metastasis of solid tumors, including those of gastrointestinal tract, is facilitated by neoangiogenesis. Vascular Endothelial Growth Factor (VEGF) is one of the most powerful known inducer of endothelial cell growth. Therefore, VEGF is likely to contribute to tumor growth by promoting angiogenesis and stroma formation both directly, through its neovascularization inducing activity, and indirectly, by increasing vascular permeability. In addition, VEGF facilitates tumor diffusion favouring metastatic spread of cancer cells. In view of these implications, it is important to understand the physiopathological role played by this factor. In this review the authors present the accumulating body of data on the biological and functional properties of VEGF, paying special reference to new evidence on its contribution in tumor immune escape, through a marked inhibition of differentiation and activity of the professional antigen presenting cells (APC), namely dendritic cells (DC). As the molecular and cellular events that underlie the functional role of VEGF in tumor angiogenesis and immune suppression become better defined, rational pharmacological and/or gene therapies can be derived in order to treat those neoplasms, such as pancreatic adenocarcinoma, not well amenable to chemo- and radiotherapy or immunotherapy.

The aim of this review is to summarize the current concepts concerning the active role of the endothelium in the pathogenesis of atherosclerosis. Activated endothelium may promote the adhesion of monocytes and their transmigration into the intima. The coordinated expression of adhesion molecules of the selectin, integrin or immunoglobulin superfamily on the surface of endothelial cells and of monocytes modulates these events. The role of lipoproteins and their oxidative derivatives as well as that of selected cytokines and platelet activated factor in initiating changes on the endothelial cell surface has been investigated: these events are associated with an increased endothelial permeability to lipids and lipoproteins with their accumulation in the subendothelium. Once migrated into the intima, monocytes undergo morphological and functional modifications leading to the generation of a polypeptide mediator network which is instrumental in the migration, differentiation and proliferation of smooth muscle cells. Mediators produced by macrophages infiltrating the atherosclerotic plaque and by the endothelium may render the surface of the endothelial cells thrombogenic thus favoring thrombotic occlusion. In conclusion, the most recent studies suggest that the endothelium plays an active role in the pathogenesis of atherosclerosis.

A case of a 72-year-old woman affected by angioimmunoblastic lymphadenopathy with dysproteinemia is described. She was admitted to the hospital for serious cutaneous lesions and dementia. The patient had been treated with corticosteroids for the previous two years. Cryptococcosis was diagnosed by cutaneous biopsy. Antimycotic therapy together with corticosteroid withdrawal cured the cutaneous lesions and improved her psychiatric symptoms.

Andrologic problems were considered as nutrition is concerned: vitamin and oligo-element deficiencies, metabolic alterations, and toxic intake. Ethanol role was examined and discussed for its relevance in psychological and organic impairment due to both chronic abuse and acute intake, mainly for its role on hypothalamic-pituitary-gonadal axis. Rational nutrition is a clue in sexual disturbance prevention, correction and integrated care.

We report a case of primary sclerosing cholangitis associated with Crohn disease of the large intestine and marked eosinophilia in a 64 year old woman. Clinical features, histologic findings at biopsy of the intestine and liver and the endoscopic retrograde cholangiopancreatography are described. The case report is discussed, particularly as regards treatment with biliary salts and aminosalicilic acid.

A normally functioning vascular endothelium is required for vascular tone modulation and blood fluidity. Systemic and local circulatory and coagulation alterations, even to the point of renal failure, may be observed in obstructive jaundice; bile salts are included among the potential pathogenetic factors. To assess the effects of taurocholic acid, glycocholic acid, and cholic acid on the integrity and properties of the endothelium, cultured human endothelial cells (HUVEC) were studied. Taurocholic and glycocholic acids (up to 2000 mumoles/L) did not exhibit any significant effect on 51Cr release from HUVEC after 6 h incubation. Following HUVEC exposure to 2000 mumoles/L of the unconjugated compound, cholic acid, a significant discharge of the radiolabel and LDH leakage in the supernatant were observed, to some extent prevented by the presence of human plasma or albumin (physiologic carrier). Prostacyclin spontaneous release from HUVEC was significantly depressed by both taurocholic and glycocholic acid; the action was related to bile salt concentration (200-1000 mumoles/L) and to the time of exposure (1 to 24 h); the reduced production of PGI2 was demonstrated to be reversible. Conversely, spontaneous TxA2 generation and fVIII release were not affected by the presence of bile salts in culture medium. Previous investigations showed that experimental obstructive jaundice could impair prostacyclin release from rat aortic tissue. The same effect was also demonstrated after in vitro exposure of the vessel wall to jaundiced serum and bile salts alone; furthermore, bile salts exert toxic effects on the integrity of several cells and impair the prostaglandin system of different tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

The incidence of immunological disorders seems to play a primary, significative role in the genesis of insulin-dependent diabetes mellitus (IDDM). Auto-immunological anti-pancreas alterations, both cell-mediated and humoral, have been detected in course of IDDM; moreover, the presence of antipancreatic antibodies seems to correlate with progressive destruction of islet cells and increased insulin deficiency. Animal models and human studies, revealing the pathologic entity of "insulitis", are consistent with an autoimmune component playing a part in the pathogenesis of diabetes mellitus. Furthermore, genotypic factors may be considered: recent studies prove the association between HLA system and IDDM; specifically, HLA antigens B8 and BW15 are found in significantly higher frequencies in juvenile onset insulin-dependent diabetics. Therefore, it can be hypothesized, in the pathogenesis of the disease, an altered immune response to an additional environmental diabetogenic factor; it has been postulated, on the ground of epidemiologic and experimental studies, the interference of a viral infection, that may act as a triggering event to pancreatic cell damage with a latent period of variable duration.

The discovery of hepatitis B surface antigen by Blumberg in 1965 offered a specific marker that could readily be employed in the clinical, epidemiological and experimental investigation of type B viral hepatitis. It has since been followed by the continuous gathering of further knowledge concerning this disease. The morphology and immunological and biochemical features of virus B, the epidemiology and prevention of hepatitis B, and marker determination techniques are examined in an overview of the present situation.

Different methods available for investigating patients for pancreatic disease are discussed. They first include measurement of pancreatic enzymes in biological fluids. Basal amylase and/or lipase in blood are truly diagnostic in acute pancreatitis but their utility is low in chronic pancreatic diseases. Evocative tests have been performed to increase the sensitivity of blood enzyme measurement. The procedure is based on enzyme determination following administration of pancreozymin and secretin, and offers a valuable aid in diagnosis of chronic pancreatitis and cancer of the pancreas. They are capable of discerning pancreatic lesions but are not really discriminatory because similar changes are observed in both diseases. The measurement of urinary enzyme levels in patients with acute pancreatitis is a sensitive indicator of disease. The urinary amylase excretion rises to abnormal levels and persists at significant values for a longer period of time than the serum amylase in acute pancreatitis. The fractional urinary amylase escretion seems to be more sensitive than daily urinary measurement. The pancreatic exocrin function can be assessed by examining the duodenal contents after intravenous administration of pancreozymin and secretin. Different abnormal secretory patterns can be determinated. Total secretory deficiency is observed in patients with obstruction of excretory ducts by tumors of the head of the pancreas and in the end stage of chronic pancreatitis. Low volume with normal bicarbonate and enzyme concentration is another typical pattern seen in neoplastic obstruction of escretory ducts. In chronic pancreatitis the chief defect is the inability of the gland to secrete a juice with a high bicarbonate concentration; but in the advanced stage diminution of enzyme and volume is also evident. Diagnostic procedures for pancreatic diseases include digestion and absorption tests. The microscopic examination and chemical estimation of the fats in stool specimens in different conditions of intake are still important screening tests. Isotopic estimates of steatorrhea and distinction between labeled triolein and oleic acid absorption do not provide greater diagnostic discrimination than traditional procedures. 131I labeled proteins permit a good evaluation of a negative nitrogen balance. Sophisticated procedures to estimate exocrine pancreatic insufficiency are based on the study of endoluminal digestive processes at several times and different level of the small intestine. They permite esclusion of extrapancreatic factors interfering in digestion and absorption functions. The endocrin pancreatic function is evaluated by mean of oral tolerance test an radioimmunoassay of blood insulin. It is generally agreed that "diabetes" caused by insulin deficiency and digestion and absorption defects are the result of diffuse pancreatic destruction. Many methods are now available investigating patients with pancreatic disease but the single use of one of them is never satisfactory...

The discovery of Australian antigen (HBsAg) has led to an increasing deal of knowledges about the virus of type B hepatitis (HBV); several markers of HBV have been detected and are becoming disposable for clinical and epidemiological purposes. The HBsAg is carried by 3 types of particulate structures discovered by electron microscopy as small spherical particles having diameter around 22 nm, long filaments and spherical particles having an overall diameter of the 42 nm (Dane-particle) with an electron-dense core. Dane-particle core contains circular double-stranded DNA molecules and an enzyme, the DNA polymerase. At present, Dane-particle is thought to represent the HBV, having properties consistent with those of a complete virus. Four antigen/antibody systems related to viral type B hepatitis have been discovered; they have been designated with the following nomenclature: HBsAg/anti-HBs, HBcAg/anti-HBc, HBeAg/anti-HBe, epilon antigen/anti epilson. The availability of the HBV markers for clinical purposes will permit a better understanding of the sequence of the biological reactions as well as of the clinical and epidemiological features concerning this viral infection: incubation period, acute disease, resolution, chronic carrier state, actively or passively immunized subject, persistent or subsided infectivity, prognosis.

Lymphocyte subsets have been examined in 23 patients affected by idiopathic dilated cardiomyopathy (IDCM). Patients were divided according to their functional class showing that compromised subjects exhibited high T-lymphocyte helper/suppressor ratio whereas the contrary was observed in the other patients. It has therefore suggested that IDCM is characterized by 2 distinct phases, each of them with different helper/suppressor ratio.