The incidence of HPV infection in anal cancer patients in Greece.

BACKGROUND AND AIM OF THE STUDY: Although anal cancer represents a relatively uncommon malignancy, its incidence over the last five decades, has been reported as increased for both sexes, worldwide. Human papillomavirus (HPV) infection has been shown to be a major cause for its development. The aim of the present study is to report on clinical, epidemiological and virological data of squamous anal cancer in Greek patients. PATIENTS AND METHOD: Between January 2002 and December 2010, 11 Greek patients (6 females) who were diagnosed as suffering from squamous cell anal or perianal cancer, were treated in our Hospital. Formalin fixed paraffin embedded tissue samples, obtained at the time of the anal biopsy or surgery, were analyzed by PCR in order to identify the presence as well as the type of HPV infection. RESULTS: Overall, the presence of HPV DNA was detected in 6 out of the 11 patients (54.5%). The "high risk" HPV DNA was detected in 3 of them (2 women and 1 man), while the "low risk" HPV DNA was detected in the remaining three (2 women and 1 man). CONCLUSION: The incidence of HPV infection in squamous cell anal cancer Greek patients, is lower than other Western countries, probably reflecting differences in sexual habits in the Greek population.

Does Helicobacter pylori identification in the mucosa of the gallbladder correlate with cholesterol gallstone formation? / ¿Existe una correlación de la identificación de Helicobacter pylori en la mucosa de la vesícula biliar con la formación de cálculos biliares de colesterol?

OBJECTIVE: Helicobacter pylori (H pylori) represents a potential initiator of cholesterol crystallization and it has been proposed that it is related to gallstone formation. In this study, any possible association between the H pylori identification in the mucosa of gallbladder and cholesterol gallstone formation was evaluated. METHODS: Gallbladders containing pure or mixed cholesterol gallstones (cholelithiasis group, n = 89) and gallbladders without gallstones (control group, n = 42) were submitted to standard histopathological examination for H pylori detection, as well as to nested polymerase chain reaction amplification for H pylori DNA detection. RESULTS: Helicobacter pylori was identified in the gallbladder's epithelium in four patients with cholelithiasis and in two patients in the control group by histology. In all the cases which were found to be H pylori positive by histological examination, H pylori DNA were also detected. No correlation between gallstone formation and H pylori detection in the biliary epithelium was found. A higher incidence of acute inflammation in the cholelithiasis (22.5% vs 9.5%, p = not significant [ns]) and in the H pylori positive groups (33% vs 17.6%, p = ns) were histologically detected. A higher incidence (10% vs 0%), p = ns) of H pylori in gallbladders with gallstones and acute inflammation, compared to gallbladders with acute inflammation but without gallstones, was noticed. CONCLUSION: Helicobacter pylori is detectable in low frequency in the mucosa of the gallbladder and it does not seem to act as a lithogenic component for cholesterol gallstone formation. Its higher incidence in gallbladders with gallstones and acute inflammation, suggests a possible accessory role in a subset of patients with cholelithiasis.

OBJETIVO: Helicobacter pylori (H pylori) representa un iniciador potencial de la cristalización del colesterol, y se ha propuesto que guarda relación con la formación del cálculo biliar. En este estudio, se evaluó cualquier posible asociación entre la identificación de H pylori en la mucosa de la vesícula y la formación del cálculo biliar de colesterol. MÉTODOS: Las vesículas que contienen cálculos biliares de colesterol puros o mixtos (grupo de colelitiasis, n = 89) y vesículas sin cálculos biliares (grupo control, n = 42) fueron sometidos a un examen histopatológico estándar con el fin de detectar el H pylori descubrimiento, así como a la amplificación de la reacción en cadena de polimerasa para la detección de ADN H pilori. RESULTOS: El Helicobacter pylori fue identificado mediante histología en el epitelio de la vesícula en cuatro pacientes con el colelitiasis y en dos pacientes en el grupo de control. En todos los casos que resultaron ser H pylori positivo por el examen histológico, se halló también DNA H pylori. No se halló correlación ninguna entre la formación del cálculo biliar y la detección de H pylori en el epitelio biliar. Se detectó histológicamente una incidencia más alta de inflamación aguda en la colelitiasis (22.5% contra 9.5%, p = no significativo [ns]) y en los grupos H pylori positivos (33% contra 17.6%, p = ns). Se observó una incidencia más alta (10% contra 0%), p = ns) de H pylori en las vesículas con los cálculos biliares e inflamación aguda, en comparación con las vesículas con la inflamación aguda pero sin cálculos biliares. CONCLUSIÓN: Helicobacter pylori es detectable en baja frecuencia en la mucosa de la vesícula y no parece actuar como un componente litogénico en la formación del cálculo biliar de colesterol. Su mayor incidencia en las vesículas con cálculo biliar e inflamación aguda, hace pensar en un posible papel auxiliar en un subconjunto de pacientes con colelitiasis.

Implications for a role of interleukin-23 in the pathogenesis of chronic gastritis and of peptic ulcer disease.

The present study aimed to investigate the role of gastric mucosa for the secretion of interleukin (IL)-23 in chronic gastritis. One hundred and one patients were enrolled; 47 with duodenal ulcer, 33 with gastric ulcer and 31 with chronic gastritis. Biopsies were incubated in the absence/presence of endotoxins. Supernatants were collected and IL-23 and IL-1beta were measured by enzyme-linked immunosorbent assay. Scoring of gastritis was performed according to the updated Sydney score. Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis. IL-23 was higher in supernatants of tissue samples of Helicobacter pylori-positive than of H. pylori-negative patients. No differences were recorded in concentrations of IL-23 and IL-1beta between patients with duodenal ulcer, gastric ulcer and chronic gastritis. Positive correlations were found between IL-23 of patients with both duodenal and gastric ulcer and chronic gastritis and the degree of infiltration of neutrophils and monocytes. Similar correlations were observed between IL-23 and IL-1beta. IL-23 secreted by the gastric mucosa could be implicated in the pathogenesis of chronic gastritis. IL-23 was released in the presence of H. pylori from the inflamed gastric mucosa and followed the kinetics of IL-1beta.

CEA and CA-19.9 serum tumor markers as prognostic factors in patients with locally advanced (unresectable) or metastatic pancreatic adenocarcinoma: a retrospective analysis.

Most pancreatic adenocarcinoma patients present with locally advanced or metastatic disease at diagnosis. in this retrospective study the authors evaluated the prognostic significance of the CEA and CA-19.9 serum tumor markers in advanced (unresectable) pancreatic cancer in correlation to other prognostic factors (demographic data, clinical parameters, treatment modality) and survival time using univariate and multivariate methods, in 215 patients with locally advanced (unresectable) or metastatic pancreatic adenocarcinoma. median survival was 29.0 weeks, with 21.9% of patients surviving 36 weeks. Among 24 potential prognostic variables, 19 were associated with shorter survival. Multivariate analysis indicated that ten factors had a significant independent effect on survival: chemotherapy, surgery, tumor localization, elevated C-reactive protein, elevated CeA, CA 19-9 (>30 x nl), jaundice at diagnosis, weight loss >10%, distant metastases, and Karnofsky performance status. Patients who had only palliative therapy had a hazard ratio of 8.94 versus those who underwent palliative surgery and chemotherapy. Although certain clinical, biochemical and biological factors remain important predictors of survival in patients with advanced pancreatic cancer, CA-19.9 serum tumor marker levels retain independent prognostic value for poor survival.

Does Helicobacter pylori identification in the mucosa of the gallbladder correlate with cholesterol gallstone formation?

OBJECTIVE: Helicobacter pylori (H pylori) represents a potential initiator of cholesterol crystallization and it has been proposed that it is related to gallstone formation. In this study, any possible association between the H pylori identification in the mucosa of gallbladder and cholesterol gallstone formation was evaluated METHODS: Gallbladders containing pure or mixed cholesterol gallstones (cholelithiasis group, n = 89) and gallbladders without gallstones (control group, n = 42) were submitted to standard histopathological examination for H pylori detection, as well as to nested polymerase chain reaction amplification for H pylori DNA detection. RESULTS: Helicobacter pylori was identified in the gallbladder's epithelium in four patients with cholelithiasis and in two patients in the control group by histology. In all the cases which were found to be H pylori positive by histological examination, H pylori DNA were also detected. No correlation between gallstone formation and H pylori detection in the biliary epithelium was found. A higher incidence of acute inflammation in the cholelithiasis (22.5% vs 9.5%, p = not significant [ns]) and in the H pylori positive groups (33% vs 17.6%, p = ns) were histologically detected. A higher incidence (10% vs 0%), p = ns) of H pylori in gallbladders with gallstones and acute inflammation, compared to gallbladders with acute inflammation but without gallstones, was noticed CONCLUSION: Helicobacter pylori is detectable in low frequency in the mucosa of the gallbladder and it does not seem to act as a lithogenic component for cholesterol gallstone formation. Its higher incidence in gallbladders with gallstones and acute inflammation, suggests a possible accessory role in a subset of patients with cholelithiasis.

c-FLIP expression in colorectal carcinomas: association with Fas/FasL expression and prognostic implications.

AIMS: Disruption of apoptotic cell death has been implicated in tumour aggressiveness in colonic carcinogenesis. The Fas-Fas ligand (FasL) system is involved in the execution of apoptosis induced by the immune system. c-FLIP protein constitutes an inhibitor of Fas and other (TRAIL) death receptor-mediated apoptosis. The aim of this study was to investigate the simultaneous expression of Fas, FasL and c-FLIP in relation to standard clinicopathological parameters and patients' outcome in colorectal cancer. METHODS AND RESULTS: Levels of Fas, FasL and c-FLIP protein expression were quantified immunohistochemically in paraffin-embedded tissues from 90 patients. Immunopositivity was detected for Fas, FasL and c-FLIP in 71%, 35.5% and 68.8% of cases, respectively. Concurrent expression of Fas/FasL was seen in 28 samples (31%), of which 24 (85.7%) also displayed c-FLIP positivity (P = 0.04). c-FLIP overexpression (> 10%) tended to prevail marginally in higher stage tumours (P = 0.09). Additionally, FasL and c-FLIP adversely affected survival on both univariate (P = 0.001 and P = 0.0024, respectively) and multivariate analysis [hazard ratio (HR) 3.491, P = 0.005 and HR 2.960, P = 0.036, respectively]. CONCLUSIONS: The frequent expression and coexpression of Fas, FasL and c-FLIP in colorectal carcinoma implicates c-FLIP as an inhibitor of the Fas-FasL-induced death pathway in these tumours. Moreover, c-FLIP conveys independent prognostic information in the presence of classical prognosticators.

H3 Propranolol serum levels following lidocaine administration in rats with CCL4 induced liver damage.

Liver disease alters the pharmacokinetic and pharmacodynamic properties of hepatically eliminated drugs. The main factors influenced are plasma albumin levels, enzyme balance (induction & inhibition) and drug binding to tissue proteins. The influence of lidocaine on serum, heart and liver propranolol levels in Wistar rats after liver injury induced by carbon tetrachloride CCl4 0.4 ml/kg x 2/wkl, was investigated. 40 male Wistar rats were divided into four groups (I, II, III, IV; n=10), Group I animals received only propranolol (labelled + cold substance) 40 mg/kg/12 h p.o., group II propranolol plus lidocaine in a single dose of 4mg/kg s.c., group III was treated with CCl4 for 6 weeks and received propranolol x2 at the same dosage as group I, while group VI was treated with CCl4 and the same drug dosage as group II. The simultaneous administration of H3-propranolol and lidocaine increased propranolol levels in the serum and tissues. The liver in damaged animals showed an increase of propranolol level under lidocaine co-administration, probably due to CCl4 induced liver enzyme activity, resulting in a rapid propranolol metabolism or to competition between both drug protein binding sites. The increased propranolol levels in the heart after lidocaine administration were probably due to attributed to its high affinity for heart tissue. Consequently, as regards the therapeutic approach for patients with liver disease receiving propranolol their propranolol dosage should be reduced when lidocaine is co-administered.

Effects of hemodialysis on serum lipids and phospholipids of end-stage renal failure patients.

Patients with chronic renal failure undergoing periodic maintenance hemodialysis frequently present dyslipoproteinaemia which has been linked to the sharply increased risk of cardiovascular disease in these subjects. Reported defects on lipoprotein-related enzyme activities suggest a possible influence of hemodialysis not just to plasma lipid and lipoprotein levels but also to the composition of cell membranes. In this study, it was investigated whether the reported lipid abnormalities are accompanied by changes in serum phospholipids levels. Blood samples were obtained from 140 patients undergoing maintenance hemodialysis treatment and 122 normolipidemic healthy controls and analyzed for total serum phospholipids and their individual subclasses, as well as for total cholesterol and triglycerides, HDL-cholesterol and its subclasses. A significant decrease was observed in serum HDL cholesterol levels (p < 0.001) and its subclasses, HDL2-cholesterol (p < 0.01) and HDL3-cholesterol (p < 0.01) in patients when compared with healthy controls. A critical increase in the serum triglyceride content (p < 0.001) of patients was also observed. In addition, the serum levels of sphingomyelin (p < 0.01) and diphosphatidylglycerol (p < 0.001) were increased in the patient group, while the levels of phosphatidylcholine (p < 0.01) and phosphatidylinositol (p < 0.01) were significantly decreased in the patient group compared to healthy controls. In conclusion, this work clearly demonstrates that hemodialysis treatment contributes significantly to the dyslipidemic profile of end-stage renal failure patients by altering serum lipoprotein and phospholipids concentrations.

Computer-aided tumor detection in endoscopic video using color wavelet features.

We present an approach to the detection of tumors in colonoscopic video. It is based on a new color feature extraction scheme to represent the different regions in the frame sequence. This scheme is built on the wavelet decomposition. The features named as color wavelet covariance (CWC) are based on the covariances of second-order textural measures and an optimum subset of them is proposed after the application of a selection algorithm. The proposed approach is supported by a linear discriminant analysis (LDA) procedure for the characterization of the image regions along the video frames. The whole methodology has been applied on real data sets of color colonoscopic videos. The performance in the detection of abnormal colonic regions corresponding to adenomatous polyps has been estimated high, reaching 97% specificity and 90% sensitivity.

Jejunogastric intussusception presented with hematemesis: a case presentation and review of the literature.

BACKGROUND: Jejunogastric intussusception (JGI) is a rare but potentially very serious complication of gastrectomy or gastrojejunostomy. To avoid mortality early diagnosis and prompt surgical intervention is mandatory. CASE PRESENTATION: A young man presented with epigastric pain and bilous vomiting followed by hematemesis,10 years after vagotomy and gastrojejunostomy for a bleeding duodenal ulcer. Emergency endoscopy showed JGI and the CT scan of the abdomen was compatible with this diagnosis. At laparotomy a retrograde type II, JGI was confirmed and managed by reduction of JGI without intestinal resection. Postoperative recovery was uneventful. CONCLUSIONS: JGI is a rare condition and less than 200 cases have been published since its first description in 1914. The clinical picture is almost diagnostic. Endoscopy performed by someone familiar with this rare entity is certainly diagnostic and CT-Scan of the abdomen could also help. There is no medical treatment for acute JGI and the correct treatment is surgical intervention as soon as possible.

Rapid urease test is less sensitive than histology in diagnosing Helicobacter pylori infection in patients with non-variceal upper gastrointestinal bleeding.

BACKGROUND AND AIMS: The validity of the rapid urease (CLO) test to diagnose Helicobacter pylori infection in patients with bleeding ulcers has been questioned. The aim of this paper is to evaluate the validity of the CLO test in comparison with histology in diagnosing H. pylori infection in patients with acute upper gastrointestinal bleeding (UGB), irrespective of non-steroidal anti-inflammatory drug (NSAID) use. METHODS: Upper gastrointestinal endoscopy was performed within 24 h of admission for all patients with UGB admitted to the Department of Pathophysiology, Medical School, Athens, for a period of 12 months. Patients with variceal bleeding, previous gastric operation, recent treatment with proton pump inhibitors (< 2 months) and those with a history of H. pylori eradication therapy were excluded from the study. At least four biopsies (two from the antrum and two from the body) were obtained for the CLO test and histology (modified Giemsa). RESULTS: Seventy-two consecutive patients (aged 18-90 years, 51 men, 21 women) were included. Forty-six patients (64%) used NSAID. Thirty-two patients (44%) were found to be positive for H. pylori infection by the CLO test, while 44 patients (61%) were found to be positive on histology (P<0.045, 95% CI, 0.004-0.331). The sensitivity and specificity of the CLO test were 68 and 93% respectively; positive and negative predictive values were 94 and 65%, respectively. The age of the patient and visible blood in the stomach did not influence results of either the CLO or histology. CONCLUSIONS: The CLO test, performed within 24 h of hospital admission in patients with UGB, irrespective of NSAID use, is unreliable for the detection of H. pylori infection. The age of the patient and the presence of blood in the stomach do not seem to influence these results.

Neural network application in the discrimination of benign from malignant gastric cells.

OBJECTIVE: To investigate the potential value of morphometry and neural networks for the discrimination of benign from malignant gastric lesions. STUDY DESIGN: One thousand cells from 19 cases of cancer, 19 cases of gastritis and 56 cases of ulcer were selected as a training set, and an additional 4,000 cells from the same cases of cancer, gastritis and ulcer were used as a test set. Images of routinely processed gastric smears stained by the Papanicolaou technique were analyzed by a custom-made image analysis system. RESULTS: Application of the neural network gave correct classification in 96% of benign cells and 89% of malignant cells. CONCLUSION: The results indicate that the use of neural networks and image morphometry may offer useful information concerning the potential of malignancy in gastric cells.

The CLO test is unreliable in diagnosing H. pylori infection in post-surgical stomach; is there any role of H. pylori in peptic ulcer recurrence?

AIM: To evaluate the validity of the CLO test in detecting Helicobacter pylori in patients with gastric operation and to investigate the relationship of H. pylori with peptic ulcer recurrence in these patients. METHODS: In this prospective study, 110 consecutive patients, the majority of whom had undergone gastric operation for benign disease (n = 102), were included. Eighty patients (62 males), aged 38-87 years, had had a gastrectomy (10 Billroth I, 70 Billroth II), and 30 patients (27 males), aged 36-73 years, had had a vagotomy (13 vagotomy plus gastroenterostomy, 17 vagotomy plus pyloroplasty). H. pylori was sought on multiple biopsy specimens, using CLO test and histology (modified Giemsa stain). The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of the CLO test were estimated using histology as 'gold standard'. RESULTS: Overall, 21 gastrectomy patients (26%) were H. pylori-positive by CLO and 25 (31 %) were H. pylori-positive by histology. The estimated sensitivity, specificity, PPV and NPV of the CLO test, using histology as 'gold standard', were 68%, 91%, 77% and 86%, respectively. The CLO test was positive in 67% of vagotomy patients (20 of 30), while 50% (15 of 30) were H. pylori-positive by histology. The estimated sensitivity, specificity, PPV and NPV of the CLO test were 87%, 53%, 65% and 80%, respectively. H. pylori prevalence by histology was 50% in patients with vagotomy and 31% in those with gastrectomy (P = 0.0787). Recurrent ulcers were observed in 8/30 patients (27%) after vagotomy and in 10/72 patients (14%) after gastrectomy. Recurrent ulcer was documented in 6/15 H. pylori-positive patients with vagotomy (40%), and in one of 25 H. pylori-positive patients with gastrectomy (4%). This difference was significant (Fisher's exact test, P = 0.007, relative risk 5.091, 95% CI 0.819-31.64). CONCLUSION: The CLO test seems to be unreliable in diagnosing H. pylori in post-surgical stomach. The H. pylori prevalence is higher, although not significantly, in vagotomized patients compared with gastrectomized patients, and in this group is closely related to the presence of recurrent ulcer. So, at least in this group of patients, it is strongly recommended to look for and eradicate H. pylori.

Expression of HLA-DR, costimulatory molecules B7-1, B7-2, intercellular adhesion molecule-1 (ICAM-1) and Fas ligand (FasL) on gastric epithelial cells in Helicobacter pylori gastritis; influence of H. pylori eradication.

There is evidence that Helicobacter pylori infection up-regulates the expression of HLA class II molecules by gastric epithelial cells (GEC). In this study we evaluated whether GEC are capable of expression of costimulatory molecules in H. pylori gastritis. The expression of FasL by GEC, before and after eradication of H. pylori, was also studied. Thirty patients (23 men) aged 27-81 years (53.67 +/- 13.99 years (mean +/- s.d.)) with dyspepsia were studied. Upper gastrointestinal endoscopy was performed and six biopsies were obtained (antrum, n = 3; corpus, n = 3) for Campylobacter-Like Organisms (CLO) test and histology; 23 (16 men) were H. pylori+ and seven (all men) were H. pylori- by both methods and served as controls. Helicobacter pylori eradication therapy was given to H. pylori+ patients and all patients were re-endoscoped after 116 +/- 9 days. Formalin-fixed paraffin-embedded tissue sections were stained by the ABC immunoalkaline phosphatase method. In H. pylori gastritis HLA-DR was expressed and correlated with disease activity (P < 0.01). No HLA-DR was observed in controls. In H. pylori-eradicated patients significant decrease of HLA-DR was found (antrum, P < 0. 001). ICAM-1 was expressed by GEC in 80% of H. pylori+ patients; ICAM-1 expression did not correlate with gastritis parameters and decreased significantly after eradication (antrum, P < 0.01). B7-1 and B7-2 were expressed on H. pylori+ samples and their expression decreased after eradication, albeit not significantly. Weak epithelial expression of both B7 molecules was observed in all the controls. FasL was steadily expressed by GEC in both H. pylori+ and H. pylori- patients and remained almost unchanged after eradication. These findings suggest that GEC may acquire antigen-presenting cell properties in H. pylori infection through de novo expression of HLA-DR and costimulatory molecules. This seems to be attenuated after eradication and resolution of mucosal inflammation. The same cells exhibit the capacity to control the inflammatory process, probably by inducing apoptotic cell death to Fas-bearing infiltrating lymphocytes.

Ranitidine versus ranitidine plus octreotide in the treatment of acute non-variceal upper gastrointestinal bleeding: a prospective randomised study.

AIM: To compare the efficacy of ranitidine with that of ranitidine plus octreotide in the treatment of non-variceal upper gastrointestinal (UGI) bleeding. DESIGN: Prospective, randomised, open study. PATIENTS AND METHODS: Upper GI endoscopy was carried out during the first 24 hours in all patients with UGI bleeding who had been admitted within a period of 18 months. Patients with variceal bleeding, and those who had undergone any type of gastric operation, were excluded. Eighty-four patients (58 men and 26 women) aged 21-92 years (mean age: 61.2 +/- 15.0 SD) were included. Patients were randomised to receive ranitidine 50 mg tid intravenously alone (Group A: 44 patients, 29 men), or in combination with octreotide 100 micrograms tid subcutaneously, the second drug given for three days only (Group B: 40 patients, 29 men). The study end-points were discharge without operation, emergency surgical intervention or death. The number of blood units given and the days of hospitalization were also recorded. RESULTS: Aspirin and non-aspirin NSAID use before bleeding was reported by 16/44 (36%) patients in Group A and by 19/40 (47.5%) patients in Group B (p = 0.38, OR = 0.63, 95% CI = 0.26-1.51). The endoscopically detected pathology and bleeding stigmata did not differ between the groups (p = 0.86, p = 0.64, OR = 0.78, 95% CI = 0.3-1.99, respectively). Mean use of blood units (p = 0.16) and days of hospitalization (p = 0.25) did not differ. Three patients in Group A (6.8%) and three in Group B (7.5%) required surgical intervention (p = 1.0, OR = 1.1, 95% CI = 0.21-5.84). CONCLUSION: Ranitidine plus subcutaneous octreotide is not superior to ranitidine alone in the management of patients with acute non-variceal UGI bleeding.

Diazepam treatment in rats induces changes in the concentrations of different phospholipid classes in liver and liver mitochondria.

Liver phospholipid concentrations were determined in rats after the administration of diazepam (5 mg/Kg/day), for a period of two months. Increased concentrations of total phospholipids (P < 0.05), phosphatidylcholine (P < 0.05) and phosphatidylinositol (P < 0.05) were found in the rats taking diazepam. In contrast, a decreased concentration of phosphatidylserine (P < 0.01) was observed in the same group of animals. In addition, changes in the concentration of rat liver mitochondrial phospholipids after the administration of diazepam during the same period of time were determined. Increased concentrations of total phospholipids (P < 0.01), phosphatidylcholine (P < 0.001) and diphosphatidylglycerol (P < 0.001) were found in the rats treated with diazepam. In contrast, decreased phosphatidylserine (P < 0.001) and phosphatidylinositol (P < 0.01) concentrations were observed in the same group of animals. The considerable changes observed in liver phospholipids and individual classes of liver mitochondrial phospholipids induced by long-term administration of diazepam, possibly suggest a stimulation of liver phospholipid biosynthesis. This effect may be related to enzymatic systems which are involved in phospholipid pathways, and are linked to benzodiazepinergic binding sites.

Clinical significance of plasma HDL subfractions (HDL2, HDL3) in patients with peripheral arterial disease (PAD) in the Greek population.

OBJECTIVE: In this study the major high density lipoprotein (HDL) subfractions (HDL2, HDL3) were examined, in angiographically selected patients with peripheral arterial disease (PAD). RESULTS: Patients with PAD have significantly high triglyceride levels. HDL2 and HDL3 levels were found significantly reduced in patients with PAD. Also, the ratio HDL2-C/HDL3-C was significantly reduced in patients with PAD. CONCLUSIONS: The aim of the present study is to provide additional support to the hypothesis that the determination of HDL subfractions could be useful to elucidate possible mechanism(s) for a better assessment of the risk profile for PAD.