PubMed Health⌕ Search

Biomedical subjects

D Sorrentino

Publications and source records attributed to D Sorrentino.

At least 19 recordsLinked to original sources
PubMed2004

Cavernous transformation of the portal vein associated to multiorgan developmental abnormalities.

Initial diagnosis of cavernous transformation of the portal vein (portal cavernoma) is rarely made in adults. Its main clinical manifestation is upper gastrointestinal hemorrhage due to variceal bleeding. More rarely, diagnosis is made from obstructive jaundice. In children, this condition is frequently associated to prehepatic portal hypertension and congenital anomalies, the most frequent of which are atrial septal defects or malformations of the biliary tract or of the inferior vena cava. We describe here a case of a 23-year-old female presenting with massive hematemesis due to the presence of esophageal and small intestinal varices. She had a cavernous transformation of the portal vein with prehepatic portal hypertension associated with heretofore unreported malformations such as right pulmonary hypoplasia, cardiac dextroposition, and right renal ectopia. A unifying hypothesis (e.g. an intrauterine vascular insult) to explain the pathogenesis of these defects seems unlikely. Appropriate tests failed to identify specific functional abnormalities in these organs. Although she bled more than once, the combination of sclerotherapy and beta-blockers has been, thus far, able to control the major clinical consequences of this disease.

Abnormalities, Multiple↗
PubMed2000

Gastric mucosa as an additional extrahepatic localization of hepatitis C virus: viral detection in gastric low-grade lymphoma associated with autoimmune disease and in chronic gastritis.

The hepatitis C virus (HCV) has been linked to B-cell lymphoproliferation and autoimmunity, and has been localized in several tissues. The clinical observation of an HCV-infected patient with Sjögren's syndrome (SS) and Helicobacter pylori (HP) positive gastric low-grade B-cell non-Hodgkin's lymphoma (NHL), which did not regress after HP eradication, led us to investigate the possible localization of HVC in the gastric microenvironment. HCV genome and antigens were searched in gastric biopsy specimens from the previously mentioned case, as well as from 9 additional HCV-infected patients (8 with chronic gastritis and 1 with gastric low-grade B-cell NHL). HCV-specific polymerase chain reaction (PCR) and immunohistochemistry procedures were used. The gastric B-cell NHL from the patient with SS was characterized by molecular analyses of B-cell clonality. HCV RNA was detected in both the gastric low-grade B-cell NHL and in 3 out of 6 gastric samples from the remaining cases. HCV antigens were detected in the residual glandular cells within the gastric B-cell NHL lesions, in glandular cells from 2 of the 3 additional gastric lesions that were HCV positive by PCR, and in 1 additional chronic gastritis sample in which HCV-RNA studies could not be performed. By molecular analyses, of immunoglobulin genes, the B-cell NHL from the patient with SS was confirmed to be a primary gastric lymphoma, subjected to ongoing antigenic stimulation and showing a significant similarity with rheumatoid factor (RF) and anti-HCV- antibody sequences. Our results show that HCV can localize in the gastric mucosa.

Aged↗
PubMed2000

Scientific publications in gastroenterology and hepatology in Western Europe, USA and Japan in the years 1992-1996: a global survey.

AIM: To evaluate number and quality of publications in gastroenterology, hepatology and digestive endoscopy from Western Europe (Belgium, Denmark, France, Germany, Great Britain, Italy, the Netherlands, Spain, Sweden, Switzerland), Japan and USA over a recent 5-year period. METHODS: We screened by computer for full liver/gastrointestinal-related articles and reviews the top 40% of journals (according to the annual rating of the SCI Journal Citation Reports; Institute for Scientific Information database) in most clinical and basic science disciplines in the years 1992-1996. To be credited with an article, a given country had to be the site of the first institution where the work was conducted. Papers were rated according to the impact factor of the Institute for Scientific Information and to the ratio impact factor/mean European impact factor. Data were also normalized for nondefense research and development expenditure. RESULTS AND CONCLUSIONS: As randomly tested, the computer search had an error of +/- 5-10%. In Europe, Great Britain achieved the highest total impact factor and the highest number of papers. Most of the British impact factor came from publications in British journals. The total USA impact factor exceeded that of Europe by 20%. The average impact factor for a single paper was highest for the USA and, in Europe, for Germany. The temporal trend of total impact factor showed Spain improving by 9% per year, with Germany and Italy also displaying a substantial growth. Expressed per funds allocated in nondefense research and development, Great Britain and the USA had the highest cumulative impact factor.

Data Collection↗
PubMed1999

Colorectal cancer screening in Italy: feasibility and cost-effectiveness in a model area.

OBJECTIVE: To evaluate the feasibility and cost-effectiveness of screening programmes for colorectal cancer in Italy. DESIGN; We compared five types of programmes: annual faecal occult blood testing, sigmoidoscopy (every 5 years), faecal occult blood testing plus sigmoidoscopy (every 1 and 5 years), colonoscopy (every 10 years) (all in the age group 55-69 years, last examination at 70 years) and 'filter' colonoscopy. The latter had to be performed in persons at 50 years of age and repeated every 10 years until the age of 70. Costs for the tests and colon cancer care were paid by the Regional Health Office to the hospitals performing the procedures/treatments. SETTING: Data were applied to a small model area in northern Italy (Gemona, 80,000 inhabitants) with well-known demographic (age distribution) and epidemiological (colon cancer incidence) features. RESULTS: All-inclusive 10-year costs per screenee and per death prevented (in US dollars) were: 965 and 77,200 for faecal occult blood testing; 436 and 15,500 for sigmoidoscopy; 1521 and 35,000 for sigmoidoscopy plus faecal occult blood testing; 510 and 15,100 for colonoscopy; 510 and 14,000 for 'filter' colonoscopy. With 'filter' colonoscopy the programme required 870 colonoscopies per year, while with colonoscopy 13,700 colonoscopies were needed at time zero. CONCLUSIONS: In Italy, screening programmes based on sigmoidoscopy/colonoscopy are more cost effective than those based on faecal occult blood testing. 'Filter' colonoscopy at age 50 appears superior to the other types of endoscopy-based screening programmes because it utilizes, at any point in time, a much smaller fraction of available resources.

Colonic Neoplasms↗
PubMed1999

Family burden and coping strategies in schizophrenia: are key relatives really different to other relatives?

Subjective and objective burden, psychiatric symptoms and coping strategies in a sample of 90 key relatives and other relatives of patients with schizophrenia, living in two European countries, were explored by means of well-validated questionnaires. The levels of burden on key relatives did not differ significantly from those on other relatives. Moreover, the risk of developing psychiatric symptoms was similar in the two subject groups at both centres. Significant correlations were found between key relatives and other relatives concerning the adoption of emotion-focused coping strategies. These data contrast with the current belief that family burden in schizophrenia is mainly a burden of key relatives, and they emphasize the need to provide supportive interventions for as many relatives as possible.

Adaptation, Psychological↗
PubMed1998

Helicobacter pylori infection and autoimmune processes: an emerging field of study.

Evidence is accumulating that Helicobacter pylori infection may be closely associated with autoimmunity. However, whether autoimmunity plays a causal role in the pathogenesis of some of the diseases attributed to this bacterium or whether it is rather an epiphenomenon remains to be determined. In this brief review, a summary is made of current knowledge regarding the potential general mechanisms by which Helicobacter pylori causes mucosal damage. A review is then made of the evidence linking this bacterium to the production of different gastric autoantibodies. Finally, the reported association between Helicobacter pylori infection and some known autoimmune diseases is discussed. Although the data are still not sufficiently complete to draw definite conclusions, autoimmunity appears to be an important aspect of this infection and will certainly become a major field of study in the next few years.

Antigens, Bacterial↗
PubMed1997

Characterization of prelymphomatous stages of B cell lymphoproliferation in Sjögren's syndrome.

OBJECTIVE: To determine whether the prelymphomatous stages of B cell lymphoproliferation in Sjögren's syndrome (SS) may be better characterized by the integration of clinical, pathologic, and molecular data, the latter focusing on the expansion, persistence, and dissemination of clonal B cells in the course of the disease. METHODS: Multiple tissue lesions (synchronous from different tissues and metachronous from the same tissue) were evaluated in biopsy specimens obtained from 6 consecutive patients with SS who had an associated lymphoproliferative disorder. Fully benign gastric lesions were evaluated in tissue from an additional 11 patients with SS who had no associated lymphoproliferative disorder. Multiple and complementary molecular analyses of B cell clonality were used: Southern blot, polymerase chain reaction, single-strand conformation polymorphism, DNA sequencing, and hybridization with clonospecific oligoprobes. All the patients were then strictly followed up for the appearance of lymphoma. RESULTS: Different scenarios of SS-associated B cell lymphoproliferation were identified: 1) the ongoing expansion of the same dominant clone, localized or disseminated, in tissue from 2 patients, 1 of whom later developed an overt B cell lymphoma; 2) different dominant clones in different synchronous or metachronous tissues from the remaining 4 patients with an associated lymphoproliferative disorder; and 3) small oligoclonal expansions in 7 of the 11 benign gastric lymphoid infiltrates. CONCLUSION: Prelymphomatous B cell lymphoproliferation in SS was better characterized following integration of the findings. The different types of B cell clonal expansion (oligoclonal or monoclonal, smaller or larger in size, fluctuating or established, localized or disseminated) may imply a different risk of lymphoma progression. An accurate clinical, histopathologic, and molecular characterization may therefore be crucial in future studies aimed at clarifying the pathobiology of SS-associated lymphoproliferation.

Adult↗
PubMed1997

Gastric B-cell clonal expansion and Helicobacter pylori infection in patients with autoimmune diseases and with dyspepsia. A follow-up study.

BACKGROUND: It is not clear whether gastric B-cell clonal expansion, a possible precursor of mucosa-associated lymphatic tissue (MALT) lymphoma, is exclusively linked to Helicobacter pylori infection and virulence. METHODS: In this study we followed up, for up to 33 months, 16 VDJ polymerase chain reaction-positive patients (4 with dyspepsia, 9 with Sjögren's syndrome, and 3 with other autoimmune diseases). Of these, 12 were H. pylori-positive. In addition, in H. pylori-positive patients we tested whether the serum anti-cag-A (a potential marker of virulence) was preferentially associated with B-cell clonality. RESULTS: In all but one patient clonality appeared temporally unrelated to H. pylori infection. The prevalence of anti-cagA was not higher in H. pylori/VDJ-positive patients than in controls. CONCLUSIONS: These data indicate that, in addition to H. pylori, gastric B-cell clonality may be sustained by other agents/mechanisms. Anti-cag-A does not appear to be involved in the pathogenesis of clonality.

Adult↗
PubMed1996

Hepatocellular sulfobromophthalein uptake at physiologic albumin concentrations: kinetic evidence for a high affinity/low capacity sinusoidal membrane system.

BACKGROUND/AIMS: Controversy exists regarding the nature of the hepatocyte membrane transport system for sulfobromophthalein and other organic anions and its driving forces. Most studies have been performed in the absence of albumin, the plasma sulfobromophthalein binding protein, or using very low albumin concentrations. We have shown that in the latter case uptake kinetics reflect dissociation/diffusion events and not membrane transport. In contrast, without albumin very high sulfobromophthalein concentrations reach the cell surface and may overwhelm a high affinity/low capacity system operating in vivo. The aim of this study was to test the latter hypothesis. METHODS: Sulfobromophthalein uptake was measured by rapid filtration in isolated hepatocytes without albumin (up to 13 microM sulfobromophthalein) and with 600 microM albumin (sulfobromophthalein:albumin from 0.03:1 to 1:1), a physiologic setting which greatly reduces the unbound BSP concentration. Unbound sulfobromophthalein concentration was estimated according to a three binding site model. RESULTS: In the absence of albumin, kinetic parameters for sulfobromophthalein uptake were similar to those reported in the literature (K(m):7.1 +/- 1.2 microM; V(max): 452 +/- 37 pmol/min/5 x 10(4) cells). In the presence of albumin, sulfobromophthalein uptake displayed much greater affinity and much lower capacity (K(m): 80 +/- 11 nM; V(max): 60 +/- 9 pmol/min/5 x 10(4) cells). CONCLUSIONS: These findings suggest that in the absence of albumin, resulting high sulfobromophthalein concentrations overload (and make undetectable) a high affinity/low capacity system operating at physiologic albumin concentrations (i.e. at low unbound sulfobromophthalein concentrations). Previously characterized transport systems may be operating only under defined conditions. These findings could explain the apparent controversy regarding the nature of the sulfobromophthalein transport system and its driving forces.

Animals↗
PubMed1996

Widespread clonal B-cell disorder in Sjögren's syndrome predisposing to Helicobacter pylori-related gastric lymphoma.

Helicobacter pylori has been identified as a critical antigenic stimulus to the development of gastric lymphoma, but additional factors should be required for such evolution. This topic is now of major importance to clarify the pathobiology of gastric lymphomagenesis. Peculiar autoimmune diseases, such as Sjögren's syndrome, are well known to predispose to B-cell lymphomas. We report on a patient with Sjögren's syndrome and a widespread B-cell lymphoproliferative disorder. A pathological picture of low-grade lymphoma was observed in the stomach, concomitantly with H. pylori infection. However, the B-cell disorder was definitely nonmalignant in the other tissues involved, i.e., the parotid gland and lymph nodes, which are the characteristic targets of Sjögren's syndrome-associated lymphoproliferation. After H. pylori eradication, a dramatic regression of gastric lymphoma into chronic gastritis was observed, but no amelioration occurred in the parotid and nodal involvement. Multiple molecular analyses showed the expansion of the same B-cell clone in synchronous and metachronous lymph node, parotid, and gastric lesions before and after H. pylori eradication. Thus, H. pylori played a crucial role in the local boosting of B-cell lymphoproliferation, but the underlying B-cell disorder was that associated with the autoimmune disease and was nonmalignant. The comprehensive clinical, pathological, and molecular approach allowed us to then distinguish the role of peculiar individual predisposing factors and of local infection in the pathobiology of mucosa-associated lymphoid tissue-associated lymphoproliferation.

Aged↗
PubMed1996

B cell clonality in gastric lymphoid tissues of patients with Sjögren's syndrome.

OBJECTIVE: To determine the prevalence of mucosa associated lymphoid tissue (MALT) in the stomach and of a possible antigen driven proliferation, in patients with Sjögren's syndrome (SS). METHODS: Twenty one patients with primary SS and 80 dyspeptic controls underwent upper endoscopy. Lymphoid tissue and Helicobacter pylori were assessed by histopathological analysis. Epstein-Barr virus (EBV) or human herpes virus-6 (HHV-6) genome were studied by polymerase chain reaction (PCR) DNA amplification. Two PCR VDJ procedures were used to detect immunoglobulin heavy chain (IgH) gene rearrangement. RESULTS: Organised MALT was found in 33.3% of the patients, compared with 21.5% of the controls (NS). H pylori infection was seen in 71% of patients and 63% of controls. Genomic EBV or HHV-6 was found in a minor portion of SS gastric tissues. B cell expansion was detected in nine of the 21 patients. Infectious agents in the stomach might have contributed to B cell clonality only in 55.5% of the cases. No strict relationship was found between lymphoid follicles and clonality. CONCLUSION: Lymphoid accumulation in the gastric mucosa is common in Sjögren's syndrome, but full evidence for an antigen driven B cell expansion could not be demonstrated. Only a portion of those with clonal B cell expansion had evidence of an infectious agent. Other unknown infectious agents or factors related to the underlying disease (autoantigen) and its tissue environment may have a further role as possible causes of B clonal expansion in the gastric mucosa.

Adult↗
PubMed1996

B-cell clonality and infection with Helicobacter pylori: implications for development of gastric lymphoma.

BACKGROUND: Although Helicobacter pylori has been implicated in the pathogenesis of gastric mucosa associated lymphoid tissue (MALT) and MALT lymphoma, it is not known how it may trigger these lesions and whether there is an identifiable pre-neoplastic stage. AIMS: To investigate the relation between MALT, H pylori infection, and B-cell clonality (a potential marker of pre-neoplastic lesions). PATIENTS: 141 subjects with simple dyspepsia. METHODS: Gastric biopsy specimens from all patients were examined for MALT and H pylori. Of these, 25 consecutive MALT positive specimens were scored for features of MALT lymphoma and VDJ clonality studied by polymerase chain reaction. RESULTS: Overall, prevalence was 62% for H pylori and 46% for MALT. VDJ clonality was frequent in the sub-group studied (nine of 25), mostly associated with lymphoid follicles (eight of nine or 89%), and with a high scoring for MALT lymphoma. VDJ clonality was equally frequent in patients with and without H pylori (seven of 20 and two of five or 35% and 40% respectively). CONCLUSIONS: B-cell clonality is unexpectedly common in subjects with simple dyspepsia and MALT raising clinical management questions. These findings also suggest that the cascade MALT formation--B-cell clonality--MALT lymphoma may not be uniquely associated with H pylori infection.

Adolescent↗
PubMed1996

Oleate uptake by isolated hepatocytes and the perfused rat liver is competitively inhibited by palmitate.

Competition for uptake between long-chain free fatty acids has been difficult to document, because there has been no algorithm for computing unbound concentrations of two fatty acids simultaneously in solution with albumin. We modified an iterative procedure to permit this computation and studied initial [3H]oleate uptake by isolated hepatocytes and steady-state uptake by the single-pass perfused rat liver from 600 microM bovine serum albumin solutions containing various concentrations of oleate in the presence and absence of palmitate. In both systems, the Michaelis-Menten constant was significantly higher in the presence of palmitate than in its absence, whereas the maximal reaction velocity was unaltered, indicating competitive inhibition. In additional experiments employing the multiple transhepatic indicator-dilution technique, the influx rate constant and permeability-surface area product for oleate influx were significantly reduced by palmitate, confirming that the competition observed in the conventional perfused liver studies was at the influx step. Long-chain fatty acid uptake has now been shown to exhibit all the kinetic properties of facilitated transport and cannot be attributed solely to passive diffusion.

Animals↗
PubMed1994

The hepatocellular uptake of free fatty acids is selectively preserved during starvation.

BACKGROUND/AIMS: The liver loses protein during fasting. This study sought to determine if hepatic protein loss during fasting selectively preserves functions important to survival such as uptake of fatty acids, which are major energy substrates in that condition. METHODS: Initial [3H]oleate uptake and efflux rates in hepatocytes from starved (for 48 hours) and fed male rats were measured in media containing 250 mumol/L albumin at oleate/albumin ratios of 0.2:1-2:1. Uptake rates of sulfobromophthalein, taurocholate, and glucose were also determined. RESULTS: Initial oleate uptake rate was saturable with respect to unbound oleate concentration. Maximum initial velocity expressed per cell number did not differ between fasted and fed animals, but measured cell volume and estimated surface area were decreased in starved vs. fed hepatocytes (921 +/- 21 vs. 1623 +/- 58 microns2, respectively; P < 0.001). Consequently, when expressed per surface area, maximum initial velocity was greater in starved cells (17 +/- 3 vs. 10 +/- 2 [pmol.min-1.micron2] x 10(-7); P < 0.02). Expressed similarly, oleate efflux was also greater from starved hepatocytes and was inhibited by an antibody to plasma membrane fatty acid binding protein (FABPpm). FABPpm concentration per unit area of plasma membrane also increased in starved hepatocytes (P < 0.05). By contrast, uptake rates of sulfobromophthalein, taurocholate, and glucose by starved hepatocytes were decreased when expressed per cell number and unchanged per unit area. CONCLUSIONS: During fasting, the hepatocellular uptake mechanism for oleate is selectively preserved compared with those for sulfobromophthalein, taurocholate, or glucose.

Animals↗
PubMed1994

Oleate uptake kinetics in the perfused rat liver are consistent with pseudofacilitation by albumin.

We measured uptake of a representative free fatty acid, oleate, by the single-pass perfused rat liver at oleate:albumin molar ratios of 0.01 to 2:1. For each ratio, uptake was studied at albumin concentrations from 50 to 600 microM. When uptake velocity was plotted as a function of the albumin concentration, the data at each ratio exhibited a pseudosaturation pattern as previously observed in isolated cells (J Clin Invest 84: 1325). At a physiologic albumin concentration of 600 microM, a plot of uptake vs. unbound oleate concentrations was best fitted by the Michaelis-Menten equation (Vmax = 235 +/- 8.8 nmol.min-1.g.liver-1; Km = 130 +/- 12 nM). As the albumin concentration was increased from 50 to 250 microM, the unbound oleate clearance, calculated by either the undistributed sinusoidal or venous equilibrium models, increased progressively, in violation of conventional pharmacokinetic theory, indicating an enhancing effect of albumin on ligand uptake at low albumin concentrations. In contrast, there was no significant difference between measures of unbound clearance at albumin concentrations of 350 and 600 microM. To explain this phenomenon, the clearance data were examined for evidence of facilitation (accelerated dissociation of ligand:albumin complexes) by the clearance ratio test ("square root rule"). All deviations from the predictions of conventional theory were entirely attributable to pseudofacilitation. No data required explanation by a true facilitation model.

Animals↗