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1.
  • Amin, Kawa, et al. (författare)
  • Autoantibody profiles in autoimmune hepatitis and chronic hepatitis C identifies similarities in patients with severe disease
  • 2017
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327 .- 2219-2840. ; 23:8, s. 1345-1352
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: To determine how the auto-antibodies (Abs) profilesoverlap in chronic hepatitis C infection (CHC) andautoimmune hepatitis (AIH) and correlate to liverdisease.METHODS: Levels of antinuclear Ab, smooth muscle antibody (SMA)and liver/kidney microsomal-1 (LKM-1) Ab and markersof liver damage were determined in the sera of 50 patients with CHC infection, 20 AIH patients and 20healthy controls using enzyme linked immunosorbentassay and other immune assays. RESULTS: We found that AIH patients had more severe liverdisease as determined by elevation of total IgG,alkaline phosphatase, total serum bilirubin and serumtransaminases and significantly higher prevalence ofthe three non-organ-specific autoantibodies (auto-Abs)than CHC patients. Antinuclear Ab, SMA and LKM-1 Abwere also present in 36% of CHC patients and relatedto disease severity. CHC cases positive for auto-Abswere directly comparable to AIH in respect of mostmarkers of liver damage and total IgG. These caseshad longer disease duration compared with auto-Abnegative cases, but there was no difference in gender,age or viral load. KLM-1+ Ab CHC cases showed bestoverlap with AIH. CONCLUSION: Auto-Ab levels in CHC may be important markers ofdisease severity and positive cases have a diseasesimilar to AIH. Auto-Abs might have a pathogenic roleas indicated by elevated markers of liver damage.Future studies will unravel any novel associationsbetween these two diseases, whether genetic or other.
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2.
  • Bergquist, Annika, et al. (författare)
  • Perinatal events and the risk of developing primary sclerosing cholangitis
  • 2006
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327 .- 2219-2840. ; 12:37, s. 6037-6040
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: To investigate whether perinatal events, intrauterine or postpartum, are associated with the development of primary sclerosing cholangitis (PSC) later in life.METHODS: Birth records from 97 patients with adult PSC in Sweden were reviewed. Information on perinatal events including medications and complications during pregnancy, gestation length, birth weight and length were collected. Two control children of the same sex were selected for each subject. Conditional multiple logistic regression was used to assess associations of the perinatal measures with development of PSC.RESULTS: No significant associations were found between gestational age, birth length, breastfeeding, and the majority of medical complications including infections or medication during pregnancy for the mothers or postpartum for the children. Vaginal bleeding and peripheral oedema showed associations with PSC, with matched odds ratios of 5.70 (95% CI, 1.13-28.83) and 2.28 (95% CI, 1.04-5.03), respectively. CONCLUSION: The associations of vaginal bleeding and oedema with subsequent PSC cannot readily be explained, so our findings do not strongly support the hypothesis of a significant role of perinatal events as a risk for the development of PSC later in life.
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3.
  • Gao, Jingfang, et al. (författare)
  • Relationships of tumor inflammatory infiltration and necrosis with microsatellite instability in colorectal cancers
  • 2005
  • Ingår i: World Journal of Gastroenterology. - 1007-9327. ; 11:14, s. 2179-2183
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: The relationships between microsatellite instability (MSI) and survival in colorectal cancer patients are not consistent. The favorable survival of patient with MSI has been suggested to be related to pronounced inflammatory infiltration; however, the reason for non-association of MSI with survival is unclear. Our aims were to investigate the associations of inflammatory infiltration and tumor necrosis (TN) with microsatellite status and clinicopathological factors in colorectal cancer patients in whom MSI was not related to survival. Methods: Three hundred and one colorectal adenocar-cinomas were evaluated for inflammatory infiltration and 300 for TN under light microscope. Results: Low infiltration at invasive margin (c2 = 3.94, P = 0.047) and in whole tumor stroma (c2 = 3.89, P = 0.049) was associated with MSI, but TN was not (c2 = 0.10, P = 0.75). Low infiltration was related to advanced stage (c2 = 8.67, P = 0.03), poorer differentiation (c2 = 8.84, P = 0.03), DNA non-diploid (c2 = 10.04, P = 0.002), higher S-phase fraction (c2 = 11.30, P = 0.004), positive p53 expression (c2 = 7.94, P = 0.01), and worse survival (P = 0.03 for both univariate and multivariate analyses). Abundant TN was related to advanced stage (c2 = 17.74, P = 0.001) and worse survival (P = 0.02 for univariate, and P = 0.05 for multivariate analysis). Conclusion: The result that high inflammatory infiltration was not related to MSI might help explain the non-association of MSI with survival in colorectal cancer patients.
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4.
  • He, Lu-Jun, et al. (författare)
  • Genetic polymorphisms of N-acetyltransferase 2 and colorectal cancer risk.
  • 2005
  • Ingår i: World Journal of Gastroenterology. - 1007-9327 .- 2219-2840. ; 11:27, s. 4268-4271
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: To identify the distribution of N-acetyltrasferase 2(NAT2) polymorphism in Hebei Han Chinese and the effects of the polymorphism on the development of colorectal cancer. METHODS: We performed a hospital-based case-control study of 237 healthy individuals and 83 colorectal cancer patients of Hebei Han Chinese. DNA was extracted from peripheral blood and cancer tissues. The genotypes of the polymorphisms were assessed by PCR-restriction fragment length polymorphism (RFLP). RESULTS: There were four NAT2 alleles of WT, M1, M2, and M3 both in the healthy subjects and in the patients, and 10 genotypes of WT/WT, WT/M1, WT/M2, WT/M3, M1/M1, M1/M2, M1/M3, M2/M2, M2/M3, M3/M3. M2 allele was present in 15.61% of healthy subjects and 29.52% of patients (chi(2) = 15.31, P<0.0001), and M3 allele was present in 30.59% of healthy subjects and 16.87% of patients (chi(2) = 25.33, P<0.0001). There were more WT/M2 (chi(2) = 34.42, P<0.0001, odd ratio = 4.99, 95%CI = 2.27-9.38) and less WT/M3 (chi(2) = 3.80, P = 0.03) in the patients than in the healthy subjects. In 70.3% of the patients, there was a difference in NAT2 genotype between their tumors and blood cells. Patients had more WT/M2 (chi(2) = 5.11, P = 0.02) and less M2/M3 (chi(2) = 4.27, P = 0.039) in their blood cells than in the tumors. Furthermore, 53.8% (7/13) of M2/M3 in tumors were from WT/M2 of blood cells. CONCLUSION: There is a possible relationship between the NAT2 polymorphisms and colorectal cancer in Hebei Han Chinese. The genotype WT/M2 may be a risk factor for colorectal cancer.
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6.
  • Ogren, M., et al. (författare)
  • Portal vein thrombosis: prevalence, patient characteristics and lifetime risk: a population study based on 23,796 consecutive autopsies
  • 2006
  • Ingår i: World J Gastroenterol. - 1007-9327 .- 2219-2840. ; 12:13, s. 2115-9
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: To assess the lifetime cumulative incidence of portal venous thrombosis (PVT) in the general population. METHODS: Between 1970 and 1982, 23,796 autopsies, representing 84% of all in-hospital deaths in the Malmo city population, were performed, using a standardised protocol including examination of the portal vein. PVT patients were characterised and the PVT prevalence at autopsy, an expression of life-time cumulative incidence, assessed in high-risk disease categories and expressed in terms of odds ratios and 95% CI. RESULTS: The population prevalence of PVT was 1.0%. Of the 254 patients with PVT 28% had cirrhosis, 23% primary and 44% secondary hepatobiliary malignancy, 10% major abdominal infectious or inflammatory disease and 3% had a myeloproliferative disorder. Patients with both cirrhosis and hepatic carcinoma had the highest PVT risk, OR 17.1 (95% CI 11.1-26.4). In 14% no cause was found; only a minority of them had developed portal-hypertension-related complications. CONCLUSION: In this population-based study, PVT was found to be more common than indicated by previous clinical series. The markedly excess risk in cirrhosis and hepatic carcinoma should warrant an increased awareness in these patients for whom prospective studies of directed intervention might be considered.
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7.
  • Ren, J, et al. (författare)
  • Expression of sphingosine kinase gene in the interactions between human gastric carcinoma cell and vascular endothelial cell
  • 2002
  • Ingår i: World Journal of Gastroenterology. - 1007-9327. ; 8:4, s. 602-607
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: To study the interactions between human gastric carcinoma cell (HGCC) and human vascular endothelial cell (HVEC), and if the expression of sphingosine kinase (SPK) gene was involved in these interactions. METHODS: The specific inhibitor to SPK, dimethyl sphingosine (DMS), was added acting on HGCC and HVEC, then the cell proliferation was measured by MTT. The conditioned mediums (CMs) of HGCC and HVEC were prepared. The CM of one kind of cell was added to the other kind of cell, and the cell proliferation was measured by MTT. After the action of CM, the cellular expression of SPK gene in mRNA level was detected with in situ hybridization (ISH). RESULTS: DMS could almost completely inhibit the proliferation of HGCC and HVEC. The growth inhibitory rates could amount to 97.21%, 83.42%, respectively (P<0.01). The CM of HGCC could stimulate the growth of HVEC (2.70 +/- 0.01, P<0.01) while the CM of HVEC could inhibit the growth of HGCC (52.97 +/- 0.01%, P<0.01). There was no significant change in the mRNA level of SPK gene in one kind of cell after the action of the CM of the other kind of cell. CONCLUSION: SPK plays a key role in regulating the proliferation of HGCC and HVEC. There exist complicated interactions between HGCC and HVEC. HGCC can significantly stimulate the growth of HVEC while HVEC can significantly inhibit the growth of HGCC. The expression of SPK gene is not involved in the interactions.
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8.
  • Ren, J, et al. (författare)
  • The role of KDR in the interactions between human gastric carcinoma cell and vascular endothelial cell
  • 2002
  • Ingår i: World Journal of Gastroenterology. - 1007-9327. ; 8:4, s. 596-601
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM:To study the interactions between human gastric carcinoma cell (HGCC) and human vascular endothelial cell (HVEC), and the role of KDR in these interactions. METHODS:Antisense oligodexynucleotide(ASODN) specific to KDR gene was devised and added to the culture medium of HGCC and HVEC. After the action of ASODN, the proliferation of two cells was measured by MTT method. The role of KDR in regulating the proliferation of two kinds of cells was known through observing the effect of ASODN on them. The conditioned mediums (CMs) of HGCC and HVEC were prepared. The CM of one kind of cell was added acting on the other kind of cell, then the cell proliferation was measured by MTT. After the action of ASODN or CM, the cellular expression of KDR gene was detected with in situ hybridization(ISH) for mRNA level and with immunohistochemical staining for protein level. ABC-ELISA was used to detect hVEGF in the CMs of two cells. RESULTS: KDR ASODN could specifically inhibit the proliferation of HGCC and HVEC significantly. The growth inhibitory rate amounted to 55.35 % and 54.83 %, respectively (P <0.01). HGCC and HVEC could secret a certain level of hVEGF(92.06 +/- 1.69 ng/L, 77.70 +/- 8.04 ng/L. The CM of HGCC could significantly stimulate the growth(2.70 +/- 0.01 times) and KDR gene expression of HVEC( P<0.01) while the CM of HVEC could significantly inhibit the growth(52.97 +/- 0.01%) and KDR gene expression of HGCC (P <0.01). CONCLUSION: KDR plays a key role in regulating the proliferation of HGCC and HVEC. There exist complicated interactions between HGCC and HVEC. HGCC can significantly stimulate the growth of HVEC while HVEC can significantly inhibit the growth of HGCC. KDR is involved in the interactions between them.
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9.
  • Wagner, Michael, 1957-, et al. (författare)
  • Fecal markers of inflammation used as surrogate markers for treatment outcome in relapsing inflammatory bowel disease
  • 2008
  • Ingår i: World Journal of Gastroenterology. - : WJG Press. - 1007-9327 .- 2219-2840. ; 14:36, s. 5584-5589
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims: To evaluate fecal calprotectin (FC) as a surrogate marker for treatment outcome of a relapse of inflammatory bowel disease (IBD) and, secondly, to compare FC to fecal myeloperoxidase (MPO) and fecal eosinophil protein X (EPX). Methods: Thirty-eight patients with IBD, whereof twenty-seven with ulcerative colitis (UC) and 11 with Crohn´s disease (CD) were studied before treatment (inclusion), and after four and eight weeks of treatment. Treatment outcome, based on clinical activity and endoscopy in UC patients, and clinical activity in CD patients, were evaluated together with fecal samples analysed for FC with ELISA and MPO and EPX with RIA. Results: At inclusion 37/38 (97%) patients had elevated FC levels (>94.7 µg/g). At the end of the study 31/38 (82%) patients fulfilled predefined criteria of a complete response [UC 21/27 (78%); CD 10/11 (91%)].  Overall, a normalised FC level at the end of the study predicted a complete response in 100% whereas elevated FC level predicted noncomplete response in 30%. Normalised MPO or EPX levels predicted a complete response in 100% and 90%, respectively. However, elevated MPO or EPX levels predicted noncomplete response in 23% and 22%, respectively. Conclusion: A normalised FC level poses the potential to be used as a surrogate marker for successful treatment outcome in IBD patients, but cases with persistent elevated FC levels needs further evaluation. FC and MPO appears to discriminate better than EPX to treatment outcome in IBD.
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11.
  • Vaz, Juan, et al. (författare)
  • Intervention on toll-like receptors in pancreatic cancer
  • 2014
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327. ; 20:19, s. 5808-5817
  • Forskningsöversikt (refereegranskat)abstract
    • Pancreatic ductal adenocarcinoma (PDA) is a devastating disease with pronounced morbidity and a high mortality rate. Currently available treatments lack convincing cost-efficiency determinations and are in most cases not associated with relevant success rate. Experimental stimulation of the immune system in murine PDA models has revealed some promising results. Toll-like receptors (TLRs) are pillars of the immune system that have been linked to several forms of malignancy, including lung, breast and colon cancer. In humans, TLRs are expressed in the pancreatic cancer tissue and in several cancer cell lines, whereas they are not expressed in the normal pancreas. In the present review, we explore the current knowledge concerning the role of different TLRs associated to PDA. Even if almost all known TLRs are expressed in the pancreatic cancer microenvironment, there are only five TLRs suggested as possible therapeutic targets. Most data points at TLR2 and TLR9 as effective tumor markers and agonists could potentially be used as e.g. future adjuvant therapies. The elucidation of the role of TLR3 in PDA is only in its initial phase. The inhibition/blockage of TLR4-related pathways has shown some promising effects, but there are still many steps left before TLR4 inhibitors can be considered as possible therapeutic agents. Finally, TLR7 antagonists seem to be potential candidates for therapy. Independent of their potential in immunotherapies, all existing data indicate that TLRs are strongly involved in the pathophysiology and development of PDA.
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12.
  • Jiang, Jing-Ting, et al. (författare)
  • Metabolism of high density lipoproteins in liver cancer
  • 2007
  • Ingår i: World Journal of Gastroenterology. - 1007-9327. ; 13:23, s. 3159-3163
  • Forskningsöversikt (refereegranskat)abstract
    • Liver plays a vital role in the production and catabolism of plasma lipoproteins. It depends on the integrity of cellular function of liver, which ensures homeostasis of lipid and lipoprotein metabolism. When liver cancer occurs these processes are impaired and high-density lipoproteins are changed. (C) 2007 The WJG Press. All rights reserved.
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13.
  • Aabenhus, Rune, et al. (författare)
  • First attempt to produce experimental Campylobacter concisus infection in mice
  • 2008
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327. ; 14:45, s. 6954-6959
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: To infect mice with atypical Campylobacter concisus (C concisus) for the first time. METHODS: Three separate experiments were conducted in order to screen the ability of five clinical C concisus isolates of intestinal origin and the ATCC 33237 type strain of oral origin to colonize and produce infection in immunocompetent BALB/cA mice. The majority of the BALB/cA mice were treated with cyclophosphamide prior to C concisus inoculation to suppress immune functions. Inoculation of C concisus was performed by the gastric route. RESULTS: C concisus was isolated from the liver, ileum and jejunum of cyclophosphamide-treated mice in the first experiment. No C concisus strains were isolated in the two subsequent experiments. Mice infected with C concisus showed a significant loss of body weight from day two through to day five of infection but this decreased at the end of the first week. Histopathologicalexamination did not consistently find signs of inflammation in the gut, but occasionally microabscesses were found in the liver of infected animals. CONCLUSION: Transient colonization with C concisus was observed in mice with loss of body weight. Future studies should concentrate on the first few days after inoculation and in other strains of mice. (C) 2008 The WJG Press. All rights reserved.
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15.
  • Acosta, Stefan (författare)
  • Surgical management of peritonitis secondary to acute superior mesenteric artery occlusion.
  • 2014
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327. ; 20:29, s. 9936-9941
  • Tidskriftsartikel (refereegranskat)abstract
    • Diagnosis of acute arterial mesenteric ischemia in the early stages is now possible using modern computed tomography with intravenous contrast enhancement and imaging in the arterial and/or portal phase. Most patients have acute superior mesenteric artery (SMA) occlusion, and a large proportion of these patients will develop peritonitis prior to mesenteric revascularization, and explorative laparotomy will therefore be necessary to evaluate the extent and severity of intestinal ischemia, and to perform bowel resections. The establishment of a hybrid operating room in vascular units in hospitals is most important to be able to perform successful intestinal revascularization. This review outlines current frontline surgical strategies to improve survival and minimize bowel morbidity in patients with peritonitis secondary to acute SMA occlusion. Explorative laparotomy needs to be performed first. Curative treatment is based upon intestinal revascularization followed by bowel resection. If no vascular imaging has been carried out, SMA angiography is performed. In case of embolic occlusion of the SMA, open embolectomy is performed followed by angiography. In case of thrombotic occlusion, the occlusive lesion can be recanalized retrograde from an exposed SMA, the guidewire snared from either the femoral or brachial artery, and stented with standard devices from these access sites. Bowel resections and sometimes gall bladder removal due to transmural infarctions are performed at initial laparotomy, leaving definitive bowel reconstructions to a planned second look laparotomy, according to the principles of damage control surgery. Patients with peritonitis secondary to acute SMA occlusion should be managed by both the general and vascular surgeon, and a hybrid revascularization approach is of utmost importance to improve outcomes.
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16.
  • Andersen, Vibeke, et al. (författare)
  • Colorectal cancer in patients with inflammatory bowel disease : can we predict risk?
  • 2012
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327 .- 2219-2840. ; 18:31, s. 4091-4094
  • Tidskriftsartikel (refereegranskat)abstract
    • The inflammatory bowel diseases (IBD), Crohn's disease (CD) and ulcerative colitis (UC), may be complicated by colorectal cancer (CRC). In a recent population-based cohort study of 47 347 Danish patients with IBD by Tine Jess and colleagues 268 patients with UC and 70 patients with CD developed CRC during 30 years of observation. The overall risk of CRC among patients with UC and CD was comparable with that of the general population. However, patients diagnosed with UC during childhood or as adolescents, patients with long duration of disease and those with concomitant primary sclerosing cholangitis were at increased risk. In this commentary, we discuss the mechanisms underlying carcinogenesis in IBD and current investigations of genetic susceptibility in IBD patients. Further advances will depend on the cooperative work by epidemiologist and molecular geneticists in order to identify genetic polymorphisms involved in IBD-associated CRC. The ultimate goal is to incorporate genotypes and clinical parameters into a predictive model that will refine the prediction of risk for CRC in colonic IBD. The challenge will be to translate these new findings into clinical practice and to determine appropriate preventive strategies in order to avoid CRC in IBD patients. The achieved knowledge may also be relevant for other inflammation-associated cancers.
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17.
  • Andersson, Bodil, et al. (författare)
  • Pancreatic function, quality of life and costs at long-term follow-up after acute pancreatitis.
  • 2010
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327. ; 16:39, s. 4944-4951
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: To evaluate long-term endocrine and exocrine pancreatic function, quality of life and health care costs after mild acute pancreatitis and severe acute pancreatitis (SAP). METHODS: Patients prospectively included in 2001-2005 were followed-up after 42 (36-53) mo. Pancreatic function was evaluated with laboratory tests, the oral glucose tolerance test (OGTT), fecal elastase-1 and a questionnaire. Short Form (SF)-36, was completed. RESULTS: Fourteen patients with a history of SAP and 26 with mild acute pancreatitis were included. Plasma glucose after OGTT was higher after SAP (9.2 mmol/L vs 7.0 mmol/L, P = 0.044). Diabetes mellitus or impaired glucose tolerance in fasting plasma glucose and/or 120 min plasma glucose were more common in SAP patients (11/14 vs 11/25, P = 0.037). Sick leave, time until the patients could take up recreational activities and time until they had recovered were all longer after SAP (P < 0.001). No significant differences in SF-36 were seen between the groups, or when comparing with age and gender matched reference groups. Total hospital costs, including primary care, follow-up and treatment of complications, were higher after SAP (median €16 572 vs €5000, P < 0.001). CONCLUSION: Endocrine pancreatic function was affected, especially after severe disease. SAP requires greater resource use with long recovery, but most patients regained a good quality of life.
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18.
  • Andersson, Ellen, et al. (författare)
  • Tissue factor in predicted severe acute pancreatitis.
  • 2010
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327. ; 16:48, s. 6128-6134
  • Tidskriftsartikel (refereegranskat)abstract
    • To study tissue factor (TF) in acute pancreatitis and evaluate the role of TF as a predictive marker of severity.
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19.
  • Anlauf, Martin, et al. (författare)
  • Sporadic versus hereditary gastrinomas of the duodenum and pancreas : distinct clinico-pathological and epidemiological features.
  • 2006
  • Ingår i: World Journal of Gastroenterology. - 1007-9327 .- 2219-2840. ; 12:34, s. 5440-6
  • Tidskriftsartikel (refereegranskat)abstract
    • Gastrinomas are defined as gastrin secreting tumors that are associated with Zollinger-Ellison syndrome (ZES). ZES is characterized by elevated fasting gastrin serum levels, positive secretin stimulation test and clinical symptoms such as recurrent peptic ulcer disease, gastroesophageal reflux disease and occasional diarrhea. Genetically, nonhereditary (sporadic) gastrinomas are distinguished from hereditary gastrinomas, which are associated with multiple endocrine neoplasia type 1 (MEN1) syndrome. In general, duodenal gastrinomas are small and solitary if they are sporadic and multiple as well as hereditary. The sporadic gastrinomas occur in the duodenum or in the pancreas while the hereditary gastrinomas almost all occur in the duodenum. Our series of 77 sporadic duodenal neuroendocrine tumors (NETs) includes 18 patients (23.4%) with gastrinomas and ZES. Of 535 sporadic NETs in the pancreas collected from the NET archives of the departments of pathology in Zurich, Switzerland, and Kiel, Germany, 24 patients (4.5%) suffered from sporadic pancreatic gastrinomas and ZES. These NETs have to be distinguished from tumors with immunohistochemical positivity for gastrin but without evidence of ZES. An additional 19 patients suffered from MEN1 and ZES. These patients showed exclusively duodenal gastrinomas, but not pancreatic gastrinomas. The prognosis of sporadic and MEN1-associated duodenal gastrinomas is better than that of pancreatic gastrinomas, since they progress slowly to liver metastasis. In summary, sporadic and MEN1-associated gastrinomas in the duodenum and pancreas show different clinico-pathological and genetic features. The incidence of sporadic duodenal gastrin-producing tumors is increasing, possibly due to optimized diagnostic procedures. In contrast, pancreatic MEN1-associated gastrinomas seem to be extremely rare. A considerable subset of tumors with immunohistochemical expression of gastrin but without evidence of ZES should be designated as functionally inactive NETs expressing gastrin, but not as gastrinomas.
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20.
  • Ansari, Daniel, et al. (författare)
  • Pancreatic cancer: Translational research aspects and clinical implications.
  • 2012
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327. ; 18:13, s. 1417-1424
  • Tidskriftsartikel (refereegranskat)abstract
    • Despite improvements in surgical techniques and adjuvant chemotherapy, the overall mortality rates in pancreatic cancer have generally remained relatively unchanged and the 5-year survival rate is actually below 2%. This paper will address the importance of achieving an early diagnosis and identifying markers for prognosis and response to therapy such as genes, proteins, microRNAs or epigenetic modifications. However, there are still major hurdles when translating investigational biomarkers into routine clinical practice. Furthermore, novel ways of secondary screening in high-risk individuals, such as artificial neural networks and modern imaging, will be discussed. Drug resistance is ubiquitous in pancreatic cancer. Several mechanisms of drug resistance have already been revealed, including human equilibrative nucleoside transporter-1 status, multidrug resistance proteins, aberrant signaling pathways, microRNAs, stromal influence, epithelial-mesenchymal transition-type cells and recently the presence of cancer stem cells/cancer-initiating cells. These factors must be considered when developing more customized types of intervention ("personalized medicine"). In the future, multifunctional nanoparticles that combine a specific targeting agent, an imaging probe, a cell-penetrating agent, a biocompatible polymer and an anti-cancer drug may become valuable for the management of patients with pancreatic cancer.
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21.
  • Ansari, Daniel, et al. (författare)
  • Radiofrequency ablation or percutaneous ethanol injection for the treatment of liver tumors.
  • 2012
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327. ; 18:10, s. 1003-1008
  • Tidskriftsartikel (refereegranskat)abstract
    • The liver is a common location of both primary and secondary malignancies. For unresectable liver cancer, many local ablative therapies have been developed. These include e.g., percutaneous ethanol injection (PEI), percutaneous acetic acid injection, radiofrequency ablation (RFA), cryoablation, microwave ablation, laser-induced thermotherapy, and high-intensity focused ultrasound. RFA has recently gained interest and is the most widely applied thermoablative technique. RFA allows more effective tumor control in fewer treatment sessions compared with PEI, but with a higher rate of complications. However, there are certain circumstances where PEI therapy represents a better strategy to control liver tumors than RFA, especially in situations where RFA is difficult, for example when large vessels surround the tumor. In the context of hepatocellular carcinoma (HCC), both RFA and PEI are feasible and of benefit in non-operable patients. RFA seems superior to PEI in HCC > 2 cm, and the combination of interventions may be of benefit in selected patients. Liver resection is superior to RFA for patients with HCC meeting the Milan criteria, but RFA can be employed in tumors ≤ 3 cm and where there is an increased expected operative mortality. In addition, some lines of evidence indicate that RFA and PEI can be employed as a bridge to liver transplantation. The use of RFA in colorectal liver metastases is currently limited to unresectable disease and for patients unfit for surgery. The aim of this article is to summarize the current status of RFA in the management of liver tumors and compare it to the cheap and readily available technique of PEI.
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22.
  • Ansari, Daniel, et al. (författare)
  • Update on the management of pancreatic cancer: Surgery is not enough.
  • 2015
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327. ; 21:11, s. 3157-3165
  • Tidskriftsartikel (refereegranskat)abstract
    • Pancreatic ductal adenocarcinoma (PDAC) represents the fourth cause of death in cancer and has a 5-year survival of < 5%. Only about 15% of the patients present with a resectable PDAC with potential to undergo "curative" surgery. After surgery, local and systemic recurrence, is though very common. The median survival of resected patients with adjuvant chemotherapy after surgery is only 20-23 mo. This underscores the significant need to improve PDAC management strategies. Increased survival rate is dependent on new breakthroughs in our understanding of not at least tumor biology. The aim of this review is to update and comment on recent knowledge concerning PDAC biology and new diagnostics and treatment modalities. One fundamental approach to improve survival rates is by earlier and improved diagnosis of the disease. In recent years, novel blood-based biomarkers have emerged based on genetic, epigenetic and protein changes in PDAC with very promising results. For biomarkers to enter clinical practice they need to have been developed using adequate control groups and provide high sensitivity and specificity and by this identify patients at risk already in a pre-symptomatic stage. Another way to improve outcomes, is by employing neoadjuvant treatments thereby increasing the number of resectable cases. Novel systemic treatment regimes like FOLFIRINOX and nab-paclitaxel have demonstrated improvements in prolonging survival in advanced cases, but long-term survival is still scarce. The future improved understanding of PDAC biology will inevitably render new treatment options directed against both the cancer cells and the surrounding microenvironment.
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23.
  • Anthoni, Sari, et al. (författare)
  • Milk protein IgG and IgA : the association with milk-induced gastrointestinal symptoms in adults
  • 2009
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327 .- 2219-2840. ; 15:39, s. 4915-4918
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: To study the association between serum levels of milk protein IgG and IgA antibodies and milk-related gastrointestinal symptoms in adults. METHODS: Milk protein IgG and IgA antibodies were determined in serum samples of 400 subjects from five outpatient clinics in Southern Finland. Subjects were randomly selected from a total of 1900 adults undergoing laboratory investigations in primary care. All 400 participants had completed a questionnaire on abdominal symptoms and dairy consumption while waiting for the laboratory visit. The questionnaire covered the nature and frequency of gastrointestinal problems, the provoking food items, family history and allergies. Twelve serum samples were disqualified due to insufficient amount of sera. The levels of specific milk protein IgG and IgA were measured by using the ELISA technique. The association of the milk protein-specific antibody level was studied in relation to the milk-related gastrointestinal symptoms and dairy consumption. RESULTS: Subjects drinking milk (n = 265) had higher levels of milk protein IgG in their sera than non-milk drinkers (n = 123, P < 0.001). Subjects with gastrointestinal problems related to milk drinking (n = 119) consumed less milk but had higher milk protein IgG levels than those with no milk-related gastrointestinal symptoms (n = 198, P = 0.02). Among the symptomatic subjects, those reporting dyspeptic symptoms had lower milk protein IgG levels than non-dyspeptics (P < 0.05). However, dyspepsia was not associated with milk drinking (P = 0.5). The association of high milk protein IgG levels with constipation was close to the level of statistical significance. Diarrhea had no association with milk protein IgG level (P = 0.5). With regard to minor symptoms, flatulence and bloating (P = 0.8), were not associated with milk protein IgG level. Milk protein IgA levels did not show any association with milk drinking or abdominal symptoms. The levels of milk protein IgA and IgG declined as the age of the subjects increased (P < 0.004). CONCLUSION: Milk protein IgG but not milk IgA seems to be associated with self-reported milk-induced gastrointestinal symptoms.
  •  
24.
  • Antonodimitrakis, Pantelis, et al. (författare)
  • Gastric carcinoid in a patient infected with Helicobacter pylori : A new entity?
  • 2011
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327 .- 2219-2840. ; 17:25, s. 3066-3068
  • Tidskriftsartikel (refereegranskat)abstract
    • There are four types of gastric carcinoid tumors, classified according to their histology and malignant potential. Only a few cases of carcinoid tumors in patients infected with Helicobacter pylori (H. pylon) have been reported so far. We report a patient infected with H. pylori presenting with a small solitary gastric carcinoid tumor with very low proliferative rate and normal gastrin levels. The tumor was endoscopically removed and the patient received an eradication therapy against H. pylori. No signs of metastatic disease have been found so far during more than 3 year of follow-up. Infection with H. pylon may cause chronic gastritis with normal or elevated gastrin levels, leading to the development of gastric carcinoids by mechanisms unrelated to gastrin. Enterochromaffin-like cell tumors related to a chronic H. pylori infection may be considered as a distinct type of gastric carcinoid tumors.
  •  
25.
  • Baldaque-Silva, F., et al. (författare)
  • Impact of gastroesophageal reflux control through tailored proton pump inhibition therapy or fundoplication in patients with Barrett's esophagus
  • 2017
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327 .- 2219-2840. ; 23:17, s. 3174-3183
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM To determine the impact of upwards titration of proton pump inhibition (PPI) on acid reflux, symptom scores and histology, compared to clinically successful fundoplication. Two cohorts of long-segment Barrett's esophagus (BE) patients were studied. In group 1 (n = 24), increasing doses of PPI were administered in 8-wk intervals until acid reflux normalization. At each assessment, ambulatory 24 h pH recording, endoscopy with biopsies and symptom scoring (by a gastroesophageal reflux disease health related quality of life questionnaire, GERD/HRLQ) were performed. Group 2 (n = 30) consisted of patients with a previous fundoplication. In group 1, acid reflux normalized in 23 of 24 patients, resulting in improved GERD/HRQL scores (P = 0.001), which were most pronounced after the starting dose of PPI (P < 0.001). PPI treatment reached the same level of GERD/HRQL scores as after a clinically successful fundoplication (P = 0.5). Normalization of acid reflux in both groups was associated with reduction in papillary length, basal cell layer thickness, intercellular space dilatation, and acute and chronic inflammation of squamous epithelium. This study shows that acid reflux and symptom scores co-vary throughout PPI increments in long-segment BE patients, especially after the first dose of PPI, reaching the same level as after a successful fundoplication. Minor changes were found among GERD markers at the morphological level.
  •  
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