Can Helicobacter pylori eradication therapy be shortened to 4 days?
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Comment↗
Biomedical subjects
Ernst J Kuipers
Publications and source records attributed to Ernst J Kuipers.
Attendance at surveillance endoscopy of patients with adenoma or colorectal cancer.
OBJECTIVE: Surveillance of patients treated for adenoma or colorectal cancer (CRC) is intended to reduce the incidence of CRC. Responsibility for the adherence to surveillance advice is often left to the patients and family physician. It is not known whether this type of passive policy affects the efficacy of surveillance. The aim of this study was to determine the yield of surveillance without active invitation to follow-up endoscopy. MATERIAL AND METHODS: The study comprised a cohort follow-up of patients under 75 years of age with adenomas or CRC at index endoscopy in the period 1997-99. Adherence and intervals of follow-up endoscopy were determined up to December 2004. RESULTS: During the inclusion period 2946 patients underwent lower endoscopy. In total, 393 patients were newly diagnosed with colorectal polyps (n=280) or CRC (n=113). Polyps were classified as adenomas in 167/280 (61%) patients. Forty-five (27%) of the adenoma patients underwent surveillance endoscopy within the guideline interval, 63 (38%) underwent delayed endoscopy, and 59 (35%) did not have any follow-up at all. CRC was diagnosed in 113 patients. Thirty-six patients who died during the first year or were diagnosed with metastases were excluded from the analysis. Twenty-three (30%) of the remaining 77 patients underwent endoscopic surveillance according to the guidelines, 40 (52%) had delayed surveillance endoscopy, and 14/77 (18%) did not undergo surveillance endoscopy at all. CONCLUSIONS: In surveillance for colorectal neoplasia, active follow-up invitation is important. Given the low follow-up rate in our series, passive follow-up policies may lead to under-performance of surveillance programs. An active and controlled follow-up is advisable.
Adenocarcinoma↗
Inhibition of viral replication reduces regulatory T cells and enhances the antiviral immune response in chronic hepatitis B.
Regulatory T cells (Treg) play a key role in the impaired immune response that is typical for a chronic Hepatitis B virus (HBV) infection. To gain more insight in the mechanism that is responsible for this impaired immune response, the effect of viral load reduction resulting from treatment with the nucleotide analogue adefovir dipivoxil on the percentages of Treg and HBV-specific T-cell responses was analyzed. Peripheral blood mononuclear cells (PBMC) of 12 patients were collected at baseline and during treatment. In parallel to the decline in viral load, we found a decline in circulating Treg, combined with an increase in HBV core antigen-specific IFN-gamma production and proliferation. The production of IL10 did not decrease during therapy. In conclusion, adefovir induced viral load reduction results in a decline of circulating Treg together with a partial recovery of the immune response.
Adenine↗
Iron-responsive repression of urease expression in Helicobacter hepaticus is mediated by the transcriptional regulator Fur.
Persistent colonization of mucosal surfaces by bacteria in the mammalian host requires concerted expression of colonization factors, depending on the environmental conditions. Helicobacter hepaticus is a urease-positive pathogen that colonizes the intestinal and hepatobiliary tracts of rodents. Here it is reported that urease expression of H. hepaticus is iron repressed by the transcriptional regulator Fur. Iron restriction of growth medium resulted in a doubling of urease activity in wild-type H. hepaticus strain ATCC 51449 and was accompanied by increased levels of urease subunit proteins and ureA mRNA. Insertional inactivation of the fur gene abolished iron-responsive repression of urease activity, whereas inactivation of the perR gene did not affect iron-responsive regulation of urease activity. The iron-responsive promoter element was identified directly upstream of the H. hepaticus ureA gene. Recombinant H. hepaticus Fur protein bound to this ureA promoter region in a metal-dependent matter, and binding resulted in the protection of a 41-bp, Fur box-containing operator sequence located at positions -35 to -75 upstream of the transcription start site. In conclusion, H. hepaticus Fur controls urease expression at the transcriptional level in response to iron availability. This represents a novel type of urease regulation in ureolytic bacteria and extends the already diverse regulatory repertoire of the Fur protein.
Bacterial Proteins↗
Genomic analysis of a case of multifocal adenocarcinoma in ulcerative colitis.
Long-standing ulcerative colitis is associated with an elevated risk of developing colonic adenocarcinoma. A very limited group of patients present with multiple synchronous cancers. This could be due to either a multifocal presentation of the same neoplastic clone or different tumors arising in a large area of polyclonal dysplastic colonic mucosa ("field cancerization"). Here, we describe a patient with long-standing colitis and three different tumors in the rectosigmoid part of the large bowel. Clonal evaluation of the lesions was performed by array-based comparative genomic hybridization. These three neoplasms showed a comparable pattern of genomic alterations characterized by gains of chromosomes 12, 13, and 20. Noteworthy, dysplastic mucosa distal to the three cancers displayed a completely different pattern of genomic changes indicating that different cell lineages were present. In addition, all three carcinomas were microsatellite stable and revealed identical immunoprofiles for several cancer-associated genes. We conclude that these three multifocal tumors must have originated from the same preneoplastic lineage.
Adenocarcinoma↗
NikR mediates nickel-responsive transcriptional repression of the Helicobacter pylori outer membrane proteins FecA3 (HP1400) and FrpB4 (HP1512).
The transition metal nickel plays an important role in gastric colonization and persistence of the important human pathogen Helicobacter pylori, as it is the cofactor of the abundantly produced acid resistance factor urease. Nickel uptake through the inner membrane is mediated by the NixA protein, and the expression of NixA is controlled by the NikR regulatory protein. Here we report that NikR also controls the nickel-responsive expression of the FecA3 (HP1400) and FrpB4 (HP1512) outer membrane proteins (OMPs), as well as the nickel-responsive expression of an ExbB-ExbD-TonB system, which may function in energization of outer membrane transport. Transcription and expression of the frpB4 and fecA3 genes were repressed by nickel in wild-type H. pylori 26695, but they were independent of nickel and derepressed in an isogenic nikR mutant. Both the frpB4 and fecA3 genes were transcribed from a promoter directly upstream of their start codon. Regulation by NikR was mediated via nickel-dependent binding to specific operators overlapping either the +1 or -10 sequence in the frpB4 and fecA3 promoters, respectively, and these operators contained sequences resembling the proposed H. pylori NikR recognition sequence (TATWATT-N(11)-AATWATA). Transcription of the HP1339-1340-1341 operon encoding the ExbB2-ExbD2-TonB2 complex was also regulated by nickel and NikR, but not by Fur and iron. In conclusion, H. pylori NikR controls nickel-responsive expression of the HP1400 (FecA3) and HP1512 (FrpB4) OMPs. We hypothesize that these two NikR-regulated OMPs may participate in the uptake of complexed nickel ions and that this process is energized by the NikR-regulated ExbB2-ExbD2-TonB2 system, another example of the specific adaptation of H. pylori to the gastric lifestyle.
Bacterial Outer Membrane Proteins↗
Superior immunomodulatory effects of intravenous immunoglobulins on human T-cells and dendritic cells: comparison to calcineurin inhibitors.
BACKGROUND: Prophylactic administration of anti-HBs intravenous immunoglobulins (IVIg) in hepatitis B infected-liver transplant patients protects against acute rejection. To explore the suitability of intravenous immunoglobulins (IVIg) as prophylaxis of acute rejection and graft-versus-host disease (GVHD) after allograft transplantation, the effects of IVIg and calcineurin inhibitors (CNI) on human blood-derived T-cells and DC were compared. METHODS: T-cells were stimulated with phytohemagglutinin (PHA) or allogeneic spleen antigen-presenting cells (APC) and T-cell proliferation and cytokine production were determined in presence or absence of IVIg or CNI. Immature blood dendritic cells (DC) were stimulated in presence or absence of IVIg or CNI, and allogeneic T-cell stimulatory capacity, cell death, and phenotypic maturation were established. RESULTS: IVIg and CNI equally inhibited T-cell proliferation and IFN-gamma production after PHA stimulation or allogeneic stimulation. CD8+ T-cells were preferentially affected by both IVIg and CNI after allogeneic stimulation. Like CNI, addition of IVIg at later time points after T-cell activation suppressed mitotic progression of responding T-cells. IVIg-treated DC were suppressed in their capacity to stimulate allogeneic T-cell proliferation by 73+/-12%, whereas DC-function was not affected by CNI. The decreased allogeneic T-cell stimulatory capacity of IVIg-treated DC correlated to induction of cell death in DC and decreased up-regulation of CD40 and CD80. CONCLUSIONS: In vitro IVIg functionally inhibit the two principal immune cell-types involved in rejection and GVHD, i.e. T-cells and DC, whereas CNI only suppress T-cells. By targeting both T-cells and DC, IVIg may be a promising candidate for immunosuppressive treatment after allograft transplantation.
Calcineurin↗
Genomic analysis of Barrett's esophagus after ablative therapy: persistence of genetic alterations at tumor suppressor loci.
Barrett's esophagus (BE) is a major predisposing factor for the development of esophageal adenocarcinoma. Current strategies for treatment of BE, both dysplastic and nondysplastic, include photodynamic therapy (PDT) and argon plasma coagulation (APC). However, the effect of ablative therapy at the genetic level is unclear. We performed loss of heterozygosity (LOH) analysis of BE in baseline and follow-up biopsy specimens from 21 patients with BE (17 male, 4 female) treated with PDT and/or APC. At baseline, 14 patients had intestinal metaplasia without dysplasia (MET), 4 low-grade dysplasia (LGD) and 3 high-grade dysplasia (HGD). LOH was assessed using a panel of 9 polymorphic markers for evaluation of the P53 gene on 17p, P16 on 9p, DCC and SMAD4 on 18q and the APC gene on 5q. The tissue specimens obtained at baseline (t = 0) were analysed, as well as the first (t = 1; mean interval: 4 months) and last (t = 2; mean interval: 8 months) available biopsy with residual or recurrent BE after ablation. At t = 0, allelic loss was detected of 5q in 27%, 9p in 56%, 17p in 31% and 18q in 6% of informative cases. At t = 1 (18 patients with persistent MET and 3 with LGD) and at t = 2 (8 MET, 2 LGD), the LOH patterns were not statistically different from t = 0. Further, multiple genetic lineages before and after therapy were detected in 15 cases illustrating the multiclonal nature of BE. We conclude that recurrent and/or persistent BE after ablative therapy still contains genetic alterations associated with malignant progression to cancer. Therefore, the goal of treatment should be the complete elimination of Barrett's mucosa.
Adenocarcinoma↗
Characterization of human liver dendritic cells in liver grafts and perfusates.
It is generally accepted that donor myeloid dendritic cells (MDC) are the main instigators of acute rejection after organ transplantation. The aim of the present study was to characterize MDC in human donor livers using liver grafts and perfusates as a source. Perfusates were collected during ex vivo vascular perfusion of liver grafts pretransplantation. MDC, visualized in wedge biopsies by immunohistochemistry with anti-BDCA-1 monoclonal antibody (mAb), were predominantly observed in the portal fields. Liver MDC, isolated from liver wedge biopsies, had an immature phenotype with a low expression of CD80 and CD83. Perfusates were collected from 20 grafts; perfusate mononuclear cells (MNC) contained 1.5% (range, 0.3-6.6%) MDC with a viability of 97 +/- 2%. Perfusates were a rich source of hepatic MDC since 0.9 x 10(6) (range, 0.11-4.5 x 10(6)) MDC detached from donor livers during vascular perfusion pretransplantation. Perfusate MDC were used to further characterize hepatic MDC. Perfusate MDC expressed less DC-LAMP (P = 0.000), CD80 (P = 0.000), CD86 (P = 0.003), and CCR7 (P = 0.014) than mature hepatic lymph node (LN) MDC, and similar CD86 (P = 0.140) and CCR7 (P = 0.262) as and more DC-LAMP (P = 0.007) and CD80 (P = 0.002) than immature blood MDC. Perfusate MDC differed from blood MDC in producing significantly higher amounts of interleukin (IL)-10 in response to lipopolysaccharide (LPS), and in being able to stimulate allogeneic T-cell proliferation. In conclusion, human donor livers contain exclusively immature MDC that detach in high numbers from the liver graft during pretransplantation perfusion. These viable MDC have the capacity to stimulate allogeneic T-cells, and thus may represent a major player in the induction of acute rejection.
Antigens, CD↗
Electrocautery therapy for refractory anastomotic strictures of the esophagus.
BACKGROUND: Anastomotic esophageal stenoses after esophageal resection are common and sometimes are refractory to Savary bougie dilation. The efficacy of electrocautery needle-knife treatment in these patients is described. METHODS: Twenty patients with a refractory anastomotic stricture of the esophagus were treated with electrocautery and were followed for 12 months. All patients had recurrence of dysphagia despite repeated bougienage. OBSERVATIONS: All 12 patients with a stricture shorter than 1 cm remained without dysphagia after a single treatment. In all 8 patients with a long-segment stenosis of 1.5 to 5 cm, dysphagia recurred, and a mean of 3 treatments were necessary. The interval between electrocautery treatments was significantly longer compared with bougienage. There were no complications. The body weight of all patients increased. CONCLUSIONS: Electrocautery seems to be a good single-treatment modality for refractory short-segment anastomotic strictures, whereas longer-segment stenoses appear to require repeated treatment sessions before similar results are obtained.
Adult↗
A new esophageal stent design (Niti-S stent) for the prevention of migration: a prospective study in 42 patients.
BACKGROUND: Covered, rather than uncovered, metal stents are used for the palliation of dysphagia from esophageal cancer, but a major drawback is the risk of stent migration, which occurs in up to 20% of patients. To overcome this problem, a double-layered stent, the Niti-S stent (Taewong Medical, Seoul, Korea), has been developed. The Niti-S stent consists of an inner polyurethane layer to prevent tumor ingrowth and an outer uncovered nitinol wire tube to allow the mesh of the stent to embed itself in the esophageal wall. METHODS: Between June 2003 and May 2004, 42 patients with malignant dysphagia caused by inoperable carcinoma of the esophagus or gastric cardia were treated with a Niti-S stent. Patients were prospectively followed and data collection focused on recurrent dysphagia, functional outcome, complications, and survival. RESULTS: At 4 weeks, the dysphagia score had significantly improved from a median of 3 (liquids only) to 0 (ability to eat a normal diet). Five of 42 (12%) patients with a Niti-S stent developed recurrent dysphagia, mainly due to tissue overgrowth (2 of 42; 5%) and stent migration (3 of 42; 7%). Major complications (perforation, 1; aspiration pneumonia, 2; hemorrhage, 2) occurred in 5 of 42 (12%) patients. Pain following stent placement was observed in 5 of 42 (12%) patients, and symptomatic gastroesophageal reflux occurred in 2 of 42 (5%) patients. CONCLUSIONS: The Niti-S stent provides symptomatic relief of malignant dysphagia and effectively reduces recurrent dysphagia. Its double-layered design is probably important in preventing migration. In addition, the complete covering of the Niti-S stent may be a factor in preventing tissue overgrowth at both ends of the stent.
Adenocarcinoma↗
Colorectal neoplasia in veterans is associated with Barrett's esophagus but not with proton-pump inhibitor or aspirin/NSAID use.
BACKGROUND: It has been suggested that Barrett's esophagus (BE) is associated with an increased risk of developing colorectal neoplasia, but this has not been reported consistently. AIM: To study whether BE is associated with an increased risk of colorectal neoplasia, and if it is, whether it is dependent on use of proton-pump inhibitors (PPIs) or aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs). DESIGN: Case-control study. SETTING: Endoscopic database of the Palo Alto Veterans Affairs Health Care System. POPULATION: 268 veterans with BE were matched with 268 controls without BE. INTERVENTION: Controls had undergone upper GI endoscopy within 14 days of the corresponding case. Colonoscopy was performed within 6 months in cases and controls. MAIN OUTCOME MEASURE: Development of colorectal neoplasia. RESULTS: Colorectal neoplasia was present in 162 of 268 (60%) BE patients and in 105 of 268 (40%) controls (p < 0.001). The presence of BE (odds ratio [OR] 2.02: 95% CI [1.35, 3.04]), but also increasing age (OR 1.24 per decade: 95% CI [1.04, 1.48]) and alcohol use (OR 1.70: 95% CI [1.16, 2.50]) were associated with an increased risk of colorectal neoplasia in multivariable logistic regression analysis, whereas PPIs (OR 0.99: 95% CI [0.66, 1.48]) and aspirin/NSAIDs (OR 0.90: 95% CI [0.61, 1.33]) had no meaningful effect. LIMITATIONS: This was a retrospective study in mostly male veterans. CONCLUSIONS: Veterans with BE are at an increased risk of developing colorectal neoplasia. This association is independent from the use of PPIs or aspirin/NSAIDs.
Aged↗
Staging of esophageal carcinoma in a low-volume EUS center compared with reported results from high-volume centers.
BACKGROUND: It is well known that a learning curve exists for performing EUS. OBJECTIVE: To determine whether the number of EUS investigations performed in a center affects the results of esophageal cancer staging. DESIGN: We compared EUS in the evaluation of T stage and the presence of regional and celiac lymph nodes in a low-volume center where <50 EUS/endoscopist/y were performed with reported results from 7 high-volume EUS centers. SETTING: A reference center for esophageal cancer (>90 cases/y) but a low-volume center for EUS when it comes to individual endoscopists. PATIENTS: From 1994 to 2003, 244 patients underwent EUS, without specific measures to pass a stenotic tumor or FNA and with postoperative TNM stage as the criterion standard in the low-volume EUS center. In the high-volume centers, 670 EUS investigations for esophageal cancer were performed, if needed, with dilation, and with postoperative TNM stage and/or FNA as the criterion standard. INTERVENTIONS: Retrospective analysis. MAIN OUTCOME MEASUREMENTS: Sensitivity and specificity of EUS for esophageal cancer staging. RESULTS: In the low-volume center, results of EUS for T3 staging in patients in whom passage of the EUS probe was possible were almost comparable for sensitivity (85% vs 88%-94%) but were lower for specificity (57% vs 75%-90%), whereas both sensitivity (58% vs 75%-90%) and specificity (87% vs 94%-97%) for T1 or T2 stages were lower than those reported in the high-volume centers. In the low-volume center, sensitivities of EUS for regional (45% vs 63%-89%) and celiac (19% vs 72%-83%) lymph nodes were lower, whereas specificities (75% vs 63%-82% and 99% vs 85%-100%, respectively) were comparable with those from high-volume centers. Results in the low-volume EUS center were worse if the EUS probe could not pass the stricture, which occurred in almost 30% of patients. LIMITATIONS: Both FNA and dilation before EUS for stenotic tumors were not performed in the low-volume EUS center. CONCLUSIONS: The results of EUS performed in a low-volume EUS center compared unfavorably with those reported from high-volume EUS centers. The results of this study suggest that preoperative staging by EUS should be performed by experienced and dedicated EUS endoscopists to optimize staging of esophageal cancer.
Aged↗
Detection of small-bowel neuroendocrine tumors by video capsule endoscopy.
OBJECTIVES: Carcinoid tumors are the most common GI neuroendocrine tumors (NET). They often originate in the small intestine. The primary tumor is often difficult to locate, and resection in an early phase is recommended to prevent complications. This study evaluated the value of videocapsule endoscopy (VCE) in the detection of small-intestinal primary carcinoid tumor. DESIGN: Prospective descriptive study. SETTING: Tertiary referral center. PATIENTS: Twenty consecutive patients (13 men, 7 women; 60.5 +/- 9.3 years) with metastatic NET of unknown primary tumor. INTERVENTIONS: All patients underwent CT, enteroclysis, nuclear imaging, and VCE of the small bowel. RESULTS: CTs and enteroclysis did not detect a primary small-intestinal carcinoid tumor. Nuclear imaging demonstrated abnormalities in the abdominal area in 13 patients but was unable to relate this to an intestinal localization in any patient. VCE revealed a small-intestinal tumor in 9 patients. Three other patients showed external compression and erosions. At surgery, 5 patients had a small-intestinal carcinoid tumor, and, in 2 patients, a small-intestinal ischemic segment was present. LIMITATIONS: The number of false-positive VCE findings was not clear, because not all patients underwent surgery. The absence of abnormalities at VCE in patients with abnormalities at nuclear imaging might be related to the presence of carcinoid tumor restricted to the mesenterium or to a false-negative VCE. CONCLUSIONS: VCE had a high diagnostic yield of 45% for identification of primary small-intestinal carcinoid tumors. Although nuclear imaging had a comparable diagnostic yield, it could not differentiate between intestinal and mesenterial localization of the carcinoid.
Adult↗
Helicobacter pylori and antimicrobial resistance: molecular mechanisms and clinical implications.
Helicobacter pylori is an important human pathogen that colonises the stomach of about half of the world's population. The bacterium has now been accepted as the causative agent of several gastroduodenal disorders, ranging from chronic active gastritis and peptic ulcer disease to gastric cancer. The recognition of H pylori as a gastric pathogen has had a substantial effect on gastroenterological practice, since many untreatable gastroduodenal disorders with uncertain cause became curable infectious diseases. Treatment of H pylori infection results in ulcer healing and can reduce the risk of gastric cancer development. Although H pylori is susceptible to many antibiotics in vitro, only a few antibiotics can be used in vivo to cure the infection. The frequent indication for anti-H pylori therapy, together with the limited choice of antibiotics, has resulted in the development of antibiotic resistance in H pylori, which substantially impairs the treatment of H pylori-associated disorders. Antimicrobial resistance in H pylori is widespread, and although the prevalence of antimicrobial resistance shows regional variation per antibiotic, it can be as high as 95%. We focus on the treatment of H pylori infection and on the clinical relevance, mechanisms, and diagnosis of antimicrobial resistance.
Anti-Bacterial Agents↗
Long-term risk of oesophagitis, Barrett's oesophagus and oesophageal cancer in achalasia patients.
Achalasia is a motility disorder of the oesophagus of unknown origin in which loss of relaxation of the lower oesophageal sphincter (LOS) and aperistalsis in the distal oesophagus leads to functional oesophageal obstruction. The treatment is symptomatic, aimed at lowering of the LOS pressure, and may be accompanied by various side effects, including gastro-oesophageal reflux, a risk factor for oesophagitis and its complications. Stasis and fermentation can also lead to inflammation of the oesophageal mucosa, giving rise to hyperplasia of the epithelium, multifocal dysplasia and in some patients eventually squamous cell carcinoma. Unfortunately, the sensitivity and specificity of endoscopical inspection to assess inflammation or dysplasia of the oesophageal lining is low, such that biopsy sampling is necessary for accurate assessment. Although it is generally accepted that achalasia is a pre-malignant disorder, the reported increased risk of patients with achalasia developing a squamous cell carcinoma varies from 0 to 140 times that of the normal population. In addition, achalasia may predispose to Barrett's metaplasia and oesophageal adenocarcinoma, which have been described in case reports after myotomy. Surveillance endoscopy with tissue sampling to detect pre-neoplastic lesions has been recommended, even though this can be very difficult due to mucosal adherence of food as well as hyperplastic changes of the mucosa. In the event of moderate to severe inflammation and/or persisting stasis of food despite adequate LOS pressure-lowering therapy, the surveillance interval should be shortened and performed after a 3-day liquid diet. The exact technique and time intervals still need to be established, however.
Adenocarcinoma↗
Bile acids and Barrett's oesophagus: a sine qua non or coincidence?
BACKGROUND: Barrett's oesophagus (BO), a premalignant condition associated with the development of oesophageal adenocarcinoma (OAC), is thought to be a consequence of chronic duodeno-gastro-oesophageal reflux. Of the refluxates, bile acids, either alone or in combination with acid, are probably the most important. METHODS: Analysis of the literature on the role played by bile acids in inducing BO and/or progression to OAC. RESULTS: Combined pH and Bilitec 2000 (as a measure of bile reflux) monitoring and oesophageal aspiration studies in humans suggest a combined role for bile acids, particularly taurine conjugated bile acids, in causing oesophageal mucosal injury. Evidence from animal models has demonstrated that duodenal juice alone is also able to induce BO and/or OAC. Likewise, ex vivo studies with biopsies from BO patients show that increased proliferation and cyclo-oxygenase-2 expression are present after a pulsed exposure to acid or conjugated bile acids, but not if acid and bile acids are combined. Proton-pump inhibitors (PPIs) have been shown to decrease the biliary component of the refluxate. There is some evidence that PPIs are able to reduce neoplastic progression in BO. On the other hand, chronic PPIs can also stimulate bacterial overgrowth, which can result in increased production of secondary bile acids, particularly deoxycholic acid, in the stomach. Deoxycholic acid has been demonstrated to have a tumour-promoting capacity. CONCLUSIONS: It is unknown what factors of the refluxate (acid and/or bile) induce BO and/or promote carcinogenesis, but there is evidence that secondary bile acids play a role. A better understanding of the molecular steps involved in the induction of BO, and the role of bile acids herein, may identify targets at which preventive therapies can be directed.
Adenocarcinoma↗
Argon plasma coagulation for radiation proctitis.
BACKGROUND: Rectal blood loss is a common late sequel of radiation proctitis. Teleangiectasias appear in the mucosa in 2-5% of patients after radiotherapy of the pelvis. Since pharmacotherapy is usually not beneficial, local treatment modalities with formalin irrigation, Nd:YAG laser and argon plasma coagulation (APC) have been advocated, but experience is still limited. METHODS: Between January 1997 and August 2001, 50 consecutive patients with rectal bleeding due to radiation proctitis were included for treatment with APC. Thirteen patients suffered from anaemia, six of whom required blood transfusion. Nine patients were receiving anticoagulant therapy and 10 patients used low-dose aspirin. APC was performed, applying the no-touch spotting technique at an electrical power of 50 Watt and an argon gas flow of 2.0 l/min. Pulse duration was less than 0.5 s. Treatment sessions were carried out at intervals of 3 weeks. RESULTS: In 47 out of 48 patients (98%) in whom the effect could be assessed, APC led to persistent clinical and endoscopic remission of rectal bleeding after a median of three sessions. One patient developed recurrent blood loss after resuming anticoagulant therapy for his aortic valve prosthesis. No adverse effects were encountered after initial treatment. One serious complication occurred in a patient with recurrent blood loss when he was prescribed aspirin for a transient ischaemic attack 2 years after the initial APC. Re-treatment resulted in a major rectal bleeding from a small ulcer with a visible vessel. CONCLUSIONS: APC is a safe, effective and well-tolerated treatment for blood loss due to radiation proctitis. The use of anticoagulants and aspirin seems to be a co-factors that induces bleeding.
Aged↗