Association of Chronic Periodontitis with Helicobacter pylori Infection in Stomach or Mouth: A Systematic Review and Meta-Analysis.

Helicobacter pylori (H. pylori) infection and periodontitis are both inflammatory conditions associated with systemic diseases. Researchers have attempted to investigate the correlation between them. This systematic review and meta-analyses were conducted to investigate the association of H. pylori infection in the stomach and/or in subgingival plaque and gingival crevicular fluid with chronic periodontitis. The protocol was created according to the Preferred Reporting Items for Systematic review and Meta-Analysis Protocols (PRISMA-P) statement. The study was designed according to the Cochrane criteria. A comprehensive literature search was performed in MEDLINE, Scopus, and CENTRAL, combined with hand-searching and assessment of gray literature. The meta-analysis of the included studies was made by the Review Manager (RevMan) 5.4 software. The effect measure of the outcome was odds ratios with 95% confidence intervals. Heterogeneity was assessed by chi-square and I2. Four observational studies involving 818 subjects were included in this meta-analysis. The odds of oral H. pylori presence were higher in patients with chronic periodontitis, compared to healthy controls, with an odds ratio of 1.87 (95% confidence interval 0.85-4.10; p = 0.12). The odds of the presence of H. pylori in the stomach also were higher in patients with chronic periodontitis, with an odds ratio of 1.80 (95% confidence interval 0.82-3.95; p = 0.15). There is no evidence for an association between chronic periodontitis and the prevalence of H. pylori, detected either in subgingival plaque and gingival crevicular fluid or in the stomach.

Periodontitis and Helicobacter pylori Infection: Eradication and Periodontal Therapy Combination.

OBJECTIVES: This study was aimed to assess (1) the prevalence of salivary and gastric Helicobacter pylori (HP) infection in patients with and without periodontitis, (2) the prevalence of HP infection in patients with periodontitis according to its clinical classification, (3) the effect of periodontitis treatment in patients with or without gastric HP infection, and (4) if gastric HP eradication in combination with periodontitis treatment influences periodontitis clinical outcome. MATERIALS AND METHODS: Thirty-three adults with periodontitis treated by quadrant scaling and root planning (QSRP). The simplified plaque index (PI), bleeding on probing index (BOP), probing pocket depth (PPD), and clinical attachment level (CAL) were assessed pretreatment and 3 months of posttreatment. The patients were tested for oral and gastric HP. Gastric HP (+) patients received eradication therapy. A control group of 32 periodontically healthy volunteers was tested for oral and gastric HP. Saliva samples were evaluated by real-time polymerase chain reaction (rtPCR); gastric HP was detected by urea breath test (UBT). STATISTICAL ANALYSIS: Normality of variables assessed by the Kolmogorov-Smirnov test, while the differences of pre- and post-treatment were analyzed by paired samples t-test. Differences between subgroups were compared by a Student's t-test or a Mann-Whitney U-test. Comparisons of nominal variables were made by Pearson's Chi-square test. RESULTS: No saliva samples were positive for HP. Gastric HP was detected in six patients with periodontitis and seven controls (p > 0.05). HP infection affected patients with higher disease stages and grades. All HP (+) patients underwent successful eradication treatment. All clinical periodontitis indices improved following QSRP. HP (+) patients who received QSRP as adjunctive to eradication treatment showed improvement in BOP (p < 0.001), PI (p < 0.013), and CAL (p < 0.004) compared with HP (-) patients who received QSRP alone. CONCLUSION: Periodontitis was not associated with gastric HP infection. Saliva was not a gastric HP supply reservoir. Gastric HP infection was associated with advanced stages and grades of periodontitis. Although all periodontal clinical markers improved after QSRP, BOP, PI, and CAL, they were further improved when combined with eradication treatment. Periodontal evaluation and treatment combined with HP eradication are recommended in patients with HP gastric infection.

Management of low rectal gastrointestinal stromal tumor with neoadjuvant therapy and transanal excision: a rare case report and review of the literature.

BACKGROUND: Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract. However, rectal GISTs represent only 5% of this category. We report a case of a rectal GIST treated with local excision after neoadjuvant therapy. CASE PRESENTATION: A 41-year-old male patient presented with anal bleeding. Colonoscopy revealed a mass located 5 cm from the anal verge. Histological examination showed a GIST with immunohistochemical positivity for CD117 and CD34. Transanal local excision was performed after neoadjuvant therapy. CONCLUSION: Neoadjuvant immunotherapy for GISTs with unfavorable localization may facilitate local excision and avoid complications of more demanding operations.

Endoscopically Assisted Laparoscopic Gastric Resection for Benign and Malignant Lesions: A Report of Two Cases.

BACKGROUND The first gastric resection for stomach cancer was performed in 1879, and the first gastric resection for gastric ulcer disease was performed in 1882. During the 1990s, the first laparoscopic gastrostomies were reported. During the past decade, laparoscopic techniques have developed rapidly, gaining wide clinical acceptance. Minimally invasive surgery is now shifting the balance away from traditional open methods. We report 2 cases of endoscopically assisted laparoscopic local gastric resections for both gastric cancer and gastric ulcer disease. CASE REPORT The first case involves a 67-year-old male patient who suffered from recurrent bleeding from a gastric ulcer located 4-5 cm from the gastroesophageal junction. The patient was subjected to endoscopically assisted laparoscopic wedge resection of the affected part of the stomach, had an uneventful recovery and was discharged on the third postoperative day. The second case involves a 60-year-old female patient who was diagnosed with intramucosal gastric adenocarcinoma and was also subjected to endoscopically assisted laparoscopic wedge gastrectomy. This patient also had an uneventful recovery and was discharged on the second postoperative day. CONCLUSIONS Endoscopically assisted laparoscopic local gastric resection is a minimally invasive procedure which allows the surgeon to operate under direct visualization of the internal part of the stomach. Thus, it enables the surgeon to safely remove the affected part within healthy margins, providing the patient with all the advantages of laparoscopic surgery.

Cytokine Receptor Profiling in Human Colonic Subepithelial Myofibroblasts: A Differential Effect of Th Polarization-Associated Cytokines in Intestinal Fibrosis.

Background: Colonic subepithelial myofibroblasts (cSEMFs) are mesenchymal cells with a pivotal role in the pathophysiology of Crohn's disease (CD) fibrosis. Here, we demonstrate for the first time a complete expression mapping of cytokine receptors, implicated in inflammatory bowel diseases, in primary human cSEMFs and how pro-inflammatory cytokines regulate this expression. Furthermore, we show the effect of Th1-, Th2-, Th17- and Treg-related cytokines on a fibrosis-related phenotype of cSEMFs. Methods: Colonic subepithelial myofibroblasts were isolated from healthy individuals' colonic biopsies. Interleukin (IL)-1α- and/or tumor necrosis factor (TNF)-α-induced mRNA and protein expression of cytokine receptors was assayed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunofluorescence, respectively. Th-related cytokine effects on mRNA and protein profibrotic factor expression were analyzed by qRT-PCR and/or colorimetric assays and on the wound-healing capacity of cSEMFs by scratch test. Results: In cSEMFs, we observed basal cytokine receptor expression, which was modified by IL-1α and TNF-α. Th1-related cytokines upregulated tissue factor (TF), collagen, fibronectin and matrix metalloproteinase (MMP)-1 and downregulated α-smooth muscle actin (α-SMA), MMP-9, and wound healing rate. Th2-related cytokines upregulated collagen, TF, α-SMA, MMP-1, and wound healing rate and downregulated fibronectin and MMP-9. IL-17 and IL-23 upregulated fibronectin, and IL-22 downregulated TF. IL-17 and IL-22 decreased wound healing rate. Similar to TGF-ß, IL-23 upregulated MMP-1, tissue inhibitor of metalloproteinases-1, collagen expression, and wound healing rates. Conclusions: Our results suggest that cSEMFs have a central role in inflammation and fibrosis, as they express a great variety of Th-related cytokine receptors, making them responsive to pro-inflammatory cytokines, abundant in the inflamed mucosa of CD patients.

REDD1/Autophagy Pathway Is Associated with Neutrophil-Driven IL-1ß Inflammatory Response in Active Ulcerative Colitis.

Infiltration of neutrophils into colonic mucosa has been associated with the severity of ulcerative colitis (UC). We investigated the effect of disease microenvironment on the release of neutrophil extracellular traps (NETs) as well as the involved mechanisms in NETosis and whether certain NET proteins are correlated with disease phenotype. Peripheral blood neutrophils, sera, and colonic tissue were collected from treatment-naive and mesalazine-treated patients with active UC, treatment-naive patients with active Crohn's disease, patients suffering from infectious colitis, or healthy individuals (controls). Analysis of colonic biopsy specimens and peripheral blood neutrophils for the presence of NET-related markers using immunofluorescence confocal microscopy, ELISA, immunoblotting, flow cytometry, and quantitative PCR were performed. In vitro cell and tissue culture systems were further deployed. The local inflammatory response in colon in UC, but not Crohn's disease, is characterized by the presence of NETs carrying bioactive IL-1ß and thrombogenic tissue factor. The inflammatory environment of UC is able to induce neutrophil activation, IL-1ß expression, and NET release, as shown both ex vivo and in vitro. REDD1 expression, as a mediator linking inflammation, autophagy, and NET release, was also specifically associated with the inflammatory response of UC. We show that neutrophil expression of REDD1 in colon tissue and the presence of IL-1ß in neutrophils/NETs provide candidate biomarkers for the differential diagnosis of inflammatory colitis and possible targets for the treatment of UC, suggesting that UC shares common features with autoinflammatory disorders.

Regulated in development and DNA damage responses 1 (REDD1) links stress with IL-1ß-mediated familial Mediterranean fever attack through autophagy-driven neutrophil extracellular traps.

BACKGROUND: Familial Mediterranean fever (FMF) is an IL-1ß-dependent autoinflammatory disease caused by mutations of Mediterranean fever (MEFV) encoding pyrin and characterized by inflammatory attacks induced by physical or psychological stress. OBJECTIVE: We investigated the underlying mechanism that links stress-induced inflammatory attacks with neutrophil activation and release of IL-1ß-bearing neutrophil extracellular traps (NETs) in patients with FMF. METHODS: RNA sequencing was performed in peripheral neutrophils from 3 patients with FMF isolated both during attacks and remission, 8 patients in remission, and 8 healthy subjects. NET formation and proteins were analyzed by using confocal immunofluorescence microscopy, immunoblotting, myeloperoxidase-DNA complex ELISA, and flow cytometry. Samples from patients with Still's disease and bacterial infections were used also. RESULTS: The stress-related protein regulated in development and DNA damage responses 1 (REDD1) is significantly overexpressed during FMF attacks. Neutrophils from patients with FMF during remission are resistant to autophagy-mediated NET release, which can be overcome through REDD1 induction. Stress-related mediators (eg, epinephrine) decrease this threshold, leading to autophagy-driven NET release, whereas the synchronous inflammatory environment of FMF attack leads to intracellular production of IL-1ß and its release through NETs. REDD1 in autolysosomes colocalizes with pyrin and nucleotide-binding domain, leucine-rich repeat/pyrin domain-containing 3. Mutated pyrin prohibits this colocalization, leading to higher IL-1ß levels on NETs. CONCLUSIONS: This study provides a link between stress and initiation of inflammatory attacks in patients with FMF. REDD1 emerges as a regulator of neutrophil function upstream to pyrin, is involved in NET release and regulation of IL-1ß, and might constitute an important piece in the IL-1ß-mediated inflammation puzzle.

Crohn's disease-associated mucosal factors regulate the expression of TNF-like cytokine 1A and its receptors in primary subepithelial intestinal myofibroblasts and intestinal epithelial cells.

Intestinal subepithelial myofibroblasts (SEMFs) exert a profibrotic role in Crohn's disease (CD). Tumor necrosis factor-like cytokine 1A (TL1A) and its receptors, death-domain receptor 3 (DR3) and decoy receptor 3 (DcR3), are mucosal factors with significant involvement in experimental inflammation and CD. We aimed to determine the regulation of expression of this system of proteins in SEMFs and intestinal epithelial cells. The relative amount of mRNA transcripts for TL1A, DR3, and DcR3 was measured by real-time reverse transcription polymerase chain reaction in cultured primary SEMFs, colonic myofibroblast cell line 18CO, and epithelial cell line HT29. Protein expression was determined by immunofluorescence. The effect of various proinflammatory stimuli in mRNA and protein expression was studied. TL1A mRNA and protein expression in primary SEMFs (and 18CO cells) was significantly upregulated after stimulation with interleukin 1-alpha and/or tumor necrosis factor alpha (TNF-α) (32- to 44-fold increase, P < 0.05 vs unstimulated). Following stimulation with interleukin 1-alpha + TNF-α + IFN-γ, HT-29 cells highly expressed DR3 (4.1-fold over unstimulated, P = 0.008) and DcR3 (56-fold, P = 0.009) and secreted soluble factors that led to induction of TL1A mRNA in primary SEMFs (28-fold, P = 0.008). Activated epithelial cells significantly upregulated IL-8 expression in response to stimulation with recombinant TL1A. Supernatants from mucosal cultures of patients with CD were able to stimulate the expression of TL1A in cultured primary SEMFs, in comparison to supernatants from healthy controls (3.8-fold increase, P < 0.05) or culture media alone (P < 0.05). In conclusion, we found that proinflammatory cytokines are important regulators of the expression of TL1A in SEMFs and of its receptors in intestinal epithelial cells. Our results raise the possibility for involvement of TL1A/DR3/DR3-mediated mechanisms in epithelial-mesenchymal interactions and the development of inflammation-induced intestinal fibrosis in CD.

Post-laparoscopic cholecystectomy Mirizzi syndrome induced by polymeric surgical clips: a case report and review of the literature.

BACKGROUND: Laparoscopic cholecystectomy is the gold standard treatment of gallbladder disease. Post-cholecystectomy syndrome is a severe postoperative complication which can be caused by multiple mechanisms and can present with multiple disorders. The wide use of laparoscopy induces the need to understand more clearly the presentation and pathophysiology of this syndrome. Post-cholecystectomy Mirizzi syndrome is one form of this syndrome and, according to literature, this is the first report that clearly describes it. CASE PRESENTATION: We describe the case of a 62-year-old Greek woman who underwent laparoscopic cholecystectomy because of gallstone disease. A few days after surgery, post-cholecystectomy syndrome gradually developed with mild bilirubin increase in association with epigastric pain, nausea, and vomiting. After performing ultrasound, magnetic resonance cholangiopancreatography, and endoscopic retrograde cholangiopancreatography, we conducted a second laparoscopic surgery to manage the obstruction, which was converted to open surgery because of the remaining inflammation from the post-endoscopic retrograde cholangiopancreatography acute pancreatitis. Four polymeric laparoscopic clips were removed because they were identified as the cause of her post-cholecystectomy syndrome. She had a quick recovery without further complications. CONCLUSIONS: Postoperative Mirizzi syndrome induced by the migration of polymer laparoscopic clips is a rare (only one case referring to polymeric clips has been published in the literature) but a well-identified complication of laparoscopic cholecystectomy which can confuse the diagnostic and therapeutic field requiring simultaneous immediate management.

Update on ischemic colitis: from etiopathology to treatment including patients of intensive care unit.

Ischemic colitis is the result of colonic hypoperfusion and is regarded as a relatively rare condition. It can be roughly classified as occlusive and non-occlusive. Pathogenesis includes a usually transient compromise in the colonic vasculature, with a parallel activation of an inflammatory cascade caused primarily by reperfusion. Diagnosis of ischemic colitis remains often difficult and requires a combination of diagnostic techniques, whereas clinical signs are occasionally only seen late as complications. Gold standard is considered to be colonoscopy. Clinical presentation and treatment of ischemic colitis vary widely depending on the degree of ischemia. Patients of intensive care unit (ICU) with ischemic colitis are often under-diagnosed, since the parallel co-morbidities and the nonspecific nature of symptoms that mimic almost any abdominal pathology, can mislead the doctor. Moreover, sedated or ventilated patients can mask many of the characteristic features of ischemic colitis and make the diagnosis challenging. Bedside colonoscopy and diagnostic laparoscopy in ICUs are two options, which seem lately to be reliable and promising in diagnosing ischemic colitis in critically ill patients.

Immunomodulatory Role of Clarithromycin in Acinetobacter baumannii Infection via Formation of Neutrophil Extracellular Traps.

Macrolide antibiotics have been shown to act as immunomodulatory molecules in various immune cells. However, their effect on neutrophils has not been extensively investigated. In this study, we investigated the role of macrolide antibiotics in the generation of neutrophil extracellular traps (NETs). By assessing ex vivo and in vivo NET formation, we demonstrated that clarithromycin is able to induce NET generation both in vitro and in vivo. Clarithromycin utilizes autophagy in order to form NETs, and these NETs are decorated with antimicrobial peptide LL-37. Clarithromycin-induced NETs are able to inhibit Acinetobacter baumannii growth and biofilm formation in an LL-37-dependent manner. Additionally, LL-37 antimicrobial function depends on NET scaffold integrity. Collectively, these data expand the knowledge on the immunomodulatory role of macrolide antibiotics via the generation of LL-37-bearing NETs, which demonstrate LL-37-dependent antimicrobial activity and biofilm inhibition against A. baumannii.

Endoscopically Assisted Transumbilical Single-Incision Laparoscopic Gastric Resection for GIST Treatment.

PURPOSE: Complete surgical resection with negative margins without lymphadenectomy is the treatment of choice for nonmetastatic Gastrointestinal Stromal Tumors (GISTs). Laparoscopic resection of gastric GISTs <5 cm is an acceptable and oncologically feasible, safe, and effective treatment. We present our experience of an endoscopically assisted minimally invasive transumbilical single-incision laparoscopic (SILS) technique for gastric GISTs resection. METHODS: Four patients with small gastric GISTs ≤5 cm located on the greater curvature or the anterior wall were resected with SILS by using a lesion-lifting technique under the guidance of flexible gastroscopy. RESULTS: The technique was feasible and safe and offered significant advantages in locating the tumor and controlling the resection margins. There were no major intraoperative or postoperative complications, conversions, or tumor ruptures. Pathology showed low-risk GISTs resected with disease-free margins without tumor rupture. No recurrences have been observed. CONCLUSION: The endoscopically assisted SILS wedge gastrectomy is a feasible, safe, and advantageous technique for the treatment of the greater curvature or anterior wall gastric GISTs.

Single-incision assisted laparoscopic surgery (SILS) in the treatment of an intussusception induced by a solitary hamartomatous polyp: a case report and review of the literature.

INTRODUCTION: In this case report, we describe the successful treatment of a small-bowel intussusception, which was caused by a 3 cm solitary hamartomatous polyp, with single-incision laparoscopic surgery. Single-incision laparoscopic surgery is a minimally invasive surgical procedure with important advantages that allows the reduction of the intussusception and the resection of the polyp. This case report contributes to the medical literature by describing the advantages of this surgical technique that warrant its consideration as a treatment of choice in similar cases. CASE PRESENTATION: We report a case of a 19-year-old Greek woman who complained about intermittent, non-specific abdominal pain in her left lateral abdomen. She had been admitted to the hospital because of incomplete obstructive ileus. Ultrasound and computed tomography were carried out, which revealed an intussusception of the small bowel. This pathogenic situation was treated by single-incision laparoscopic surgery. Her pathology report revealed a benign, hamartomatous excised polyp of the Peutz-Jeghers type. The patient had a quick recovery without any post-operative complications. CONCLUSION: We recommend single-incision laparoscopic surgery for the safe excision of solitary hamartomatous polyps and the management of their complications, as it represents a potential advance in minimally invasive approaches.

Inflammatory bowel disease and thromboembolism.

Patients with inflammatory bowel disease (IBD) have an increased risk of vascular complications. Thromboembolic complications, both venous and arterial, are serious extraintestinal manifestations complicating the course of IBD and can lead to significant morbidity and mortality. Patients with IBD are more prone to thromboembolic complications and IBD per se is a risk factor for thromboembolic disease. Data suggest that thrombosis is a specific feature of IBD that can be involved in both the occurrence of thromboembolic events and the pathogenesis of the disease. The exact etiology for this special association between IBD and thromboembolism is as yet unknown, but it is thought that multiple acquired and inherited factors are interacting and producing the increased tendency for thrombosis in the local intestinal microvasculature, as well as in the systemic circulation. Clinicians' awareness of the risks, and their ability to promptly diagnose and manage tromboembolic complications are of vital importance. In this review we discuss how thromboembolic disease is related to IBD, specifically focusing on: (1) the epidemiology and clinical features of thromboembolic complications in IBD; (2) the pathophysiology of thrombosis in IBD; and (3) strategies for the prevention and management of thromboembolic complications in IBD patients.

Coagulation and fibrinolysis activation after single-incision versus standard laparoscopic cholecystectomy: a single-center prospective case-controlled pilot study.

Laparoscopic cholecystectomy is associated with attenuated acute-phase response and hypercoagulable state compared with the open procedure. Single-incision laparoscopic cholecystectomy is a new technique aiming to minimize the invasiveness of the procedure. By comparing the degree of coagulation and fibrinolysis activation after conventional multiport (CLC) and single-incision (SILC) laparoscopic cholecystectomy, we aimed to determine whether the reduced incision size induces a lower thrombophilic tendency. Thirty-two adult patients with noncomplicated symptomatic cholelithiasis were nonrandomly assigned to CLC or SILC. Prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin complexes (TAT), D-dimers, fibrinogen, and von Willebrand factor levels were measured at baseline, at 1st, and 24th hour, postoperatively. Twenty-six patients were finally included in the study. Fifteen patients underwent CLC (male/female: 5/10) and 11 underwent SILC (male/female: 1/10). There were no perioperative complications. An almost similar postoperative pattern and degree of activation of coagulation and fibrinolysis pathways was noted in both groups. No statistically significant differences were found between SILC and CLC for F1 + 2, TAT, D-dimers, fibrinogen, and von Willebrand factor levels, duration of surgery, length of hospital stay, and postoperative morbidity. A similar pattern and extent of coagulation and fibrinolysis activation is present in SILC and CLC, and therefore there is no difference in tendency for thrombosis. Thromboembolic prophylaxis should be considered in SILC as recommended for CLC, pharmacologic or mechanical, considering the hemorrhagic risk and the presence of additional thromboembolism risk factors. SILC appears to be a safe, feasible technique that can be recommended for its potential advantages in cosmesis and reduced incisional pain.

Spontaneous colo-umbilical fistula complicating diverticulitis of the sigmoid colon.

Colocutaneous fistula caused by diverticulitis is relatively uncommon with colo-umbilical fistulas being even rarer. We herein report a rare case of a spontaneous colo-umbilical fistula due to diverticulitis of the sigmoid colon. The fistula developed from a diverticulum of the sigmoid colon that discharged through the umbilicus after two episodes of acute diverticulitis. The condition was successfully treated by resectional surgery.

Peripheral neuropathy electrophysiological screening in inflammatory bowel disease.

AIM: Peripheral neuropathy is often described in inflammatory bowel disease (IBD). The aim of this study was to assess the need for neurophysiological testing in IBD patients without neurological symptoms or signs to detect early subclinical neuropathy and its possible correlations with clinical and demographic characteristics. MATERIALS AND METHODS: Ninety-seven consecutive IBD patients were screened for neurological symptoms and clinical signs, and those without symptoms or signs were included. Also, patients with comorbidities associated with peripheral neuropathy or a history of neurological disease were excluded. The remaining 45 asymptomatic patients were tested electrophysiologically for peripheral nerve involvement. RESULTS: None of the examined patients showed evidence for subclinical neuropathy. CONCLUSION: IBD patients with a normal neurological clinical examination and no symptoms have no evidence for neuropathy. Therefore, proper electrophysiological testing is not considered necessary.

Interleukin-1 associations in inflammatory bowel disease and the enteropathic seronegative spondylarthritis.

PURPOSE: This study aims to investigate any associations of the proinflammatory cytokine IL-1 in treated patients with inflammatory bowel disease (IBD) and the enteropathic seronegative spondylarthritis (eSpA). METHODS: Thirty-four patients with Crohn's disease (CD), 26 with ulcerative colitis (UC) and 14 patients with SpA participated in the study. Valid clinical indexes, CRP values and the endoscopic and histologic examination were used for the determination of disease activity. IL-1α, IL-1ß, IL-1 receptor antagonist (IL-1Ra) were measured by ELISA. Nonparametric tests were used for continuous and categorical data. RESULTS: Enteropathic SpA diagnosed in 29.4 % CD and 30.8 % UC patients. Active disease had 58.8 % CD (aCD), 76.9 % UC and 50 % SpA patients. Active and inactive CD (iCD) significantly differ on IL-1α levels (11.2 vs. 3.9 pg/ml; p = 0.034). Active and inactive UC significantly differ on IL-1ß (3.7 vs. 2.3 pg/ml; p = 0.054) and IL-1Ra levels (15.9 vs. 12.7 pg/ml; p = 0.023). Active and inactive SpA (iSpA) significantly differ on IL-1Ra (16.9 vs. 14.8 pg/ml; p = 0.033) and marginally on IL-1α levels (20 vs. 3.9 pg/ml; p = 0.06). Patients with aCD/ieSpA exhibited significant differences on IL-1α (p = 0.022) compared to those with iCD/ieSpA. CONCLUSIONS: IL-1α is associated with CD activity, while IL-1ß and IL-1Ra are associated with UC activity in treated patients with IBD. Prominent cytokine in SpAs seems to be IL-1α.

Common bile duct obstruction secondary to a periampullary diverticulum.

Periampullary duodenal diverticula are not uncommon and are usually asymptomatic although complications may occasionally occur. Here, we report the case of a 72-year-old woman who presented with painless obstructive jaundice. Laboratory tests showed abnormally elevated serum concentrations of total and direct bilirubin, of alkaline phosphatase, of γ-glutamyl transpeptidase, and of aspartate and alanine aminotransferases. Serum concentrations of the tumor markers carbohydrate antigen 19-9 and carcinoembryonic antigen were normal. Abdominal ultrasonography showed dilatation of the common bile duct (CBD), but no gallstones were found either in the gallbladder or in the CBD. The gallbladder wall was normal. Computed tomography failed to detect the cause of CBD obstruction. Magnetic resonance imaging and magnetic resonance cholangiopancreatography revealed a periampullary diverticulum measuring 2 cm in diameter and compressing the CBD. The pancreatic duct was normal. Hypotonic duodenography demonstrated a periampullary diverticulum with a filling defect corresponding to the papilla. CBD compression by the diverticulum was considered as the cause of jaundice. The patient was successfully treated by surgical excision of the diverticulum. In conclusion, the presence of a periampullary diverticulum should be considered in elderly patients presenting with obstructive jaundice in the absence of CBD gallstones or of a tumor mass. Non-interventional imaging studies should be preferred for diagnosis of this condition, and surgical or endoscopic interventions should be used judiciously for the effective and safe treatment of these patients.