Acute peripancreatic fluid collection in acute pancreatitis: Incidence, outcome, and association with inflammatory markers.

Background: The hospital outcomes and predictors of acute peripancreatic fluid collection (APFC) have not been well-characterized. In this study, we aimed to investigate the clinical outcomes of APFC in patients with acute pancreatitis (AP) and the role of the systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), and C-reactive protein (CRP) level in predicting the occurrence of APFC. Methods: In this retrospective study, the complicated group (patients with APFC) and the uncomplicated group (patients without APFC) were compared for their clinical characteristics, hospital outcomes (mortality rate, intensive care unit admission rate, and length of hospital stay), pseudocyst formation, CRP levels, SII, and SIRI on admission and at 48 hours. Results: Of 132 patients with AP, 51 (38.6%) had APFC and eight (6.1%) had pancreatic pseudocysts. Of 51 patients with APFC, 15.7% had pancreatic pseudocysts. Pseudocyst did not develop in the uncomplicated group. SII value at 48 h [median 859 (541-1740) x 109/L vs. 610 (343-1259) x 109/L, P = 0.01] and CRP level at 48 h [89 (40-237) mg/L vs. 38 (12-122) mg/L, P = 0.01] were higher in the complicated group than in the uncomplicated group. The length of hospital stay was longer in the complicated group, compared with the uncomplicated group [median 8 days (5-15), vs. 4 days (3-7), P < 0.001, respectively]. No significant difference was detected between the two study groups' mortality rates and intensive care unit admission rates. Conclusions: While 38.6% of the AP patients had APFC, 6.1% of all patients and 15.7% of the patients with APFC had pancreatic pseudocysts. APFC was found to lengthen the hospital stay and to be associated with the SII value and CRP level measured at 48 h.

Effect of Direct-acting Oral Anticoagulants and Warfarin on Hospital Outcomes in Upper Gastrointestinal Bleeding.

OBJECTIVE: To evaluate the comparison of direct-acting oral anticoagulants (DOACs) and warfarin for their effects on major bleeding and hospital outcomes in patients with acute nonvariceal upper gastrointestinal bleeding (NVUGIB). STUDY DESIGN: An observational study. PLACE AND DURATION OF STUDY: Tekirdag Namik Kemal University Hospital, Hitit University Erol Olçok Education and Research Hospital, between January and December 2021. METHODOLOGY: Adult patients prescribed warfarin and DOACs were followed up for one year. Their length of hospital stay, need for intensive care unit admission, need for red blood cell transfusion, and major bleeding rates were compared. RESULTS: Thirty-two patients (61.5%) were user of DOACs (DOAC group), and 20 patients (38.5%) were users of warfarin (warfarin group). No statistically significant difference was determined between patients in warfarin group and DOAC group for the number of packed red blood cells transfused [median 3 (0-6) units, 3 (0-10) units, p=0.229, respectively], length of hospital stay [median 5 days (3-10), and 4.5 days (2-20), p=0.739, respectively], rate of intensive care unit admission [(n=9, 45%; and n=10 (31%), p=0.623, respectively] and the occurrence of major bleeding events (warfarin-70%; DOACs-78%; p=0.529). CONCLUSION: Major bleeding episodes and hospital outcomes of acute NVUGIB were similar between patients receiving warfarin and DOACs. KEY WORDS: Direct-acting oral anticoagulants, Warfarin, Gastrointestinal bleeding, Outcome, Mortality.

Ki67 as a prognostic factor for long-term outcome following surgery in gastrointestinal stromal tumors.

OBJECTIVE: This study aimed to examine the value of Ki67 expression along with other potential prognostic factors for predicting overall survival and disease-free survival in patients with gastrointestinal stromal tumors who underwent curative resection. PATIENTS AND METHODS: Sixty-eight histologically confirmed and operated patients with gastrointestinal stromal tumors were included. Clinical and follow-up data were retrieved from medical records and patients were contacted at the end of the study. The effects of certain clinical and histopathological parameters on survival outcomes were examined. RESULTS: Sixty-eight patients were followed for a mean duration of follow-up of 2923.3 patient-months. Twelve deaths (17.6%), seven metastasis (10.3%), and two local recurrences (2.9%) occurred. Overall survival was 102.5 months [95% confidence interval (CI), 88.3-116.8] and disease-free survival was 91.8 months (95% CI, 76.5-107.2). Multivariate analyses identified a high Ki67 index (≥ 10%) as an independent predictor of both poor overall survival (hazard ratio, 4.8; 95% CI 1.2-19.2; P=0.027) and poor disease-free survival (hazard ratio, 15.3; 95% CI, 4.7-50.2). CONCLUSION: A high Ki67 expression seems to be a useful prognostic factor that would aid in predicting disease course in gastrointestinal stromal tumors. These findings deserve further investigation in larger studies.

Serum annexin A2 levels in patients with colon cancer in comparison to healthy controls and in relation to tumor pathology.

BACKGROUND: The deregulation and localization of the Annexins is consistently reported to have close relation to tumor cell malignancy, invasion, and metastasis as well as clinical progression of tumors. This study aimed to evaluate serum Annexin A2 (Anx A2) levels in patients with colon cancer in comparison to healthy controls and in relation to demographics and tumor pathology. MATERIAL AND METHODS: A total of 100 patients (mean (SD) age: 58 (5.8) years, 55.0% females) with colon cancer and 70 controls (mean (SD) age: 59 (5.4) years, 50.0% females) were included. Serum levels for Anx A2 were evaluated in relation to study group, demographics, and tumor pathology. RESULTS: Serum levels for Anx A2 were significantly lower in patients with colon cancer than in controls (13.1 (4.5) vs. 22.8 (2.1) ng/mL, p<0.001) and significantly decreased with increase in tumor size (p=0.003), and at higher stages of TNM (p=0.004), tumor invasion (p=0.005), lymph node metastasis (p=0.003), and distant metastasis (p=0.005). CONCLUSIONS: Our findings indicate a significant decrease in Anx A2 expression in colon cancer patients compared to healthy controls and in parallel with tumor progression.

Isolated hepatic tuberculosis: a rare cause of hepatic mass lesions.

Hepatic tuberculosis usually accompanies pulmonary and extrapulmonary tuberculosis. Although isolated hepatic tuberculosis is a very rare condition, it should be considered in the differential diagnosis of a hepatic mass. Here, we report a 42-year-old woman presenting with weight loss, fever, night sweats, and a hepatic mass on the abdominal ultrasonography and magnetic resonance imaging (MRI). Ultrasonography-guided percutaneous needle biopsy demonstrated a caseating granuloma with epithelioid histiocytes and giant cells compatible with the diagnosis of tuberculosis. The patient was treated with four anti-tuberculous drugs for 1 year. She recovered clinically, and her post-treatment abdominal MRI was normal.

Foreign material in the gastrointestinal tract: cocaine packets.

Smuggling drugs by swallowing or inserting into a body cavity is not only a serious and growing international crime, but can also lead to lethal medical complications. The most common cause of death in 'body packers', people transporting drugs by ingesting a packet into the gastrointestinal tract, is acute drug toxicity from a ruptured packet. However, more than 30 years after the initial report of body packing, there is still no definitive treatment protocol for the management of this patient group. The treatment strategy is determined according to the particular condition of the patient and the clinical experience of the treatment center. Surgical intervention is also less common now, due to both the use of improved packaging materials among smugglers and a shift towards a more conservative medical approach. Herein, we report a case of toxicity from ingested packets of cocaine that leaked and, despite surgery, resulted in exitus of the patient.

Immunohistochemical analysis of Ki-67, p53 and Bcl-2 expression related to histological features in gastroesophageal reflux disease.

BACKGROUND/AIMS: The endoscopic and histologic findings of gastroesophageal reflux disease are usually indistinct. The current study was designed to define accurately the histology in gastroesophageal reflux disease and to develop a hypothesis that reflux produces immunohistochemical changes. METHODS: The study was based on the examination of endoscopic esophageal biopsy specimens obtained from 20 patients with evidence of reflux with 24-hour pH-meter monitoring and from 20 control subjects without clinical or endoscopic reflux. The pathogenesis of reflux esophagitis was discussed by comparing the histopathologic changes with determined Ki-67, p53 and Bcl-2 immunoreactivity. RESULTS: In this study, the presence of esophagitis was determined endoscopically in only 55% of the patients with gastroesophageal reflux disease, while microscopic esophagitis was detected in 60% of them. No correlation was found between presence of endoscopic esophagitis and microscopic esophagitis in the patients with gastroesophageal reflux disease. There was a significant difference between control cases and the patients according to histological parameters, which included basal activity (p=0.006), height of papillae (p=0.006), intraepithelial neutrophils (p=0.000), intraepithelial eosinophils (p=0.006), congestion (p=0.001), and dilated intercellular spaces (p=0.006). Immunohistochemically, there was a significant difference in the expression of p53 and Ki-67 between the three study groups (patients with/without microscopic esophagitis, controls) (p<0.05). However, there was no difference in Bcl-2 between the patients with reflux and control cases. CONCLUSIONS: In this study, we considered that microscopic esophagitis does not always accompany reflux, and the lack of reliable diagnostic histologic criteria is still a serious problem for pathologists. Immunohistochemically, an increase in cell proliferative activity and p53 protein accumulation to repair oxidative DNA damage related to reflux were observed. However, the close Bcl-2 immunoreactivity in all groups that was indicated by a weak positivity suggests that the inhibition of apoptosis may not be involved in reflux esophagitis.

The role of pRB, p16 and cyclin D1 in colonic carcinogenesis.

BACKGROUND/AIMS: This study is aimed to investigate abnormal expression of the Rb protein (pRb), p16(INK4a) (p16) and cyclin D1 in colorectal adenomas and adenocarcinomas and to assess the possible alterations in Rb pathway in colorectal carcinogenesis. METHODOLOGY: 44 cases of colorectal adenoma and 44 cases of colorectal adenocarcinoma were examined histopathologically and immunohistochemically using monoclonal antibodies to identify abnormalities of pRb, p16, and cyclin D1 expression. Staining degree of above-mentioned markers was assessed by using a semi-quantitative method in all cases in order to determine any staining differences. RESULTS: In 70.5% of the adenomas and 97.7% of the adenocarcinomas, an overexpression of pRb was found. There was a statistically significant relationship between the immunoreactivity of pRb and villous/tubulovillous types of adenomas (p < 0.05). There was a loss of p16 expression in 84.1% of adenomas and 61.4% of adenocarcinomas. Statistically significantly, the p16 overexpression was not seen in any of tubular adenomas (p < 0.001). Overexpression of cyclin D1 was found in only 9.1% of adenomas, while 31.8% of adenocarcinomas overexpressed this protein. Loss of expression of cyclin D1 was similar in adenomas and adenocarcinomas (27.3% and 25%, respectively). Staining degrees of all three cell cycle proteins were shown to be statistically different in adenomas and adenocarcinomas, for pRb (p = 0.001), for p16 ( p = 0.045), and cyclin D1 ( p = 0.05). Also, there was only a mild agreement with respect to p16 and cyclin D1 relationship between for adenomas ( K = +0.28 p = 0.051) and for adenocarcinomas ( K = +0.35 p = 0.017). Besides, there was no correlation between the expression of pRb, p16, and cyclin D1 and clinicopathological tumor characteristics and prognostic data such as stage or lymph node/liver metastasis. CONCLUSIONS: pRb, p16 and cyclin D1 are shown to be aberrantly expressed in both colorectal adenomas and adenocarcinomas. It can be claimed that disturbances in Rb pathway take part in colonic carcinogenesis and pRb, p16 and cyclin D1 play an ever increasing role in the further stages of adenoma-carcinoma sequence.

Features of chronic inflammation at the gastric cardia and the relationship with Helicobacter pylori infection and oesophagitis.

BACKGROUND: The etiopathogenesis of chronic inflammation at the gastric cardia is still debated. It is suggested that carditis may be a finding of gastro-oesophageal reflux disease (GORD) or it may occur as a result of the gastritis caused by Helicobacter pylori (H. pylori) infection. AIM: To examine morphological features of carditis, as well as the associations of carditis with Helicobacter pylori gastritis and oesophagitis as a marker of gastro-oesophageal reflux disease. PATIENTS AND METHODS: Endoscopic biopsy specimens obtained systematically from oesophagus, cardia, corpus and antrum of 135 dyspeptic patients were retrospectively evaluated. In biopsies, we have searched for any correlations between clinical, endoscopic, and histological features. RESULTS: Carditis was detected in 123 (91.1%) of the cases. The mean age of the carditis group was 47.9 years and the male-to-female ratio was 1.08:1. The relation of carditis with age and sex was not significant (p = 0.19 and p = 0.24, respectively). All cases of the carditis group had concomitant chronic gastritis. In these cases, chronic inflammation, degree of neutrophil-mediated activity and H. pylori colonisation were significantly correlated in cardia, corpus and antrum (p < 0.001). Intestinal metaplasia was observed in 14 cases (11.3%) and, was associated with H. pylori colonisation (p < 0.001). Microscopic oesophagitis detected in 37.7% cases also showed correlation with reflux symptoms and endoscopic oesophagitis but not carditis. When all cases with carditis were evaluated for H. pylori infection and oesophagitis, which are presumed risk factors for carditis, H. pylori infection appeared to be an independent risk factor for carditis (p = 0.012), while oesophagitis did not. CONCLUSIONS: This study suggests that carditis is commonly found in patients presenting with dyspepsia and the histological features of carditis were similar to those seen in H. pylori gastritis in antrum and corpus. In addition, our data have also shown that carditis was significantly associated with H. pylori infection but not with symptoms or signs of GORD.

Somatostatin infusion and hemodynamic changes in patients with non-variceal upper gastrointestinal bleeding: a pilot study.

BACKGROUND: Intravenous somatostatin decreases acid secretion, splanchnic blood flow, and portal pressure, but the evidence for its efficacy in the treatment of non-variceal upper gastrointestinal bleeding has been mixed. We aimed to evaluate the vasoactive effect and possible mechanisms of somatostatin infusion in the cessation of non-variceal upper gastrointestinal bleeding. MATERIAL/METHODS: Patients with non-variceal upper gastrointestinal bleeding without portal hypertension were enrolled in the study. They were given somatostatin infusion in a dose of 250 microgr/hour for 72 hours. Superior mesenteric arterial average flow velocity (SMA-V), SMA pulsatility index (SMA-PI), portal venous volume flow (PV-F), and renal artery resistance index (RA-RI) were measured two times for each patient by Doppler ultrasound; once on the first day of infusion therapy and again 6 hours or more after stopping the infusion. RESULTS: 21 patients (12 male, mean age 44.1 +/- 9.9) with bleeding peptic ulcer were enrolled. During somatostatin infusion, PV-F was 33.7 +/- 12.7 cm3/sec. After stopping infusion, it increased to 56.3 +/- 16.0 cm3/sec (p=0.001). SMA-V was 39.7 +/- 13.1 cm/sec and 64.4 +/- 15.1 cm/sec during somatostatin infusion and after cessation of somatostatin respectively (p=0.01). SMA-PI was 2.0 +/- 0.8 during somatostatin infusion but 2.8 +/- 0.8 without somatostatin infusion (p=0.02). However, RA-RI showed no difference between states with or without somatostatin infusion (p>0.05). CONCLUSIONS: Somatostatin infusion causes a decrease in arterial blood flow to the stomach and duodenum in patients with non-variceal upper gastrointestinal bleeding without portal hypertension. Somatostatin therapy also decreases portal blood flow while not altering renal blood.

The effect of perendoscopic sclerosing agent injection in Forrest's II ulcers -- a pilot study from Turkey.

BACKGROUND: We aimed to clarify the outcome of perendoscopic prophylactic injection of sclerosing agent in Forrest's II ulcers. MATERIAL/METHODS: Patients with upper gastrointestinal bleeding in last 6 hours were performed emergency endoscopy and were enrolled. The patients in group-1 were performed prophylactic injection therapy with 1% aethoxysclerol and then given medical treatment with intravenous 40 mg omeprazole twice a day and somatostatin infusion at the dose of 6 mg/day during 3 days. Group-2 patients were only given medical treatment with same agents and at same doses without having any perendoscopic therapy. RESULTS: There were 32 patients in group-1 and 20 in group-2. In emergency endoscopy, 20 (62.5%) patients had IIa ulcers and 12 (37.5%) patients had IIb ulcers in group-1. These patients underwent prophylactic perendoscopic hemostasis by 1% aethoxysclerol in addition to medical treatment. Early rebleeding occurred in 9 (28.1%) patients of group-1 and 3 (15%) in group-2 (p<0.001). At the endoscopic control after 48 hours 13 (40.6%) patients in the group-1 and 15 (75%) patients in group-2 showed improved local ulcer stigmata (p<0.001). The numbers of blood units transfused were lower in the group-2 (p=0.002). The hospital stay was longer in group-1 (p=0.01). In the group-1, more endoscopic intervention was needed. Any death and the need for surgical intervention did not occurred in any groups. CONCLUSIONS: According to our results; the indication of perendoscopic prophylactic injection of sclerosing agent in non-bleeding ulcers with high risk of rebleeding must be reviewed by large population based, prospective, randomized trials.

Combination thymosin-alpha 1 and interferon-alpha 2b in the treatment of anti-HBe-positive chronic hepatitis B in Turkey.

BACKGROUND/AIMS: The most prevalent type of chronic hepatitis B in Turkey is anti-HBe-positive. No consistently effective therapy is yet available for the treatment of these patients. The aim of this study was to assess the efficacy and safety of interferon-alpha and thymosin-alpha 1 combination in the treatment of naive anti-HBe-positive and HBV DNA-positive chronic hepatitis B patients. METHODOLOGY: Twenty-one patients were enrolled in the study. All patients had documented anti-HBe-positive, HBV DNA-positive chronic active hepatitis B without evidence of cirrhosis. Patients received a 26-week combination course of 1.6 mg thymosin-alpha 1 subcutaneously twice a week and 10 MIU interferon-alpha subcutaneously three times a week, followed by interferon-alpha monotherapy at the same dose for another 26 weeks. After treatment patients were observed for a further 26 weeks. Endpoints were a normalization of alanine aminotransferase and negativity of HBV DNA at weeks 52 and 78, as well as an improvement in liver histology at week 78. RESULTS: Eighteen (87.7%) of the 21 patients responded by losing serum HBV DNA and normalizing alanine aminotransferase values at the end of the 52-week treatment period. Sixteen (76.2%) of these patients became sustained responders, with normal alanine aminotransferase and negative HBV DNA at the end of 78 weeks. Two patients were non-responders, two relapsed and one had a breakthrough during therapy. Significant improvements in the Knodell histological activity index were observed in the responders. No adverse events other than those seen previously with interferon monotherapy were reported. CONCLUSIONS: Combination interferon-alpha 2b and thymosin-alpha 1 treatment may provide a safe and effective therapeutic approach for the difficult-to-treat anti-HBe-positive chronic hepatitis B patients. Further controlled studies are needed to assess the full role of this treatment strategy.

Histological and clinical predictive value of determination of tissue CagA status by PCR in Helicobacter pylori infected patients; results of the large population based study in western Turkey.

BACKGROUND/AIMS: Early experimental and epidemiological studies have suggested that the presence of cagA gene was a virulence factor for Helicobacter pylori. We aimed to investigate the clinical significance of tissue CagA status in Helicobacter pylori infected patients and to assess its association with histological changes in gastric mucosa. METHODOLOGY: Three hundred and forty-five patients with Helicobacter pylori infection established by both urease test and histological examination were included in the study. The symptoms of the patients were recorded according to the Glasgow dyspepsia scale. Biopsies (cardia, corpus, angulus and antrum) were evaluated histologically according to the Sidney system. The cagA status was determined by polymerase chain reaction method from an antral biopsy. Polymerase chain reaction studies were performed by Wizard genomic DNA purification system (promega). We also determined the serum levels of tumor necrosis factor-alpha, and gastrin. They were all prescribed lansoprazole (30 mg b.i.d.), clarithromycin (500 mg b.i.d.), and amoxycillin (1 g b.i.d.) for a week. At the 8th week a second endoscopy was performed and further biopsy specimens were obtained from the same sites. Mann-Whitney U and chi 2 tests were used for statistical analyses. RESULTS: Two hundred and thirty-five patients (68.1%) were infected with cagA-positive strains of Helicobacter pylori and the other 110 patients (31.8%) were infected with cagA-negative strains. We compared the parameters and measurements studied in this trial between the patients infected with cagA-positive and negative Helicobacter pylori strains. Helicobacter pylori density was greater in the cagA-positive group by 1.9 +/- 0.9 than in the cagA-negative group by 1.2 +/- 0.7 (P = 0.01). Helicobacter pylori activity and chronic inflammation also were significantly higher in the cagA-positive group with the values of 1.4 +/- 0.8 and 2.1 +/- 1.1 than in the cagA-negative group with 0.7 +/- 0.2 and 1.3 +/- 0.5, respectively (P = 0.001, P = 0.002). The presence of atrophy and lymphoid aggregate was not different between the two groups (P > 0.05). However intestinal metaplasia was shown to be significantly frequent in patients infected with cagA-positive Helicobacter pylori strains (0.001). Serum tumor necrosis factor-alpha and gastrin levels which were accepted as the markers of inflammation in Helicobacter pylori infection were increased in the cagA-positive group compared with the cagA-negative group. Serum tumor necrosis factor-alpha level was 11.3 +/- 7.0 pg/mL in the cagA-positive group and 4.9 +/- 2.7 pg/mL in the cagA-negative group (P = 0.001). Gastrin level also showed a significant difference between two groups by 66.8 +/- 31.1 pg/mL and 37.2 +/- 19.2 pg/mL, respectively, in the cagA-positive and negative groups (P = 0.001). The virulent strains seem to cause peptic ulcer more frequently. Peptic ulcer was determined in 17% of patients in the cagA-positive group but this ratio was 9% in the cagA-negative group (P = 0.608). Although, all these differences of the degree of inflammation, clinical spectrum and biochemical parameters were seen, interestingly there was no significant difference in the severity of the symptoms of the patients in both groups according to Glasgow dyspepsia severity score (P = 0.20). CONCLUSIONS: Our results confirm that cagA-positive strains of Helicobacter pylori cause greater histological changes. However this virulence is not associated with more severe symptoms. The histological changes can be predictable by determining the tissue cagA status.