Investigation of Clinical, Laboratory, Imaging Findings and Histopathological Features of Patients with Gastric Neuroendocrine Cell Hyperplasia.

BACKGROUND/AIMS: Neuroendocrine cell hyperplasia is a non-neoplastic proliferation of enterochromaffin-like cells and is considered a premalignant lesion because of their potential to progress to neuroendocrine tumor. In this study, we aimed to evaluate the demographic and clinical features, laboratory, radiological and endoscopic findings, gastric biopsy histopathological features, follow-up frequency, and histopathological findings of patients diagnosed with gastric neuroendocrine cell hyperplasia as well as to investigate the factors that play a role in the development of neuroendocrine tumors on the basis of neuroendocrine cell hyperplasia. MATERIALS AND METHODS: The study has been conducted in 2 centers with 282 patients that were grouped as those with and without neuroendocrine tumor. Individuals with control endoscopy were separated as those with regression of neuroendocrine cell hyperplasia and those without regression, and the determined parameters were evaluated between the groups. RESULTS: The most common histological subtype of neuroendocrine cell hyperplasia was linear+micronodular (50.4%). Neuroendocrine tumor developed in 4.3% (12/282) of the patients with neuroendocrine cell hyperplasia after a mean of 36 months. The presence of polyps as confirmed via endoscopy and dysplasia as confirmed via histopathological examination was significantly higher in favor of the group with neuroendocrine tumor (P = .01). In patients with neuroendocrine cell hyperplasia regressed and patients in whom it did not regress were examined, the rate of asymptomatic patients and increased sedimentation rate were found in favor of the group that did not regress (P = .02 and P = .02), but no difference was found in other parameters. CONCLUSION: Neuroendocrine tumor development rate was found to be 4.3% in the background of neuroendocrine cell hyperplasia. Two factors predicting progression from neuroendocrine cell hyperplasia to neuroendocrine tumor can be elaborated as the presence of polypoid appearance due to neuroendocrine cell hyperplasia as confirmed via endoscopy and dysplasia as confirmed via histopathological examination.

What Is the Place of Intermediate Care Unit in Patients with COVID-19? A Single Center Experience.

Introduction: COVID-19 pandemic has led to an increased rate of intensive care unit (ICU) stays. Intermediate care units (IMCUs) are a useful resource for the management of patients with severe COVID-19 that do not require ICU admission. In this research, we aimed to determine survival outcomes and parameters predicting mortality in patients who have been admitted to IMCU. Materials and Methods: Patients who were admitted to IMCU between April 2019 and January 2021 were analyzed retrospectively. Sociodemographics, clinical characteristics, and blood parameters on admission were compared between the patients who died in IMCU and the others. Blood parameters at discharge were compared between survived and deceased individuals. Survival analysis was performed via Kaplan-Meier analysis. Blood parameters predicting mortality were determined by univariate and multivariate Cox regression analysis. Results: A total of 140 patients were included within the scope of this study. The median age was 72.5 years, and 77 (55%) of them were male and 63 (45%) of them were female. A total of 37 (26.4%) patients deceased in IMCU, and 40 patients (28.5%) were transferred to ICU. Higher platelet count (HR 3.454; 95% CI 1.383-8.625; p=0.008), procalcitonin levels (HR 3.083; 95% CI 1.158-8.206; p=0.024), and lower oxygen saturation (HR 4.121; 95% CI 2.018-8.414; p < 0.001) were associated with an increased risk of mortality in IMCU. At discharge from IMCU, higher procalcitonin levels (HR 2.809; 95% CI 1.216-6.487; p=0.016), lower platelet count (HR 2.269; 95% CI 1.012-5.085; p=0.047), and noninvasive mechanic ventilation requirement (HR 2.363; 95% CI 1.201-4.651; p=0.013) were associated with an increased risk of mortality. Median OS was found as 41 days. The overall survival rate was found 40% while the IMCU survival rate was 73.6%. Conclusions: IMCU seems to have a positive effect on survival in patients with severe COVID-19 infection. Close monitoring of these parameters and early intervention may improve survival rates and outcomes.

Can Ischemia Modified Albumin (IMA) Levels Be a Predictor of Acute Pancreatitis?

BACKGROUND: We aimed to evaluate the value of ischemia modified albumin (IMA) as a prognostic marker in acute pancreatitis (AP) patients, determine whether it is efficient in assessing the disease severity or not, and to estimate the correlation between IMA and the inflammatory markers, prognostic markers and scoring systems routinely used in clinical practice. METHODS: 100 adult patients (18 years and older) who have been hospitalized and evaluated with AP diagnosis in Tepecik Training and Research Hospital,, Department of Gastroenterology, between April 1, 2017 and April 1, 2018 have been enrolled in the study. Patients have been stratified disease etiology (biliary or non-biliary). The non-biliary group has been divided into subgroups as alcoholic, lipemic, or idiopathic. Disease severity has been categorized as mild, moderate, or severe pancreatitis according to the Atlanta classification. Ranson, Harmless Acute Pancreatitis Score (HAPS), Bedside Severity Index for Acute Pancreatitis (BISAP) scores have been determined for each patient. Patients have been grouped as necrotizing or edematous according to the Atlanta classification. RESULTS: According to our findings, IMA has been found to be correlated with disease severity, Ranson and BISAP scores, and procalcitonin levels. We have observed that some laboratory parameters including blood urea nitrogen and hematocrit levels and HAPS scoring system are not correlated to IMA. CONCLUSION: Our study is the first study to compare multiple prognostic factors with IMA in AP patients. In our study, the association between IMA and AP has been evaluated in the context of prognostic scoring and disease severity.

The validity and reliability study of the University of California, Los Angeles Scleroderma Clinical Trial Consortium Gastrointestinal Tract (UCLA SCTC GIT) 2.0 questionnaire for the Turkish society.

BACKGROUND/AIMS: To translate the University of California, Los Angeles Scleroderma Clinical Trial Consortium Gastrointestinal Tract (UCLA SCTC GIT) 2.0 questionnaire from English to Turkish and to validate it. MATERIALS AND METHODS: UCLA SCTC GIT 2.0 was translated into Turkish using the translation-retranslation method. The available Turkish GIT 2.0 and the Short Form 36 (SF-36) were administered to 97 Turkish-speaking patients with systemic sclerosis (Ssc). Internal consistency reliability and structural validity were assessed by analyzing the correlations between the UCLA SCTC GIT 2.0 and the SF-36 scales. Internal consistency was determined by calculating Cronbach's alpha. For evaluation of reliability, the questionnaire scale was repeatedly applied to a subgroup of patients with a 2-week interval, and the intraclass correlation coefficient (ICC) was calculated. The Spearman's correlation coefficients between the GIT and the SF-36 scores were calculated. RESULTS: A group of 97 patients with Ssc with a mean age of 55.37±11.35 years and a female predominance (87.6%) were included in the study. The Cronbach's alpha value for the UCLA SCTC GIT 2.0 scale was 0.894. ICC was 0.821 (p=0.000). The scale showed acceptable reliability, with the exception of the diarrhea subscale (alpha=0.356). There was a moderate correlation between the total GIT score and the Short Form 36 (SF-36) subscales. All of the items in the scale were included in the validity analysis owing to their reliability. CONCLUSION: The Turkish GIT 2.0 scale showed good internal consistency, high reliability, and an acceptable validity.

Mucosal healing effect of nilotinib in indomethacin-induced enterocolitis: A rat model.

AIM: To investigate the effects of nilotinib in a rat model of indomethacin-induced enterocolitis. METHODS: Twenty-one Wistar albino female rats obtained from Dokuz Eylul University Department of Laboratory Animal Science were divided into the following three groups: control (n = 7), indomethacin (n = 7) and nilotinib (n = 7). A volume of 0.25 mL of physiological serum placebo was administered to the control and indomethacin groups through an orogastric tube for 13 d. To induce enterocolitis, the indomethacin and nilotinib groups received 7.5 mL/kg indomethacin dissolved in 5% sodium bicarbonate and administered subcutaneously in a volume of 0.5 mL twice daily for three days. Nilotinib was administered 20 mg/kg/d in two divided doses to the nilotinib group of rats for 13 d through an orogastric tube, beginning on the same day as indomethacin administration. For 13 d, the rats were fed a standard diet, and their weights were monitored daily. After the rats were sacrificed, the intestinal and colonic tissue samples were examined. The macroscopic and microscopic pathology scores were evaluated. The pathologist stained all tissue samples using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling method. Mucosal crypts and apoptotic cells were quantified. The platelet-derived growth factor receptor (PDGFR) α and ß scores assessed by immunohistochemical staining method and tissue and serum tumor necrosis factor (TNF) α levels were determined by enzyme-linked immunosorbent assay. RESULTS: Between days 1 and 13, the rats in the nilotinib and indomethacin groups lost significantly more weight than the controls (-11 g vs +14.14 g, P = 0.013; -30 g vs +14.14 g, P = 0.003). In the small intestinal and colonic tissues, the macroscopic scores were significantly lower in the nilotinib group than in the indomethacin group (1.14 ± 0.38 and 7.29 ± 2.98, P = 0.005; 1.14 ± 0.38 and 7.43 ± 2.64, P = 0.001, respectively), but the values of the nilotinib and indomethacin groups were similar to the control group. In the small intestinal and colonic tissues, the microscopic scores were significantly lower in the nilotinib group than in the indomethacin group (3.43 ± 2.99 and 7.67 ± 3.67, P = 0.043; 2.29 ± 0.76 and 8.80 ± 2.68, P = 0.003, respectively), but the values were similar to the control group. The PDGFR ß scores in the small intestine and colon were significantly lower in the nilotinib group than in the indomethacin group (1.43 ± 0.79 and 2.43 ± 0.54, P = 0.021; 1.57 ± 0.54 and 3 ± 0, P =0.001), and the values were similar to controls. The colonic PDGFR α scores were significantly lower in the nilotinib group than in the indomethacin group (1.71 ± 0.49 and 3 ± 0, P = 0.001). The colonic apoptosis scores were significantly lower in the controls than in the nilotinib group (1.57 ± 1.13 and 4 ± 1.29, P = 0.007). Furthermore, the serum and tissue TNF-α levels were similar between the nilotinib and indomethacin groups. CONCLUSION: In the indomethacin-induced enterocolitis rat model, nilotinib has a positive effect on the macroscopic and microscopic pathologic scores, ensuring considerable mucosal healing. Nilotinib decreases PDGFR α and ß levels and increases the colonic apoptotic scores, but it has no significant effects on weight loss and the TNF-α levels.

The validity and reliability of "The liver disease symptom index 2.0" for Turkish society.

BACKGROUND/AIMS: Chronic liver diseases have been shown to adversely affect the quality of life. Standardized tools for patient assessment are of great importance for treatment and follow-up of these patients. In this study, we aimed to determine the validity and reliability of the Liver Symptom Index 2.0 (LDSI 2.0) for Turkish society, for use in other studies and in daily clinical practice. MATERIALS AND METHODS: A total of 308 patients with chronic liver disease attending to the outpatient liver clinic of the Department of Gastroenterology, Faculty of Medicine, Dokuz Eylül University between September 2011 and May 2012 were included in this study. A sociodemographic data questionnaire, the LDSI 2.0 comprising 24 items, and the Short Form-36 (SF-36) were completed by the participating patients. After 6 weeks, these tools were re-administered to a total of 115 patients. After obtaining the required permissions, LDSI 2.0 was translated into Turkish using the translation/re-translation method. RESULTS: Of the 308 participants, 160 (51.9%) were male and 184 (43.1%) were female, with an average age of 48.67±13.31 years. Of all cases, 70.5% had viral hepatitis. The average Child-Pugh score was 5.9±1.2, and the average Model For End-Stage Liver Disease (MELD) score was 10.2±3.2. The assessment tool comprised the following sub-items: itching, joint pain, abdominal pain, sleepiness, worry, appetite, depression, fear, jaundice, memory, personality, financial status, use of time, sexual desire, and sexual activity. For more than 50% of the patients, worry (68.8%), depression (65.3%), joint pain (62.3%), itch (56.5%), sleepiness (54.2%), memory problems (53.6), and sexual problems (50%) were present. The internal coefficient of consistency (Cronbach alpha coefficient) was 0.908, which indicates a very high level of consistency. The correlation coefficient for the intraobserver test/re-test reliability was 0.746 (p<0.000), which denotes a significant and good level of reliability. The construct validity between each sub-item of the tool and sub-items of SF-36 was assessed using Spearman's correlation test, which showed a weak to moderate correlation (<0.04 and 0.4-0.7) in the reverse direction. CONCLUSION: Our study findings provide supportive evidence of the reliability of the assessment tool. Its validity is similar to the original construct validity and was confirmed in our sample. Therefore, it was concluded that LDSI 2.0 was an appropriate tool for daily clinical use and research purposes. Simultaneous use of this life-quality assessment tool and SF-36 will enable a comprehensive but practical assessment of our patients.

Nilotinib-mediated mucosal healing in a rat model of colitis.

AIM: To investigate the effects of nilotinib in a rat model of trinitrobenzene sulfonic acid (TNBS)-induced colitis. METHODS: Twenty-one Wistar albino female rats obtained from Dokuz Eylul University Department of Laboratory Animal Science were categorized into a control (n = 7), TNBS (n = 7) and nilotinib group (n = 7). Saline was administered orally for 14 d to the control and the TNBS group. The TNBS group received rectal TNBS on the first day while saline was administered to the control group. The nilotinib group received 20 mg/kg nilotinib for 14 d in 2 divided doses, starting the same day as TNBS administration. For 14 d, the rats were fed a standard diet, and their weights were recorded daily. After sacrifice, colon tissue samples from each group were scored for macroscopic and microscopic pathology. Apoptotic indices were determined by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling method. Platelet-derived growth factor receptor (PDGFR) alpha and beta levels were assessed through immunohistochemistry staining scores and compared among the groups. Tissue and serum tumor necrosis factor (TNF) alpha levels were determined by enzyme-linked immunosorbent assay. RESULTS: Between days 1 and 14, the nilotinib group rats lost significantly less weight than the TNBS group rats (-0.7 g vs -14.0 g, P = 0.047). The difference in weight between the control and nilotinib groups was also statistically significant (+8.3 g vs -0.7 g, P = 0.031). From day 7 to day 14, the weight differences of the control group vs the TNBS group, the TNBS group vs the nilotinib group, and the control group vs the nilotinib group were all statistically significant (+8.0 g vs -11.1 g, P = 0.007; -11.1 g vs +2.9 g, P = 0.015; +8.0 g vs +2.9 g, P = 0.042, respectively). Macroscopic and microscopic scores were significantly lower in the nilotinib group than in the TNBS group (0.00 ± 0.00 vs 1.43 ± 0.65, P = 0.009; 2.86 ± 0.55 vs 7.71 ± 1.48, P = 0.030, respectively). However, these scores were similar between the nilotinib and control groups. While no significant difference for the nilotinib vs control groups could be determined for PDGFR alpha and beta scores, PDGFR alpha and beta scores were lower in the nilotinib group than in the TNBS group. Furthermore, the TNF alpha levels in the serum, tissue and apoptosis scores were similar between the nilotinib and TNBS groups. CONCLUSION: Nilotinib prevents weight loss, facilitates mucosal healing by improving the pathological scores without introducing variation into the apoptotic scores or TNF alpha levels.