Nese Imeryuz

Botulinum toxin injection versus lateral internal sphincterotomy in the treatment of chronic anal fissure: a non-randomized controlled trial

BackgroundAlthough lateral internal sphincterotomy is the gold-standard treatment for chronic anal fissure, intrasphincteric injection of botulinum toxin seems to be a reliable new option. The aim of this non-randomized study is to compare the effect of lateral internal sphincterotomy and botulinum toxin injection treatments on the outcome and reduction of anal sphincter pressures in patients with chronic anal fissure.MethodsPatients with chronic anal fissure were treated with either botulinum toxin injection or lateral internal sphincterotomy by their own choice. Maximal resting pressure and maximal squeeze pressure measurements were performed before and 2 weeks after treatments by anal manometry. Patients were followed for fissure relapse during 14 months.ResultsTwenty-one consecutive outpatients with posterior chronic anal fissure were enrolled. Eleven patients underwent surgery and ten patients received botulinum toxin injection treatment. Before the treatment, anal pressures were found to be similar in both groups. After the treatment, the maximal resting pressures were reduced from 104 ± 22 mmHg to 86 ± 15 mmHg in the surgery group (p < 0.05) and from 101 ± 23 mmHg to 83 ± 24 mmHg in the botulinum toxin group (p < 0.05). The mean maximal squeeze pressures were reduced from 70 ± 27 mmHg to 61 ± 32 mmHg (p > 0.05) in the surgery group, and from 117 ± 62 mmHg to 76 ± 34 (p < 0.01) in the botulinum toxin group. The fissures were healed in 70 percent of patients in the botulinum group and 82 percent in the surgery group (p > 0.05). There were no relapses during the 14 months of follow up.ConclusionLateral internal sphincterotomy and botulinum toxin injection treatments both seem to be equally effective in the treatment of chronic anal fissure.

Clinical characteristics of inflammatory bowel disease in Turkey: a multicenter epidemiologic survey.

Aim To investigate the epidemiologic and clinical characteristics of inflammatory bowel disease (IBD) patients in a large multicenter, countrywide, hospital-based study in Turkey. Materials and Methods Twelve centers uniformly distributed throughout Turkey reported through a questionnaire the new IBD cases between 2001 and 2003. The incidence of ulcerative colitis (UC) and Crohns disease (CD) has been reported per 100,000 people. Epidemiologic features and clinical characteristics of both diseases were analyzed. Results During the study period, 661 patients of UC and 216 patients of CD were identified. The incidence in the referral population was 4.4/100,000 and 2.2/100,000 for UC and CD, respectively. The age of the patients showed the characteristic biphasic distribution with 2 peaks between 20 and 30 and 50 and 70 years. A male predominance was observed in both diseases. A history of smoking was detected in 15.5% of UC patients and 49.3% of patients with CD. Family history was positive in 4.4% in UC and 8.3% in CD patients. Concomitant amebiasis was observed in 17.3% of patients with UC and 1.3% of patients with CD. A history of appendectomy was reported in 15% of patients with CD and only 3% of patients with UC. Both extraintestinal and local complications were more frequent in CD patients, whereas arthritis was most common in both diseases. Conclusions IBDs are frequently encountered in Turkey. IBD incidence is lower than North and West Europe but close to Middle East in our country. The majority of IBD cases are diagnosed in young people (20 to 40 y) with predominance in males. The rate of both intestinal and extraintestinal complications in our population was low when compared with the data reported in the literature. IBD and especially UC, can coexist with amebiasis or become manifest with amebic infestation. The presence of concomitant ameba may create confusion and cause dilemmas in the diagnosis and treatment of UC.

Orlistat accelerates gastric emptying and attenuates GIP release in healthy subjects

Orlistat, an inhibitor of digestive lipases, is widely used for the treatment of obesity. Previous reports on the effect of orally ingested orlistat together with a meal on gastric emptying and secretion of gut peptides that modulate postprandial responses are controversial. We investigated the effect of ingested orlistat on gastric emptying and plasma responses of gut peptides in response to a solid mixed meal with a moderate energy load. In healthy subjects, gastric emptying was determined using scintigraphy and studies were performed without and with 120 mg of orlistat in pellet form in random order. Orlistat shortened t lag and t half and decreased the area under the gastric emptying curve. Orlistat significantly attenuated the secretion of glucose-dependent insulinotropic polypeptide (GIP) but did not alter the plasma responses of cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), pancreatic polypeptide (PP), and insulin. There was no peptide YY (PYY) response. Area under the curve of gastric emptying was positively correlated with integrated secretion of GIP (r=0.786) in orlistat and was negatively correlated with integrated plasma response of GLP-1 (r=-0.75) in control experiments, implying that inhibition of fat absorption modifies determinants of gastric emptying of a meal. Orlistat administered similar to its use in obesity treatment accelerates gastric emptying of a solid mixed meal with a moderate energy load and profoundly attenuates release of GIP without appreciably altering plasma responses of CCK, GLP-1, and PP. Since GIP is being implemented in the development of obesity, its role in weight control attained by orlistat awaits further investigation.

Corticosteroid therapy augments gastroduodenal permeability to sucrose

Objective:The aim of the present study was to investigate whether corticosteroid therapy alters gastroduodenal mucosal permeability and whether permeability alteration is associated with macroscopic mucosal damage.Methods:Eight patients taking oral corticosteroid therapy (total prednisone-equivalent dose, 1.5 ± 0.1 g; duration, ∼30 days), nine patients with multiple sclerosis taking high-dose intravenous methyl-prednisolone therapy (total dose, 11.7 ± 0.5 g; duration, ∼9 days), and 20 age- and gender-matched controls were studied. Gastroduodenal permeability was determined using sucrose as a site-specific permeability probe. Five-hour urine was collected after ingesting 100 g of sucrose and its urinary excretion rate was measured using high-pressure liquid chromatography. Gastroduodenal endoscopy was performed before steroid therapy to exclude subjects with evidence of macroscopic mucosal lesions. The sucrose test and endoscopy were repeated after completion of corticosteroid therapy.Results:The urinary sucrose excretion rates were similar in the control group and in patient groups before corticosteroid therapy. The median excretion rate of sucrose increased four (one to 28)- and eight (two to 35)-fold, respectively, as compared with pretreatment values in patients taking oral steroid and high-dose intravenous methyl-prednisolone therapy (p < 0.01). Considering all patients together, subjects who received a mean prednisone-equivalent dose of 8.4 ± 1.5 g exhibited mucosal lesions, whereas patients who received 3.3 ± 1.8 g did not (p= 0.06). The posttherapy increments in sucrose excretion rates were associated with neither the presence of macroscopic lesions nor with the total steroid dose received.Conclusion:Corticosteroid therapy augments gastroduodenal permeability and high doses are associated with macroscopic mucosal lesions. Steroid-induced permeability increase does not appear to be associated with the presence of macroscopic mucosal lesions.

Noninvasive detection of hepatic steatosis in patients without ultrasonographic evidence of fatty liver using the controlled attenuation parameter evaluated with transient elastography.

Objective Although ultrasound is a useful technique for detecting hepatic steatosis, it cannot provide a precise determination of hepatic fat content. A novel attenuation parameter named controlled attenuation parameter (CAP) has been developed to process the raw ultrasonic signals acquired by Fibroscan. The aim of this study was to determine the percentage of hepatic steatosis in apparently healthy Turkish individuals using the proposed diagnostic cut-off points for CAP. In addition, we sought to investigate the association of CAP with the traditional risk factors for nonalcoholic fatty liver disease in a screening setting. Materials and methods In the present study, 102 Turkish individuals without evidence of fatty liver on ultrasound and normal aminotransferase levels underwent CAP measurements by means of Fibroscan. Results The mean (SD), median (minimum−maximum), and 5th and 95th percentile values of CAP values in this cohort of 102 individuals were 206.99 (48.12), 210.5 (100.0−314.0), 113.4 and 280.2 dB/m, respectively. Using the cut-offs of 222, 238, and 283 dB/m for CAP, there were 39 (38.2%), 23 (22.5%), and five (4.9%) individuals out of 102 who had at least 10% steatosis despite normal liver findings on ultrasound. After allowance for potential confounders, CAP was independently associated with BMI (&bgr;=0.39, t=3.5, P<0.001) and the number of metabolic syndrome criteria (&bgr;=0.24, t=2.1, P<0.05). Conclusion These results hold promise for early noninvasive detection of hepatic steatosis on the basis of CAP assessment.

The effects of psychiatric treatment on depression, anxiety, quality of life, and sexual dysfunction in patients with inflammatory bowel disease

Objective Depression and anxiety are common disorders in inflammatory bowel disease (IBD). Our aim is to prospectively determine the effect of psychiatric treatment on scores for depression, anxiety, quality of life (QoL), and sexual dysfunction in an outpatient population diagnosed with IBD and also anxiety and/or depression disorder. Patients and methods Patients who scored higher than the cutoff point on the Hospital Anxiety Depression Scale were referred for further structured psychiatric evaluation and determination of the need for psychiatric drug treatment. Patients who underwent drug therapy completed Short Form-36 (SF-36) and the Arizona Sexual Experience Scale at baseline and after 6 months of follow-up. Results Major depressive disorder and generalized anxiety disorder were the most common diagnoses. After 6 months, 47 patients had completely adhered to drug treatment (group A), whereas 20 were nonadherent (group B). In group A, all domains of SF-36, Arizona Sexual Experience Scale, depression/anxiety scores, and Crohn’s disease activity index were statistically improved after treatment when compared with the baseline. In group B, the three domains of SF-36, platelet count, and mean corpuscular volume were worse between baseline and at 6 months. Conclusion In IBD patients having any psychiatric disorder, 6 months of antidepressant drug treatment is associated with an improvement in depression, anxiety, QoL, and sexual functioning scores, as well as an improvement in Crohn’s disease activity index. On the other hand, insufficient psychiatric treatment seems to be related to a poor QoL.

Serum zinc-α2-glycoprotein concentrations in patients with non-alcoholic fatty liver disease

Abstract Background: Evidence suggests that zinc-α2-glycoprotein (ZAG) might serve as a biomarker for human metabolic alterations. We measured serum ZAG in patients with non-alcoholic fatty liver disease (NAFLD), a hepatic manifestation of the metabolic syndrome, and examined its association with clinical, biochemical, and histological phenotypes. Methods: Serum ZAG was determined using ELISA in 90 patients with biopsy-proven NAFLD and 81 controls. Results: Serum ZAG concentrations did not differ in patients with NAFLD (median 61 μg/mL; interquartile range: 56–73 μg/mL) compared with healthy controls (median 66 μg/mL; interquartile range: 56–78 μg/mL, Mann-Whitney U-test, p=NS). However, among patients with NAFLD serum ZAG concentrations were significantly higher in males and in those with the metabolic syndrome. After stepwise linear regression analysis, serum ZAG concentrations were the only independent predictor of the number of metabolic syndrome components in patients with NAFLD (β=0.22; t=2.001, p<0.05). Conclusions: In summary, the hypothesis of an association between NAFLD and serum ZAG concentrations is not supported by the present results. However, ZAG remains an interesting molecule for further research in the field of human metabolic disorders.

Mechanisms of basolateral Na+ transport in rabbit esophageal epithelial cells

We examined the mechanisms of cellular Na+ transport, both Cl- dependent and Cl- independent, in the mammalian esophageal epithelium. Rabbit esophageal epithelium was dissected from its muscular layers and mounted in a modified Ussing chamber for impalement with ion-selective microelectrodes. In bicarbonate Ringer, transepithelial potential difference was -14.9 ± 0.9 mV, the transepithelial resistance ( R TE) was 1,879 ± 142 Ω ⋅ cm2, the basolateral membrane potential difference ( V mBL) was -53 ± 1.5 mV, and the intracellular activity of Na+([Formula: see text]) was 24.6 ± 2.1 mM. Removal of Na+ and Cl- from the serosal and luminal baths decreased [Formula: see text] to 6.6 ± 0.6 mM. Readdition of Na+ to the serosal bath in the absence of Cl- increased[Formula: see text] by 21.8 ± 3.0 mM, whereas V mBL and R TE remained unchanged. When serosal Na+ was readded in the presence of amiloride the increase in[Formula: see text] and the rate of Na+ entry were decreased by ∼50%. 5-( N-ethyl- N-isopropyl)amiloride mimicked the effect of amiloride, whereas phenamil did not. Subsequent readdition of Cl- to the serosal bath further increased [Formula: see text] by 4.4 ± 1.9 mM. When the cells were acid loaded by pretreatment with[Formula: see text] in nominally[Formula: see text]-free Ringer, intracellular pH measurements showed a pHi recovery that is dependent on the presence of Na+ in the serosal bath and that can be blocked by amiloride. These data indicate that esophageal epithelial cells possess a Na+-dependent, amiloride-sensitive electroneutral mechanism for Na+entry consistent with the presence of a basolateral Na+/H+ exchanger. The ability of Cl- to further enhance Na+ entry supports the existence of at least one additional Cl--dependent component of basolateral Na+entry.We examined the mechanisms of cellular Na+ transport, both Cl- dependent and Cl- independent, in the mammalian esophageal epithelium. Rabbit esophageal epithelium was dissected from its muscular layers and mounted in a modified Ussing chamber for impalement with ion-selective microelectrodes. In bicarbonate Ringer, transepithelial potential difference was -14.9 +/- 0.9 mV, the transepithelial resistance (RTE) was 1,879 +/- 142 Omega. cm2, the basolateral membrane potential difference (VmBL) was -53 +/- 1.5 mV, and the intracellular activity of Na+ (aNai) was 24.6 +/- 2.1 mM. Removal of Na+ and Cl- from the serosal and luminal baths decreased aNai to 6.6 +/- 0.6 mM. Readdition of Na+ to the serosal bath in the absence of Cl- increased aNai by 21.8 +/- 3.0 mM, whereas VmBL and RTE remained unchanged. When serosal Na+ was readded in the presence of amiloride the increase in aNai and the rate of Na+ entry were decreased by approximately 50%. 5-(N-ethyl-N-isopropyl)amiloride mimicked the effect of amiloride, whereas phenamil did not. Subsequent readdition of Cl- to the serosal bath further increased aNai by 4.4 +/- 1.9 mM. When the cells were acid loaded by pretreatment with NH+4 in nominally HCO-3-free Ringer, intracellular pH measurements showed a pHi recovery that is dependent on the presence of Na+ in the serosal bath and that can be blocked by amiloride. These data indicate that esophageal epithelial cells possess a Na+-dependent, amiloride-sensitive electroneutral mechanism for Na+ entry consistent with the presence of a basolateral Na+/H+ exchanger. The ability of Cl- to further enhance Na+ entry supports the existence of at least one additional Cl--dependent component of basolateral Na+ entry.

Serum insulin-like growth factor-1 and insulin-like growth factor binding protein-3 levels in patients with chronic hepatitis B / Kronik hepatit B hastalarında serum insülin benzeri büyüme faktörü 1 (IGF-1) ve insülin benzeri büyüme faktörü bağlayıcı protein 3 (IGFBP-3) düzeyleri

Abstract Objective: Decreased serum insulin-like growth factor-1 (IGF-1) and insulin like growth factor binding protein-3 (IGFBP-3) levels have been found in patients with chronic liver disease of different etiologies, but these factors have not been studied extensively in patients with hepatitis B virus (HBV)-induced chronic liver disease. Methods: We have investigated serum IGF-1 and IGFBP-3 levels in 40 patients with chronic HBV and 40 patients with HBV-induced cirrhosis. According to Child-Pugh classification cirrhotic patients were divided into three groups. Forty age-and sex-matched healthy subjects served as controls. IGF-1 and IGFBP-3 levels were measured by immunochemiluminescence. The results were compared with those for serum albumin, total bilirubin, transaminase activity, and with prothrombin time. Results: IGF-1 and IGFBP-3 levels were significantly lower in patients with cirrhosis than in those with chronic HBV and in controls (p<0.001). In chronic HBV patients, IGFBP-3 levels were significantly lower than in controls (p=0.013). IGF-1 and IGFBP-3 levels were significantly lower in cirrhotic patients with Child-Pugh stage B and Child-Pugh stage C compared with Child-Pugh stage A (for IGF-1 p=0.037 and p<0.001, for IGFBP-3 p=0.036 and p<0.001, respectively). In patients with Child-Pugh stage C significantly IGF-1 levels were lower than in patients with Child-Pugh stage B (p=0.003). IGF-1 and IGFBP-3 levels were positively correlated with serum albumin concentrations and negatively correlated with serum total bilirubin and prothrombin time concentrations in cirrhotic patients. IGF-1 and IGFBP-3 levels in chronic HBV patients were negatively correlated with serum transaminases. Conclusion: We conclude that serum levels of IGF-1 and IGFBP-3 may be useful markers for liver dysfunction in patients with HBV-induced chronic liver disease. Özet Amaç: Farklı etyolojilere bağlı kronik karaciğer hastalığı olan hastalarda serum insülin benzeri büyüme faktörü 1 (IGF-1) ve insülin benzeri büyüme faktörü bağlayıcı protein 3 (IGFBP-3) düzeyleri düşük bulunmuştur, fakat bu parametreler hepatit B virüsüne (HBV) bağlı kronik karaciğer hastalığı olan hastalarda geniş capta calışılmamıştır. Metod: Bu çalışmada kronik HBV’li 40 hasta ve HBV’ye bağlı sirozu olan 40 hasta calışmaya dahil edildi. Child- Pugh sınıflandırmasına göre sirozlu hastalar üç gruba ayrıldı. Yaş ve cinsiyet uyumlu 40 sağlıklı birey kontrol grubu olarak kullanıldı. IGF-1 ve IGFBP-3 düzeyleri immünokemilüminesans yöntemle ölçüldü. Sonuçlar serum albümini, total bilirübin, transaminaz aktiviteleri ve protrombin zamanı ile karşılaştırıldı. Bulgular: IGF-1 ve IGFBP-3 düzeyleri sirozlu hastalarda kronik HBV’li ve kontrollere göre belirgin olarak düşüktü (p<0.001). Kronik HBV’li hastalarda IGFBP-3 duzeyleri kontrollere göre belirgin olarak düşüktü (p=0.013). Serum IGF-1 ve IGFBP-3 düzeyleri siroz hastalarında Child-Pugh B ve Child-Pugh C gruplarında Child-Pugh A grubuna göre belirgin olarak düşüktü (sırasıyla IGF-1 için p=0.037 ve p<0.001; IGFBP-3 için p=0.036 ve p<0.001). Serum IGF-1 düzeyleri Child-Pugh C grubunda Child-Pugh B grubuna göre belirgin olarak düşüktü (p=0.003). Siroz hastalarında IGF-1 ve IGFBP-3 duzeyleri serum albümin konsantrasyonu ile pozitif, protrombin zamanı ve serum total bilirübin konsantrasyonu ile negatif korelasyon göstermekteydi. Kronik HBV’li hastalarda IGF 1 ve IGFBP-3 düzeyleri serum transaminazlarıyla ise negatif korelasyon göstermekteydi. Sonuç: HBV’ye bağlı kronik karaciğer hastalığı olan hastalarda IGF-1 ve IGFBP-3 karaciğer bozukluğunu değerlendirmekte yararlı belirtecler olabilir.

Association of MDR1 Gene and Helicobacter pylori in the Development of Gastric Cancer and Gastritis

G A A b st ra ct s colonized bacteria in stomach was estimated as the copy number of 16S rRNA gene by the real-time PCR analysis using theH. heilmannii-specific primer pair of 16S rRNA gene.Results: Gastric MALT lymphoma formation by infection with H. heilmannii was observed in C57BL/ 6J mice, but it was not detected in IL-10 knockout mice. In the IL-10 knockout mice, a large number of infected bacteria were observed as much as the same amounts of C57BL/6J mice. Microarray and KEGG pathway analyses revealed that cell migration related pathways, namely the Intestinal immune network for IgA production (hsa04672) and the Leukocyte transendothelial migration (hsa04670), were activated in the H. heilmannii TKY infected C57BL/6J mice. Quantitative RT-PCR analysis confirmed that the expression of several integrin genes (α4, αL, αM, β2, and β7) and TNF-receptor super family genes (BCMA, TACI, and BAFFR), were significantly upregulated by infection with H. heilmannii in C57BL/ 6 mice. However, these induced gene expressions were not shown in IL-10 knockout mice. Conclusion: Cell migration related pathway cascade is activated in the H. heilmannii TKY infected gastric mucosa through IL-10 dependent signaling. These might be the cause of gastric MALT lymphoma by infection with H. heilmanii.