Otoimmün karaciğer hastalıklarında Helicobacter pylori ve üst gastrointestinal endoskopi bulgularının sıklığı

Giriş ve Amaç: Helicobacter pylori birçok gastrik hastalığın nedenidir. Otoimmün karaciğer hastalıklarına diğer hastalıklar ile ilişkisiz olan çeşitli üst gastrointestinal sistem mukozal bulguları eşlik edebilir. Çalışmamızdaki amacımız retrospektif olarak otoimmun karaciğer hastalıklarında üst gastro- intestinal endoskopi bulgularını taramak ve Helicobacter pylori ile ilişkisini araştırmaktır. Gereç ve Yöntem: Bu çalışmaya 99 otoimmün karaciğer has- tası ve 110 kontrol grubu hastası dahil edilmiştir. Her hastanın antrumdan ve gastrik yüzeyden alınan endoskopik biyopsileri incelenmiş ve Helicoba- cter pylori varlığı değerlendirilmiştir. Hastalar daha öncesinde asit süpres- yon, antibiyotik ya da steroid dışı inflamatuvar baskılayıcı ajan tedavisi almış ise ve veya çeşitli nedenler ile gastrik biyopsi alınmamış ise çalışmaya dahil edilmedi. Bulgular: Helicobacter pylori otoimmün hepatit hastalarında %60, primer biliyer siroz hastalarında %57 ve kontrol grubunda %63 saptandı. Üç grup arasında belirgin bir farklılık yoktu. Patolojik endoskopik bulgular otoimmün hepatit hastalarında %45, primer biliyer siroz hastalarında %52 ve kontrol grubunda %43 saptandı. Sonuç: Helicobacter pylori otoimmün hastalar ile kontrol grubu arasında benzer bulundu. Endoskopik antral gast- rit otoimmün hepatit hastalarında yüksek saptansa da otoimmün karaciğer hastalarında dispeptik gruba göre belirgin bir endoskopik bulgu farklılığı saptanmadı.Background and Aims: Helicobacter pylori is the main cause of gastric le- sions in chronic gastritis, autoimmune gastritis, peptic ulcer disease, and gastric cancer. Autoimmune liver disease is associated with various upper gastrointestinal mucosal lesions, which are not linked to the severity of the disease. The aim of this study was to retrospectively investigate upper gas- trointestinal mucosal lesions in relation to the prevalence of Helicobacter pylori infection in autoimmune liver disease. Materials and Methods: This study included 99 patients with autoimmune liver disease and 110 dyspep- tic patients as the control group. Endoscopy was performed in all patients, with biopsy specimens taken from the antrum and gastric body for histolog- ical examination and Helicobacter pylori detection. Patients were excluded if they had a history of acid suppression therapy, antibiotic or non-steroi- dal anti-inflammatory drug treatment, or if antrum and gastric body biopsy specimens could not be taken. Results: Helicobacter pylori was detected in 60% of autoimmune hepatitis cases, 57% of primary biliary cirrhosis cases, and 63% of controls. There was no statistically significant difference between the three groups. Abnormal findings during upper gastrointestinal endosco- py were found in 45% of autoimmune hepatitis cases, 52% primary biliary cirrhosis cases, and 43% of dyspeptic controls. Conclusion: Helicobacter pylori was detected in autoimmune liver disease cases at a similar frequency as in the control group. Endoscopic antral gastritis was more prevalent in autoimmune hepatitis than in primary biliary cirrhosis, but autoimmune liv- er disease was not significantly characterized by more upper gastrointestinal mucosal lesions than in dyspeptic controls

Prevalence of gastroesophageal reflux disease in a country with a high occurrence of Helicobacter pylori

WOS: 000391956000016PubMed ID: 28210089AIM To evaluate the prevalence of gastroesophageal reflux disease (GERD) with additional symptoms, relationship with Helicobacter pylori (H. pylori) of this country-wide study. METHODS Data from 3214 adults were obtained with validated questionnaire. Eight hundred and forty-one subjects were randomized to be tested for H. pylori via the urea breath test. "Frequent symptoms" were defined heartburn and/or regurgitation occurring at least weekly. RESULTS The prevalence of GERD was 22.8%, frequent and occasional heartburn were 9.3%-12.7%, regurgitation were 16.6%-18.7%, respectively. Body mass index (BMI) 30 was 28.5%. The GERD prevalence was higher in women (26.2%) than men (18.9%) (P < 0001). Overall prevalence of H. pylori was 75.7%. The prevalence was 77.1% in subjects without symptoms vs 71.4% in subjects with GERD (chi(2) = 2.6, P = 0.27). Underprivileged with the lowest income people exhibit a higher risk. CONCLUSION GERD is common in Turkey which reflects both Western and Eastern lifestyles with high rate of H. pylori. The presence of H. pylori had no effect on either the prevalence or the symptom profile of GERD. Subjects showing classical symptoms occasionally exhibit more additional symptoms compared with those without classical symptoms.Sanovel, TurkeySupported by This study partially support from Sanovel, Turkey

İrritabl barsak sendromu ve kolonoskopi

Background and Aims: The diagnosis of irritable bowel syndrome is symptom-based and the use of colonoscopy for diagnosis is not clearly defined. The aim of this study was to compare the colonoscopic findings in patients with irritable bowel syndrome and a control group and to evaluate the diagnosis by colonoscopy in patients with irritable bowel syndrome.&nbsp; Materials and Methods: The study included 210 irritable bowel syndrome patients and 166 controls identified retrospectively from among 2485 patients who underwent colonoscopy in Celal Bayar University Faculty of Medicine, Gastroenterology Department, between 2006 and 2010.&nbsp; Results:&nbsp; Colonoscopy findings were normal in 65% in the irritable bowel syndrome group and in 74% in the control group. The frequency of polyps was found to be more common in patients with irritable bowel syndrome (17.1%) than in the control group (7.4%).&nbsp; Conclusions: Although the statistical probability of normal colonoscopic findings is greater than of pathologic findings in irritable bowel syndrome patients, we believe the requirement of performing a colonoscopy should be revised once again.</p

The Importance of Apoptosis in Cancer Development and Treatment

Cancer is one of the most important causes of death in our era. Multifactorial causes are involved in the formation of cancer. The reduction of apoptosis is one of these reasons. Failure to activate apoptosis pathways can lead to resistance to the current treatment approaches of cancers. A better understanding of the molecular events that regulate apoptosis in cancers and cancer therapy form the basis of a more rational approach to the development of molecular targeted therapies in the fight against cancer

Hepatit B’ye Bağlı Kronik Karaciğer Hastalığında Safra Kesesi Motilitesinin Değerlendirilmesi

Amaç: Çalışmamızda hepatit B’ye bağlı kronik karaciğer hastalarında portal hipertansiyonla ilişkili faktörlerin safra kesesi duvar kalınlığı ve motilitesi üzerindeki etkilerine bakıldı. Aynı zamanda antrum duvar kalınlığı ve mide motilitesi üzerindeki etkilerine bakılması amaçlandı. Yöntemler: Çalışmaya portal hipertansiyon bulguları olmayan 10 hasta kontrol, portal hipertansiyon gelişmiş 20 hasta olgu grubu olarak alındı. Batın ultrasonografiyle açlık, test yemeği sonrası 15.dk, 30.dk, 60.dk, 90.dk, 120.dk safra kesesi ve antrum duvar kalınlığı, postprandiyal safra kesesi volümleri ve ejeksiyon fraksiyonları ölçüldü. Bulgular: Hastaların 15’i Child Pugh A (%50), 10’u Child Pugh B (%35), 5’i Child Pugh C (%15) olarak sınıflandırıldı. Her iki grupta zamanla safra kesesi ejeksiyon fraksiyon oranlarının arttığı, safra kesesi volümlerin de azalma olduğu gösterildi. Sirozlu hastaların safra kesesi duvar kalınlık değişimi kontrol grubuna göre 30 ve 90. dk’ larda istatistiksel anlamlı ölçüde arttığı gösterildi. Sirozlu hastalarda antrum duvar kalınlığındaki değişim oranının 15, 30. ve 120. dakikalarda istatistiksel olarak anlamlı şekilde arttığı gösterildi. Sonuç: Kronik karaciğer hastalığında safra kesesi duvar kalınlığında artma ve motilitesinde azalma olduğu saptandı. Bu sonuçlardan portal hipertansiyonun tek başına sorumlu olmadığı gösterildi. Portal hipertansiyon olan ve olmayan kronik karaciğer hastalarında safra kesesi hipomotilitesi yönünden bir fark olmadığı saptandı. Safra kesesi hipomotilitesi ve kese duvar kalınlaşmasında portal hipertansiyonla ilişkili karaciğer yetmezliğine bağlı rezervin azalması, hipoalbuminemi, safra stazı bilinen önemli nedenlerdir. Ancak portal hipertansiyon dışı nörohumoral faktörlerin de sorumlu olabileceğini düşündürdüğünden bununla ilgili ileri çalışmaların yapılması gerektiğini düşünmekteyiz.Objective: In our study, the effects of factors related to portal hypertension on gallbladder wall thickness and motility in chronic liver patients due to hepatitis B were investigated. At the same time, it was aimed to investigate the effects on antrum wall thickness and stomach motility. Method: 10 patients without portal hypertension findings were included in the study as control and 20 patients with portal hypertension were included as the case group. The gallbladder and antrum wall thickness, postprandial gallbladder volumes and ejection fractions were measured by abdominal ultrasonography, 15 minutes, 30 minutes, 60 minutes, 90 minutes, 120 minutes after the test meal. Results: 15 of the patients were classified as Child Pugh A (50%), 10 as Child Pugh B (35%), 5 as Child Pugh C (15%). It was shown that ejection fraction rates increased and gall bladder volumes decreased in time in both groups. It was shown that gallbladder wall thickness change in cirrhotic patients increased statistically significantly at 30 and 90 minutes compared to the control group. It was shown that the rate of change in antrum wall thickness in patients with cirrhosis significantly increased at 15, 30 and 120 minutes. Conclusion: Increased gallbladder wall thickness and decreased motility were found in chronic liver disease. It has been shown that portal hypertension alone is not responsible from these results. It was found that there was no difference in terms of gall bladder hypomotility in chronic liver patients with and without portal hypertension. In gallbladder hypomotility and bladder wall thickening, decreased reserve due to liver failure associated with portal hypertension, hypoalbuminemia, and bile stasis are known important causes. However, we think that further studies should be carried out, as it suggests that neurohumoral factors other than portal hypertension may also be responsible