Peripheral lymphocyte DNA damage and oxidative status after eradication therapy in patients infected with Helicobacter pylori.

INTRODUCTION: Helicobacter pylori infection has been shown to cause inflammation, increased production of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. However, the effect of eradication treatment on DNA damage in patients infected with H. pylori is unclear. OBJECTIVES: The objective of this study was to investigate the effect of eradication treatment on peripheral DNA damage and oxidative status in patients wth H. pylori infection. PATIENTS AND METHODS: The study involved 42 patients positive for H. pylori (Hp+) and 25 patients negative for H. pylori (Hp-). Peripheral lymphocyte DNA damage was assessed using the alkaline comet assay and plasma oxidative status was determined. Measurements were conducted at baseline and 2 weeks after eradication treatment. RESULTS: The total antioxidant status (TAS) was lower in Hp+ patients than in Hp- patients (P <0.05), while the total oxidant status (TOS), oxidative stress index (OSI), and peripheral lymphocyte DNA damage were higher (P <0.001 for all parameters). TOS, OSI, and peripheral lymphocyte DNA damage were significantly lower after eradication treatment (P <0.001 for all parameters), while TAS was significantly higher (P <0.05). There was no correlation between TOS, OSI, peripheral lymphocyte DNA damage, and TAS and the histopathological degree of antral gastric inflammation in the Hp+ group (P >0.05). CONCLUSIONS: Our results suggest that H. pylori eradication significantly decreases peripheral lymphocyte DNA damage and oxidative stress. Eradication treatment might help prevent the development of gastric cancer in patients with H. pylori infection.

Peripheral lymphocyte DNA damage and oxidative stress in patients with ulcerative colitis.

INTRODUCTION: Ulcerative colitis (UC) is a fairly common chronic inflammatory disorder. Chronic inflammation may contribute to the risk of colorectal cancer through the accumulation of specific products resulting from DNA damage. Previous studies reported that DNA damage and oxidative stress play a significant role in the pathophysiology of UC, but the results are inconsistent. OBJECTIVES: In the present study, we investigated peripheral DNA damage and oxidative stress in patients with UC. PATIENTS AND METHODS: The study included 20 patients with UC and 20 controls. Peripheral lymphocyte DNA damage was measured using the alkaline comet assay. Plasma total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) were determined. RESULTS: DNA damage levels, TOS, and OSI were significantly higher in patients with UC than in controls (P <0.001 for all parameters), while TAC was significantly lower (P <0.001). DNA damage was significantly correlated with TOS, TAC, and OSI (r = 0.604, P <0.001; r = -0.593, P <0.001; and r = 0.716, P <0.001, respectively). Moreover, TAC levels were significantly correlated with TOS and OSI (r = 0.604, P <0.001; r = -0.399, P <0.05; and r = -0.513, P <0.05, respectively). CONCLUSIONS: Our results show that increased peripheral DNA damage and oxidative stress seem to be associated with decreased antioxidant levels and thus may in part contribute to the development of colorectal cancer associated with UC.

Serum prolidase enzyme activity and its relation to histopathological findings in patients with non-alcoholic steatohepatitis.

The aim of this study was to investigate serum prolidase enzyme activity and to find out its association with liver biopsy specimens' histopathological findings in patients with nonalcoholic steatohepatitis (NASH), which may progress to liver fibrosis and cirrhosis. Thirty-six patients with biopsy-proven NASH and 29 healthy controls were enrolled. Serum prolidase enzyme activity was measured spectrophotometrically. Serum prolidase enzyme activity was significantly higher in patients with NASH than controls (P=0.016). A significant correlation was observed between serum prolidase enzyme activity and fibrosis score in patients with NASH (r=0.661, P<0.001). Serum prolidase activity seems to be correlated with the level of fibrosis. Monitoring serum prolidase activity may be a useful adjunctive tool in predicting liver fibrosis, especially in the absence of advanced fibrosis and other conditions, which may affect the interpretation of prolidase activity.

Prevalence and importance of amebic infestation in patients with ulcerative colitis in two regions in Turkey.

We investigated the prevalence of amebiasis in patients with ulcerative colitis residing in two geographical regions with different socioeconomic status and climatic conditions, and its effect on the age of onset, duration, localization, and activity of disease. Ninety patients from a high socioeconomic location (group I) and 28 cases from a low socioeconomic location (group II) were enrolled. Median age at disease onset was significantly higher in group I compared with in group II. Prevalence of amebiasis in group I was significantly lower than in group II. A considerably number of patients with amebiasis in group I had a history of travel to the cities with a lower socioeconomic level, mainly located in the east of Turkey. There was a strong relationship between presence of amebiasis and history of travel to eastern parts of Turkey among residents from the northwestern part of Turkey. Median age and age at time of diagnosis were significantly lower in patients with amebiasis compared with those without infection. In patients with mild disease activity, prevalence of amebiasis was significantly lower compared with those with moderate or severe disease activity. In conclusion, prevalence of amebiasis was markedly higher in the southeast compared to the northwest of Turkey. Travel to regions with low socioeconomic status may be considered a risk factor for amebiasis in patients with ulcerative colitis. Amebiasis enhances disease activity in ulcerative colitis.

Serum paraoxonase-1 activity in Helicobacter pylori infected subjects.

Previous studies have suggested that Helicobacter pylori (H. pylori) infection may play an important role in the process of atherosclerosis. The objective of this study was to investigate serum paraoxonase and arylesterase activities, and lipid hydroperoxide (LOOH) and total thiol (SH) levels along with lipid parameters in H. pylori infected subjects. Fifty-six H. pylori positive subjects and 43 H. pylori negative subjects were enrolled. Serum paraoxonase and arylesterase activities were measured spectrophotometrically. LOOH levels were measured by FOX-2 assay. Serum SH levels, paraoxonase and arylesterase activities were significantly lower in H. pylori positive group than H. pylori negative group (all p<0.05), while LOOH levels were significantly higher (p<0.05). In H. pylori positive subjects, serum LOOH levels were correlated with SH levels (r=-0.247, p<0.05), serum paraoxonase (r=-0.432, p<0.05) and arylesterase activities (r=-0.404, p<0.001), and triglyceride (r=0.305, p<0.05), total cholesterol (r=0.568, p<0.05), high-density lipoprotein-cholesterol (HDL-C) (r=-0.300, p<0.05) and low-density lipoprotein-cholesterol (LDL-C) (r=0.577, p<0.05) levels. Serum paraoxonase and arylesterase activities were also correlated with HDL-C levels (r=0.221, p<0.05 and r=0.291, p<0.05, respectively), while no correlation was observed with triglyceride, total cholesterol and LDL-C levels (both p>0.05). In conclusion, paraoxonase and arylesterase activities decrease significantly in H. pylori infected subjects. Lower serum paraoxonase-1 (PON1) activity seems to be related to decrease in HDL-C and, in part, to increased oxidative stress and inflammatory condition induced by H. pylori infection. Measurement of serum PON1 activity may help in the early identification of H. pylori infected subjects with increased risk of atherosclerotic disease.

Serum prolidase activity and oxidative status in Helicobacter pylori infection.

OBJECTIVES: During the course of Helicobacter pylori infection, increased oxidative stress plays an important role in the pathogenesis of gastroduodenal mucosal inflammation, which can cause gastric mucosal atrophy that characterized by the replacement of the gastric mucosal glands by collagen fibers. In the present study, we aimed to determine serum prolidase activity and oxidative status, and to find out if there is any association between serum prolidase activity and oxidative status in H. pylori infection. DESIGN AND METHODS: Forty H. pylori-positive and 32 H. pylori-negative subjects were enrolled. Serum prolidase activity was measured spectrophotometrically. Oxidative status was determined using total antioxidant capacity and total oxidant status measurement and calculation of oxidative stress index. RESULTS: Total antioxidant capacity level was lower in H. pylori-positive group than H. pylori-negative group (p<0.001), whereas total oxidant status, oxidative stress index and prolidase activity were higher (all p<0.05). Significant correlation was observed between serum prolidase activity, and total antioxidant capacity, total oxidant status and oxidative stress index (p<0.01, r=-0.367; p<0.05, r=0.283; p<0.01, r=0.379; respectively) in H. pylori-positive subjects. CONCLUSION: H. pylori infection may be associated with increased oxidative stress and increased serum prolidase activity. Increased oxidative stress seems to be associated with increased serum prolidase activity and this association may help to provide a better understanding about the pathogenesis of H. pylori infection.

Relationship between Helicobacter pylori status and serum pepsinogens as serologic markers in atrophic gastritis.

BACKGROUND/AIMS: Serum pepsinogen levels are considered as a non-endoscopic blood test in the diagnosis of atrophic gastritis. The objective of the present study was to investigate whether there is any difference between pepsinogen levels in Helicobacter pylori-positive and -negative patients with atrophic gastritis, and to analyze the relationship between histopathology and pepsinogen levels after treatment in H. pylori-positive patients with atrophic gastritis. METHODS: The study enrolled a total of 30 cases with atrophic gastritis (18 H. pylori-positive and 12 H. pylori-negative). The H. pylori-positive cases received a one-week eradication treatment. Initially for all and after the treatment for H. pylori-positive cases, serum pepsinogen I and II levels, anti-H. pylori IgG titration and histopathologic analysis were carried out. RESULTS: In the H. pylori-positive patients with atrophic gastritis, the levels of pepsinogen I and pepsinogen I/II ratio were lower while the levels of pepsinogen II were higher compared to the H. pylori-negative patients (p<0.05 for all). The post-treatment serum pepsinogen I levels and pepsinogen I/II ratios did not change in the H. pylori-positive group, while the levels of pepsinogen II, H. pylori antibody titration and gastric atrophy degree remarkably decreased (p<0.05 for all). CONCLUSIONS: In atrophic gastritis, the levels of serum pepsinogen and pepsinogen I/II ratio show a difference in H. pylori-negative versus -positive cases. Additionally, the usage of pepsinogen II as a serum marker in predicting the eradication of H. pylori with atrophic gastritis could be more reliable than pepsinogen I or the I/II ratio.

Relationship between levels of DNA damage in lymphocytes and histopathological severity of chronic hepatitis C and various clinical forms of hepatitis B.

BACKGROUND AND AIM: A significant proportion of cancer is attributable to DNA damage caused by chronic infection and inflammation. Because both hepatitis B and C viruses (HBV and HCV, respectively) cause chronic infection and inflammatory disease, the aim of the present study was to investigate whether there is a difference in peripheral DNA damage in patients with chronic HCV compared with patients with chronic HBV; and whether there is an association in the level of peripheral DNA damage with a natural history of HBV infection. METHODS: Twenty patients with chronic hepatitis C, 20 patients with chronic hepatitis B, 11 patients with cirrhosis secondary to hepatitis B, 12 inactive hepatitis B s antigen (HBsAg) carriers and 21 healthy subjects were included in the study. The DNA damage in lymphocytes was determined using the alkaline comet assay. RESULTS: Although the chronic hepatitis C group had similar levels of DNA damage compared with patients with cirrhosis due to hepatitis B (P > 0.05) and non-cirrhotic patients with chronic hepatitis B (P > 0.05), they had higher levels of DNA damage compared with inactive HBsAg carriers (P = 0.021) and controls (P = 0.001). Hepatitis B cirrhotic patients and patients with chronic hepatitis B had significantly higher levels of DNA damage than inactive HBsAg carriers (P = 0.002 and P = 0.012, respectively) and controls (both P = 0.001). Linear logistic regression analysis showed that chronic hepatitis C and HBV-related cirrhosis were discriminators in determining DNA damage in lymphocytes (beta 0.424 and P = 0.013, beta 0.393 and P = 0.016, respectively). CONCLUSIONS: Chronic hepatitis C, based on the severity of liver disease, or cirrhosis as an advanced form of HBV infection increase DNA damage in lymphocytes independently of confounding factors such as age, gender, body mass index and smoking habits.

Measurement of the total antioxidant response using a novel automated method in subjects with nonalcoholic steatohepatitis.

BACKGROUND: Oxidative stress, an increase in oxidants and/or a decrease in antioxidant capacity, is one of the potential biochemical mechanisms involved in the pathogenesis of nonalcoholic steatohepatitis. We aimed to investigate the total antioxidant response using a novel automated method in nonalcoholic steatohepatitis subjects. As a reciprocal measure, we also aimed to determine total peroxide level in the same plasma samples. METHODS: Twenty-two subjects with biopsy proven nonalcoholic steatohepatitis and 22 healthy controls were enrolled. Total antioxidant response and total peroxide level measurements were done in all participants. The ratio percentage of total peroxide level to total antioxidant response was regarded as oxidative stress index. RESULTS: Total antioxidant response of subjects with nonalcoholic steatohepatitis was significantly lower than controls (p < 0.05), while mean total peroxide level and mean oxidative stress index were higher (all p < 0.05). In subjects with nonalcoholic steatohepatitis, fibrosis score was significantly correlated with total peroxide level, total antioxidant response and oxidative stress index (p < 0.05, r = 0.607; p < 0.05, r = -0.506; p < 0.05, r = 0.728, respectively). However, no correlation was observed between necroimflamatory grade and those oxidative status parameters (all p > 0.05). CONCLUSION: Nonalcoholic steatohepatitis is associated with increased oxidant capacity, especially in the presence of liver fibrosis. The novel automated assay is a reliable and easily applicable method for total plasma antioxidant response measurement in nonalcoholic steatohepatitis.

High rate of seropositivity of Chlamydia pneumoniae IgA in male patients with nonalcoholic steatohepatitis.

The aim of this study was to investigate if there was any relationship between nonalcoholic steatohepatitis and the rate of Chlamydia pneumoniae seropositivity in a male population. Fifteen men with nonalcoholic steatohepatitis and 20 healthy men were enrolled in the study. The seropositivity rate of Chlamydia pneumoniae immunoglobulin A in the nonalcoholic steatohepatitis and control groups was 53.3 and 5%, respectively. The rate of Chlamydia pneumoniae immunoglobulin A positivity was significantly higher in the nonalcoholic steatohepatitis group than the controls (P = 0.002), while such a difference did not occur for Chlamydia pneumoniae immunoglobulin G positivity (P > 0.05). There is an association between nonalcoholic steatohepatitis and persistent Chlamydia pneumoniae infection as a probable causative or triggering agent. These findings suggest that further studies are necessary to clarify this association.

Clinical presentation of abdominal tuberculosis in HIV seronegative adults.

BACKGROUND: The accurate diagnosis of abdominal tuberculosis usually takes a long time and requires a high index of suspicion in clinic practice. Eighty-eight immune-competent patients with abdominal tuberculosis were grouped according to symptoms at presentation and followed prospectively in order to investigate the effect of symptomatic presentation on clinical diagnosis and prognosis. METHODS: Based upon the clinical presentation, the patients were divided into groups such as non-specific abdominal pain & less prominent in bowel habit, ascites, alteration in bowel habit, acute abdomen and others. Demographic, clinical and laboratory features, coexistence of pulmonary tuberculosis, diagnostic procedures, definitive diagnostic tests, need for surgical therapy, and response to treatment were assessed in each group. RESULTS: According to clinical presentation, five groups were constituted as non-specific abdominal pain (n = 24), ascites (n = 24), bowel habit alteration (n = 22), acute abdomen (n = 9) and others (n = 9). Patients presenting with acute abdomen had significantly higher white blood cell counts (p = 0.002) and abnormalities in abdominal plain radiographs (p = 0.014). Patients presenting with alteration in bowel habit were younger (p = 0.048). The frequency of colonoscopic abnormalities (7.5%), and need for therapeutic surgery (12.5%) were lower in patients with ascites, (p = 0.04) and (p = 0.001), respectively. There was no difference in gender, disease duration, diagnostic modalities, response to treatment, period to initial response, and mortality between groups (p > 0.05). Gastrointestinal tract alone was the most frequently involved part (38.5%), and this was associated with acid-fast bacteria in the sputum (p = 0.003). CONCLUSION: Gastrointestinal tract involvement is frequent in patients with active pulmonary tuberculosis. Although different clinical presentations of patients with abdominal tuberculosis determine diagnostic work up and need for therapeutic surgery, evidence based diagnosis and consequences of the disease does not change.

The optimal starting time of postoperative intraperitoneal mitomycin-C therapy with preserved intestinal wound healing.

BACKGROUND: There is controversy about the effect of the timing of intraperitoneal administration of chemotherapeutic agents on the healing of intestinal anastomosis. We have investigated the effect on intestinal wound healing of mitomycin-C administered at different times post-operatively. METHODS: Eighty-four Wistar-Albino female rats underwent ileal resection and end-to-end anastomosis. The rats were randomly selected for intraperitoneal administration of mitomycin-C or saline as follows: mitomycin-C group (n = 65), 2 mg/kg mitomycin-C; control group (n = 13), 10 ml saline. The former was sub-divided into 5 equal groups (A 1-5) and mitomycin-C was administered postoperatively as follows: day 0 (A1), day 3 (A2), day 5 (A3), day 7 (A4) and day 10 (A5). All the rats were sacrificed on the 14th postoperative day and anastomotic bursting pressures and tissue hydroxyproline levels were determined. RESULTS: Five of the animals died postoperatively: 2 (15.4%) in group A1, 2 (15.4%) in group A2 and 1(7.7%) in group A3. Non-lethal anastomotic leakage was observed in a further five animals: 1 in group A1, 2 in group A2, 1 in group A5 and 1 in the control group. Groups A1 and A2 had significantly lower anastomotic bursting pressures than the other groups (P was <0.05 for each comparison). The anastomotic bursting pressures of group A3, A4 and A5 were comparable with those of the controls (P was >0.05 for each comparison). Tissue hydroxyproline levels in group A1 and A2 were significantly lower than in the controls (P values were <0.05 for each comparison) or the other mitomycin-C sub-groups (P was <0.05 for each comparison). CONCLUSIONS: Intraperitoneal chemotherapy impairs intestinal wound healing when applied before the 5th postoperative day. Additional therapeutic approaches are needed to prevent this potentially lethal side effect of early intraperitoneal mitomycin-C administration.

Child-Pugh classification dependent alterations in serum leptin levels among cirrhotic patients: a case controlled study.

BACKGROUND: As anorexia and hypermetabolism are common in cirrhosis, leptin levels may be increased in this disease. In this study, we investigated the relation between the severity of disease and serum leptin levels in post-hepatitis cirrhosis and the role of body composition, gender and viral aetiology of cirrhosis in this association. METHODS: Thirty-five cases with post-hepatitis cirrhosis and 15 healthy controls were enrolled in this study. Body composition including body mass index, body fat percentage and body fat mass were determined. Serum leptin levels were assayed. RESULTS: Leptin levels were significantly higher among cirrhotic patients independent of sex compared to controls (p = 0.001). Female patients in both groups have had higher leptin levels than males (in cirrhotics p = 0.029, in controls p = 0.02). Cirrhotic patients in each of A, B and C subgroups according to the Child- Pugh classification revealed significantly different levels compared to controls (p = 0.046, p = 0.004, p = 0.0001, respectively). Male cirrhotics in Child-Pugh Class B and C subgroups had significantly higher leptin levels compared to male controls (p = 0.006, p = 0.008). On the other hand, female patients only in Child Pugh class C subgroup have had higher levels of serum leptin compared to controls (p = 0.022).Child-Pugh classification has been found to be the sole discriminator in determination of leptin levels in cirrhotics by linear regression (beta: 0.435 p = 0.015). CONCLUSION: Serum leptin levels increase in advanced liver disease independently of gender, body composition in posthepatitic cirrhosis. The increase is more abundant among patients that belong to C subgroup according to the Child- Pugh classification.