Murat Harputluoglu

Brain natriuretic peptide and severity of disease in non-alcoholic cirrhotic patients.

Background:  Cirrhotic patients have a hyperdynamic systemic circulation. They have insidious cardiac problems besides well‐known complications. Brain natriuretic peptide (BNP) relaxes vascular smooth muscle and has a portal hypotensive action. The relations between BNP levels and severity of disease, cardiac dysfunction and esophageal varices were studied in non‐alcoholic cirrhotic patients.

The relationship of heart rate variability with severity and prognosis of cirrhosis.

Many studies have demonstrated that cirrhosis is frequently associated with autonomic dysfunction. The aim of this study was to test autonomic dysfunction in cirrhotic patients by analyzing heart rate variability (HRV), to determine whether or not the degree of autonomic dysfunction is correlated with the severity of disease, and, also, to compare the changes of HRV between survivor and nonsurvivor groups after 2-year follow-up periods. HRV was analyzed using 24-hr ECG recording in 30 cirrhotic patients and 28 normal controls. The changes in HRV parameters including mean normal-to-normal (N-N) interbeat intervals (mean NN), standard deviation of all N-N intervals (SDNN), standard deviation of the average of N-N intervals for each 5-min period over 24 hr (SDANN), root mean square succesive differences (r-MSSD; msec), and percentage of adjacent N-N intervals that are >50 msec apart (pNN50), all as time domain parameters, were evaluated. The cirrhotic patients were also evaluated according to Child-Pugh classification scores as markers of the disease severity. The time-domain measures of HRV in cirrhotic patients were significantly reduced compared with those in the control group (for all parameters; P < 0.001). The severity of disease was associated with reduced HRV measures (for all parameters; P < 0.001). After the 2-year follow-up periods, HRV measurements in cirrhotic patients were significantly much lower in nonsurvivors than in survivors (P < 0.001 for all). We conclude that increasing severity of cirrhosis is associated with a reduction in HRV. This finding may be an indicator of poor prognosis and mortality for cirrhosis.

Epicardial adipose tissue, hepatic steatosis and obesity

Objective: Hepatic steatosis is a common companion of obesity. Moreover, the measurement of epicardial adipose tissue (EAT) has been reported to be related with both obesity and insulin resistance. Therefore, we aimed to evaluate the relationship between hepatic steatosis, EAT and insulin resistance in obese patients. Methods: Sixty-three obese subjects were enrolled in the study. Patients were divided into 3 groups according to body mass index (BMI) as follows: 20 patients with 30≤BMI<35 kg/m2 (Group 1, mean age 39.3±12.9 yr), 25 patients with 35≤BMI<40 kg/m2 (Group 2, mean age 41.7±9.3 yr), and 18 patients with BMI≥40 kg/m2 (Group 3, mean age 36.8±13.9 yr). EAT and grade of hepatic steatosis were assessed sonographically. Anthropometrical measurements were assessed with the foot-to-foot bioelectrical impedance analysis. Insulin resistance was assessed according to basal insulin, quantitative insulin sensitivity check index (QUICKI) and homeostasis model assessment (HOMA) equations. Results: Although EAT was similarly higher in both groups 2 and 3, these groups were found to be similar in terms of the grade of hepatic steatosis. Both EAT and the grade of hepatic steatosis were correlated with whole body fat mass, abdominal adiposity, insulin resistance, and triglyceridemia but waist circumference was the only factor affecting EAT thickness. Highly sensitive C-reactive protein (hsCRP) was the only metabolic parameter that was significantly higher in Group 3 than in Group 1 (p=0.02). Conclusion: Hepatic steatosis should be assessed as a valuable predictor that reflects the increments of whole body fat mass as well as abdominal adiposity. However, in an attempt to demonstrate marginal differences between patients with similar obesity levels, epicardial adipose tissue appears to be a more sensitive marker compared to hepatic steatosis.

Protective effects of Gingko biloba on thioacetamide-induced fulminant hepatic failure in rats.

Gingko biloba (GB) has antioxidant and platelet-activating factor (PAF) antagonistic effects. We investigated the protective effects of GB on thioacetamide (TAA)induced fulminant hepatic failure in rats. Fulminant hepatic failure was induced in treatment groups by three intraperitoneal (ip) injections of TAA (350 mg/kg) at 24-hour intervals. Treatments with GB (100 mg/kg per day, orally) and N-acetylcysteine (20 mg/kg twice daily, sc) were initiated 48 hours prior to TAA administration. The liver was removed for histopathological examinations. Serum and liver thiobarbituric acid-reactive substance (TBARS) levels were measured for assessment of oxidative stress. Liver necrosis and inflammation scores and serum and liver TBARS levels were significantly higher in the TAA group compared to the control group (P <0.001,<0.001, 0.001,<0.001, respectively). Liver necrosis and inflammation scores and liver TBARS levels were significantly lower in the GB group compared to the TAA group (P <0.001,<0.001 and 0.01, respectively). GB ameliorated hepatic damage in TAA-induced fulminant hepatic failure. This may be due to the free radical-scavenging effects of GB.

Gastric Tissue Oxidative Changes in Portal Hypertension and Cirrhosis

Gastric mucosal lesions are very common in portal hypertension and cirrhosis. The aim of this study was to assess for oxidative gastric tissue damage in cirrhosis and evaluate relations with portal hypertension and cirrhosis parameters. The study included 30 patients with cirrhosis and 30 controls. Each patients history, physical examination, and laboratory findings were recorded, and multiple biopsies of the gastric antrum were obtained at endoscopy. A set of antral biopsies was also collected from each control subject. Each tissue specimen was analyzed for levels of glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase (CAT) activity and level of malondialdehyde (MDA). Patients’ gastric GPX, SOD, and CAT levels were significantly lower, and MDA levels were higher, than in the control group. The GPX activity level in the specimens was moderately negatively correlated with portal vein diameter (P < 0.05, r=−0.45) and spleen length (P < 0.05, r=−0.45). In this study gastric tissue oxidative markers showed that antral oxidative factors worsen in cirrhosis. Oxidative stress may not be a clinical condition but it obviously shows gastric tissue damage and may explain many patients’ gastric lesions and hemorrhage.

Quantifying the necrotic areas on liver tissues using support vector machine (SVM) algorithm and Gabor filters

Liver is a vital organ of a body that has numerous functions. Severe malfunctioning of these functions causes a liver necrosis. The diagnosis of this necrosis is performed by a specialist who uses appropriate microscopic analysis. However, because this analysis is based on specialists opinion, the results could be subjective and error prone. The aim of this study is to quantify the hepatic necrotic areas using computer aided algorithms and provide quantitative results that are not prone to errors.

Lighter Ingestion as an Uncommon Cause of Severe Vomiting in a Schizophrenia Patient.

Background. Foreign bodies in the gastrointestinal tract are important morbid and mortal clinical conditions. Particularly, emergency treatment is required for cutting and drilling bodies. The majority of ingested foreign bodies (80–90%) leave gastrointestinal tract without creating problems. In 10–20% of cases, intervention is absolutely required. Less than 1% of cases need surgery. In this paper, we present a schizophrenia patient who swallowed multiple lighters. Case. A 21-year-old male schizophrenic patient who uses psychotic drugs presented to the emergency department with the complaints of abdominal pain, severe vomiting, and inability to swallow for a week. His physical examination revealed epigastric tenderness. A plain radiograph of the abdomen revealed multiple tiny metallic densities. Gastroscopy was performed. The lighters were not allowing the passage, and some of them had penetrated the gastric mucosa, and bezoars were observed. One lighter was extracted with the help of the polypectomy snare. Other lighters as a bezoar were removed by surgery. Conclusion. Excessive vomiting of swallowed foreign bodies in the etiology of psychotic patients should be kept in mind. Endoscopic therapy can be performed in the early stages in these patients, but in the late stage surgery is inevitable.

An antibody of TNF-alpha did not prevent thioacetamide-induced hepatotoxicity in rats.

Tumor necrosis factor (TNF)-α antibodies have been shown to reduce liver damage in different models. We investigated the effects of infliximab (a TNF-α antibody) on liver damage in thioacetamide (TAA)-induced hepatotoxicity in rats. Group 1 (n = 8) was the control group. In group 2 (n = 8), the TAA group, the rats received 300 mg/kg intraperitoneal (ip) TAA daily for 2 days. In group 3 (n = 8), the TAA + Infliximab (INF) group, infliximab (5 mg/kg ip daily) was administered 48 hours before the first dose of TAA daily for 2 days and was maintained for 4 consecutive days. In group 4 (n = 8), the INF group, the rats received only ip infliximab (5 mg/kg) daily. Livers were excised for histopathological and biochemical tests (thiobarbituric-acid-reactive substances [TBARS], and myeloperoxidase [MPO]). Serum ammonia, aspartate transaminase (AST), alanine transaminase (ALT), TNF-α, liver TBARS and MPO levels, and liver necrosis and inflammation scores in the TAA group were significantly higher than in the control and INF groups (all p < 0.01). All parameters except AST were not significantly different between TAA and TAA + INF. In conclusion, our results suggest that oxidative stress plays an important role in TAA-induced hepatotoxicity, and infliximab does not improve oxidative liver damage.