Preoperative detection of insulinomas: two case reports

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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

Serum cystatin C measurement in differential diagnosis of intra and extrahepatic cholestatic diseases

Objective. Cystatin C is a very potent inhibitor of cysteine proteinases and, it has been clinically applied as a sensitive marker in monitoring of renal and liver functions. The aim of this study was to reveal whether cystatin C may be a useful marker for distinguishing intra-versus extrahepatic cholestasis.Materials and methods. Serum cystatin C concentrations were determined by nephelometric immunoassay using N latex cystatin C kit in 53 patients with cholestatic disorder that included 18 patients with intrahepatic cholestasis, 17 patients with malignant extrahepatic cholestasis, 18 patients with benign extrahepatic cholestasis. Serum cystatin C concentration was also determined in 20 healthy volunteers.Results. Mean serum cystatin C concentration was 2.82 ± 0.24 mg/l (SD) in patients with intrahepatic cholestasis, 2.05 ± 0.15 mg/l in patients with extrahepatic malignant cholestasis, 1.37 ± 0.13 mg/l in extrahepatic benign cholestatic patients and 0.93 ± 0.24 mg/l in control group. Serum cystatin C concentrations in patients with cholestatic disease were significantly higher than those in the healthy controls (p < 0.001). Moreover, mean serum cystatin C concentration in patients with intrahepatic cholestasis was higher than those in extrahepatic cholestasis groups (p < 0.001). Serum cystatin C concentrations were significantly higher in patients with malignant extrahepatic cholestasis than in patients with benign extrahepatic cholestasis (p < 0.001). There were no correlations patients among serum cystatin C concentrations and serum levels of AST, ALT, ALP, GGT, total and conjugated bilirubin.Conclusion. Our results suggested that serum cystatin C level may be a potential biochemical marker both to point out an intrahepatic origin by excluding an extrahepatic source of cholestasis in patients with jaundice and to possibly differentiate bening and malignant extrahepatic cholestatic disorders

Kolorektal kanser tanısında insülin benzeri büyüme faktörü-1 (IGF-1) ve insülin benzeri büyüme faktör bağlayıcı protein-3 (IGFBP-3)’ün kullanılabilirliği

İnsülin benzeri büyüme faktörü-1 (IGF-1), etkisi insülin benzeri büyüme faktör bağlayıcı protein-3 (IGFBP-3) tarafından düzenlenen, potent bir mitojen ve antiapoptotik ajandır. IGFBP-3, IGF-1’i dolaşımda taşır, hedef dokulara yönlendirir, onu proteolitik degradasyondan korur. IGFBP-3 in vitro şartlarda kolon kanser hücrelerinin tümörojenik potansiyellerini azaltır. IGFBP-3 hedef hücreleri doğrudan inhibe edebilir. Çalışmamızda kolorektal kanserli hastalarda IGF-I, IGFBP-3’ün tümör markırı olarak kullanılıp, kullanılamayacağı ve bilinen tümör markırlarından karsinoembriyonik antijen (CEA), karbonhidrat antijeni 19-9 (CA19-9) ile olan ilişkisi incelendi. Çalışmamıza histopatolojik olarak kolorektal kanser teşhisi konulmuş 40 hasta ile, kontrol grubu olarak benzer yaş grubundan ve tamamen sağlıklı 40 kişi dahil edildi. Kontrol grubu ile kıyaslandığında kolorektal kanserli hastalarda IGF-I düzeyi anlamlı derecede yüksek bulundu (p< 0.01). IGFBP-3 düzeyleri kolorektal kanserde kontrol grubu ile kıyaslandığında anlamlı derecede düşük bulundu (p< 0.05). Yine aynı vakalarda çalışılan CEA ve CA19-9 düzeylerinde gözlenen artış kontrol grubu ile kıyaslandığında istatistiki açıdan anlamlı olarak yüksek bulundu (p< 0.05). Fakat IGF-1 ve IGFBP-3 düzeylerindeki değişimi ile CEA ve CA 19-9 arasında anlamlı ilişki tespit edilemedi. Sonuç olarak, IGF-I düzeyindeki artış, kolorektal kanser şüphesi olan hastalarda tümör varlığı yönünden anlamlı bir gösterge olarak kabul edilebilir. IGFBP-3 düzeyini artışına neden olabilecek ajanlar kolorektal kanser tedavisinde yeni ufuklar açabilir.Insulin-like growth factor (IGF-1) is a potent mitogen and an anti-apoptotic agent which is regulated by insulin-like growth factor binding protein-3 (IGFBP-3). IGFBP-3 carries IGF-1 through the bloodstream to the target tissues and protects it from proteolytic degradation. IGFBP-3 reduces tumorigenic potential of colon cancer cells in vitro. IGFBP- 3 may inhibit target cells directly. In the present study, we assessed whether serum levels of IGF-I and IGFBP-3 could be used as tumor markers in patients with colorectal cancers and evaluated its relationship with known tumor markers, carcinoembryogenic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9). Our study enrolled 40 patients diagnosed with colorectal cancer histopathologically and 40 completely healthy, agematched subjects (control group). Serum IGF-I levels were found significantly higher in patients with colorectal cancers compared to control group (p< 0.01). Serum IGFBP-3 levels were significantly lower in patients with colorectal cancers compared to control group (p< 0.05). The observed increase in CEA and CA19-9 levels in the same subjects were found statistically significantly higher compared to control group (p< 0.05). However, no significant association could be found between change in IGF-1 and IGFBP-3 levels and CEA or CA 19-9. Increased serum levels of IGFI might be considered as a significant predictor of tumor presence in patients with suspected colorectal cancer. Agents that could increase IGFBP-3 levels might be promising for the treatment of colorectal cancers

Therapeutic effect of caffeic acid phenethyl ester on cerulein-induced acute pancreatitis

AIM: To evaluate the therapeutic role of caffeic acid phenethyl ester (CAPE) in a rat model of cerulean-induced acute pancreatitis (AP)

The beneficial effect of propolis on cerulein-induced experimental acute pancreatitis in rats

Background/aims: Inflammatory cytokitzes and oxidative stress have a central role in the pathogenesis of acute pancreatitis. Propolis is a resinous hive product collected by honeybees from various plant sources and has anti-inflammatory and anti-oxidant effects. The present work aimed to investigate the therapeutic role of ethanolic extract of propolis on a cerulein-induced acute pancreatitis model in rats. Methods: Seventy male Wistar albino rats were used in the study. Acute edematous pancreatitis was induced by subcutaneous cerulein injection (20 mu g/kg) four times at one-hour intervals. Ethanolic extract of propolis 300 mg/kg was given subcutaneously at the beginning of the procedure (ethanolic extract of propolis-1 group) or 12 h after the last cerulein injection (ethanolic extract of propolis-2 group). Serum amylase and lipase levels, white blood cell count and serum tumor necrosis factor-alpha levels were measured and pancreatic tissue was evaluated histologically. Results: In the acute pancreatitis group, serum amylase and lipase levels were found to be elevated and the histopathological evaluation of the tissue revealed massive edema and inflammation with less fatty necrosis when compared to the sham and control groups. Serum amylase and lipase levels and edema formation were significantly decreased in the ethanolic extract of propolis-treated groups (p<0.001). In the ethanolic extract of propolis-2 group, in particular, tissue edema was improved markedly (p=0.001). Tissue inflammation and fatty necrosis were decreased with ethanolic extract of propolis treatment; however, the improvement was not statistically significant. Conclusions: Treatment with ethanolic extract of propolis improved the biochemical and histopathological findings in a rat model of experimental pancreatitis. Although our findings suggest that ethanolic extract of propolis might be considered an effective agent for the treatment of acute pancreatitis, this notion should be supported with further experimental and clinical investigations

A comparison of the effects of desflurane, sevoflurane and propofol on QT, QTc, and P dispersion on ECG.

The aim of this prospective, randomized, and double-blinded study was to compare the effects of desflurane, sevoflurane, propofol on both atrial and ventricular wall function by measurement of QT dispersion (QTd), corrected QT dispersion (QTcd), and P dispersion (Pd) on electrocardiogram (ECG). Forty-six patients from the American Society of Anesthesiologists class I-II undergoing noncardiac surgery, were enrolled in this study. Patients were randomly allocated to receive desflurane, sevoflurane or propofol anesthesia. ECG recordings were taken before and after 5 minutes of drug administration. Induction with desflurane significantly increased the QTd compared to baseline (38 +/- 2 ms vs. 62 +/- 6 ms, P < 0.05). Sevoflurane and propofol anesthesia was not associated with any changes in QTd. QTcd was increased with desflurane induction and decreased with sevoflurane and propofol induction, but this decrease was only significant in the propofol group (67 +/- 5 ms vs. 45 +/- 3 ms, P < 0.05). Pd was significantly increased after induction with desflurane (34 +/- 3 vs. 63 +/- 6 ms, P < 0.05). There was a significant increase in QTd and Pd in desflurane group, but this increment did not cause any dangerous arrhythmias. QTcd significantly decreased in propofol group. We believe that further investigations are required for using desflurane as safe as sevoflurane and propofol in noncardiac surgery patients who have high cardiac arrhythmia and ischemia risk