Browsing by Author "Tuzcuoglu I."

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    The effect of perendoscopic sclerosing agent injection in Forrest's II ulcers- A pilot study from Turkey
    (2002) Saruc M.; Ozden N.; Kucukmetin N.; Tuzcuoglu I.; Yuceyar H.
    Background: We aimed to clarify the outcome of perendoscopic prophylactic injection of sclerosing agent in Forrest's II ulcers. Material/Methods: Patients with upper gastrointestinal bleeding in last 6 hours were performed emergency endoscopy and were enrolled. The patients in group-1 were performed prophylactic injection therapy with 1% aethoxysclerol and then given medical treatment with intravenous 40 mg omeprazole twice a day and somatostatin infusion at the dose of 6 mg/day during 3 days. Group-2 patients were only given medical treatment with same agents and at same doses without having any perendoscopic therapy. Results: There were 32 patients in group-1 and 20 in group-2. In emergency endoscopy, 20 (62.5%) patients had IIa ulcers and 12 (37.5%) patients had IIb ulcers in group-1. These patients underwent prophylactic perendoscopic hemostasis by 1% aethoxysclerol in addition to medical treatment. Early rebleeding occurred in 9 (28.1%) patients of group-1 and 3 (15%) in group-2 (p<0.001). At the endoscopic control after 48 hours 13 (40.6%) patients in the group-1 and 15 (75%) patients in group-2 showed improved local ulcer stigmata (p<0.001). The numbers of blood units transfused were lower in the group-2 (p=0.002). The hospital stay was longer in group-1 (p=0.01). In the group-1, more endoscopic intervention was needed. Any death and the need for surgical intervention did not occurred in any groups. Conclusion: According to our results; the indication of perendoscopic prophylactic injection of sclerosing agent in non-bleeding ulcers with high risk of rebleeding must be reviewed by large population based, prospective, radomized trials.
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    Midazolam-Induced Sedation for Upper Gastrointestinal Endoscopy:Assessment of Endoscopist and Patient Satisfaction
    (2003) Saruc M.; Sertdemir A.; Turkel N.; Tuzcuoglu I.; Ozden N.; Yuceyar H.
    Upper gastrointestinal endoscopy can be performed without intravenous sedation but the evidence suggests most patients and endoscopists prefer some form of premedication. Intravenous diazepam or midazolam are used by the majority of endoscopists in the United States, though it is not common practice in Turkey where this study was conducted. This study aimed to evaluate the efficacy and safety of midazolam in performing upper gastrointestinal endoscopy. A total of 352 patients undergoing upper gastrointestinal endoscopy were sedated with midazolam given as a bolus injection over 5 seconds. Ages of the patients ranged between 16 and 79 years (average: 41.6 ± 12.7 years). The course of endoscopy, anterograde memory, degree of cooperation, degree of sedation, side effects, and acceptability of further intervention were evaluated by a questionnaire given to the patients and endoscopists. © 2003 Lippincott Williams & Wilkins, Inc.
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    The association of dehydroepiandrosterone, obesity, waist-hip ratio and insulin resistance with fatty liver in postmenopausal women - A hyperinsulinemic euglycemic insulin clamp study
    (2003) Saruç M.; Yüceyar H.; Ayhan S.; Türkel N.; Tuzcuoglu I.; Can M.
    Background/Aims: The relationship between insulin resistance and the occurrence of fatty acid has been documented. Recently DHEA (dehydroepiandrosterone) was shown to have a protective effect against development of fatty liver in rats. We aimed to investigate the association of nonalcoholic fatty liver and serum levels of DHEA, obesity, fat distribution and insulin resistance and to evaluate the effect of DHEA on fatty liver, obesity and insulin resistance. Methodology: Thirteen postmenopausal women with nonalcoholic fatty liver and 14 postmenopausal women with normal liver histology were included into the study. Body mass index, waist-hip ratio, serum DHEA, DHEAS, triglyceride, cholesterol levels and insulin resistance were determined. Fatty liver was determined by ultrasound and established by liver biopsy and histology. Hyperinsulinemic euglycemic clamp studies were performed. Results: The subjects in both groups were age matched (p>0.05). Body mass index showed obesity in patients with fatty liver but not in control group (p=0.01). Central obesity was present in women with fatty liver (p=0.039). As expected, insulin resistance was significantly present in patients with fatty liver (p=0.001). DHEA and DHEAS levels of women with fatty liver were greater than those of control group (p1=0.001 and p2=0.0001, respectively). DHEA and DHEAS were positively correlated with both body mass index and waist-hip ratio. However, glucose disposal rate was inversely and significantly correlated with DHEA and DHEAS levels. Conclusions: These data do not support the hypothesis that DHEA or DHEAS protect postmenopausal women against fatty liver, diabetes and obesity. Indeed, DHEA and DHEAS may be the cause of fatty liver, obesity (especially abdominal obesity) and diabetes in estrogen-deficient women.
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    Functional dyspepsia: Relationship between clinical subgroups and Helicobacter pylori status and Western Turkey
    (Associacao Brasileira de Divulgacao Cientifica, 2003) Saruc M.; Ozden N.; Turkel N.; Ayhan S.; Demir M.A.; Tuzcuoglu I.; Akarca U.S.; Yuceyar H.
    The etiology of functional dyspepsia is not known. The objective of the present study was to determine the characteristics of functional dyspepsia in Western Turkey. We divided 900 patients with functional dyspepsia into three subgroups according to symptoms: ulcer-like (UL), 321 (35.6%), motility disorder-like (ML), 281 (31.2%), and the combination (C) of these symptoms, 298 (33.1%). All patients were submitted to endoscopic evaluation, with two biopsies taken from the cardia and corpus, and four from the antrum of the stomach. All biopsy samples were studied for Helicobacter pylori (Hp) density, chronic inflammation, activity, intestinal metaplasia, atrophy, and the presence of lymphoid aggregates by histological examination. One antral biopsy was used for the rapid urease test. Tissue cagA status was determined by PCR from an antral biopsy specimen by a random sampling method. We also determined the serum levels of tumor necrosis factor-a (TNF-α) and gastrin by the same method. Data were analyzed statistically by the Kolmogorov-Smirnov test and by analysis of variance. Hp and cagA positivity was significantly higher in the UL subgroup than in the others. The patients in the ML subgroup had the lowest Hp and cagA positivity and Hp density. The ML subgroup also showed the lowest level of Hp-induced inflammation among all subgroups. The serum levels of TNF-α and gastrin did not reveal any difference between groups. Our findings show a poor association of Hp with the ML subgroup of functional dyspepsia, but a stronger association with the UL and C subgroups.
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    Long-term outcomes of thymosin-α1 and interferon α-2b combination therapy in patients with hepatitis B e antigen (HBeAg) negative chronic hepatitis B
    (John Wiley and Sons Inc., 2003) Saruc M.; Ozden N.; Turkel N.; Ayhan S.; Hock L.M.; Tuzcuoglu I.; Yuceyar H.
    Hepatitis B e antibody (HbeAb) and hepatitis B virus (HBV) DNA positive chronic hepatitis is a clinical entity, distinct from classical hepatitis B e antigen (HbeAg) positive chronic hepatitis B. Our aim was to evaluate the long-term therapeutic efficacy of the combination of interferon α-2b and thymosin-α1 compared with lamivudine plus interferon α-2b and interferon α-2b alone. Fifty-two patients with HbeAg-negative chronic hepatitis B were assigned to three different groups in a nonrandomized manner. Group 1 (n = 27) received thymosin-α1 [1.6 mg subcutaneously (sc), twice a week] and interferon α-2b (10 MIU sc, three times per week) for 26 weeks, subsequently followed by interferon α-2b monotherapy at the same dosage for an additional 26 weeks. Group 2 (n = 10) received interferon α-2b (10 MIU sc, three times per week) for 52 weeks. Group 3 (n = 15) received interferon α-2b (10 MIU sc, three times per week) and lamivudine [100 mg orally (po), q.d.] for 52 weeks, followed by continuous lamivudine (100 mg po, q.d.) therapy. By the end of 78 weeks, a sustained response (SR-6 mo) was seen in 74% (20/27) of the patients within Group 1. On the contrary, Groups 2 and 3 had sustained response rates of 40 (4/10) and 53.3% (8/15), respectively (p = 0.13). At the end of 12 months post-treatment in Group 1, a virological and biochemical response rate was seen in 70.3% of patients (19/27); in contrast, Groups 2 and 3 had response rates of 20 (2/10) and 26.6% (4/15), respectively (p = 0036). At the end of the 18-month post-treatment follow-up period, 71.4% (19/27) of patients in Group 1, 10% of patients in Group 2 (1/10), and 20% of patients in Group 3(3/15) preserved their sustained response (p = 0.0003). Interferon α-2b and thymosin-α1 combination therapy results in significant virological and biochemical response rates compared with standard therapeutic regimens and is well tolerated. © 2003 Wiley-Liss, Inc. and the American Pharmacists Association.
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    Somatostatin infusion and hemodynamic changes in patients with non-variceal upper gastrointestinal bleeding: A pilot study
    (2003) Saruç M.; Can M.; Küçükmetin N.; Tuzcuoglu I.; Tarhan S.; Göktan C.; Yüceyar H.
    Background: Intravenous somatostatin decreases acid secretion, splanchnic blood flow, and portal pressure, but the evidence for its efficacy in the treatment of non-variceal upper gastrointestinal bleeding has been mixed. We aimed to evaluate the vasoactive effect and possible mechanisms of somatostatin infusion in the cessation of non-variceal upper gastrointestinal bleeding. Material/Methods: Patients with non-variceal upper gastrointestinal bleeding without portal hypertension were enrolled in the study. They were given somatostatin infusion in a dose of 250 μgr/hour for 72 hours. Superior mesenteric arterial average flow velocity (SMA-V), SMA pulsatility index (SMA-PI), portal venous volume flow (PV-F), and renal artery resistance index (RA-RI) were measured two times for each patient by Doppler ultrasound; oncee on the first day of infusion therapy and again 6 hours or more after stopping the infusion. Results: 21 patients (12 male, mean age 44.1±9.9) with bleeding peptic ulcer were enrolled. During somatostatin infusion, PV-F was 33.7±19.7 cm3/sec. After stopping infusion, it increased to 56.3±16.0 cm3/sec (p=0.001). SMA-V was 39.7±13.1 cm/ sec and 64.4±15.1 cm/sec during somatostatin infusion and after cessation of somatostatin respectively (p=0.01). SMA-PI was 2.0±0.8 during somatostatin infusion but 2.8±0.8 without somatostatin infusion (p=0.02). However, RA-RI showed no difference between states with or without somatostatin infusion (p>0.05). Conclusions: Somatostatin infusion causes a decrease in arterial blood flow to the stomach and duodenum in patients with non-variceal upper gastrointestinal bleeding without portal hypertension. Somatostatin therapy also decreases portal blood flow while not altering renal blood.
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    An experimental model of hemolysis-induced acute pancreatitis
    (Associacao Brasileira de Divulgacao Cientifica, 2003) Saruc M.; Yuceyar H.; Turkel N.; Ozutemiz O.; Tuzcuoglu I.; Yuce G.; Huseyinov A.
    The literature indicates that acute pancreatitis is a complication of massive hemolysis with a prevalence of about 20%. We describe an experimental model of hemolysis-induced acute pancreatitis. Hemolytic anemia was induced in rats by a single ip injection of 60 mg/kg of 20 mg/ml acetylphenylhydrazine (APH) in 20% (v/v) ethanol on the first experimental day (day 0). One hundred and fifty Wistar albino rats weighing 180-200 g were divided into three groups of 50 animals each: groups 1, 2 and 3 were injected ip with APH, 20% ethanol, and physiological saline, respectively. Ten rats from each group were sacrificed on study days 1, 2, 3, 4 and 5. Serum amylase, lipase levels and pancreatic tissue tumor necrosis factor-α (TNF-α) and platelet-activating factor (PAF) contents were determined and a histological examination of the pancreas was performed. No hemolysis or pancreatitis was observed in any of the rats in groups 2 and 3. In group 1, massive hemolysis was observed in 35 (70%) of 50 rats, moderate hemolysis in seven (14%), and no hemolysis in eight (16%). Thirty-three of 35 (94.2%) rats with massive hemolysis had hyperamylasemia, and 29 of these rats (82.8%) had histologically proven pancreatitis. The most severe pancreatitis occurred on day 3, as demonstrated by histology. Tissue TNF-α and PAF levels were statistically higher in group 1 than in groups 2 and 3. Acute massive hemolysis induced acute pancreatitis, as indicated by histology, in almost 80% of cases. Hemolysis may induce acute pancreatitis by triggering the release of proinflammatory and immunoregulatory cytokines.
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    The role of heme in hemolysis-induced acute pancreatitis
    (2007) Saruç M.; Yuceyar H.; Turkel N.; Ozutemiz O.; Tuzcuoglu I.; Ayhan S.; Yuce G.; Coker I.; Huseyinov A.
    Background: The aim was to reveal the mechanism of hemolysis-induced acute pancreatitis and to evaluate the role of heme and heme oxygenase activity in inducing pancreatic inflammation in an experimental hemolysis model. Material/Methods: Hemolytic anemia was induced in rats by intraperitoneal injection of 60 mg/kg acetylphenylhydrazine (APH). To evaluate the toxic effect of free heme after hemolysis, heme oxygenase inhibitor (HOI) was used to inhibit the enzyme which decreases the free heme concentration after hemolysis. One hundred and fifty rats were divided into two treatment and three control groups. Rats in the hemolysis group were given APH intraperitoneally. Rats in the HOI+hemolysis group were given Cr(III)mesoporphyrin IX chloride as HOI and then APH intraperitoneally. Serum amylase and lipase levels as well as pancreatic tissue cytokine content were determined and histological examination performed. Results: No hemolysis or pancreatitis was seen in the control groups. Massive hemolysis was seen in 22 of the 30 rats of the hemolysis group and 20 of the 30 rats of the HOI+hemolysis group. The total pancreatitis rates were 60% and 76.6% in the hemolysis and HOI+hemolysis groups, respectively (p<0.05). Pancreatic cytokine levels were significantly higher in the HOI+hemolysis and hemolysis groups than in all control groups. The highest ICAM-1 and MCP-1 levels were in the HOI+hemolysis group. Histological signs of acute pancreatitis were also more severe in this group. Conclusions: Acute massive hemolysis can induce acute pancreatitis. Excess of free vascular heme seems to be an inducer of inflammation by modulating ICAM-1 and MCP-1. © Med Sci Monit, 2007.