A retrospective study demonstrating properties of nonvariceal upper gastrointestinal bleeding in Turkey.

BACKGROUND/AIMS: Helicobacter pylori infection, non-steroidal anti-inflammatory drugs and peptic ulcer are considered as the major factors for upper gastrointestinal system bleeding. The objective of the study was to determine the sociodemographic and etiologic factors, management and outcome of patients with non-variceal upper gastrointestinal system bleeding in Turkey. METHODS: Patients who admitted to hospitals with upper gastrointestinal system bleeding and in whom upper gastrointestinal endoscopy was performed were enrolled in this retrospective study. The detailed data of medical history, comorbid diseases, medications, admission to intensive care units, Helicobacter pylori infection, blood transfusion, upper gastrointestinal endoscopy, and treatment outcome were documented. RESULTS: The most frequent causes of bleeding (%) were duodenal ulcer (49.4), gastric ulcer (22.8), erosion (9.6), and cancer (2.2) among 1,711 lesions in endoscopic appearances of 1,339 patients from six centers. Seven hundred and four patients were evaluated for Helicobacter pylori infection and the test was positive in 45.6% of those patients. Comorbid diseases were present in 59.2% of the patients. The percentage of patients using acetylsalicylic acid and/or other non-steroidal anti-inflammatory drug was 54.3%. Bleeding was stopped with medical therapy in 66.9%. Only 3.7% of the patients underwent emergency surgery, and a 1.1% mortality rate was determined. CONCLUSIONS: Patients with upper gastrointestinal system bleeding were significantly older, more likely to be male, and more likely to use non-steroidal anti-inflammatory drugs. Though most of the patients were using gastro-protective agents, duodenal and gastric ulcers were the contributing factors in more than 70% of the upper gastrointestinal bleeding. The extensive use of non-steroidal anti-inflammatory drug is a hazardous health issue considering the use of these drugs in half of the patients.

Protection against cisplatin-induced nephrotoxicity by recombinant human erythropoietin.

Cisplatin (CDDP) is a potent nephrotoxin, and nephrotoxicity is its most important dose-limiting toxicity. In this study, we aimed to investigate the role of recombinant human erythropoietin (rhEPO) in the protection of cisplatin-induced nephrotoxicity and compare its efficacy with the cell-protective agent amifostine. All experiments were conducted on female Wistar albino rats. Animals were randomly assigned to four groups, each including six rats. Group A received only CDDP, group B received CDDP plus rhEPO, group C received CDDP plus amifostine, and group D received only rhEPO. At the end of 7 wk, hemoglobin (Hgb), hematocrite (Htc), blood urea nitrogen (BUN), and creatinine (Cr) levels were determined and kidneys of the rats were removed. The weights of the kidneys were measured and sent for histopathological examination. Proximal tubules from four areas of the kidney (outer cortex, inner cortex, the medullary ray, and outer stripe of outer medulla [OSOM]) were evaluated. There were statistically significant differences among the groups in terms of tubular scores, including overall renal tubular score, cortex, inner cortex, OSOM, and medullary ray tubular scores, and Htc levels. Group A rats had the worse tubular scores in all categories when compared to group D rats. When the results of groups B and C were compared, there were no differences in terms of BUN, Cr levels, and tubular scores, but the Htc level was significantly higher in group B. Group B rats had better overall and OSOM tubular scores when compared to group A. Group C also had better overall and OSOM tubular scores compared to group A. The present study showed for the first time that rhEPO plays an important role in the prevention of cisplatin-induced nephrotoxicity and it is as effective as amifostine.

Protective effect of amifostine against cisplatin-induced motor neuropathy in rat.

Cisplatin (CDDP) is a potent anticancer drug. Neurotoxicity is one of the most important dose-limiting toxicity of CDDP. We investigated the role of amifostine in the protection against CDDP-induced neurotoxicity especially on the motor nerves. All experiments were conducted on female Wistar albino rats. Animals were randomly assigned to two groups, each including six rats. Group A received CDDP plus amifostine and Group B received CDDP only. Electroneurography (ENG) was carried out in the beginning and at the end of 7 wk; then, the rats were sacrificed and the sciatic nerve was removed for histopathological examination. The mean initial latency was 2.4667 msn for group A and 2.44833 msn for group B. After 7 wk of treatment, the latency was 2.9167 for group A and 2.6333 for group B. The difference in latencies was not statistically significant. The amplitude was 11.7853 mV and 13.533 mV for groups A and B, respectively. After 7 wk of treatment, the amplitude was 9.400 mV and 9.000 mV, respectively. The decrease of amplitude in compound muscle action potential (CMAP) was 20% in the amifostine group and the decrease was 33% in the untreated group. The mean area of the CMAP in group A was 9.400 mVsn initially and 9.666 mVsn at the end of the treatment; there was a 0.3% increase despite CDDP treatment. In group B, the mean area of the CMAP was 13.816 mVsn initially and 11.857 mVsn at the end of the treatment; this corresponded to a statistically significant 14% decrease as a result of CDDP treatment. The ENG and histopathological studies showed that at the given dose and schedule CDDP-induced motor neuropathy and amifostine reduced this neuropathy both by protection of the amplitude and area of the CMAP in ENG studies and by sparing a larger number of nerve fibers.