Bunyamin Aydin

The Role of Carnitine in Preventing Renal Damage Developed as a Result of Infrarenal Aortic Ischemia–Reperfusion

Background: This study was designed to use carnitine for preventing deposition of end products of lipid peroxidation in rat models in the prevention of ischemia–reperfusion (IR) damage frequently seen following operations of infrarenal abdominal aorta (AA). Methods: Forty male rats of Sprague-Dawley type were evenly (n = 8) randomized to five groups: sham laparotomy (SHAM), carnitine control (CC), aortic IR (AIR), AIR + low-dose carnitine (AIR+LDC), and AIR + high-dose carnitine (AIR+HDC). Results: Compared to other groups, serum creatinine levels of AIR group were significantly higher. Also tissue malondialdehyde (MDA) levels of AIR group were significantly higher compared to SHAM, CC, and AIR+HDC groups. In histopathological examination, although tubular necrosis atrophy and tubular degeneration observed in AIR group showed regression with low-dose carnitine, tubular necrosis atrophy, tubular degeneration, glomerular damage, and vascular congestion thrombosis decreased with high-dose carnitine. Total score of histological damage was significantly higher in AIR, AIR+LDC, and AIR+HDC groups compared to SHAM and CC groups. Moreover, total score of histological damage was significantly lower in AIR+HDC group than AIR+LDC group. Conclusions: In this study, we showed carnitine can partially prevent renal damage in infrarenal AIR models of rats. This result may open new prospects to us in the prevention of renal IR damage during surgery of aorta.

Investigation of pulmonary involvement in inflammatory bowel disease in an experimental model of colitis.

Background/Aims: Inflammatory bowel disease (IBD) may also involve various extra-intestinal organs. Clinical studies have found asymptomatic/symptomatic pulmonary involvement in 1% to 6% of patients with IBD. The present study histopathologically investigated pulmonary involvement in an experimental model of colitis in order to demonstrate pulmonary tissue involvement in IBD and to expose potential etiological factors. It also explored the relation between inflammation and tissue concentrations of vascular endothelial growth factor (VEGF) and tumor necrosis factor α (TNF-α). Methods: The study comprised 24 male Wistar albino rats. The rats were divided into four groups of six rats each. Acute colitis was induced in two separate groups using either the dextran sulphate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) method, while the other two groups were used as controls for each model of colitis. Wallace scoring was used for macroscopic assessment of colitis, and the lungs were histopathologically examined. Concentrations of VEGF and TNF-α in pulmonary tissue were measured by the enzyme-linked immunosorbent assay method. Results: The number of animals that had alveolar hemorrhage was significantly higher in the TNBS-induced colitis and DSS-induced colitis groups compared to their own control groups (p = 0.015 and p = 0.015, respectively). VEGF and TNF-α concentrations in pulmonary tissues were significantly increased in both the TNBS colitis and DSS colitis groups compared to their own control groups (p = 0.002 and p = 0.004, respectively; and p = 0.002 and p = 0.002, respectively). Conclusions: The present study demonstrated that significant and serious histopathological changes directly associated with colitis occur in the lungs in IBD.

Amyloid Goiter Secondary to Ulcerative Colitis.

Diffuse amyloid goiter (AG) is an entity characterized by the deposition of amyloid in the thyroid gland. AG may be associated with either primary or secondary amyloidosis. Secondary amyloidosis is rarely caused by inflammatory bowel diseases. Secondary amyloidosis is relatively more common in the patients with Crohns disease, whereas it is highly rare in patients with ulcerative colitis. Diffuse amyloid goiter caused by ulcerative colitis is also a rare condition. In the presence of amyloid in the thyroid gland, medullary thyroid cancer should be kept in mind in the differential diagnosis. Imaging techniques and biochemical tests are not very helpful in the diagnosis of secondary amyloid goiter and the definitive diagnosis is established based on the histopathologic analysis and histochemical staining techniques. In this report, we present a 35-year-old male patient with diffuse amyloid goiter caused by secondary amyloidosis associated with ulcerative colitis.

SP663THE RELATIONSHIP BETWEEN SERUM FETUIN A LEVELS AND FETUIN GENE POLYMORPHISM IN HEMODIALYSIS PATIENTS

Introduction: Fetuin A, also called Heramans Schmid alpha 2 glycoprotein (AHSG), is one of the important proteins that inhibit vascular calcification. In this study, we aimed to evaluate relationship between AHSG gene polymorphism and fetuin A levels. Materials and methods: 152 patients receiving regular hemodialysis treatment and 61 healthy controls were included to this cross-sectional study. Serum fetuin-A levels were assessed by ELISA method. Thr256Ser and Thr248Met gene polymorphisms are determined by PCR-RFLP. Results: Serum fetuin A level in hemodialysis patients (330.5 ± 171.2 mg/L) was significantly lower as compared to control group (382.9 ± 138.5 mg/L) (p=0.001). Significant negative correlation between fetuin-A and C-reactive protein (CRP) (r=-0.28, p<0.0001) was found. The distribution of Thr256Ser and Thr248Met gene polymorphisms in hemodialysis and control groups were similar. In hemodialysis group, serum fetiun A levels in the patients with genotype Thr/Thr (n=94, 366.9 ± 184.2 mg/L) were found to be singnificantly higher than in the patients with genotype Thr/Ser (n=52, 278.1 ± 132.7 mg/L) and Ser/Ser (n=6, 212.5 ± 63.3 mg/L) (respectively; p=0.005, p=0.022). Unlike Thr256Ser polymorphism, serum Fetuin-A levels did not differ between Thr248Met gene polymorphism genotypes. Conclusion: The current study showed that HD patients with altered polymorphism of the AHSG Thr256Ser gene appear to be a negative prognostic factor on serum Fetuin-A levels. In other words, it can be speculated that fetuin-A Thr256Ser gene polymorphism, particularly genotypes Thr/Ser and Ser/ Ser, may be an additional promoting risk factor for vascular ossification in HD patients.

Insulinoma-Induced Hypoglycemia in a Patient with Insulinoma after Gastrojejunostomy for Prepyloric Ulcer

Hyperinsulinism due to dumping syndrome following gastric surgery is an uncommon condition. It is specified with hypoglycemic attacks. However, linking symptoms to dumping syndrome in each patient to whom gastric surgery was performed leads to inappropriate diagnosis and therapy. Insulinoma and other causes that give rise to hyperinsulinemia should not be ignored and these diagnoses should be excluded. In this paper, 71-year-old male patient who was followed up for 2 years with a false conclusion of dumping syndrome and operated on due to insulinoma diagnosed at endoscopic ultrasonography is presented in the light of the literature.