Ayhan Eralp

The significance of immunohistochemistry in the skin pathergy reaction of patients with Behçet's syndrome.

Background  Behçets syndrome is a chronic systemic immuno‐inflammatory disorder affecting multiple organs with generalized vasculitis of arteries and veins. Although the aetiology is still unknown, endothelial dysfunction is one of the most prominent features in Behçets syndrome. The skin pathergy reaction (SPR) is a non‐specific hyperreactive lesion formation that is one of the major features and diagnostic criteria of the disease. It develops after 24–48 h at the site of the needle‐prick, especially in the exacerbation period, and it is very similar to the erythematous papules or pustules that appear spontaneously in patients with Behçets syndrome. Therefore, an investigation into the formation of the SPR lesion may contribute to the pathophysiology of skin lesions of this unique disorder.

Chorangiosis : The potential role of smoking and air pollution

Chorangiosis is considered to be strongly associated with various fetal, maternal, and placental disorders, including pre-eclampsia, diabetes, hypertension, and major congenital anomalies, and has been found to correlate with increased fetal morbidity and mortality. In this study, we investigated the pathologic effects of maternal smoking and air pollution on the pathogenesis of chorangiosis. We investigated 92 placentas macroscopically and microscopically over a 3-month period (March 2006-May 2006) at Denizli State Hospital to identify the frequency of chorangiosis and the potential role of maternal smoking and air pollution. Placental changes were examined by light microscopy after hematoxylin and eosin (H&E) staining and immunohistochemical evaluation of CD 34 and CD 68; muscle-specific actin was used to confirm the diagnosis. Among the 92 mothers included in the study, 33 were smokers (group I), 31 were thought to have been exposed to air pollution (group II), and 28 were living in rural areas free of air pollution and maternal smoking (group III). Chorangiosis was found in 14% (13/92) of all placentas: 7 (53.8%) cases were assigned to group I, 5 (38.5%) to group II, and 1 (7.7%) to group III. Vascular changes were found mainly in the smoking and air pollution groups. There appeared to be no correlation of these vascular changes with placental weight, parity, gestational age, major congenital anomalies, and maternal factors, including diabetes and pre-eclampsia. We presume that smoking and air pollution may contribute to the development of chorangiosis. We suggest that chorangiosis may be an adaptive response to maternal hypoxia, and studies addressing the role of smoking and air pollution in chorangiosis may provide new insights into the pathogenesis of this condition.

Effect of Vitamin A against Methotrexate-Induced Damage to the Small Intestine in Rats

Objective: The aim of the present study was to examine whether or not the administration of vitamin A (VA) protects against methotrexate (MTX)-induced damage to small intestinal epithelium. Materials and Methods: Sixty-three male Wistar albino rats, 10–12 weeks old, weighing 240–280 g, were divided into three groups: (1) controls, (2) rats receiving MTX treatment alone, and (3) rats receiving MTX plus VA treatment. A single dose of MTX (20 mg/kg MTX in 20 ml vehicle) was administered to the rats intraperitoneally. For MTX plus VA treated groups, retinol palmitate (VA) 5,000 IU/kg dissolved in 0.5 ml sunflower oil was administered by intragastric tube 3 days prior to MTX treatment and continued till the rats were sacrificed. The control group was treated with vehicle. Both control and MTX-alone groups were also treated with sunflower oil as a placebo. The rats were sacrificed on the 2nd, 4th and 6th day after MTX treatment. Tissue samples from the jejunum were taken for histopathological analysis. Results: MTX treatment induced villus shortening and fusion, epithelial atrophy, crypt loss, inflammatory infiltrate in the lamina propria, and goblet cell depletion. The pre- and post-treatment administration of VA decreased the severity of jejunal damage caused by MTX treatment. Conclusion: Our results confirmed that administration of VA decreased the MTX-induced damage to the small intestine. This protective effect of VA may have clinical applications in cancer chemotherapy.

Preventative Effect of Vitamin E on Mast Cells in Carbon Tetrachlorideinduced Acute Liver Damage

BACKGROUND Preventing liver damage that might lead to cirrhosis is very important in the early stages of injury to that organ. The role of mast cells (MCs) in liver injuries has been long debated, and vitamin E is a well-known antioxidant used to treat those injuries. This study aimed to determine the protective role of vitamin E on MCs in injury to the liver that is triggered by carbon tetrachloride (CCl4). There is a correlation between MC deposits and improvement in fibrosis tissues. METHODS To further examine this, 68 male Albino Wistar rats were divided randomly into five groups: the control group, the vitamin E group, the CCl4 group, the CCl4 + vitamin E group, and the vitamin E + CCl4 group. Malondialdehyde (MDA) analysis, MC counts, histopathological investigation, and statistical analyses were used to evaluate the findings. RESULTS The administration of CCl4 resulted in an increase in the accumulation of MCs, degenerative parenchyma cells, MDA level, steatosis and inflammation. Additionally, proliferation of the bile ducts in the portal area and porto-portal and porto-central fibrosis were observed in the CCl4 group. In contrast, in the vitamin E group and in the groups administered a combination of vitamin E and CCl4, vitamin E prevented these increases. CONCLUSION It was concluded that the significant decrease in the MC counts, in the level of MDA and the number of degenerative cells, as well as a decrease in the steatosis and inflammation scores showed that vitamin E could prevent liver injuries by protecting the organs histological architecture. Finally, the results indicate that vitamin E has positive effects on liver injuries.