Free oxygen radical-induced acute pancreatitis. A light and electron microscopic study

BACKGROUND/AIMS: To date direct toxic effects of free oxygen radicals in vivo on pancreatic parenchyma have not been studied thoroughly. We aimed to study: 1) the detailed histopathological changes induced by free oxygen radicals in pancreas; and 2) the preventive effect of intraductal catalase in H2O2-induced acute pancreatitis. METHODOLOGY: Wistar Albine rats were randomized into six groups. 1) First experiment: Bile-pancreatic duct was cannulated close to the liver and perfused through the duodenum with (i) normal saline solution, (ii) iron sulfate (FeSO4), (iii) hydrogen peroxide (H2O2), (iv) hydrogen peroxide and iron sulfate simultaneously. 2) Second experiment: Bile pancreatic duct was perfused either with H2O2 or H2O2 + catalase. Serum amylase and pancreas malondialdehyde levels were measured in both experiments after 3 hours of perfusion period. Tissue samples were obtained for histopathological examinations. RESULTS: 1) First experiment: Intraductal perfusion of FeSO4 or H2O2 or H2O2 + FeSO4 induced acute edematous pancreatitis with focal parenchymal necrosis. At the ultrastructural level, intracytoplasmic formation of vacuoles. fusion of the vacuoles and zymogen granules, and autophagosomes containing cellular organelles were found. Serum amylase and pancreas malondialdehyde levels, and morphological score were significantly higher in these groups than control group (p < 0.001). 2) Second experiment: Catalase perfusion simultaneously with H2O2 decreased the serum amylase and pancreas malondialdehyde levels, and morphological score significantly (p < 0.001) and prevented the desquamation of the columnar epithelium and development of gross edema but not parenchymal necrosis. CONCLUSIONS: Intraductal perfusion of FeSO4 or H2O2 or H2O2 + FeSO4-induced acute pancreatitis with marked light and electronmicroscopic changes. Intraductal perfusion of catalase and H2O2 simultaneously did not prevent or lessen the parenchymal necrosis. These findings have suggested that another mechanism of injury may also play a role in parenchymal injury in oxygen radical-induced acute pancreatitis.     

Angiographic prevalence of myocardial bridging.

OBJECTIVE: Muscle fibers overlying the intramyocardial segment of an epicardial coronary artery are termed myocardial bridging. Variable prevalence has been described at autopsy and angiographic series with small and large sample sizes. The aim of the study was to investigate the angiographic prevalence of myocardial bridging in 25982 patients from Turkey. METHODS: We performed a retrospective study, evaluated the cases with myocardial bridging among patients undergone selective coronary angiography, and searched the angiographic prevalence of myocardial bridging in a very large sample size. We studied also the correlation between the severity of the bridging and risk factors for coronary artery disease. RESULTS: Among 25982 patients we found 316 cases of myocardial bridging in a retrospective manner. The total prevalence was 1.22%. Although, 96.52% of patients with myocardial bridging had the lesion in the left anterior descending coronary artery (LAD) as expected, distribution of bridges between mid- and distal segments were almost equal (52.79% and 47.21%, respectively). We subclassified patients in two groups, Group A (<50% of systolic compression) and Group B (>or=50% of systolic compression), according to the amount of systolic compression of LAD and studied relationship of risk factors for coronary artery disease between groups. Another subclassification was also made for patients having myocardial bridging without coronary or valvular heart disease and hypertrophic obstructive cardiomyopathy; Group 1 (<50% of systolic compression) and Group 2 (>or=50% of systolic compression). In these patients we studied correlation between the severity of the myocardial bridging and risk factors for coronary artery disease. The prevalence of bridges in circumflex and right coronary arteries individually and in all arteries as combination was also studied. CONCLUSION: In a very large group of patients from Turkey undergone selective coronary artery angiography, the angiographic prevalence of myocardial bridging was slightly higher than expected. Only diabetes mellitus as a risk factor for coronary artery disease was higher in groups representing <50% of systolic compression (Group A and 1) than in groups representing >or=50% of systolic compression (Group B and 2) but the importance of this result is not known.     

Lead Exposure Is Related to Impairment of Aortic Elasticity Parameters

Arterial hypertension is one of the physical complications of chronic lead exposure. Hypertension has effects on aortic elastic properties. The aim of this study was to evaluate the aortic elastic properties in workers occupationally exposed to lead. Forty‐one workers who were exposed to lead and 39 healthy controls were included in the study. All patients underwent transthoracic echocardiography for detecting aortic elastic parameters. There were no differences in baseline characteristics between the lead‐exposure group and controls. Aortic strain (9.4%±4.5% vs 12.4%±4.2%, P=.004) and aortic distensibility (0.45±0.21 cm²/dyn vs 0.55±0.20 cm²/dyn, P=.046) were decreased in patients with lead exposure compared with controls. There was a negative significant weak correlation between aortic strain and (r=−0.294, P=.008) lead levels. There was no significant correlation between aortic distensibility and any other echocardiographic parameters. This study suggests that chronic exposure to lead is related to impairment of aortic elasticity parameters.

Lead contamination (such as that emitted from house paint, gasoline, batteries, and other sources) may cause a wide variety of body organ complications.¹ Despite the still manifested divergences of opinion, it seems that chronic exposure to lead represents a risk for arterial hypertension development. Functional changes within the arterial wall both in smooth muscles and the endothelium might result in arterial hypertension caused by chronic exposure to lead compounds.² Blood pressure (BP) was found to be increased in workers with blood lead concentrations of 7 μg/L on average.³ According to the World Health Organization (2000), the level of 400 μg/L is accepted as safe to avoid possible adverse health effects, but American Conference Governmental and Industrial Hygienists suggest an even lower value of <300 μg/L.Hypertension has effects on the aorta (decreased aortic distensibility and increased aortic stiffness). Aortic strain is a simple and useful parameter of transthoracic echocardiography. Some studies have suggested that aortic elastic parameters can be used as an independent predictor of all‐cause and cardiovascular mortality in hypertensive patients.⁴, ⁵ In previous studies, the relationship between lead exposure and arterial hypertension has been demonstrated, and findings suggest that arterial hypertension and organ complications of arterial hypertension are more frequent in workers with lead exposure. Until now, there have been no data on the effects of lead exposure on aortic stiffness. The aim of this study was to evaluate the effects of lead on aortic elasticity parameters.     

Bleeding and non-bleeding phenotypes in patients with GGCX gene mutations

Functional limitations for the vitamin K cycle, caused either by mutations in gamma-glutamyl carboxylase or vitamin K epoxide reductase genes, result in hereditary deficiency of vitamin K-dependent coagulation factors (VKCFD1 and VKCFD2, respectively). Patients suffering from VKCFD often share several other anatomical irregularities which are not related to haemostasis. Here we report on nine patients, eight of them previously unreported, who presented with VKCFD1. All were examined with special attention to vitamin K-dependent coagulation factors as well as to bone and heart development and to other anatomical signs of embryonal vitamin K deficiency. In total, we detected ten mutations in the gamma-glutamyl carboxylase gene of which seven have not been previously reported. Most interestingly, additional non-bleeding phenotypes were observed in all patients including midfacial hypoplasia, premature osteoporosis, cochlear hearing loss, heart valve defects, pulmonary stenosis, or pseudoxanthoma elasticum-like phenotype. Undercarboxylated matrix Gla protein, osteocalcin, and periostin appear to be responsible for these defects which are also observed in cases of fetal warfarin syndrome.