The expression of E-cadherin and beta-catenin was assessed with immunohistochemistry.
Results: In the colon the microvilli and their glycocalyx shortened and reduced in
density the most in necrotizing pancreatitis. In necrotizing pancreatitis JNJ-26481585 research buy adherens and tight junctions were occasionally open in the colon but rarely in the jejunum. Mitochondria in the colon epithelial cells were degenerated in necrotizing pancreatitis, swollen in edematous pancreatitis, and remained intact in the control case. In necrotizing pancreatitis, capillaries of the colon showed a broken endothelial lining with narrow lumens. The expression of E-cadherin immunoreactivity showed a trend toward this website a decrease in the colon in both edematous and necrotizing pancreatitis.
Conclusion: Ultrastructural abnormalities in acute pancreatitis appear early in the colon, where they seem to be more damaging than in jejunum. Epithelial cell
damage seems to include mitochondrial injury and an opening of tight and adherens junctions, which are more pronounced in necrotizing pancreatitis. Damage is seen in the mucosal and mesenteric endothelial cells.”
“Background: Treatment of secondary hyperparathyroidism (SHPT) with calcitriol is often limited by the occurrence of hypercalcemia, hyperphosphatemia and risk of vascular calcifications. Paricalcitol, a vitamin D analogue with lower calcemic and phosphatemic effects, is successfully utilized in dialysis patients, although some uncertainty remains about the optimal dosage. Amelioration of survival in hemodialysis patients has been correlated to the use of calcitriol and, even better, paricalcitol.
Methods: We evaluated 1-year treatment with paricalcitol in 12 chronic
hemodialysis patients with moderate-severe SHPT previously treated with intravenous calcitriol. Starting dose of paricalcitol was calculated according to the severity of the disease by the formula: LOXO-101 clinical trial intact parathyroid hormone (iPTH) / 80, and successive titration performed according to the NKF-DOQI guidelines.
Results: Paricalcitol caused a rapid decrease in serum levels of iPTH with a consistent percentage of values falling below 150 pg/mL in the first months of treatment. Although the occurrence of hypercalcemia was not significantly different between treatment with calcitriol and paricalcitol, a slight but significant increase in mean calcium levels was observed during paricalcitol treatment. A significant amelioration of erythropoiesis and acid-base balance was observed during paricalcitol treatment.
Conclusions: Paricalcitol efficiently suppresses PTH secretion in dialysis patients with SHPT, with a moderate calcemic, but not a phosphatemic, effect. The dose of paricalcitol calculated as iPTH/80 may cause acute lowering of bone turnover.